2f:I[703058,["/_next/static/immutable/chunks/3bhq_5eh1d760.js","/_next/static/immutable/chunks/1855-ogyi8eh4.js","/_next/static/immutable/chunks/2pfsjpn6k6zlg.js","/_next/static/immutable/chunks/26c7v3_3uwnwu.js","/_next/static/immutable/chunks/25a3ozcrvi1ff.js","/_next/static/immutable/chunks/2r4wx50nvjh_4.js","/_next/static/immutable/chunks/23fsw06hsi5b1.js","/_next/static/immutable/chunks/06_yt270h41rg.js","/_next/static/immutable/chunks/3ezsiz-7shkna.js","/_next/static/immutable/chunks/20x2y96ldu5wx.js","/_next/static/immutable/chunks/2lxntcm3pd1_h.js","/_next/static/immutable/chunks/00dgco8irq3jw.js","/_next/static/immutable/chunks/00nwe-kq0rboc.js","/_next/static/immutable/chunks/2051ffx3xzio9.js"],"PaperListPageClient"] 30:T7fd,The COVID-19 pandemic significantly disrupted melanoma care worldwide, raising concerns about diagnosis and treatment delays. To compare changes in incidence and prognostic factors of invasive cutaneous melanomas across two regions with contrasting COVID-19 infection control strategies. A retrospective population-based registry study using the Swedish quality registry for cutaneous melanoma (SweMR) and the Cancer Council in Victoria, Australia was performed. Incident invasive melanomas diagnosed between 2013 and 2021 were used for trend analyses considering the long-term underlying trends and seasonality. Regression models were used for analyses of prognostic variables (Breslow thickness, ulceration, lymph node status), comparing the time periods, "before COVID" and "during COVID" (using 1 March 2020 as interruption point). In Victoria, melanoma diagnoses declined during COVID across all age groups, most notably among patients <50 years. Median Breslow thickness remained 0.7mm, but the distribution shifted significantly (p<0.001), with an 8% increase in geometric mean ratio (95% CI, 5%-12%). In Sweden, measures of thickness remained unchanged during COVID, but the odds of ulceration increased slightly (OR 1.09; 95% CI 1.01-1.19). Lymph node metastasis rates were stable in both regions. A significant immediate drop in overall incidence followed COVID-19 onset in both regions, primarily driven by thin melanomas. In Victoria, the lower incidence level persisted without a subsequent slope change. In contrast, the Swedish melanoma incidence gradually realigned with the pre-COVID trend after the initial level change. The immediate incidence drop was most prominent among older age groups in both regions. COVID-19 influenced melanoma incidence and prognostic features in both Sweden and Victoria. Reduced incidence of particularly thin melanomas and modest worsening of prognostic markers were observed. Victoria showed a more sustained impact, possibly reflecting the stricter and longer-lasting pandemic control measures.31:Tb2e,Abstract Introduction The COVID-19 pandemic significantly disrupted melanoma care worldwide, raising concerns about diagnosis and treatment delays. Objectives To compare changes in incidence and prognostic factors of invasive cutaneous melanomas across two regions with contrasting COVID-19 infection control strategies. Methods A retrospective population-based registry study using the Swedish quality registry for cutaneous melanoma (SweMR) and the Cancer Council in Victoria, Australia was performed. Incident invasive melanomas diagnosed between 2013 and 2021 were used for trend analyses considering the long-term underlying trends and seasonality. Regression models were used for analyses of prognostic variables (Breslow thickness, ulceration, lymph node status), comparing the time periods, “before COVID” and “during COVID” (using 1 March 2020 as interruption point). Results In Victoria, melanoma diagnoses declined during COVID across all age groups, most notably among patients <50 years. Median Breslow thickness remained 0.7mm, but the distribution shifted significantly (p<0.001), with an 8% increase in geometric mean ratio (95% CI, 5%–12%). In Sweden, measures of thickness remained unchanged during COVID, but the odds of ulceration increased slightly (OR 1.09; 95% CI 1.01–1.19). Lymph node metastasis rates were stable in both regions. A significant immediate drop in overall incidence followed COVID-19 onset in both regions, primarily driven by thin melanomas. In Victoria, the lower incidence level persisted without a subsequent slope change. In contrast, the Swedish melanoma incidence gradually realigned with the pre-COVID trend after the initial level change. The immediate incidence drop was most prominent among older age groups in both regions. Conclusions COVID-19 influenced melanoma incidence and prognostic features in both Sweden and Victoria. Reduced incidence of particularly thin melanomas and modest worsening of prognostic markers were observed. Victoria showed a more sustained impact, possibly reflecting the stricter and longer-lasting pandemic control measures. 32:T434,The nervous system drives tumor growth directly through intra-tumoral axons and indirectly through the systemic action of hormones. Yet contexts where the nervous system inhibits tumor growth are less defined. Here, we performed optical reconstruction of axonal innervation in mouse models of cutaneous melanoma, revealing progressive innervation by sympathetic axons. Local depletion of these axons accelerates while local optogenetic activation slows melanoma growth, together consistent with these axons acting as a physiological growth brake. The sympathetic nervous system is typically associated with driving tumor growth through activation of β-adrenergic receptors (ARs). Here, we find that the initial tumor seeding conditions sensitize melanomas from βAR-driven growth promotion toward α2-AR-driven growth inhibition. Mechanistically, the axonal activation of α2 ARs restricts the number and distribution of pro-tumor myeloid cells, independently of T cell activity. Together, our data reveal context-dependent, bidirectional neural control of tumor progression.33:T7f3,It is widely accepted that definitive surgical treatment for primary cutaneous melanoma should occur promptly, but the effects of a delay between initial diagnosis and definitive surgery remain unclear. In addition, high quality evidence is lacking for an optimal time-to-surgery from initial melanoma diagnosis. The aim of this study was to determine whether the timing of surgical treatment for Stage I & II melanoma was associated with survival outcome and whether there was an optimal time interval between melanoma diagnosis and definitive surgical treatment with respect to survival. This was a retrospective cohort study of patients with primary cutaneous melanoma treated at a single institution between 1990 and 2015. The associations between time-to-surgery and clinical outcomes including overall survival (OS) and recurrence-free survival (RFS) were described using the Kaplan-Meier method. Multivariable Cox proportional hazard models were used to quantify the relationship between each time-to-surgery cohort and clinical outcome. In total 18, 242 patients were included in the analysis. Their average age was 57.5 years and 57% were male. The majority of primary melanomas were located on the trunk (32.5%) and upper limb (24.7%). Mean Breslow thickness was 1.8 mm (range 0.1-50 mm) and 64% were of superficial spreading subtype. Time to surgery was divided into ≤ 1 week, 1-4 weeks, 4-8 weeks, 8-12 weeks and > 12 weeks (n = 2453, 8882, 5906, 870 and 126, respectively). Increased delay of definitive surgical treatment was associated with poorer OS and RFS, with an OS HR of 1.23 for the 8-12 week group compared to the 1-4 week group. For RFS HR was 1.36 for the same cohorts. Definitive surgical treatment of patients with primary cutaneous melanoma between 1-4 weeks post-diagnosis with excision-biopsy was associated with improved OS & RFS compared to those treated within 1 week and greater than 4 weeks in this patient cohort treated prior to the use of adjuvant drug therapy.34:Tb13,ABSTRACT Introduction It is widely accepted that definitive surgical treatment for primary cutaneous melanoma should occur promptly, but the effects of a delay between initial diagnosis and definitive surgery remain unclear. In addition, high quality evidence is lacking for an optimal time‐to‐surgery from initial melanoma diagnosis. The aim of this study was to determine whether the timing of surgical treatment for Stage I & II melanoma was associated with survival outcome and whether there was an optimal time interval between melanoma diagnosis and definitive surgical treatment with respect to survival. Methods This was a retrospective cohort study of patients with primary cutaneous melanoma treated at a single institution between 1990 and 2015. The associations between time‐to‐surgery and clinical outcomes including overall survival (OS) and recurrence‐free survival (RFS) were described using the Kaplan–Meier method. Multivariable Cox proportional hazard models were used to quantify the relationship between each time‐to‐surgery cohort and clinical outcome. Results In total 18, 242 patients were included in the analysis. Their average age was 57.5 years and 57% were male. The majority of primary melanomas were located on the trunk (32.5%) and upper limb (24.7%). Mean Breslow thickness was 1.8 mm (range 0.1–50 mm) and 64% were of superficial spreading subtype. Time to surgery was divided into ≤ 1 week, 1–4 weeks, 4–8 weeks, 8–12 weeks and > 12 weeks ( n = 2453, 8882, 5906, 870 and 126, respectively). Increased delay of definitive surgical treatment was associated with poorer OS and RFS, with an OS HR of 1.23 for the 8–12 week group compared to the 1–4 week group. For RFS HR was 1.36 for the same cohorts. Conclusion Definitive surgical treatment of patients with primary cutaneous melanoma between 1–4 weeks post‐diagnosis with excision‐biopsy was associated with improved OS & RFS compared to those treated within 1 week and greater than 4 weeks in this patient cohort treated prior to the use of adjuvant drug therapy. 35:T884,The origins of cutaneous melanoma are often traced to visible precursor lesions (e.g., melanocytic naevi), but ∼2/3 melanomas arise from clinically normal skin with no precursor lesion. BRAF V600E drives both melanoma and naevus formation, but eruptive naevi syndromes and the disproportionate role early-life UV exposure plays in melanoma risk suggest the presence of a hidden field of oncogene-mutant melanocytes within clinically normal skin, which may represent an earlier step in tumourigenesis. We aimed to determine whether BRAF V600E-mutant melanocytes were commonly present in non-lesional skin from adults at high risk of melanoma. We examined BRAF V600E mutation in 97 histologically and clinically normal, non-lesional skin samples from a high-risk Australian melanoma cohort. The skin selected was adjacent to a naevus or a prior melanoma site, photodamaged skin proximal (∼5cm) from melanoma excision, and photoprotected skin distant from lesions, as well as a low-risk neonatal foreskin-derived melanoblasts. We used immunohistochemistry to locate BRAF V600E-mutant cells in histopathology sections, droplet digital PCR to determine the fractional abundance of BRAF V600E in whole skin, and single-cell RNA sequencing to confirm cells as melanocytes and detect their transcriptional programs. We identified BRAF V600E-mutant melanocytes in skin surrounding naevi and primary melanomas, even years after tumour excision. Fields of BRAF V600E-mutant melanocytes are commonly observed in the skin of patients at high risk for melanoma and are up to 20-fold more dense and 50% more frequent in tumour-adjacent skin. Field cells exhibit a gene expression profile characteristic of BRAF V600E-induced growth arrest, consistent with dormant yet genetically primed cells. There is a reservoir of oncogene-harbouring melanocytes in normal skin. Our observations challenge the prevailing notion that melanocyte expression of BRAF V600E is inherently tumourigenic. The presence of such fields suggests that the scope of melanoma detection and prevention efforts might be extended beyond visible lesions, to encompass potentially precancerous fields of driver-mutant cells.36:Tb99,Abstract Background The origins of cutaneous melanoma are often traced to visible precursor lesions (e.g., melanocytic naevi), but ∼2/3 melanomas arise from clinically normal skin with no precursor lesion. BRAF V600E drives both melanoma and naevus formation, but eruptive naevi syndromes and the disproportionate role early-life UV exposure plays in melanoma risk suggest the presence of a hidden field of oncogene-mutant melanocytes within clinically normal skin, which may represent an earlier step in tumourigenesis. Objectives We aimed to determine whether BRAF V600E-mutant melanocytes were commonly present in non-lesional skin from adults at high risk of melanoma. Methods We examined BRAF V600E mutation in 97 histologically and clinically normal, non-lesional skin samples from a high-risk Australian melanoma cohort. The skin selected was adjacent to a naevus or a prior melanoma site, photodamaged skin proximal (∼5cm) from melanoma excision, and photoprotected skin distant from lesions, as well as a low-risk neonatal foreskin-derived melanoblasts. We used immunohistochemistry to locate BRAF V600E-mutant cells in histopathology sections, droplet digital PCR to determine the fractional abundance of BRAF V600E in whole skin, and single-cell RNA sequencing to confirm cells as melanocytes and detect their transcriptional programs. Results We identified BRAF V600E-mutant melanocytes in skin surrounding naevi and primary melanomas, even years after tumour excision. Fields of BRAF V600E-mutant melanocytes are commonly observed in the skin of patients at high risk for melanoma and are up to 20-fold more dense and 50% more frequent in tumour-adjacent skin. Field cells exhibit a gene expression profile characteristic of BRAF V600E-induced growth arrest, consistent with dormant yet genetically primed cells. Conclusions There is a reservoir of oncogene-harbouring melanocytes in normal skin. Our observations challenge the prevailing notion that melanocyte expression of BRAF V600E is inherently tumourigenic. The presence of such fields suggests that the scope of melanoma detection and prevention efforts might be extended beyond visible lesions, to encompass potentially precancerous fields of driver-mutant cells. 37:T430,A total of 1761 patients (median [IQR] age, 64 [53-72] years; 997 male [56.6%]) underwent SLNB (310 [17.6%] SLN positive) and had a successful CP-GEP test; GEP was successful in 97.7% of samples. A total of 651 patients (37.0%) were considered low risk by CP-GEP. Among low-risk cases, 46 (7.1%) were SLN positive, and NPV was 92.9% (95% CI, 90.7%-94.8%). High-risk cases had a 23.8% (264 of 1110) SLN-positive rate. The percentage of cases with low-risk CP-GEP declined with increasing T category (T1 = 346 of 507 [68.2%]; T2 = 295 of 897 [32.9%]; T3 = 10 of 357 [2.8%]). CP-GEP results were consistent in discriminating SLN-positive rates across primary sites, histologic subtypes, and mitotic count categories. In 2 large subsets, clinical stage IB (n = 1187) and patients 65 years and older (n = 832), 6.5% (95% CI, 4.6%-8.8%) of low-risk clinical stage IB cases and 6.6% (95% CI, 4.2%-9.7%) of all low-risk cases in patients 65 years and older were SLN positive vs 18.3% (95% CI, 15.3%-21.6%) and 20.3% (95% CI, 16.8%-24.2%) for high-risk cases, respectively.38:Tbec,Contemporary guidelines recommend sentinel lymph node biopsy (SLNB) for patients with melanoma with predicted risk of SLN metastasis greater than 10% and consideration of SLNB when the risk is 5% to 10%. A gene expression profile (GEP)-based test that can accurately identify patients with a low risk of SLN metastasis would refine selection for SLNB. To establish the predictive capability of the combined clinicopathological factors and GEP (CP-GEP) test to identify patients with primary cutaneous melanoma who can safely forgo SLNB and to investigate the prognostic value of CP-GEP regarding the outcome in patients with cutaneous melanoma after a negative SLNB (not reported herein). This prognostic study was conducted from September 2021 to June 2024 at 9 academic medical centers with experienced melanoma surgeons. Included were patients with biopsy-proven invasive cutaneous melanoma with T1 to T3 tumors and clinically negative regional LNs. All patients were deemed candidates for SLNB using standard clinical criteria. GEP was performed on formalin-fixed, paraffin-embedded tissue from the primary melanoma biopsy. Analyses were performed from December 2024 to August 2025. CP-GEP testing to determine risk of having a positive SLNB in patients with T1 to T3 cutaneous melanoma who were considered appropriate candidates for the procedure based on standard clinical parameters. CP-GEP results were reported as low risk or high risk; the primary outcome measure was negative predictive value (NPV) in low-risk cases. Analyses included NPV assessment by tumor (T) subcategory, primary site, and age. A total of 1761 patients (median [IQR] age, 64 [53-72] years; 997 male [56.6%]) underwent SLNB (310 [17.6%] SLN positive) and had a successful CP-GEP test; GEP was successful in 97.7% of samples. A total of 651 patients (37.0%) were considered low risk by CP-GEP. Among low-risk cases, 46 (7.1%) were SLN positive, and NPV was 92.9% (95% CI, 90.7%-94.8%). High-risk cases had a 23.8% (264 of 1110) SLN-positive rate. The percentage of cases with low-risk CP-GEP declined with increasing T category (T1 = 346 of 507 [68.2%]; T2 = 295 of 897 [32.9%]; T3 = 10 of 357 [2.8%]). CP-GEP results were consistent in discriminating SLN-positive rates across primary sites, histologic subtypes, and mitotic count categories. In 2 large subsets, clinical stage IB (n = 1187) and patients 65 years and older (n = 832), 6.5% (95% CI, 4.6%-8.8%) of low-risk clinical stage IB cases and 6.6% (95% CI, 4.2%-9.7%) of all low-risk cases in patients 65 years and older were SLN positive vs 18.3% (95% CI, 15.3%-21.6%) and 20.3% (95% CI, 16.8%-24.2%) for high-risk cases, respectively. In this multicenter, prospective, blinded, prognostic study, the CP-GEP test reliably identified patients with melanoma with less than 10% SLN metastasis risk. SLN metastasis rates were approximately 3-fold greater for high-risk vs low-risk CP-GEP cases. In appropriately selected patients, the CP-GEP test may add value for shared patient-surgeon decision-making.39:T10c5, Importance Contemporary guidelines recommend sentinel lymph node biopsy (SLNB) for patients with melanoma with predicted risk of SLN metastasis greater than 10% and consideration of SLNB when the risk is 5% to 10%. A gene expression profile (GEP)–based test that can accurately identify patients with a low risk of SLN metastasis would refine selection for SLNB. Objective To establish the predictive capability of the combined clinicopathological factors and GEP (CP-GEP) test to identify patients with primary cutaneous melanoma who can safely forgo SLNB and to investigate the prognostic value of CP-GEP regarding the outcome in patients with cutaneous melanoma after a negative SLNB (not reported herein). Design, Setting, and Participants This prognostic study was conducted from September 2021 to June 2024 at 9 academic medical centers with experienced melanoma surgeons. Included were patients with biopsy-proven invasive cutaneous melanoma with T1 to T3 tumors and clinically negative regional LNs. All patients were deemed candidates for SLNB using standard clinical criteria. GEP was performed on formalin-fixed, paraffin-embedded tissue from the primary melanoma biopsy. Analyses were performed from December 2024 to August 2025. Intervention CP-GEP testing to determine risk of having a positive SLNB in patients with T1 to T3 cutaneous melanoma who were considered appropriate candidates for the procedure based on standard clinical parameters. Main Outcomes and Measures CP-GEP results were reported as low risk or high risk; the primary outcome measure was negative predictive value (NPV) in low-risk cases. Analyses included NPV assessment by tumor (T) subcategory, primary site, and age. Results A total of 1761 patients (median [IQR] age, 64 [53-72] years; 997 male [56.6%]) underwent SLNB (310 [17.6%] SLN positive) and had a successful CP-GEP test; GEP was successful in 97.7% of samples. A total of 651 patients (37.0%) were considered low risk by CP-GEP. Among low-risk cases, 46 (7.1%) were SLN positive, and NPV was 92.9% (95% CI, 90.7%-94.8%). High-risk cases had a 23.8% (264 of 1110) SLN-positive rate. The percentage of cases with low-risk CP-GEP declined with increasing T category (T1 = 346 of 507 [68.2%]; T2 = 295 of 897 [32.9%]; T3 = 10 of 357 [2.8%]). CP-GEP results were consistent in discriminating SLN-positive rates across primary sites, histologic subtypes, and mitotic count categories. In 2 large subsets, clinical stage IB (n = 1187) and patients 65 years and older (n = 832), 6.5% (95% CI, 4.6%-8.8%) of low-risk clinical stage IB cases and 6.6% (95% CI, 4.2%-9.7%) of all low-risk cases in patients 65 years and older were SLN positive vs 18.3% (95% CI, 15.3%-21.6%) and 20.3% (95% CI, 16.8%-24.2%) for high-risk cases, respectively. Conclusions and Relevance In this multicenter, prospective, blinded, prognostic study, the CP-GEP test reliably identified patients with melanoma with less than 10% SLN metastasis risk. SLN metastasis rates were approximately 3-fold greater for high-risk vs low-risk CP-GEP cases. In appropriately selected patients, the CP-GEP test may add value for shared patient-surgeon decision-making. 3a:Ta23,Most patients who present with primary cutaneous melanomas have thin tumors (≤1.0 mm in Breslow thickness, ie, pT1a and pT1b). Although their prognosis is generally considered to be excellent, there is limited precise information on the association of risk of death with specific Breslow measurements in thin lesions. To assess the relative effect of a 0.8-mm Breslow thickness threshold with respect to the incidence of both melanoma-related and nonmelanoma-related death. Registry data for all Australians diagnosed with thin invasive primary melanomas between 1982 and 2014 were analyzed. Data were extracted from all 8 Australian state and territory population-based cancer registries. Dates and causes of death were obtained from the Australian National Death Index. Adults diagnosed with a first invasive primary melanoma of 1.0 mm or smaller in thickness were included. First invasive primary melanoma between 1982 and 2014. The primary outcomes were melanoma-related deaths and nonmelanoma-related deaths. Competing-risk regression analyses and cause-specific analyses were performed to investigate the relationships between Breslow thickness subcategory (<0.8 mm versus ≥0.8 mm by 0.1-mm increments) and the primary outcomes. Overall, a cohort of 144 447 participants was included. The median (range) age was 56 (18-101) years and 78 014 (54.0%) were men. Median (IQR) follow-up was 15.0 (9.5-23.3) years. Crude incidence rates of melanoma-related death 20 years after diagnosis were 6.3% (95% CI, 6.1%-6.5%) for the whole cohort, 6.0% (95% CI, 5.7%-6.2%) for tumors smaller than 0.8 mm, and 12.0% (95% CI, 11.4%-12.6%) for tumors 0.8 to 1.0 mm. The corresponding 20-year melanoma-specific survival rates were 91.9% (95% CI, 91.6%-92.1%), 94.2% (95% CI, 94.0%-94.4%), and 87.8% (95% CI, 87.3%-88.3%), respectively. On multivariable analysis, tumor thickness of 0.8 to 1.0 mm was significantly associated with both a greater absolute risk of melanoma-related death (subdistribution hazard ratio, 2.92; 95% CI, 2.74-3.12) and a greater rate of melanoma-related death (hazard ratio, 2.98; 95% CI, 2.79-3.18) than thinner tumors (<0.8 mm). Risk of death from nonmelanoma-related causes was not associated with Breslow thickness. In this study, the risk of melanoma-related death increased significantly for patients with primary tumors of 0.8 to 1.0 mm in thickness. The risk of death from nonmelanoma-ralated causes was similar across Breslow thicknesses of 0.1 to 1.0 mm. This analysis suggests that a 0.8-mm threshold for guiding the care of patients with thin primary melanomas.3b:Tcef,ImportanceMost patients who present with primary cutaneous melanomas have thin tumors (≤1.0 mm in Breslow thickness, ie, pT1a and pT1b). Although their prognosis is generally considered to be excellent, there is limited precise information on the association of risk of death with specific Breslow measurements in thin lesions.ObjectiveTo assess the relative effect of a 0.8-mm Breslow thickness threshold with respect to the incidence of both melanoma-related and nonmelanoma-related death.Design, Setting, and ParticipantsRegistry data for all Australians diagnosed with thin invasive primary melanomas between 1982 and 2014 were analyzed. Data were extracted from all 8 Australian state and territory population-based cancer registries. Dates and causes of death were obtained from the Australian National Death Index. Adults diagnosed with a first invasive primary melanoma of 1.0 mm or smaller in thickness were included.ExposureFirst invasive primary melanoma between 1982 and 2014.Main Outcomes and MeasuresThe primary outcomes were melanoma-related deaths and nonmelanoma-related deaths. Competing-risk regression analyses and cause-specific analyses were performed to investigate the relationships between Breslow thickness subcategory (&lt;0.8 mm versus ≥0.8 mm by 0.1-mm increments) and the primary outcomes.ResultsOverall, a cohort of 144 447 participants was included. The median (range) age was 56 (18-101) years and 78 014 (54.0%) were men. Median (IQR) follow-up was 15.0 (9.5-23.3) years. Crude incidence rates of melanoma-related death 20 years after diagnosis were 6.3% (95% CI, 6.1%-6.5%) for the whole cohort, 6.0% (95% CI, 5.7%-6.2%) for tumors smaller than 0.8 mm, and 12.0% (95% CI, 11.4%-12.6%) for tumors 0.8 to 1.0 mm. The corresponding 20-year melanoma-specific survival rates were 91.9% (95% CI, 91.6%-92.1%), 94.2% (95% CI, 94.0%-94.4%), and 87.8% (95% CI, 87.3%-88.3%), respectively. On multivariable analysis, tumor thickness of 0.8 to 1.0 mm was significantly associated with both a greater absolute risk of melanoma-related death (subdistribution hazard ratio, 2.92; 95% CI, 2.74-3.12) and a greater rate of melanoma-related death (hazard ratio, 2.98; 95% CI, 2.79-3.18) than thinner tumors (&lt;0.8 mm). Risk of death from nonmelanoma-related causes was not associated with Breslow thickness.Conclusions and RelevanceIn this study, the risk of melanoma-related death increased significantly for patients with primary tumors of 0.8 to 1.0 mm in thickness. The risk of death from nonmelanoma-ralated causes was similar across Breslow thicknesses of 0.1 to 1.0 mm. This analysis suggests that a 0.8-mm threshold for guiding the care of patients with thin primary melanomas.3c:T87b,Over the past decades, many global regions have experienced a steady increase in the incidence of cutaneous melanoma. However, more recently, a downward trend has been observed in the younger age groups in Australia and the US. Yet, in Europe, none of the countries have reported any significant decline in melanoma incidence for any age group. To assess melanoma incidence and mortality trends in Sweden, with a focus on individuals younger than the average age of melanoma onset. This cohort study used data on the national population from the Swedish Melanoma Registry and the Swedish Cancer Registry, which cover more than 99% of all primary invasive cutaneous melanomas diagnosed in the country. All patients diagnosed from 1990 to 2022 were included. Incidence and mortality rates per 100 000 inhabitants were calculated for each year and shown as average annual rates for every 5-year period from 1990 to 2022. Joinpoint regression models were used to evaluate statistical significance of temporal trends and points of change. There were 34 800 primary invasive cutaneous melanomas (19 582 [56.3%] in females and 15 218 [43.7%] in males) reported in 33 324 individuals younger than 60 years (median [IQR] age, 48 [36-58] years) from 1990 to 2022. A consistent rise in melanoma incidence was observed among those 50 to 59 years old. The age groups from 20 to 29 years, 30 to 39 years, and 40 to 49 years showed an incidence peak in 2013 to 2015 followed by stable or significantly declining rates until 2022. In patients younger than 20 years, melanoma incidence remained low with no significant trends. There was also a significant decline in melanoma mortality among 30- to 59-year-old individuals, but not in those 60 years and older. The findings of this cohort study showed a significant recent downward trend in both melanoma incidence and melanoma mortality in the age group 30 to 49 years in Sweden. The reasons for these declines are unclear but may include UV protection, public health campaigns, changing population demographics, and the introduction of effective melanoma treatment. None of these possibilities were evaluated; further study is needed.3d:Tad6,ImportanceOver the past decades, many global regions have experienced a steady increase in the incidence of cutaneous melanoma. However, more recently, a downward trend has been observed in the younger age groups in Australia and the US. Yet, in Europe, none of the countries have reported any significant decline in melanoma incidence for any age group.ObjectiveTo assess melanoma incidence and mortality trends in Sweden, with a focus on individuals younger than the average age of melanoma onset.Design, Setting, and ParticipantsThis cohort study used data on the national population from the Swedish Melanoma Registry and the Swedish Cancer Registry, which cover more than 99% of all primary invasive cutaneous melanomas diagnosed in the country. All patients diagnosed from 1990 to 2022 were included.Main Outcomes and MeasuresIncidence and mortality rates per 100 000 inhabitants were calculated for each year and shown as average annual rates for every 5-year period from 1990 to 2022. Joinpoint regression models were used to evaluate statistical significance of temporal trends and points of change.ResultsThere were 34 800 primary invasive cutaneous melanomas (19 582 [56.3%] in females and 15 218 [43.7%] in males) reported in 33 324 individuals younger than 60 years (median [IQR] age, 48 [36-58] years) from 1990 to 2022. A consistent rise in melanoma incidence was observed among those 50 to 59 years old. The age groups from 20 to 29 years, 30 to 39 years, and 40 to 49 years showed an incidence peak in 2013 to 2015 followed by stable or significantly declining rates until 2022. In patients younger than 20 years, melanoma incidence remained low with no significant trends. There was also a significant decline in melanoma mortality among 30- to 59-year-old individuals, but not in those 60 years and older.Conclusions and RelevanceThe findings of this cohort study showed a significant recent downward trend in both melanoma incidence and melanoma mortality in the age group 30 to 49 years in Sweden. The reasons for these declines are unclear but may include UV protection, public health campaigns, changing population demographics, and the introduction of effective melanoma treatment. None of these possibilities were evaluated; further study is needed.3e:T50d,A PS-matched cohort of 731 patients (mean [SD] age, 67.9 [14.8] years; 437 [59.8%] male) with melanoma from 2018 to 2019 and 731 patients (mean [SD] age, 67.9 [14.4] years; 440 [60.2%] male) from 2007 to 2012 were evaluated. The 2018 to 2019 patients had greater mean (SD) health care (including systemic therapy) costs compared with the 2007 to 2012 patients ($47 886 [$55 176] vs $33 347 [$31 576]), specifically for stage III ($67 108 [$57 226] vs $46 511 [$30 622]) and stage IV disease ($117 450 [$79 272] vs $47 739 [$37 652]). Mean (SD) systemic therapy costs were greater among 2018 to 2019 patients: stage II ($40 823 [$40 621] vs $10 309 [$12 176]), III ($55 699 [$41 181] vs $9764 [$12 771]), and IV disease ($79 358 [$50 442] vs $9318 [$14 986]). Overall survival was greater for the 2018 to 2019 cohort compared with the 2007 to 2012 cohort (3-year OS: 74.2% [95% CI, 70.8%-77.2%] vs 65.8% [95% CI, 62.2%-69.1%], hazard ratio, 0.72 [95% CI, 0.61-0.85]; P < .001). Time toxicity was similar between eras. Patients with stage IV disease spent more than 1 day per week (>52 days) with physical contact with the health care system by 2018 to 2019 (mean [SD], 58.7 [43.8] vs 44.2 [26.5] days; standardized difference, 0.40; P = .20).3f:Tc42,Melanoma treatment has evolved during the past decade with the adoption of adjuvant and palliative immunotherapy and targeted therapies, with an unclear impact on health care costs and outcomes in routine practice. To examine changes in health care costs, overall survival (OS), and time toxicity associated with primary treatment of melanoma. This cohort study assessed a longitudinal, propensity score (PS)-matched, retrospective cohort of residents of Ontario, Canada, aged 20 years or older with stages II to IV cutaneous melanoma identified from the Ontario Cancer Registry from January 1, 2018, to March 31, 2019. A historical comparison cohort was identified from a population-based sample of invasive melanoma cases diagnosed from the Ontario Cancer Registry from January 1, 2007, to December 31, 2012. Data analysis was performed from October 17, 2022, to March 13, 2023. Era of melanoma diagnosis (2007-2012 vs 2018-2019). The primary outcomes were mean per-capita health care and systemic therapy costs (Canadian dollars) during the first year after melanoma diagnosis, time toxicity (days with physical health care contact) within 1 year of initial treatment, and OS. Standardized differences were used to compare costs and time toxicity. Kaplan-Meier methods and Cox proportional hazards regression were used to compare OS among PS-matched cohorts. A PS-matched cohort of 731 patients (mean [SD] age, 67.9 [14.8] years; 437 [59.8%] male) with melanoma from 2018 to 2019 and 731 patients (mean [SD] age, 67.9 [14.4] years; 440 [60.2%] male) from 2007 to 2012 were evaluated. The 2018 to 2019 patients had greater mean (SD) health care (including systemic therapy) costs compared with the 2007 to 2012 patients ($47 886 [$55 176] vs $33 347 [$31 576]), specifically for stage III ($67 108 [$57 226] vs $46 511 [$30 622]) and stage IV disease ($117 450 [$79 272] vs $47 739 [$37 652]). Mean (SD) systemic therapy costs were greater among 2018 to 2019 patients: stage II ($40 823 [$40 621] vs $10 309 [$12 176]), III ($55 699 [$41 181] vs $9764 [$12 771]), and IV disease ($79 358 [$50 442] vs $9318 [$14 986]). Overall survival was greater for the 2018 to 2019 cohort compared with the 2007 to 2012 cohort (3-year OS: 74.2% [95% CI, 70.8%-77.2%] vs 65.8% [95% CI, 62.2%-69.1%], hazard ratio, 0.72 [95% CI, 0.61-0.85]; P < .001). Time toxicity was similar between eras. Patients with stage IV disease spent more than 1 day per week (>52 days) with physical contact with the health care system by 2018 to 2019 (mean [SD], 58.7 [43.8] vs 44.2 [26.5] days; standardized difference, 0.40; P = .20). This cohort study found greater health care costs in the treatment of stages II to IV melanoma and substantial time toxicity for patients with stage IV disease, with improvements in OS associated with the adoption of immunotherapy and targeted therapies. These health system-wide data highlight the trade-off with adoption of new therapies, for which there is a greater economic burden to the health care system and time burden to patients but an associated improvement in survival.40:Tf49,ImportanceMelanoma treatment has evolved during the past decade with the adoption of adjuvant and palliative immunotherapy and targeted therapies, with an unclear impact on health care costs and outcomes in routine practice.ObjectiveTo examine changes in health care costs, overall survival (OS), and time toxicity associated with primary treatment of melanoma.Design, Setting, and ParticipantsThis cohort study assessed a longitudinal, propensity score (PS)–matched, retrospective cohort of residents of Ontario, Canada, aged 20 years or older with stages II to IV cutaneous melanoma identified from the Ontario Cancer Registry from January 1, 2018, to March 31, 2019. A historical comparison cohort was identified from a population-based sample of invasive melanoma cases diagnosed from the Ontario Cancer Registry from January 1, 2007, to December 31, 2012. Data analysis was performed from October 17, 2022, to March 13, 2023.ExposuresEra of melanoma diagnosis (2007-2012 vs 2018-2019).Main Outcomes and MeasuresThe primary outcomes were mean per-capita health care and systemic therapy costs (Canadian dollars) during the first year after melanoma diagnosis, time toxicity (days with physical health care contact) within 1 year of initial treatment, and OS. Standardized differences were used to compare costs and time toxicity. Kaplan-Meier methods and Cox proportional hazards regression were used to compare OS among PS-matched cohorts.ResultsA PS-matched cohort of 731 patients (mean [SD] age, 67.9 [14.8] years; 437 [59.8%] male) with melanoma from 2018 to 2019 and 731 patients (mean [SD] age, 67.9 [14.4] years; 440 [60.2%] male) from 2007 to 2012 were evaluated. The 2018 to 2019 patients had greater mean (SD) health care (including systemic therapy) costs compared with the 2007 to 2012 patients ($47 886 [$55 176] vs $33 347 [$31 576]), specifically for stage III ($67 108 [$57 226] vs $46 511 [$30 622]) and stage IV disease ($117 450 [$79 272] vs $47 739 [$37 652]). Mean (SD) systemic therapy costs were greater among 2018 to 2019 patients: stage II ($40 823 [$40 621] vs $10 309 [$12 176]), III ($55 699 [$41 181] vs $9764 [$12 771]), and IV disease ($79 358 [$50 442] vs $9318 [$14 986]). Overall survival was greater for the 2018 to 2019 cohort compared with the 2007 to 2012 cohort (3-year OS: 74.2% [95% CI, 70.8%-77.2%] vs 65.8% [95% CI, 62.2%-69.1%], hazard ratio, 0.72 [95% CI, 0.61-0.85]; P &lt; .001). Time toxicity was similar between eras. Patients with stage IV disease spent more than 1 day per week (&gt;52 days) with physical contact with the health care system by 2018 to 2019 (mean [SD], 58.7 [43.8] vs 44.2 [26.5] days; standardized difference, 0.40; P = .20).Conclusions and RelevanceThis cohort study found greater health care costs in the treatment of stages II to IV melanoma and substantial time toxicity for patients with stage IV disease, with improvements in OS associated with the adoption of immunotherapy and targeted therapies. These health system–wide data highlight the trade-off with adoption of new therapies, for which there is a greater economic burden to the health care system and time burden to patients but an associated improvement in survival.25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Cutaneous Melanoma: condition Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Cutaneous Melanoma (condition). Clinician-written summaries and actionable practice insights. 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Results for non-BCC cancers should be interpreted with caution.","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2025-0274","tag_type":"warning","value":"The study cannot fully exclude reverse causation or detection bias, though the authors argue surveillance was comparable between cases and controls.","value_numeric":null}],"summaries":{"what_studied":"This nested case-control study evaluated whether cumulative narrow-band TL-01 UVB phototherapy exposure increases skin cancer risk in a Finnish cohort of 4,815 patients (treated 1999–2019) with psoriasis or atopic dermatitis who received TL-01 monotherapy. Cases included 38 BCC, 13 cutaneous melanoma (CM), and 9 cutaneous squamous cell carcinoma (cSCC), each matched to up to 4 controls by sex, skin disease, and birth year.","key_result":"Higher TL-01 session count was associated with increased BCC risk (OR per 20 sessions: 1.36, 95% CI 1.08–1.72); patients receiving ≥60 sessions had a >4-fold BCC risk vs. those with 1–29 sessions (OR 4.16, 95% CI 1.49–11.6). No significant association was found for CM or cSCC. Occupational outdoor UV exposure did not confound results.","limitations":"- Small case numbers (especially cSCC n=9, CM n=13) limit power for reliable conclusions on those cancer types.\n- Lag period for cancer induction could not be formally modeled; per-session dose data were often unavailable.\n- Registry-based design lacked data on sunbathing habits, skin phototype, sunscreen use, and systemic immunosuppressants.","practice_takeaway":"Clinicians should track cumulative TL-01 session counts and consider heightened BCC surveillance in patients approaching or exceeding 60 sessions. This signal does not yet apply to melanoma or cSCC, but larger studies with longer follow-up are needed before firm safety conclusions can be drawn."}},{"doi":"10.1016/j.jaad.2026.08.071","pmid":"42637051","title":"Trends in Cutaneous Melanoma in the United States Using SEER","journal_title":"Journal of the American Academy of Dermatology","journal_issn":"0190-9622","published_at":"2026-08-24T00:00:00.000Z","url":"https://doi.org/10.1016/j.jaad.2026.08.071","source_score":1,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-29T06:19:09.556Z","updated_at":"2026-08-29T06:19:09.556Z","tags":[{"paper_doi":"10.1016/j.jaad.2026.08.071","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1016/j.jaad.2026.08.071","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.1016/j.jaad.2026.08.071","tag_type":"condition","value":"Cutaneous Melanoma","value_numeric":null},{"paper_doi":"10.1016/j.jaad.2026.08.071","tag_type":"condition","value":"Skin Cancer","value_numeric":null},{"paper_doi":"10.1016/j.jaad.2026.08.071","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1016/j.jaad.2026.08.071","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1016/j.jaad.2026.08.071","tag_type":"study_design","value":"Retrospective Cohort Study (SEER Database Analysis)","value_numeric":null},{"paper_doi":"10.1016/j.jaad.2026.08.071","tag_type":"warning","value":"Full text is paywalled — only the abstract metadata, keywords, and publisher page were available. No specific results, sample sizes, time frames, subgroup data, or conclusions could be extracted.","value_numeric":null},{"paper_doi":"10.1016/j.jaad.2026.08.071","tag_type":"warning","value":"Level of evidence is estimated based on study type (population-based registry analysis); not confirmed from the paper itself.","value_numeric":null},{"paper_doi":"10.1016/j.jaad.2026.08.071","tag_type":"warning","value":"Publication date is August 24, 2026 — this is an Articles in Press item and may not yet be finalized.","value_numeric":null},{"paper_doi":"10.1016/j.jaad.2026.08.071","tag_type":"warning","value":"Study design classified as retrospective cohort/registry analysis based on SEER database use; exact design label not confirmed from full text.","value_numeric":null}],"summaries":{"what_studied":"This study analyzed trends in cutaneous melanoma incidence, mortality, and survival in the United States using SEER (Surveillance, Epidemiology, and End Results) data, employing a Cox-proportional hazards model.","limitations":"Only the publisher landing page is available — full text, methods, results, and specific data are behind a paywall and cannot be extracted."}},{"doi":"10.1007/s00417-026-07449-0","pmid":"42603175","title":"Clinicopathological characteristics, diagnostic challenges, and systemic implications of metastatic tumors to the eyelid: a systematic review","journal_title":"Graefe's Archive for Clinical and Experimental Ophthalmology","journal_issn":"0721-832X","published_at":"2026-08-15T00:00:00.000Z","url":"https://doi.org/10.1007/s00417-026-07449-0","source_score":3,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-20T06:47:53.781Z","updated_at":"2026-08-20T06:47:53.781Z","tags":[{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"category","value":"Ophthalmology","value_numeric":null},{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"condition","value":"Breast Carcinoma","value_numeric":null},{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"condition","value":"Cutaneous Melanoma","value_numeric":null},{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"condition","value":"Eyelid Metastasis","value_numeric":null},{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"condition","value":"Gastrointestinal Malignancy","value_numeric":null},{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"condition","value":"Lung Carcinoma","value_numeric":null},{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"condition","value":"Renal Cell Carcinoma","value_numeric":null},{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"condition","value":"Uveal Melanoma","value_numeric":null},{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"level_of_evidence","value":"4","value_numeric":null},{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"modality","value":"Immunohistochemistry","value_numeric":null},{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"sample_size","value":"n=95","value_numeric":95},{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"study_design","value":"Systematic Review","value_numeric":null},{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"warning","value":"BAP1 IHC findings are based on only 3 evaluable uveal melanoma cases; conclusions about its discriminatory utility are preliminary and cannot support firm diagnostic thresholds.","value_numeric":null},{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"warning","value":"Level of evidence assigned as 4 (case series/systematic review of case reports) because all included studies are case reports or small case series — no RCTs or cohort studies were eligible. Standard LOE hierarchies vary in how they classify this design.","value_numeric":null},{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"warning","value":"Survival and outcome data are exploratory only: 28.4% of patients were lost to follow-up and median follow-up was 6.5 months, so cancer-related mortality figures likely underestimate true burden.","value_numeric":null},{"paper_doi":"10.1007/s00417-026-07449-0","tag_type":"warning","value":"The title-restricted search strategy may have missed reports where eyelid involvement was described only in the abstract or body text, though supplementary non-title-restricted searches found no additional eligible studies.","value_numeric":null}],"summaries":{"what_studied":"PRISMA 2020-compliant systematic review of 73 case reports/series (95 patients) with histopathologically confirmed eyelid metastases, synthesizing clinicopathological features, IHC utility, preoperative misdiagnosis rates, temporal patterns, and oncological impact across all primary tumor sites.","key_result":"Breast carcinoma was the most common primary (39/95; 41.1%). Two-thirds of evaluable patients were misdiagnosed preoperatively (41/62; 66.1%), most often as pyogenic granuloma. At eyelid biopsy, 68.5% (61/89; 95% CI 58.6–77.0%) had synchronous distant organ metastases. Eyelid biopsy revealed an occult primary in 11.6% and changed oncologic management in 13.7% of patients. BAP1 loss distinguished uveal from cutaneous melanoma in 2 of 3 evaluable cases.","limitations":"- Publication bias is substantial: rare or unexpected presentations are over-reported, inflating misdiagnosis rates and unusual primary site frequencies.\n- No true-negative denominators exist, so IHC marker positivity rates cannot be interpreted as sensitivity or specificity.\n- 28.4% loss-to-follow-up and median follow-up of only 6.5 months make survival estimates unreliable.","practice_takeaway":"Maintain a low threshold for biopsy of any atypical, rapidly enlarging, or treatment-refractory eyelid lesion — especially in patients with a cancer history — because two-thirds are misdiagnosed clinically and over two-thirds harbor synchronous systemic metastases. Use a site-directed IHC panel (ER/PR/GATA3 for breast; TTF-1/NapsinA for lung; CDX2/CK20 for GI; PAX8/CAIX for RCC; BAP1 for melanoma subtyping) to establish the primary site and guide staging."}},{"doi":"10.1111/ijd.70610","pmid":"42545806","title":"The Biological Basis of the Merlin\n CP\n ‐\n GEP\n Assay: Integrin Signaling and Early Metastatic Competence in Cutaneous Melanoma","journal_title":"International Journal of Dermatology","journal_issn":"0011-9059","published_at":"2026-08-03T00:00:00.000Z","url":"https://doi.org/10.1111/ijd.70610","source_score":1,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-06T13:22:10.472Z","updated_at":"2026-08-06T13:22:10.472Z","tags":[{"paper_doi":"10.1111/ijd.70610","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1111/ijd.70610","tag_type":"brand","value":"Merlin CP-GEP","value_numeric":null},{"paper_doi":"10.1111/ijd.70610","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.1111/ijd.70610","tag_type":"condition","value":"Cutaneous Melanoma","value_numeric":null},{"paper_doi":"10.1111/ijd.70610","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1111/ijd.70610","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1111/ijd.70610","tag_type":"modality","value":"Gene Expression Profiling","value_numeric":null},{"paper_doi":"10.1111/ijd.70610","tag_type":"modality","value":"Molecular Diagnostics","value_numeric":null},{"paper_doi":"10.1111/ijd.70610","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1111/ijd.70610","tag_type":"warning","value":"Age group defaulted to 'adult' as no specific population demographics are reported in this review.","value_numeric":null},{"paper_doi":"10.1111/ijd.70610","tag_type":"warning","value":"Impact flag 'practice_changing' is applied based on the stated NCCN Guideline inclusion, not on novel trial data presented within this paper.","value_numeric":null},{"paper_doi":"10.1111/ijd.70610","tag_type":"warning","value":"No original patient data is presented; this is a biological rationale review and does not report sensitivity, specificity, or AUC for the CP-GEP assay.","value_numeric":null}],"summaries":{"what_studied":"This review examines the biological rationale behind the Merlin CP-GEP assay — a clinicopathologic-gene expression profile test for cutaneous melanoma — focusing on how integrin signaling, focal adhesion dynamics, ECM remodeling, and TGF-β pathways underpin its ability to predict sentinel lymph node (SLN) metastasis risk in primary tumors.","key_result":"The CP-GEP assay captures a dissemination-competent phenotype via a core gene set (ITGB3, TGFBR1, PLAT, SERPINE2, LOXL4, CXCL8, GDF15, MLANA) detectable in primary tumors before clinically apparent metastasis; the assay is now included in NCCN Melanoma Guidelines for SLN metastasis risk prediction.","limitations":"This is a narrative review — no original clinical data or validation cohort is presented, so effect sizes and predictive performance metrics are not reported here. The review does not directly compare CP-GEP performance to other GEP assays in head-to-head data.","practice_takeaway":"Clinicians managing cutaneous melanoma can now apply the NCCN-endorsed Merlin CP-GEP assay to primary tumors to stratify SLN metastasis risk at a molecular level, potentially guiding sentinel lymph node biopsy decisions. The integrin/TGF-β biological framework suggests this assay identifies truly early metastatic biology rather than generic prognostic risk."}},{"doi":"10.1097/cmr.0000000000001100","pmid":"42013053","title":"Expression and prognostic value of cyclase-associated proteins in cutaneous melanoma","journal_title":"Melanoma Research","journal_issn":"0960-8931","published_at":"2026-06-24T00:00:00.000Z","url":"https://doi.org/10.1097/cmr.0000000000001100","source_score":3,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-28T13:27:18.132Z","updated_at":"2026-06-28T13:27:18.132Z","tags":[{"paper_doi":"10.1097/cmr.0000000000001100","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001100","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001100","tag_type":"condition","value":"Cutaneous Melanoma","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001100","tag_type":"generic","value":"CAP1","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001100","tag_type":"generic","value":"CAP2","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001100","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001100","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001100","tag_type":"modality","value":"Immunohistochemistry","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001100","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001100","tag_type":"study_design","value":"Retrospective Cohort Study with Tissue Microarray","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001100","tag_type":"warning","value":"CAP1 and CAP2 are described here as protein/gene names (cyclase-associated proteins), not conventional drug generics; they are tagged as 'generic' for discoverability but are biomarker targets, not therapeutics.","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001100","tag_type":"warning","value":"Study design label is approximate; the paper uses a tissue microarray with retrospective survival analysis, which does not fit a single canonical design label cleanly.","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001100","tag_type":"warning","value":"The full text of the paper was not accessible — only the abstract was available for extraction. Key details such as exact sample size, cohort demographics, and TMA composition could not be confirmed.","value_numeric":null}],"summaries":{"what_studied":"CAP1 and CAP2 protein expression was evaluated by immunohistochemistry on a tissue microarray of benign nevi and cutaneous melanomas; public transcriptomic data were used to assess mRNA levels across tumor stages, and Kaplan-Meier/Cox regression were used to examine survival associations.","key_result":"CAP1 and CAP2 protein levels were significantly higher in melanomas than benign nevi (P < 0.0001). High CAP1 (score = 3) and CAP2 (score ≥ 2) expression were each associated with shorter disease-specific survival (P = 0.0005 and P = 0.0055, respectively). Elevated expression also correlated with greater Breslow depth, higher mitotic rate, and advanced T stage (P < 0.05), but CAPs were not independent predictors on multivariate analysis.","limitations":"- CAPs were not independent prognostic factors on multivariate Cox regression, limiting their standalone clinical utility.\n- The full text was not retrievable; key methodological details (sample size, cohort composition) could not be fully verified from the available abstract.\n- Public transcriptomic data (bulk normal skin comparator) may not perfectly reflect benign melanocytic tissue.","practice_takeaway":"CAP1 and CAP2 overexpression in cutaneous melanoma tracks with aggressive pathologic features (deep Breslow depth, high mitotic rate), but their value as independent prognostic markers is not yet established. At this stage, they are research biomarkers rather than clinical decision-making tools."}},{"doi":"10.1007/s13555-026-01819-6","pmid":"42337205","title":"Comparing the i31-SLNB and the MIA Nomogram for Sentinel Lymph Node Biopsy Positivity Prediction in Cutaneous Melanoma: A Prospective Cohort Analysis","journal_title":"Dermatology and Therapy","journal_issn":"2193-8210","published_at":"2026-06-23T00:00:00.000Z","url":"https://doi.org/10.1007/s13555-026-01819-6","source_score":47,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-27T13:27:42.069Z","updated_at":"2026-06-27T13:27:42.069Z","tags":[{"paper_doi":"10.1007/s13555-026-01819-6","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01819-6","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01819-6","tag_type":"condition","value":"Cutaneous Melanoma","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01819-6","tag_type":"generic","value":"31-gene expression profile (i31-SLNB)","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01819-6","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01819-6","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01819-6","tag_type":"modality","value":"Gene Expression Profiling","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01819-6","tag_type":"sample_size","value":"n=912","value_numeric":912},{"paper_doi":"10.1007/s13555-026-01819-6","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01819-6","tag_type":"study_design","value":"Prospective Cohort Study","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01819-6","tag_type":"warning","value":"Age group and sex were not explicitly reported in the provided abstract; 'adult' and 'mixed' are assumed based on typical melanoma cohort demographics.","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01819-6","tag_type":"warning","value":"Only 430 of 912 enrolled patients underwent SLNB; results may not generalize to the full enrolled cohort.","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01819-6","tag_type":"warning","value":"The full text content provided was largely a CAP pathology protocol for invasive melanoma excision specimens (v1.2.0.0), not the primary research article. Structured data was extracted from the abstract and results sections only.","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01819-6","tag_type":"warning","value":"The 'practice_changing' impact flag is applied cautiously — the finding is directionally strong but requires external validation before changing guidelines.","value_numeric":null}],"summaries":{"what_studied":"This prospective cohort study (DECIDE study) compared the i31-SLNB (integrated 31-gene expression profile) to the MIA nomogram for predicting sentinel lymph node (SLN) positivity in 430 SLN-assessed patients with T1–T4 cutaneous melanoma.","key_result":"The i31-SLNB had a significantly higher AUC than the MIA nomogram (0.74 vs. 0.61; p=0.001). When predicting <5% SLN positivity risk, observed positivity was 2.6% for i31-SLNB (NPV 97.4%, 95% CI 94.2–100.0%) vs. 5.8% for MIA (NPV 94.2%, 95% CI 88.1–98.7%). In head-to-head conflicts, observed positivity was 1.9–2.8% below i31-SLNB thresholds and 11.5–25.8% above them.","limitations":"- Only patients who underwent SLNB were analyzed (n=430 of 912 enrolled), potentially introducing selection bias.\n- The MIA nomogram uses only clinicopathologic variables, while i31-SLNB integrates gene expression, making direct comparison inherently asymmetric.\n- Long-term survival outcomes were not reported; the study focused solely on SLN positivity prediction.","practice_takeaway":"The i31-SLNB test more accurately identifies melanoma patients at low risk of SLN positivity than the MIA nomogram, and may help avoid unnecessary SLNB in appropriately selected patients. Clinicians can consider using it alongside standard clinicopathologic assessment when counseling patients about SLNB."}},{"doi":"10.1200/jco-26-00835","pmid":"42223134","title":"Intismeran Autogene Plus Pembrolizumab Versus Pembrolizumab Alone in High-Risk Resected Melanoma: 5-Year Update of the Randomized Phase IIb KEYNOTE-942 Study","journal_title":"Journal of Clinical Oncology","journal_issn":"0732-183X","published_at":"2026-06-01T00:00:00.000Z","url":"https://doi.org/10.1200/jco-26-00835","source_score":1110,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-09-08T06:32:11.886Z","updated_at":"2026-09-08T06:32:11.886Z","tags":[{"paper_doi":"10.1200/jco-26-00835","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1200/jco-26-00835","tag_type":"brand","value":"Keytruda","value_numeric":null},{"paper_doi":"10.1200/jco-26-00835","tag_type":"category","value":"Oncology","value_numeric":null},{"paper_doi":"10.1200/jco-26-00835","tag_type":"condition","value":"Cutaneous Melanoma","value_numeric":null},{"paper_doi":"10.1200/jco-26-00835","tag_type":"condition","value":"Resected High-Risk Melanoma","value_numeric":null},{"paper_doi":"10.1200/jco-26-00835","tag_type":"generic","value":"intismeran autogene","value_numeric":null},{"paper_doi":"10.1200/jco-26-00835","tag_type":"generic","value":"pembrolizumab","value_numeric":null},{"paper_doi":"10.1200/jco-26-00835","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1200/jco-26-00835","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1200/jco-26-00835","tag_type":"modality","value":"mRNA Neoantigen Vaccine","value_numeric":null},{"paper_doi":"10.1200/jco-26-00835","tag_type":"modality","value":"PD-1 Inhibitor","value_numeric":null},{"paper_doi":"10.1200/jco-26-00835","tag_type":"sample_size","value":"n=157","value_numeric":157},{"paper_doi":"10.1200/jco-26-00835","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1200/jco-26-00835","tag_type":"study_design","value":"Randomized Controlled Trial","value_numeric":null},{"paper_doi":"10.1200/jco-26-00835","tag_type":"warning","value":"Impact flag 'practice_changing' applied cautiously given phase IIb status — signals are strong but confirmatory phase III data are still needed.","value_numeric":null},{"paper_doi":"10.1200/jco-26-00835","tag_type":"warning","value":"The 5-year OS result (HR 0.471) did not reach statistical significance and was reported as descriptive only; the study was not powered for OS at this analysis.","value_numeric":null},{"paper_doi":"10.1200/jco-26-00835","tag_type":"warning","value":"The brand name 'Keytruda' is confirmed for pembrolizumab; intismeran autogene (formerly V940/mRNA-4157) does not yet have an approved brand name as of the paper's publication.","value_numeric":null},{"paper_doi":"10.1200/jco-26-00835","tag_type":"warning","value":"The phase IIb design with a small sample size (n=157) and 2:1 randomization limits generalizability; larger confirmatory trials are pending.","value_numeric":null}],"summaries":{"what_studied":"Patients with resected stage IIIB–IV cutaneous melanoma (n=157) were randomized 2:1 to intismeran autogene (mRNA-based individualized neoantigen therapy) plus pembrolizumab vs. pembrolizumab alone; this 5-year update (median follow-up 60.3 months) reports RFS, DMFS, OS, and safety.","key_result":"At 5 years, intismeran plus pembrolizumab significantly prolonged RFS (HR 0.510; 95% CI, 0.294–0.887) and DMFS (HR 0.411; 95% CI, 0.200–0.843) vs. pembrolizumab alone, with a favorable but non-significant OS trend (HR 0.471; 95% CI, 0.165–1.345); no new safety signals emerged.","limitations":"Small sample size (n=157) limits power, especially for OS; 5-year analyses were descriptive rather than formally hypothesis-testing; single-arm imbalance (2:1 randomization) restricts direct comparison.","practice_takeaway":"Adding intismeran autogene to pembrolizumab after resection of high-risk melanoma shows durable RFS and DMFS benefits at 5 years with a manageable safety profile. Clinicians should watch for results from larger confirmatory trials before adopting this combination as standard of care."}},{"doi":"10.1097/cmr.0000000000001108","pmid":"42186386","title":"CTLA-4 and TNFRSF1B genetic variants in clinicopathological aspects and outcome of cutaneous melanoma","journal_title":"Melanoma Research","journal_issn":"0960-8931","published_at":"2026-05-27T00:00:00.000Z","url":"https://doi.org/10.1097/cmr.0000000000001108","source_score":1,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-05T13:26:45.516Z","updated_at":"2026-06-05T13:26:45.516Z","tags":[{"paper_doi":"10.1097/cmr.0000000000001108","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001108","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001108","tag_type":"condition","value":"Cutaneous Melanoma","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001108","tag_type":"generic","value":"ipilimumab","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001108","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001108","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001108","tag_type":"modality","value":"Immune Checkpoint Modulation","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001108","tag_type":"sample_size","value":"n=428","value_numeric":428},{"paper_doi":"10.1097/cmr.0000000000001108","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001108","tag_type":"study_design","value":"Cohort Study","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001108","tag_type":"warning","value":"Study design classified as 'Cohort Study' based on context; the abstract does not explicitly state a prospective or retrospective design.","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001108","tag_type":"warning","value":"The full text of this article was not accessible — only the abstract was available. All extracted data are based solely on the abstract, which may omit key methodological details such as multivariate adjustment, cohort demographics, follow-up duration, and treatment regimens.","value_numeric":null},{"paper_doi":"10.1097/cmr.0000000000001108","tag_type":"warning","value":"The ipilimumab (CTLA-4 inhibitor) generic tag is inferred from the immunotherapeutic relevance of CTLA-4 variants discussed; the paper does not explicitly mention ipilimumab treatment in the abstract.","value_numeric":null}],"summaries":{"what_studied":"This study examined how inherited single nucleotide variants (SNVs) in CTLA-4 (rs11571316, rs62182595, rs11571315, rs4553808) and TNFRSF1B (rs3397, rs1061622, rs1061624, rs1061628) relate to clinicopathological features and survival outcomes in 428 cutaneous melanoma patients.","key_result":"Specific CTLA-4/TNFRSF1B genotype combinations were linked to worse outcomes: patients >54 years with CTLA-4 rs11571316 GG + TNFRSF1B rs3397 TT had a 3.04× greater chance of tumor-related death; head/neck/trunk melanoma patients with CTLA-4 rs4553808 AG/GG + TNFRSF1B rs1061624 GA/AA had a 2.30× greater chance of recurrence/progression/death, and up to a 2.97× greater chance of tumor-related death with certain genotype pairs.","limitations":"The full text was not available for review — only the abstract was accessible, limiting assessment of methodology, statistical adjustments, and confounders. The study is observational and single-cohort, which limits causal inference and generalizability.","practice_takeaway":"Certain CTLA-4 and TNFRSF1B genotype combinations may identify cutaneous melanoma patients at higher risk of progression and death, particularly those with head, neck, or trunk tumors. These findings are preliminary; routine genotyping for clinical risk stratification is not yet supported without further validation."}},{"doi":"10.1001/jamadermatol.2026.1305","pmid":"42201696","title":"Prevalence of Familial Melanoma Genes and Cancer Risk Among Genomically Ascertained Individuals","journal_title":"JAMA Dermatology","journal_issn":"2168-6068","published_at":"2026-05-27T00:00:00.000Z","url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC13217259/","source_score":2,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-02T13:27:20.660Z","updated_at":"2026-06-02T13:27:20.660Z","tags":[{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"condition","value":"Cutaneous Melanoma","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"condition","value":"Familial Melanoma","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"condition","value":"Hematologic Malignancy","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"condition","value":"Pancreatic Cancer","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"condition","value":"Renal Cell Carcinoma","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"generic","value":"BAP1 pathogenic variant","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"generic","value":"CDKN2A pathogenic variant","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"generic","value":"MITF E318K","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"generic","value":"POT1 pathogenic variant","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"modality","value":"Germline Genetic Testing","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"sample_size","value":"n=696665","value_numeric":696665},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"study_design","value":"Cohort Study (Genome-First)","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"warning","value":"Full text is under PMC embargo until May 27, 2027; summary is based solely on the abstract and results excerpt — specific odds ratios and confidence intervals are not available.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"warning","value":"Study design is labeled 'cohort study' but uses case-control analyses within cohorts for cancer associations — level of evidence reflects the observational nature.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1305","tag_type":"warning","value":"The cohorts are >93% European genetic ancestry, so prevalence and risk estimates may not apply to non-European populations.","value_numeric":null}],"summaries":{"what_studied":"A genome-first cohort study estimated the prevalence of germline pathogenic variants (PVs) in 8 familial melanoma genes (ACD, BAP1, CDKN2A, CDK4, MITF E318K, POT1, TERF2IP, TERT promoter) and their associated cancer risks in 696,665 population-ascertained individuals from UK Biobank (n=469,379) and Geisinger MyCode (n=227,286), linked to cancer registries from 1970–2024.","key_result":"Combined PV prevalence ranged from 0.5% (GMC) to 0.9% (UKBB); among patients with multiple cutaneous melanomas or first melanoma diagnosed before age 40, PV prevalence exceeded the 2.5% threshold that typically triggers germline testing. Beyond known associations, novel or inconsistently reported cancer links were identified: BAP1–prostate, CDKN2A–biliary tract/breast/nonmelanoma skin/small intestine, MITF E318K–cervix/nasal cavity/nonmelanoma skin, and POT1–myeloma.","limitations":"Cohorts were predominantly of European genetic ancestry (>93%), limiting generalizability to other populations. The UKBB skews older (mean age 70), which may affect lifetime risk estimates. Full-text access is under embargo, so nuances in statistical methods and effect sizes could not be fully verified.","practice_takeaway":"Consider germline testing for familial melanoma genes in patients with multiple cutaneous melanomas or a first melanoma before age 40, as PV prevalence exceeds the 2.5% clinical threshold in these groups. Counsel carriers—especially of CDKN2A and MITF E318K—about a broader cancer spectrum than traditionally recognized, including pancreatic, renal, and potentially breast and biliary tract cancers."}},{"doi":"10.1158/2159-8290.cd-24-1853","pmid":"41631877","title":"A Targetable Developmental Program Coregulates Angiogenesis and Immune Evasion in Melanoma","journal_title":"Cancer Discovery","journal_issn":"2159-8274","published_at":"2026-05-14T00:00:00.000Z","url":"https://doi.org/10.1158/2159-8290.cd-24-1853","source_score":228,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-18T13:25:38.198Z","updated_at":"2026-05-18T13:25:38.198Z","tags":[{"paper_doi":"10.1158/2159-8290.cd-24-1853","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1158/2159-8290.cd-24-1853","tag_type":"category","value":"Oncology","value_numeric":null},{"paper_doi":"10.1158/2159-8290.cd-24-1853","tag_type":"condition","value":"Cutaneous Melanoma","value_numeric":null},{"paper_doi":"10.1158/2159-8290.cd-24-1853","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1158/2159-8290.cd-24-1853","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1158/2159-8290.cd-24-1853","tag_type":"modality","value":"Adenosine Receptor Antagonist","value_numeric":null},{"paper_doi":"10.1158/2159-8290.cd-24-1853","tag_type":"modality","value":"Transcription Factor Targeting","value_numeric":null},{"paper_doi":"10.1158/2159-8290.cd-24-1853","tag_type":"modality","value":"VEGFR Inhibitor","value_numeric":null},{"paper_doi":"10.1158/2159-8290.cd-24-1853","tag_type":"study_design","value":"Preclinical/Translational Study","value_numeric":null},{"paper_doi":"10.1158/2159-8290.cd-24-1853","tag_type":"warning","value":"Study design is preclinical (in vivo models and transcriptomics); no randomized clinical trial data are reported, so the level of evidence is limited. The 'practice_changing' impact flag reflects the novelty of the dual VEGFR/adenosine receptor inhibition rationale, not established clinical practice. Sample size is not explicitly stated in the abstract, so no sample_size tag was assigned. Sex of subjects/models is not reported in the abstract.","value_numeric":null},{"paper_doi":"10.1158/2159-8290.cd-24-1853","tag_type":"warning","value":"The study compares early-stage melanoma to naevi and other cancers, but the specific comparator cohorts and patient numbers are not detailed in the available text.","value_numeric":null}],"summaries":{"what_studied":"This study examined whether the homeodomain transcription factor HOXD13 drives a coordinated pro-angiogenic and immune-evasive program in cutaneous melanoma, using transcriptomics, 3D chromatin profiling, and in vivo tumor models across early-stage melanoma, naevi, and other cancers.","key_result":"HOXD13 activates a melanoblast-like program that promotes tumor growth by upregulating VEGFA, SEMA3A, and CD73—enhancing angiogenesis and elevating immunosuppressive adenosine while excluding T cells. Combined VEGFR and adenosine receptor inhibition reversed HOXD13-driven tumor growth in vivo.","limitations":"Findings are largely mechanistic (in vivo/transcriptomic models); clinical translation and patient-level outcomes are not yet demonstrated. Study focuses on early-stage melanoma comparisons, so relevance to advanced or metastatic disease is unclear. The therapeutic reversal was shown in preclinical models only, with no human trial data.","practice_takeaway":"HOXD13 may serve as a biomarker identifying melanomas likely to resist immunotherapy via angiogenesis-driven T-cell exclusion. Combined VEGFR and adenosine receptor blockade warrants clinical investigation in HOXD13-high tumors."}},{"doi":"10.1093/bjd/ljag172","pmid":"42082381","title":"Evaluating COVID-19 Pandemic Impact on Melanoma Incidence and factors in Regions with Different Infection Control Strategies","journal_title":"British Journal of Dermatology","journal_issn":"0007-0963","published_at":"2026-05-05T00:00:00.000Z","url":"https://doi.org/10.1093/bjd/ljag172","source_score":10,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2026-05-06","doi":"10.1093/bjd/ljag172","days":"14","issn":"0007-0963","rank":"10","field":"Clinical Medicine","score":"10","category":"Dermatology","categories":["Dermatology"],"_categories":["Dermatology"]},"pubmed":{"doi":"10.1093/bjd/ljag172","title":"Evaluating COVID-19 Pandemic Impact on Melanoma Incidence and factors in Regions with Different Infection Control Strategies.","journal":"The British journal of dermatology","methods":"","results":"In Victoria, melanoma diagnoses declined during COVID across all age groups, most notably among patients <50 years. Median Breslow thickness remained 0.7mm, but the distribution shifted significantly (p<0.001), with an 8% increase in geometric mean ratio (95% CI, 5%-12%). In Sweden, measures of thickness remained unchanged during COVID, but the odds of ulceration increased slightly (OR 1.09; 95% CI 1.01-1.19). Lymph node metastasis rates were stable in both regions. A significant immediate drop in overall incidence followed COVID-19 onset in both regions, primarily driven by thin melanomas. In Victoria, the lower incidence level persisted without a subsequent slope change. In contrast, the Swedish melanoma incidence gradually realigned with the pre-COVID trend after the initial level change. The immediate incidence drop was most prominent among older age groups in both regions.","abstract":"$30","keywords":[],"pubmed_id":"42082381","conclusions":"","publication_date":"2026-05-05T00:00:00"},"crossref":{"DOI":"10.1093/bjd/ljag172","URL":"https://doi.org/10.1093/bjd/ljag172","ISSN":["0007-0963","1365-2133"],"link":[{"URL":"https://academic.oup.com/bjd/advance-article-pdf/doi/10.1093/bjd/ljag172/68209487/ljag172.pdf","content-type":"application/pdf","content-version":"am","intended-application":"syndication"},{"URL":"https://academic.oup.com/bjd/advance-article-pdf/doi/10.1093/bjd/ljag172/68209487/ljag172.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["Evaluating COVID-19 Pandemic Impact on Melanoma Incidence and factors in Regions with Different Infection Control Strategies"],"author":[{"given":"Cecilia","family":"Sand","sequence":"first","affiliation":[{"name":"Dermatology and Venereology, Department of Clinical Sciences, Lund University, and Department of Dermatology, Skane University Hospital ,"},{"name":"Lund Melanoma Study Group, Department of Clinical Sciences, Lund University , Lund ,"}]},{"given":"Dilki","family":"Jayasinghe","sequence":"additional","affiliation":[{"name":"Centre for Health Services Research, The University of Queensland , Brisbane, Queensland ,"}]},{"given":"Rory","family":"Wolfe","sequence":"additional","affiliation":[{"name":"School of Public Health and Preventive Medicine, Monash University Clinical Trials Centre , Melbourne ,"}]},{"given":"Victoria","family":"Mar","sequence":"additional","affiliation":[{"name":"Victorian Melanoma Service , Melbourne, VIC ,"}]},{"given":"Karolin","family":"Isaksson","sequence":"additional","affiliation":[{"name":"Lund Melanoma Study Group, Department of Clinical Sciences, Lund University , Lund ,"},{"name":"Division of Surgery, Department of Clinical Sciences in Lund, Lund University, Lund and Department of Surgery, Skåne University Hospital , Kristianstad ,"}]},{"given":"Åsa","family":"Ingvar","sequence":"additional","affiliation":[{"name":"Dermatology and Venereology, Department of Clinical Sciences, Lund University, and Department of Dermatology, Skane University Hospital ,"},{"name":"Lund Melanoma Study Group, Department of Clinical Sciences, Lund University , Lund 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The mechanism shifted from βAR-driven growth promotion to α2-AR-driven growth inhibition, with α2-AR activation reducing pro-tumor myeloid cell numbers and distribution, independently of T cells.","limitations":"All experiments are in mouse models only; clinical translation to human melanoma is unproven. The study does not clarify which specific myeloid cell subsets are most relevant or how early tumor-seeding conditions mechanistically flip the adrenergic switch from β to α2 signaling.","practice_takeaway":"These findings suggest that sympathetic nervous system activity in melanoma is not uniformly pro-tumor — context matters. Targeting α2-adrenergic receptors or local sympathetic signaling could be a future therapeutic angle, but no clinical data exist yet."}},{"doi":"10.1111/ans.70490","pmid":"41532394","title":"Timing of Definitive Surgical Management of Primary Cutaneous Melanoma: Association With Survival","journal_title":"ANZ Journal of Surgery","journal_issn":"1445-1433","published_at":"2026-01-14T00:00:00.000Z","url":"https://doi.org/10.1111/ans.70490","source_score":15,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2026-01-15","doi":"10.1111/ans.70490","days":"7","issn":"1445-1433","rank":"10","field":"Clinical Medicine","score":"15","category":"Surgery","categories":["Surgery"],"_categories":["Surgery"]},"pubmed":{"doi":"10.1111/ans.70490","title":"Timing of Definitive Surgical Management of Primary Cutaneous Melanoma: Association With Survival.","journal":"ANZ journal of surgery","methods":"","results":"In total 18, 242 patients were included in the analysis. Their average age was 57.5 years and 57% were male. The majority of primary melanomas were located on the trunk (32.5%) and upper limb (24.7%). Mean Breslow thickness was 1.8 mm (range 0.1-50 mm) and 64% were of superficial spreading subtype. Time to surgery was divided into ≤ 1 week, 1-4 weeks, 4-8 weeks, 8-12 weeks and > 12 weeks (n = 2453, 8882, 5906, 870 and 126, respectively). Increased delay of definitive surgical treatment was associated with poorer OS and RFS, with an OS HR of 1.23 for the 8-12 week group compared to the 1-4 week group. For RFS HR was 1.36 for the same cohorts.","abstract":"$33","keywords":[],"pubmed_id":"41532394","conclusions":"Definitive surgical treatment of patients with primary cutaneous melanoma between 1-4 weeks post-diagnosis with excision-biopsy was associated with improved OS & RFS compared to those treated within 1 week and greater than 4 weeks in this patient cohort treated prior to the use of adjuvant drug therapy.","publication_date":"2026-01-14T00:00:00"},"crossref":{"DOI":"10.1111/ans.70490","URL":"https://doi.org/10.1111/ans.70490","ISSN":["1445-1433","1445-2197"],"link":[{"URL":"https://onlinelibrary.wiley.com/doi/pdf/10.1111/ans.70490","content-type":"application/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https://onlinelibrary.wiley.com/doi/full-xml/10.1111/ans.70490","content-type":"application/xml","content-version":"vor","intended-application":"text-mining"},{"URL":"https://onlinelibrary.wiley.com/doi/pdf/10.1111/ans.70490","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["Timing of Definitive Surgical Management of Primary Cutaneous Melanoma: Association With Survival"],"author":[{"given":"Edward (Ned)","family":"Farley","sequence":"first","affiliation":[{"name":"Melanoma Institute Australia The University of Sydney Sydney Australia"}]},{"given":"Jake","family":"Hindmarch","sequence":"additional","affiliation":[{"name":"Melanoma Institute Australia The University of Sydney Sydney Australia"}]},{"given":"Janet","family":"McKeown","sequence":"additional","affiliation":[{"name":"Melanoma Institute Australia The University of Sydney Sydney Australia"}]},{"given":"Serigne N.","family":"Lo","sequence":"additional","affiliation":[{"name":"Melanoma Institute Australia The University of Sydney Sydney Australia"},{"name":"Faculty of Medicine and Health The University of Sydney Sydney Australia"}]},{"given":"Sydney","family":"Ch'ng","sequence":"additional","affiliation":[{"name":"Melanoma Institute Australia The University of Sydney Sydney Australia"},{"name":"Faculty of Medicine and Health The University of Sydney Sydney Australia"},{"name":"Royal Prince Alfred Hospital Sydney Australia"},{"name":"Chris O’Brien Lifehouse Sydney Australia"},{"name":"Mater Hospital Sydney Australia"}]},{"given":"Omgo E.","family":"Nieweg","sequence":"additional","affiliation":[{"name":"Melanoma Institute Australia The University of Sydney Sydney Australia"},{"name":"Faculty of Medicine and Health The University of Sydney Sydney Australia"}]},{"given":"Thomas E.","family":"Pennington","sequence":"additional","affiliation":[{"name":"Melanoma Institute Australia The University of Sydney Sydney Australia"},{"name":"Faculty of Medicine and Health The University of Sydney Sydney Australia"},{"name":"Royal Prince Alfred Hospital Sydney Australia"},{"name":"Mater Hospital Sydney Australia"}]},{"given":"Kerwin F.","family":"Shannon","sequence":"additional","affiliation":[{"name":"Melanoma Institute Australia The University of Sydney Sydney Australia"},{"name":"Faculty of Medicine and Health The University of Sydney Sydney Australia"},{"name":"Royal Prince Alfred Hospital Sydney Australia"},{"name":"Chris O’Brien Lifehouse Sydney Australia"},{"name":"Mater Hospital Sydney Australia"}]},{"given":"Andrew J.","family":"Spillane","sequence":"additional","affiliation":[{"name":"Melanoma Institute Australia The University of Sydney Sydney Australia"},{"name":"Faculty of Medicine and Health The University of Sydney Sydney Australia"},{"name":"Mater Hospital Sydney Australia"},{"name":"Royal North Shore Hospital Sydney Australia"}]},{"given":"John F.","family":"Thompson","sequence":"additional","affiliation":[{"name":"Melanoma Institute Australia The University of Sydney Sydney Australia"},{"name":"Faculty of Medicine and Health The University of Sydney Sydney Australia"},{"name":"Royal Prince Alfred Hospital Sydney Australia"},{"name":"Mater Hospital Sydney Australia"},{"name":"Faculty of Health and Medical Sciences The University of Western Australia Perth Australia"}]},{"given":"Robyn P. 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Time-to-surgery groups included n=2,453 (≤1 week), 8,882 (1–4 weeks), 5,906 (4–8 weeks), 870 (8–12 weeks), and 126 (>12 weeks).","limitations":"Retrospective, single-center cohort predating adjuvant melanoma therapies; residual confounding is likely. The abstract provides hazard ratios only for the 8–12 vs 1–4 week comparison, limiting insight into other intervals.","practice_takeaway":"When feasible, schedule definitive surgery for Stage I–II primary cutaneous melanoma within 1–4 weeks after diagnostic excision-biopsy; avoid delays beyond 4 weeks, particularly 8–12 weeks, given the worse OS and RFS observed in this cohort."}},{"doi":"10.1093/bjd/ljaf412","pmid":"41148046","title":"Subclinical Fields of\n BRAF V600E\n -Mutant Melanocytes Populate Human Skin and Are Enriched Around Melanoma and Naevi","journal_title":"British Journal of Dermatology","journal_issn":"0007-0963","published_at":"2025-10-28T00:00:00.000Z","url":"https://doi.org/10.1093/bjd/ljaf412","source_score":51,"is_retracted":false,"is_open_access":false,"raw_metadata":{"ooir":{"day":"2025-10-30","doi":"10.1093/bjd/ljaf412","days":"30","issn":"0007-0963","rank":"8","field":"Clinical Medicine","score":"51","category":"Dermatology","categories":["Dermatology"],"_categories":["Dermatology"]},"pubmed":{"doi":"10.1093/bjd/ljaf412","title":"Subclinical Fields of BRAF V600E-Mutant Melanocytes Populate Human Skin and Are Enriched Around Melanoma and Naevi.","journal":"The British journal of dermatology","methods":"","results":"We identified BRAF V600E-mutant melanocytes in skin surrounding naevi and primary melanomas, even years after tumour excision. Fields of BRAF V600E-mutant melanocytes are commonly observed in the skin of patients at high risk for melanoma and are up to 20-fold more dense and 50% more frequent in tumour-adjacent skin. Field cells exhibit a gene expression profile characteristic of BRAF V600E-induced growth arrest, consistent with dormant yet genetically primed cells.","abstract":"$35","keywords":[],"pubmed_id":"41148046","conclusions":"","publication_date":"2025-10-28T00:00:00"},"crossref":{"DOI":"10.1093/bjd/ljaf412","URL":"https://doi.org/10.1093/bjd/ljaf412","ISSN":["0007-0963","1365-2133"],"link":[{"URL":"https://academic.oup.com/bjd/advance-article-pdf/doi/10.1093/bjd/ljaf412/65003382/ljaf412.pdf","content-type":"application/pdf","content-version":"am","intended-application":"syndication"},{"URL":"https://academic.oup.com/bjd/advance-article-pdf/doi/10.1093/bjd/ljaf412/65003382/ljaf412.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["Subclinical Fields of\n BRAF V600E\n -Mutant Melanocytes Populate Human Skin and Are Enriched Around Melanoma and 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The primary outcome was negative predictive value (NPV) for CP-GEP low-risk results, with subgroup analyses by T category, site, and age.","key_result":"CP-GEP classified 651/1761 (37.0%) as low risk; 46/651 (7.1%) were SLN positive, giving an NPV of 92.9% (95% CI, 90.7%–94.8%). High-risk cases had 264/1110 (23.8%) SLN positivity; in stage IB, low vs high risk positivity was 6.5% vs 18.3%, and in patients ≥65 years, 6.6% vs 20.3%; the proportion labeled low risk declined from T1 68.2% to T2 32.9% to T3 2.8%.","limitations":"Outcomes after a negative SLNB were not reported. Findings apply to SLNB-eligible T1–T3 tumors; very few T3 cases were low risk (2.8%), and T4 disease was not studied.","practice_takeaway":"CP-GEP identified a subgroup with <10% SLN metastasis risk, aligning with thresholds where SLNB can often be forgone. 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The median (range) age was 56 (18-101) years and 78 014 (54.0%) were men. Median (IQR) follow-up was 15.0 (9.5-23.3) years. Crude incidence rates of melanoma-related death 20 years after diagnosis were 6.3% (95% CI, 6.1%-6.5%) for the whole cohort, 6.0% (95% CI, 5.7%-6.2%) for tumors smaller than 0.8 mm, and 12.0% (95% CI, 11.4%-12.6%) for tumors 0.8 to 1.0 mm. The corresponding 20-year melanoma-specific survival rates were 91.9% (95% CI, 91.6%-92.1%), 94.2% (95% CI, 94.0%-94.4%), and 87.8% (95% CI, 87.3%-88.3%), respectively. On multivariable analysis, tumor thickness of 0.8 to 1.0 mm was significantly associated with both a greater absolute risk of melanoma-related death (subdistribution hazard ratio, 2.92; 95% CI, 2.74-3.12) and a greater rate of melanoma-related death (hazard ratio, 2.98; 95% CI, 2.79-3.18) than thinner tumors (<0.8 mm). 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In multivariable models, 0.8–1.0 mm thickness had higher melanoma mortality (subdistribution HR 2.92 [95% CI, 2.74–3.12]; cause-specific HR 2.98 [95% CI, 2.79–3.18]); nonmelanoma death was not associated with thickness.","practice_takeaway":"Thin melanomas 0.8–1.0 mm carry markedly higher melanoma-specific mortality than <0.8 mm, supporting a 0.8‑mm threshold to guide care and counseling. Nonmelanoma mortality did not vary across thin-tumor thicknesses."}},{"doi":"10.1001/jamadermatol.2024.3514","pmid":"39245436","title":"Melanoma Incidence and Mortality Trends Among Patients Aged 59 Years or Younger in Sweden","journal_title":"JAMA Dermatology","journal_issn":"2168-6068","published_at":"2024-09-09T00:00:00.000Z","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/11382132","source_score":209,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2024-09-14","doi":"10.1001/jamadermatol.2024.3514","days":"30","issn":"2168-6068","rank":"3","field":"Clinical Medicine","score":"209","category":"Dermatology","categories":["Dermatology"],"_categories":["Dermatology"]},"pubmed":{"doi":"10.1001/jamadermatol.2024.3514","title":"Melanoma Incidence and Mortality Trends Among Patients Aged 59 Years or Younger in Sweden.","journal":"JAMA dermatology","methods":"","results":"There were 34 800 primary invasive cutaneous melanomas (19 582 [56.3%] in females and 15 218 [43.7%] in males) reported in 33 324 individuals younger than 60 years (median [IQR] age, 48 [36-58] years) from 1990 to 2022. A consistent rise in melanoma incidence was observed among those 50 to 59 years old. The age groups from 20 to 29 years, 30 to 39 years, and 40 to 49 years showed an incidence peak in 2013 to 2015 followed by stable or significantly declining rates until 2022. In patients younger than 20 years, melanoma incidence remained low with no significant trends. 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Accessed July 20, 2023. https://www.scienceopen.com/document?vid=19dd8115-435f-4586-81f3-eaec85280736","article-title":null,"journal-title":null,"doi-asserted-by":null}],"short-title":[],"journal-issue":{"issue":"11","published-print":{"date-parts":[[2023,11,1]]}},"content-domain":{"domain":[],"crossmark-restriction":false},"original-title":[],"container-title":["JAMA Dermatology"],"published-print":{"date-parts":[[2023,11,1]]},"reference-count":52,"published-online":null,"references-count":52,"short-container-title":["JAMA Dermatol"],"is-referenced-by-count":25},"unpaywall":{"doi":"10.1001/jamadermatol.2023.3179","is_oa":true,"title":"Changes in Health Care Costs, Survival, and Time Toxicity in the Era of Immunotherapy and Targeted Systemic Therapy for Melanoma","updated":"2025-07-30T00:59:52+00:00","published_date":"2023-09-06","best_oa_location":{"url":"https://jamanetwork.com/journals/jamadermatology/articlepdf/2808777/jamadermatology_bateni_2023_oi_230041_1692375282.3844.pdf","pmh_id":null,"url_for_pdf":"https://jamanetwork.com/journals/jamadermatology/articlepdf/2808777/jamadermatology_bateni_2023_oi_230041_1692375282.3844.pdf","url_for_landing_page":"https://doi.org/10.1001/jamadermatol.2023.3179"}}},"created_at":"2025-09-20T18:05:35.957Z","updated_at":"2025-09-20T18:19:17.906Z","tags":[{"paper_doi":"10.1001/jamadermatol.2023.3179","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.3179","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.3179","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.3179","tag_type":"condition","value":"Cutaneous Melanoma","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.3179","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.3179","tag_type":"modality","value":"Immunotherapy","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.3179","tag_type":"modality","value":"Targeted Therapy","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.3179","tag_type":"sample_size","value":"n=1462","value_numeric":1462},{"paper_doi":"10.1001/jamadermatol.2023.3179","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.3179","tag_type":"study_design","value":"Retrospective Cohort","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.3179","tag_type":"warning","value":"Costs are in Canadian dollars from Ontario’s health system and limited to the first year after diagnosis/initial treatment.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.3179","tag_type":"warning","value":"Design label simplified; the study used a propensity score–matched retrospective cohort with a historical comparator.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.3179","tag_type":"warning","value":"Time‑toxicity differences between eras were not statistically significant (P=0.20).","value_numeric":null}],"summaries":{"what_studied":"A longitudinal, propensity score–matched, retrospective cohort of Ontario residents aged 20 years or older with stage II–IV cutaneous melanoma compared outcomes in 2018–2019 vs 2007–2012. Outcomes were first‑year per‑capita health care and systemic therapy costs, time toxicity within 1 year of initial treatment, and overall survival.","key_result":"Mean first‑year health care costs were higher in 2018–2019 vs 2007–2012 ($47,886 vs $33,347), with larger increases in stage III ($67,108 vs $46,511) and stage IV ($117,450 vs $47,739). Systemic therapy costs rose across stages (stage II $40,823 vs $10,309; stage III $55,699 vs $9,764; stage IV $79,358 vs $9,318); 3‑year OS improved (74.2% vs 65.8%; HR 0.72, 95% CI 0.61–0.85; P<.001); time toxicity was similar, though stage IV patients averaged 58.7 vs 44.2 days with health system contact (>1 day/week; standardized difference 0.40; P=.20).","limitations":"Retrospective, propensity score–matched comparison of different eras (2007–2012 vs 2018–2019). Costs and time toxicity were measured only in the first year and within a single provincial health system.","practice_takeaway":"Adoption of immunotherapy and targeted therapy for stage II–IV melanoma was linked with higher first‑year costs and substantial time burden for stage IV patients, alongside better 3‑year survival. Discuss these trade‑offs when planning systemic therapy."}},{"doi":"10.1001/jamadermatol.2023.2712","pmid":"37672263","title":"Incidence of In Situ and Invasive Cutaneous Melanomas During the COVID-19 Pandemic in the US","journal_title":"JAMA Dermatology","journal_issn":"2168-6068","published_at":"2023-09-06T00:00:00.000Z","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/10483379","source_score":143,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2023-10-05","doi":"10.1001/jamadermatol.2023.2712","days":"30","issn":"2168-6068","rank":"5","field":"Clinical Medicine","score":"143","category":"Dermatology","categories":["Dermatology"],"_categories":["Dermatology"]},"pubmed":{"doi":"10.1001/jamadermatol.2023.2712","title":"Incidence of In Situ and Invasive Cutaneous Melanomas During the COVID-19 Pandemic in the US.","journal":"JAMA dermatology","methods":"","results":"","abstract":"This cohort study provides detailed annual rates and percentage changes of melanoma incidence before vs during the COVID-19 pandemic.","keywords":[],"pubmed_id":"37672263","conclusions":"","publication_date":"2023-09-06T00:00:00"},"crossref":{"DOI":"10.1001/jamadermatol.2023.2712","URL":"https://doi.org/10.1001/jamadermatol.2023.2712","ISSN":["2168-6068"],"link":[{"URL":"https://jamanetwork.com/journals/jamadermatology/articlepdf/2808780/jamadermatology_kim_2023_ld_230017_1697555540.44066.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":"1141","type":"journal-article","issue":"10","score":1,"title":["Incidence of In Situ and Invasive Cutaneous Melanomas During the COVID-19 Pandemic in the US"],"author":[{"given":"Daniel Y.","family":"Kim","sequence":"first","affiliation":[{"name":"Harvard–Massachusetts Institute of Technology Health Sciences and Technology Program, Harvard Medical School, Boston"}]},{"given":"Rebecca I.","family":"Hartman","sequence":"additional","affiliation":[{"name":"Department of Dermatology, Brigham and Women’s Hospital, Boston, Massachusetts"},{"name":"Dermatology Section, Veterans Affairs Integrated Service Network 1, Jamaica Plain, Massachusetts"}]}],"issued":{"date-parts":[[2023,10,1]]},"member":"10","prefix":"10.1001","source":"Crossref","volume":"159","created":{"date-time":"2023-09-06T15:04:52Z","timestamp":1694012692000,"date-parts":[[2023,9,6]]},"indexed":{"date-time":"2025-09-20T18:02:33Z","timestamp":1758391353482,"date-parts":[[2025,9,20]]},"subject":[],"abstract":"This cohort study provides detailed annual rates and percentage changes of melanoma incidence before vs during the COVID-19 pandemic.","language":"en","relation":{},"resource":{"primary":{"URL":"https://jamanetwork.com/journals/jamadermatology/fullarticle/2808780"}},"subtitle":[],"deposited":{"date-time":"2023-10-18T15:08:36Z","timestamp":1697641716000,"date-parts":[[2023,10,18]]},"issn-type":[{"type":"print","value":"2168-6068"}],"published":{"date-parts":[[2023,10,1]]},"publisher":"American Medical Association (AMA)","reference":[{"DOI":"10.1016/j.jaad.2022.06.031","key":"dld230017r1","year":"2022","issue":"5","author":"Trepanowski","volume":"87","first-page":"1217","unstructured":null,"article-title":"Delays in melanoma presentation during the COVID-19 pandemic: a nationwide multi-institutional cohort study.","journal-title":"J Am Acad Dermatol","doi-asserted-by":"publisher"},{"DOI":"10.1016/j.jaad.2023.02.046","key":"dld230017r2","year":"2023","issue":"1","author":"Kim","volume":"89","first-page":"175","unstructured":null,"article-title":"Impact of COVID-19 pandemic on melanoma presentation by facility type and region in the United States.","journal-title":"J Am Acad Dermatol","doi-asserted-by":"publisher"},{"DOI":"10.1001/jamaoncol.2022.2617","key":"dld230017r3","year":"2022","issue":"9","author":"Teglia","volume":"8","first-page":"1287","unstructured":null,"article-title":"Global association of COVID-19 pandemic measures with cancer screening: a systematic review and meta-analysis.","journal-title":"JAMA Oncol","doi-asserted-by":"publisher"},{"DOI":"10.1056/NEJMsb2019760","key":"dld230017r4","year":"2021","issue":"1","author":"Welch","volume":"384","first-page":"72","unstructured":null,"article-title":"The rapid rise in cutaneous melanoma diagnoses.","journal-title":"N Engl J Med","doi-asserted-by":"publisher"},{"DOI":"10.1016/j.jaad.2011.05.032","key":"dld230017r5","year":"2011","issue":"5","author":"Cartee","volume":"65","first-page":"S124","unstructured":null,"article-title":"Melanoma reporting to central cancer registries by US dermatologists: an analysis of the persistent knowledge and practice gap.","journal-title":"J Am Acad Dermatol","doi-asserted-by":"publisher"},{"DOI":"10.1200/CCI.20.00134","key":"dld230017r6","year":"2020","issue":null,"author":"Patt","volume":"4","first-page":"1059","unstructured":null,"article-title":"Impact of COVID-19 on cancer care: how the pandemic is delaying cancer diagnosis and treatment for American seniors.","journal-title":"JCO Clin Cancer Inform","doi-asserted-by":"publisher"}],"short-title":[],"journal-issue":{"issue":"10","published-print":{"date-parts":[[2023,10,1]]}},"content-domain":{"domain":[],"crossmark-restriction":false},"original-title":[],"container-title":["JAMA Dermatology"],"published-print":{"date-parts":[[2023,10,1]]},"reference-count":6,"published-online":null,"references-count":6,"short-container-title":["JAMA Dermatol"],"is-referenced-by-count":4},"unpaywall":{"doi":"10.1001/jamadermatol.2023.2712","is_oa":true,"title":"Incidence of In Situ and Invasive Cutaneous Melanomas During the COVID-19 Pandemic in the US","updated":"2025-07-30T00:59:52+00:00","published_date":"2023-09-06","best_oa_location":{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/10483379","pmh_id":"oai:pubmedcentral.nih.gov:10483379","url_for_pdf":null,"url_for_landing_page":"https://www.ncbi.nlm.nih.gov/pmc/articles/10483379"}}},"created_at":"2025-09-20T18:19:17.906Z","updated_at":"2025-09-20T19:08:47.255Z","tags":[{"paper_doi":"10.1001/jamadermatol.2023.2712","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.2712","tag_type":"condition","value":"Cutaneous Melanoma","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.2712","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.2712","tag_type":"sample_size","value":"n=76,846","value_numeric":76846},{"paper_doi":"10.1001/jamadermatol.2023.2712","tag_type":"study_design","value":"Cohort","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.2712","tag_type":"warning","value":"Age group and sex distributions are not reported in the provided text.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.2712","tag_type":"warning","value":"It is unclear whether the reported total (n=76,846) reflects the analytic denominator after exclusions for unknown race/rurality.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.2712","tag_type":"warning","value":"Only supplementary methods were provided; numeric age-adjusted incidence rates and confidence intervals are not in the excerpt.","value_numeric":null}],"summaries":{"what_studied":"A population-based cohort analysis using SEER assessed age-adjusted incidence rates for in situ and invasive cutaneous melanoma across 17 US registries from 2018–2020, comparing pre–COVID (2018–2019) with 2020. The cohort included 76,846 new cases (34,051 in situ; 42,795 invasive).","key_result":"New melanoma diagnoses declined from 27,296 (2018) and 27,658 (2019) to 21,892 (2020). Invasive melanoma incidence rates were significantly lower in 2020, largely due to fewer T1, non-ulcerated, non-mitogenic, and stage I tumors.","limitations":"SEER covers about 48% of US cancer diagnoses, limiting generalizability. Patients with non-Hispanic unknown race (12.40%) and unknown rurality (0.03%) were excluded; key pathology fields were missing in a minority of invasive cases (e.g., unknown Breslow thickness ~11%–12%), though sensitivity analyses reported similar findings.","practice_takeaway":"Expect a 2020 dip in diagnosed invasive cutaneous melanomas—most pronounced in early-stage categories—when benchmarking incidence or service volumes. Interpret year-over-year trends with caution for that period."}}],"initialOffset":20,"fetchConfig":{"kind":"tags","tags":[{"tag_type":"condition","value":"Cutaneous Melanoma"}]},"breadcrumbItems":[{"name":"Home","href":"/"},{"name":"Research Hub","href":"/hub"},{"name":"Conditions","href":"/hub/tag/condition"},{"name":"Cutaneous Melanoma"}],"hrefConfig":{"basePath":"/hub/papers","webViewQueryParams":{"hub_ctx":"tag","hub_tag_type":"condition","hub_tag_value":"Cutaneous Melanoma"}}}]]

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