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:T9f7,Cancer survivors have increased cardiovascular disease (CVD) risk partly due to the toxic effects of cancer therapy. Clonal hematopoiesis of indeterminate potential (CHIP), an age-associated blood disorder caused by somatic variants in blood stem cells, is more prevalent among individuals receiving cancer therapy and increases CVD risk independent of traditional risk factors. It is unknown whether CHIP amplifies therapy-related cardiovascular toxic effects in patients with cancer. To assess the association between CHIP and CVD risk, accounting for competing risks, among patients with primary solid tumors who received chemotherapy, radiotherapy, or immunotherapy. A cohort study was conducted using BioVU, Vanderbilt University Medical Center's biorepository linking electronic health records to whole-genome sequencing data from 250 038 participants from 2006 to 2025. In this cohort, participants had a primary solid tumor diagnosis, received chemotherapy, radiotherapy, and/or immunotherapy, and did not have hematologic malignant disease before treatment. Data were analyzed from June 2025 to November 2025. CHIP variants detected via whole-genome sequencing, chemotherapy, radiotherapy, and immunotherapy. Time to first cardiovascular event, defined as heart failure, ischemic CVD, or arrhythmia following cancer treatment. Among 8004 eligible participants (median [IQR] age, 61.9 [52.2-69.9] years; 4385 female individuals [54.8%]) with a primary solid tumor diagnosis, 7438 had no heart failure, 7392 no ischemic CVD, and 6002 no arrhythmia before cancer therapy. Overall, 549 (6.9%) had CHIP. In the propensity score-matched cohort, participants with CHIP had a significantly higher 10-year cumulative incidence of heart failure (20.3%; 95% CI, 16.0%-24.4% vs 14.5%; 95% CI, 13.5%-15.6%; P = .001) and ischemic CVD (25.3%; 95% CI, 20.5%-30.0% vs 18.5%; 95% CI, 17.3%-20.0%; P < .001) compared with those without CHIP. In adjusted Fine-Gray models, CHIP was associated with increased risk of heart failure (subdistribution hazard ratio [sHR], 1.26; 95% CI, 1.02-1.56; P = .03). In an exploratory 24-month landmark analysis, there was a statistically significant interaction between CHIP and intensive chemotherapy (≥7 cycles) on heart failure risk (sHR, 1.02; 95% CI, 1.00-1.04; P = .03). In this cohort study, CHIP was associated with increased CVD risk in patients with solid tumors receiving cancer therapy. This finding suggests incorporating CHIP status may improve cardio-oncology treatment of cancer survivors.31:T105a, Importance Cancer survivors have increased cardiovascular disease (CVD) risk partly due to the toxic effects of cancer therapy. Clonal hematopoiesis of indeterminate potential (CHIP), an age-associated blood disorder caused by somatic variants in blood stem cells, is more prevalent among individuals receiving cancer therapy and increases CVD risk independent of traditional risk factors. It is unknown whether CHIP amplifies therapy-related cardiovascular toxic effects in patients with cancer. Objective To assess the association between CHIP and CVD risk, accounting for competing risks, among patients with primary solid tumors who received chemotherapy, radiotherapy, or immunotherapy. Design, Setting, and Participants A cohort study was conducted using BioVU, Vanderbilt University Medical Center’s biorepository linking electronic health records to whole-genome sequencing data from 250 038 participants from 2006 to 2025. In this cohort, participants had a primary solid tumor diagnosis, received chemotherapy, radiotherapy, and/or immunotherapy, and did not have hematologic malignant disease before treatment. Data were analyzed from June 2025 to November 2025. Exposures CHIP variants detected via whole-genome sequencing, chemotherapy, radiotherapy, and immunotherapy. Main Outcomes and Measures Time to first cardiovascular event, defined as heart failure, ischemic CVD, or arrhythmia following cancer treatment. Results Among 8004 eligible participants (median [IQR] age, 61.9 [52.2-69.9] years; 4385 female individuals [54.8%]) with a primary solid tumor diagnosis, 7438 had no heart failure, 7392 no ischemic CVD, and 6002 no arrhythmia before cancer therapy. Overall, 549 (6.9%) had CHIP. In the propensity score–matched cohort, participants with CHIP had a significantly higher 10-year cumulative incidence of heart failure (20.3%; 95% CI, 16.0%-24.4% vs 14.5%; 95% CI, 13.5%-15.6%; P = .001) and ischemic CVD (25.3%; 95% CI, 20.5%-30.0% vs 18.5%; 95% CI, 17.3%-20.0%; P &lt; .001) compared with those without CHIP. In adjusted Fine-Gray models, CHIP was associated with increased risk of heart failure (subdistribution hazard ratio [sHR], 1.26; 95% CI, 1.02-1.56; P = .03). In an exploratory 24-month landmark analysis, there was a statistically significant interaction between CHIP and intensive chemotherapy (≥7 cycles) on heart failure risk (sHR, 1.02; 95% CI, 1.00-1.04; P = .03). Conclusions and Relevance In this cohort study, CHIP was associated with increased CVD risk in patients with solid tumors receiving cancer therapy. This finding suggests incorporating CHIP status may improve cardio-oncology treatment of cancer survivors. 32:T446,T cell engagers (TCEs) are antibody-based constructs designed to transiently reprogram cytotoxic T lymphocytes for target cell elimination by simultaneously binding the T cell receptor and a specific surface antigen on the target cell. Over the past 12 years, 10 TCEs were approved by the US Food and Drug Administration, and an additional two by the European Medicines Agency. Nine TCEs treat hematologic malignancies, and three target solid tumors. Over 150 TCEs are being investigated in clinical trials, recently also in autoimmune diseases. Here, we discuss the learnings from the 12 approved TCEs. A surprising variety of molecular designs and biochemical characteristics appear suitable for approval. On the clinical side, we review targets, indications, dosing, schedules, side effects, mitigation strategies for adverse events, and efficacy. High flexibility in design and choice of target, scalability, high response rates as a monotherapy in hematologic malignancies, and emerging efficacy against solid tumors and in autoimmune diseases make TCEs an attractive therapeutic modality.33:T457,T cell engagers (TCEs) are antibody-based constructs designed to transiently reprogram cytotoxic T lymphocytes for target cell elimination by simultaneously binding the T cell receptor and a specific surface antigen on the target cell. Over the past 12 years, 10 TCEs were approved by the US Food and Drug Administration, and an additional two by the European Medicines Agency. Nine TCEs treat hematologic malignancies, and three target solid tumors. Over 150 TCEs are being investigated in clinical trials, recently also in autoimmune diseases. Here, we discuss the learnings from the 12 approved TCEs. A surprising variety of molecular designs and biochemical characteristics appear suitable for approval. On the clinical side, we review targets, indications, dosing, schedules, side effects, mitigation strategies for adverse events, and efficacy. High flexibility in design and choice of target, scalability, high response rates as a monotherapy in hematologic malignancies, and emerging efficacy against solid tumors and in autoimmune diseases make TCEs an attractive therapeutic modality.25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Solid Tumors: condition Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Solid Tumors (condition). Clinician-written summaries and actionable practice insights. Updated daily.\",\"url\":\"https://www.reachrx.ai/hub/tag/condition/Solid%20Tumors\",\"breadcrumb\":{\"@type\":\"BreadcrumbList\",\"itemListElement\":[{\"@type\":\"ListItem\",\"position\":1,\"name\":\"Home\",\"item\":\"https://www.reachrx.ai\"},{\"@type\":\"ListItem\",\"position\":2,\"name\":\"Research Hub\",\"item\":\"https://www.reachrx.ai/hub\"},{\"@type\":\"ListItem\",\"position\":3,\"name\":\"Conditions\",\"item\":\"https://www.reachrx.ai/hub/tag/condition\"},{\"@type\":\"ListItem\",\"position\":4,\"name\":\"Solid Tumors\",\"item\":\"https://www.reachrx.ai/hub/tag/condition/Solid%20Tumors\"}]}}"}}]],["$","$L2f",null,{"title":"Solid Tumors: Research & Clinical Takeaways","description":"Discover peer-reviewed research on Solid Tumors with concise clinician summaries and next-step guidance.","papers":[{"doi":"10.1016/j.ccell.2026.08.007","pmid":"42679812","title":"Tumor immune microenvironment remodeling predicts response to checkpoint inhibitor therapy","journal_title":"Cancer Cell","journal_issn":"1535-6108","published_at":"2026-09-01T00:00:00.000Z","url":"https://doi.org/10.5281/zenodo.18825477","source_score":35,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-09-09T06:21:04.352Z","updated_at":"2026-09-09T06:21:04.352Z","tags":[{"paper_doi":"10.1016/j.ccell.2026.08.007","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1016/j.ccell.2026.08.007","tag_type":"category","value":"Oncology","value_numeric":null},{"paper_doi":"10.1016/j.ccell.2026.08.007","tag_type":"condition","value":"Solid Tumors","value_numeric":null},{"paper_doi":"10.1016/j.ccell.2026.08.007","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1016/j.ccell.2026.08.007","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1016/j.ccell.2026.08.007","tag_type":"modality","value":"Immune Checkpoint Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.ccell.2026.08.007","tag_type":"sample_size","value":"n=241","value_numeric":241},{"paper_doi":"10.1016/j.ccell.2026.08.007","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1016/j.ccell.2026.08.007","tag_type":"study_design","value":"Longitudinal Observational Study with Single-Cell Transcriptomics Atlas","value_numeric":null},{"paper_doi":"10.1016/j.ccell.2026.08.007","tag_type":"warning","value":"Full text was not available; summary is based solely on the abstract and repository description.","value_numeric":null},{"paper_doi":"10.1016/j.ccell.2026.08.007","tag_type":"warning","value":"Sample size tag reflects 241 patients; 441 samples were collected longitudinally — context-dependent interpretation is needed.","value_numeric":null},{"paper_doi":"10.1016/j.ccell.2026.08.007","tag_type":"warning","value":"Study design is observational/atlas-based; the 'practice_changing' flag reflects translational potential of the 59-gene signature validated across 19 cohorts, but prospective clinical trials have not yet been conducted.","value_numeric":null},{"paper_doi":"10.1016/j.ccell.2026.08.007","tag_type":"warning","value":"The DOI and Zenodo repository list a publication date of March 10, 2026 (v1), while the journal publication date is listed as September 1, 2026 — there may be a preprint-to-publication lag; the canonical reference should be verified.","value_numeric":null}],"summaries":{"what_studied":"This study built a longitudinal single-cell RNA sequencing atlas from 441 samples across 241 patients with ten cancer types to map how the tumor immune microenvironment (TIME) changes during immune checkpoint inhibitor (ICI) therapy, and whether those changes predict response and survival.","key_result":"Four conserved TIME subtypes were identified; ~40% of tumors shifted between subtypes during therapy. Shifts toward inflamed or B cell-enriched subtypes linked to better response and survival, while persistence in or shifts toward myeloid-dominant subtypes indicated resistance. A derived 59-gene signature predicted response and survival across 1,383 baseline tumors in 19 independent cohorts.","limitations":"The dataset spans ten cancer types, which may obscure tumor-type-specific biology; the longitudinal atlas is observational, so causal directionality of TIME transitions cannot be confirmed; file access is restricted, limiting independent replication from the shared dataset.","practice_takeaway":"Tracking shifts in the tumor immune microenvironment during ICI therapy — not just the baseline state — may be more informative for predicting outcomes. The 59-gene signature offers a potential tool for baseline response prediction across multiple cancer types, pending prospective validation."}},{"doi":"10.1158/0008-5472.can-26-0202","pmid":"42406997","title":"TLR9 Agonists Potentiate Adoptive T-cell Therapy in Cancer through a B-cell–CD2 Costimulatory Axis","journal_title":"Cancer Research","journal_issn":"0008-5472","published_at":"2026-08-04T00:00:00.000Z","url":"https://doi.org/10.1158/0008-5472.can-26-0202","source_score":19,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-09T13:25:15.853Z","updated_at":"2026-08-09T13:25:15.853Z","tags":[{"paper_doi":"10.1158/0008-5472.can-26-0202","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1158/0008-5472.can-26-0202","tag_type":"category","value":"Oncology","value_numeric":null},{"paper_doi":"10.1158/0008-5472.can-26-0202","tag_type":"condition","value":"Cancer","value_numeric":null},{"paper_doi":"10.1158/0008-5472.can-26-0202","tag_type":"condition","value":"Solid Tumors","value_numeric":null},{"paper_doi":"10.1158/0008-5472.can-26-0202","tag_type":"generic","value":"CpG oligodeoxynucleotide","value_numeric":null},{"paper_doi":"10.1158/0008-5472.can-26-0202","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1158/0008-5472.can-26-0202","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1158/0008-5472.can-26-0202","tag_type":"modality","value":"Adoptive T-Cell Therapy","value_numeric":null},{"paper_doi":"10.1158/0008-5472.can-26-0202","tag_type":"modality","value":"CAR T-Cell Therapy","value_numeric":null},{"paper_doi":"10.1158/0008-5472.can-26-0202","tag_type":"modality","value":"TLR9 Agonist","value_numeric":null},{"paper_doi":"10.1158/0008-5472.can-26-0202","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1158/0008-5472.can-26-0202","tag_type":"study_design","value":"Preclinical Study with Correlative Human Cohort Analysis","value_numeric":null},{"paper_doi":"10.1158/0008-5472.can-26-0202","tag_type":"warning","value":"Specific patient cohort sizes and survival statistics from human tumor data are not provided in the abstract.","value_numeric":null},{"paper_doi":"10.1158/0008-5472.can-26-0202","tag_type":"warning","value":"Study design is primarily preclinical (murine models) with human correlative survival data; no prospective clinical trial data are reported.","value_numeric":null},{"paper_doi":"10.1158/0008-5472.can-26-0202","tag_type":"warning","value":"The 'practice_changing' impact flag reflects mechanistic novelty and translational potential, not yet confirmed clinical benefit.","value_numeric":null}],"summaries":{"what_studied":"This study investigated how TLR9 agonists (class B CpG) enhance adoptive T-cell transfer (ACT) therapy in cancer, specifically whether a B-cell–CD2 costimulatory axis mediates improved CD8+ T-cell fitness and antitumor activity in murine and human models.","key_result":"Class B CpG uniquely drove superior CD8+ T-cell effector differentiation and metabolic fitness via B-cell–CD2 costimulation; disrupting CD2 signaling impaired glycolytic capacity and tumor control, while blocking CD86, CD80, CD28, or ICOS did not. Elevated CD2 expression in human tumors correlated with improved overall survival across multiple cancer patient cohorts.","limitations":"Findings rely primarily on murine models and human correlative cohort data, with limited direct clinical validation; the study does not report specific patient cohort sizes or survival statistics; CAR T-cell experiments are preclinical.","practice_takeaway":"CD2 costimulation may be a targetable pathway to boost ACT and CAR T-cell therapy in solid tumors. TLR9 agonists (class B CpG), rather than other TLR agonists, should be prioritized when combining with adoptive T-cell therapies in future trials."}},{"doi":"10.1186/s13046-026-03785-5","pmid":"42522039","title":"Tailored FcγR blockade enhances immune checkpoint therapy and overcomes resistance","journal_title":"Journal of Experimental & Clinical Cancer Research","journal_issn":"1756-9966","published_at":"2026-07-25T00:00:00.000Z","url":"https://doi.org/10.1186/s13046-026-03785-5","source_score":40,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-31T13:37:15.775Z","updated_at":"2026-07-31T13:37:15.775Z","tags":[{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"brand","value":"Keytruda","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"brand","value":"Opdivo","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"brand","value":"Yervoy","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"category","value":"Oncology","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"condition","value":"Colorectal Cancer","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"condition","value":"Melanoma","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"condition","value":"Solid Tumors","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"generic","value":"BI-1206","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"generic","value":"BI-1607","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"generic","value":"ipilimumab","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"generic","value":"nivolumab","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"generic","value":"pembrolizumab","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"modality","value":"Fc Gamma Receptor Blocker","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"modality","value":"Immune Checkpoint Inhibitor","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"sex","value":"female","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"study_design","value":"Preclinical In Vivo and In Vitro Study","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"warning","value":"Multiple authors are employed by BioInvent International, the company developing BI-1206 and BI-1607; industry funding and conflicts of interest should be weighed when interpreting results.","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"warning","value":"Sample sizes for individual in vivo experiments are not consistently reported in the abstract or full text excerpts; statistical robustness of some comparisons is uncertain.","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"warning","value":"The 'practice_changing' impact flag is applied based on the mechanistic novelty and ongoing clinical trials, not proven clinical benefit — results are still investigational.","value_numeric":null},{"paper_doi":"10.1186/s13046-026-03785-5","tag_type":"warning","value":"The study is entirely preclinical (mouse models and human cell cultures); no patient outcomes data are reported. Clinical translatability is unproven.","value_numeric":null}],"summaries":{"what_studied":"This preclinical study tested whether tailored FcγR blockade — using either FcγRIIB-selective (Fc-silenced; BI-1607/αFcγRIIΔFc) or pan-FcγR-blocking (Fc-competent; BI-1206/αFcγRIIwt) antibodies — could enhance the efficacy of anti-CTLA-4 (ipilimumab) and anti-PD-1 (nivolumab, pembrolizumab) immune checkpoint therapies in syngeneic mouse tumor models (CT26, MC38, B16) and in human cell co-culture systems.","key_result":"FcγRIIB-selective blockade (αFcγRIIΔFc/BI-1607) boosted anti-CTLA-4 efficacy by increasing intratumoral Treg depletion, M1 myeloid reprogramming, IFN-γ/CXCL10 induction, and activated CD8+ T cells; it also enhanced low-dose ipilimumab (2 mg/kg) to match the efficacy of the toxic 10 mg/kg dose and extended activity to PD-1-resistant B16 tumors. Conversely, pan-FcγR blockade (αFcγRIIwt/BI-1206) enhanced anti-PD-1 efficacy by blocking macrophage phagocytosis of PD-1-coated CD8+ T cells, increasing intratumoral activated CD8+ T cells; it also overcame resistance to FcγR-engaging anti-PD-1 antibodies in vivo.","limitations":"- All efficacy data are from murine syngeneic tumor models and in vitro human cell systems; no clinical efficacy data are presented.\n- Several authors are employed by or financially tied to BioInvent International, the developer of BI-1206 and BI-1607, representing a significant conflict of interest.\n- Mouse models may not replicate the toxicity profile of high-dose αCTLA-4 in humans, limiting conclusions about safety separation.","practice_takeaway":"Combining FcγRIIB-selective blockade (BI-1607) with anti-CTLA-4, or pan-FcγR blockade (BI-1206) with anti-PD-1, may enhance checkpoint therapy efficacy through distinct mechanisms — but this remains preclinical; clinicians should watch for results from the ongoing trials (NCT06784648, NCT04219254)."}},{"doi":"10.1158/1078-0432.ccr-26-0481","pmid":"42478960","title":"Targeting CD24 Activates Macrophages to Reduce Tumor Burden in Preclinical Models of Solid Tumors","journal_title":"Clinical Cancer Research","journal_issn":"1078-0432","published_at":"2026-07-22T00:00:00.000Z","url":"https://doi.org/10.1158/1078-0432.ccr-26-0481","source_score":39,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-28T14:02:33.926Z","updated_at":"2026-07-28T14:02:33.926Z","tags":[{"paper_doi":"10.1158/1078-0432.ccr-26-0481","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1158/1078-0432.ccr-26-0481","tag_type":"category","value":"Oncology","value_numeric":null},{"paper_doi":"10.1158/1078-0432.ccr-26-0481","tag_type":"condition","value":"Solid Tumors","value_numeric":null},{"paper_doi":"10.1158/1078-0432.ccr-26-0481","tag_type":"generic","value":"PHST001","value_numeric":null},{"paper_doi":"10.1158/1078-0432.ccr-26-0481","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1158/1078-0432.ccr-26-0481","tag_type":"level_of_evidence","value":"6","value_numeric":null},{"paper_doi":"10.1158/1078-0432.ccr-26-0481","tag_type":"modality","value":"Anti-CD24 Monoclonal Antibody","value_numeric":null},{"paper_doi":"10.1158/1078-0432.ccr-26-0481","tag_type":"modality","value":"Immunotherapy","value_numeric":null},{"paper_doi":"10.1158/1078-0432.ccr-26-0481","tag_type":"study_design","value":"Preclinical Study","value_numeric":null},{"paper_doi":"10.1158/1078-0432.ccr-26-0481","tag_type":"warning","value":"All efficacy results are preclinical; the ongoing Phase I trial (NCT06840886) has not yet reported clinical outcomes.","value_numeric":null},{"paper_doi":"10.1158/1078-0432.ccr-26-0481","tag_type":"warning","value":"No sample size tag was applied as the paper does not report a specific aggregate N across experiments — individual model cohort sizes were not stated in the abstract or results excerpt.","value_numeric":null},{"paper_doi":"10.1158/1078-0432.ccr-26-0481","tag_type":"warning","value":"PHST001 is not yet an approved or established generic/INN name; it is a proprietary investigational compound designation used here as the generic identifier. No brand name has been assigned.","value_numeric":null},{"paper_doi":"10.1158/1078-0432.ccr-26-0481","tag_type":"warning","value":"Study design is labeled 'Preclinical Study' as the paper comprises in vitro, xenograft, and syngeneic animal experiments; the Phase I trial is described as ongoing only.","value_numeric":null}],"summaries":{"what_studied":"PHST001, a humanized IgG4 monoclonal antibody targeting CD24, was evaluated for its ability to block the CD24/Siglec-10 'don't eat me' axis and restore macrophage-mediated phagocytosis across multiple solid tumor types, using in vitro assays, xenograft and syngeneic mouse models, and ex vivo human tumor systems.","key_result":"PHST001 blocked Siglec-10 engagement, enhanced macrophage phagocytosis across tumor types, inhibited primary and metastatic tumor growth, and prolonged survival in preclinical models — both as monotherapy and combined with chemotherapy, radiotherapy, or ADCs; a favorable nonclinical safety profile was observed.","limitations":"All efficacy data are preclinical (in vitro, xenograft, syngeneic mouse); no human clinical efficacy data are yet available. Syngeneic models may not fully replicate human tumor immune microenvironments. The Phase I trial (NCT06840886) is ongoing, so safety and tolerability in humans remain unestablished.","practice_takeaway":"CD24 targeting with PHST001 shows broad preclinical anti-tumor activity and a clean nonclinical safety profile, supporting its entry into a Phase I trial for relapsed/refractory solid tumors. Clinicians treating heavily pretreated solid tumor patients may watch for early results from NCT06840886."}},{"doi":"10.1136/jitc-2026-014960","pmid":"42419878","title":"Unbiased avidity-based isolation of antigen-specific T cells","journal_title":"Journal for ImmunoTherapy of Cancer","journal_issn":"2051-1426","published_at":"2026-07-08T00:00:00.000Z","url":"https://doi.org/10.1136/jitc-2026-014960","source_score":23,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-14T13:24:15.132Z","updated_at":"2026-07-14T13:24:15.132Z","tags":[{"paper_doi":"10.1136/jitc-2026-014960","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1136/jitc-2026-014960","tag_type":"category","value":"Immunology","value_numeric":null},{"paper_doi":"10.1136/jitc-2026-014960","tag_type":"category","value":"Oncology","value_numeric":null},{"paper_doi":"10.1136/jitc-2026-014960","tag_type":"condition","value":"Non-Small Cell Lung Cancer","value_numeric":null},{"paper_doi":"10.1136/jitc-2026-014960","tag_type":"condition","value":"Solid Tumors","value_numeric":null},{"paper_doi":"10.1136/jitc-2026-014960","tag_type":"generic","value":"antigen-specific CD8+ T cells","value_numeric":null},{"paper_doi":"10.1136/jitc-2026-014960","tag_type":"generic","value":"tumor-infiltrating lymphocytes","value_numeric":null},{"paper_doi":"10.1136/jitc-2026-014960","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1136/jitc-2026-014960","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1136/jitc-2026-014960","tag_type":"modality","value":"Adoptive Cell Therapy","value_numeric":null},{"paper_doi":"10.1136/jitc-2026-014960","tag_type":"modality","value":"Microfluidic T Cell Isolation","value_numeric":null},{"paper_doi":"10.1136/jitc-2026-014960","tag_type":"modality","value":"TCR-Engineered T Cells","value_numeric":null},{"paper_doi":"10.1136/jitc-2026-014960","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1136/jitc-2026-014960","tag_type":"study_design","value":"Preclinical Experimental Study","value_numeric":null},{"paper_doi":"10.1136/jitc-2026-014960","tag_type":"warning","value":"No head-to-head comparison with current gold-standard isolation methods (e.g., MHC multimers, 4-1BB selection) was performed in this study.","value_numeric":null},{"paper_doi":"10.1136/jitc-2026-014960","tag_type":"warning","value":"Sample sizes are small (n=2 to n=4 independent microfluidic chips per experiment), limiting statistical confidence.","value_numeric":null},{"paper_doi":"10.1136/jitc-2026-014960","tag_type":"warning","value":"Study is entirely preclinical — murine transgenic models and TCR-engineered T cells from healthy donors; no patient-derived TIL or clinical outcome data are reported.","value_numeric":null},{"paper_doi":"10.1136/jitc-2026-014960","tag_type":"warning","value":"The 'impact_flag: practice_changing' tag reflects the platform's novel approach to antigen-agnostic T cell isolation, but clinical validation is pending.","value_numeric":null}],"summaries":{"what_studied":"ATTACH (Assessment of T cells Tethered to Antigen Class I Histocompatibility) is a microfluidic platform that uses controlled shear stress (1–3 dyne/cm²) and live tumor cells as a natural source of MHC-peptide complexes to isolate antigen-specific CD8+ T cells — evaluated in both murine (OT-I/LLC-JSP-OVA) and human (EGFR-, FOXM1-, HER2-TCR-T cell) systems without requiring prior antigen knowledge.","key_result":"ATTACH achieved up to **10-fold enrichment** of antigen-specific T cells and could detect clonotypes present at as low as **0.1% frequency** (1:1000 ratio); FOXM1-specific cells were enriched 4.4-fold (p=0.0084) at a 5:1 non-specific:specific input ratio; anti-tumor (HER2) responses were largely preserved (~100%) while anti-viral (CEF) bystander responses were depleted to ~4–22% in the retained fraction, confirmed by IFN-γ ELISpot.","limitations":"- T cell attachment relies on stochastic cell–cell encounters; not all antigen-specific T cells form stable contacts, so some are lost during shear stress application.\n- Platform performance depends on target cell viability and HLA/antigen expression levels, which may be variable in patient-derived samples.\n- Autologous tumor cell lines are scarce in clinical settings, limiting direct translation to patient care.","practice_takeaway":"ATTACH offers a rapid, equipment-light method to enrich rare tumor-reactive CD8+ T cells from heterogeneous TIL populations — without needing to know the target antigen in advance — which could improve the purity and potency of TIL infusion products for solid tumor ACT. Recovered T cells retain functional competence, supporting their use in downstream cellular therapy workflows."}},{"doi":"10.1038/s41577-026-01322-1","pmid":"42393377","title":"A guide to CAR T cell therapies: development, current status and future prospects","journal_title":"Nature Reviews Immunology","journal_issn":"1474-1733","published_at":"2026-07-02T00:00:00.000Z","url":"https://doi.org/10.1038/s41577-026-01322-1","source_score":30,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-09T13:36:02.269Z","updated_at":"2026-07-09T13:36:02.269Z","tags":[{"paper_doi":"10.1038/s41577-026-01322-1","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01322-1","tag_type":"category","value":"Immunology","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01322-1","tag_type":"condition","value":"Autoimmune Disease","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01322-1","tag_type":"condition","value":"B Cell Leukemia","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01322-1","tag_type":"condition","value":"B Cell Lymphoma","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01322-1","tag_type":"condition","value":"Multiple Myeloma","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01322-1","tag_type":"condition","value":"Solid Tumors","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01322-1","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01322-1","tag_type":"level_of_evidence","value":"7","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01322-1","tag_type":"modality","value":"Allogeneic Cell Therapy","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01322-1","tag_type":"modality","value":"CAR T Cell Therapy","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01322-1","tag_type":"modality","value":"Gene Editing","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01322-1","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01322-1","tag_type":"warning","value":"No sample size tag was applied as this is a review article with no single study population.","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01322-1","tag_type":"warning","value":"The DOI references a 2026 publication; this is treated as accurate per the today's date context provided.","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01322-1","tag_type":"warning","value":"The full text pages were not readable from the provided PDF extraction — all page content was blank. Summary and tags are based solely on the abstract. Specific trial data, cited studies, and detailed arguments within the review could not be verified.","value_numeric":null}],"summaries":{"what_studied":"This review covers the development, current clinical status, and future directions of chimeric antigen receptor (CAR) T cell therapies — from foundational discoveries through approved indications (B cell malignancies, multiple myeloma) to next-generation designs targeting autoimmune disease and solid tumours.","key_result":"CAR T cell therapy has achieved durable remissions in B cell leukaemias, lymphomas, and multiple myeloma since first approval in 2017; next-generation strategies (gene editing, allogeneic manufacturing, in vivo delivery, multi-antigen targeting) aim to overcome antigen heterogeneity, tumour microenvironment barriers, and poor long-term persistence.","limitations":"Full text content was not extractable from the PDF (pages appear blank in the source), so specific clinical data, trial results, and nuanced arguments within the review could not be verified or summarized in detail.","practice_takeaway":"CAR T cell therapy is now an established option for relapsed/refractory B cell malignancies and multiple myeloma; clinicians should watch emerging data on allogeneic ('off-the-shelf') products and CAR T use in autoimmune diseases, which may soon broaden eligible patient populations."}},{"doi":"10.1038/s43018-026-01174-7","pmid":"42156983","title":"Targeting cysteinyl leukotriene receptor 1 reprograms tumor-promoting myelopoiesis and overcomes immune checkpoint therapy resistance","journal_title":"Nature Cancer","journal_issn":"2662-1347","published_at":"2026-05-19T00:00:00.000Z","url":"https://doi.org/10.1038/s43018-026-01174-7","source_score":325,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-23T13:24:56.414Z","updated_at":"2026-05-23T13:24:56.414Z","tags":[{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"brand","value":"Montelukast","value_numeric":null},{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"category","value":"Oncology","value_numeric":null},{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"condition","value":"Breast Cancer","value_numeric":null},{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"condition","value":"Colorectal Cancer","value_numeric":null},{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"condition","value":"Lung Cancer","value_numeric":null},{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"condition","value":"Melanoma","value_numeric":null},{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"condition","value":"Solid Tumors","value_numeric":null},{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"generic","value":"montelukast","value_numeric":null},{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"modality","value":"Immune Checkpoint Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"modality","value":"Leukotriene Receptor Antagonist","value_numeric":null},{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"sample_size","value":"n=8","value_numeric":8},{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"study_design","value":"Preclinical Animal Study","value_numeric":null},{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"warning","value":"Sample sizes per cohort are small (n=4–8 mice), which is standard for preclinical work but limits statistical power.","value_numeric":null},{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"warning","value":"The paper is dated May 2026 and is listed as supplementary/unedited format; the main figures and quantitative outcomes referenced throughout are not fully reproduced in the provided full text (only supplementary materials are shown).","value_numeric":null},{"paper_doi":"10.1038/s43018-026-01174-7","tag_type":"warning","value":"The 'practice_changing' impact flag is applied cautiously — all data are preclinical (mouse models); no human trial data exist yet. The flag reflects high translational potential, not current clinical evidence.","value_numeric":null}],"summaries":{"what_studied":"This preclinical study evaluated whether targeting cysteinyl leukotriene receptor 1 (CysLTR1) — a receptor known in asthma — can reverse tumor-promoting 'emergency' myelopoiesis (specifically immunosuppressive PMN-MDSCs/neutrophils) and overcome anti-PD1 resistance across multiple mouse tumor models.","key_result":"Genetic deletion or pharmacological blockade of CysLTR1 reduced tumor growth and enhanced antitumor immunity in EMT6, E0771, CT26, YUMMER1.7, MC38, and other syngeneic mouse models (n=4–8 per cohort). CysLTR1 inhibition reprogrammed granulopoiesis via transcription factors MXD1 and NFE2, shifting neutrophils toward an antitumor (N1-like) phenotype and overcoming anti-PD1 resistance. The effect required CD8+ T cells and was linked to de novo granule cargo reprogramming.","limitations":"- All tumor efficacy data are from mouse models only; no human clinical trial data are presented.\n- Pharmacological inhibition used montelukast (a clinically available CysLT1 antagonist) at doses/schedules not yet validated in oncology patients.\n- Findings rely heavily on single mouse tumor cell lines per strain, limiting generalizability across tumor microenvironments.","practice_takeaway":"CysLTR1 antagonists like montelukast — already approved for asthma — may have a near-term translational opportunity as add-on therapy to anti-PD1 in solid tumors, but clinical validation is needed before any practice change."}},{"doi":"10.1038/s41590-026-02505-7","pmid":"42156893","title":"Differential assembly of mouse and human tumor microenvironments","journal_title":"Nature Immunology","journal_issn":"1529-2908","published_at":"2026-05-19T00:00:00.000Z","url":"https://doi.org/10.1038/s41590-026-02505-7","source_score":32,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-23T13:24:54.368Z","updated_at":"2026-05-23T13:24:54.368Z","tags":[{"paper_doi":"10.1038/s41590-026-02505-7","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1038/s41590-026-02505-7","tag_type":"category","value":"Immunology","value_numeric":null},{"paper_doi":"10.1038/s41590-026-02505-7","tag_type":"condition","value":"Cancer","value_numeric":null},{"paper_doi":"10.1038/s41590-026-02505-7","tag_type":"condition","value":"Solid Tumors","value_numeric":null},{"paper_doi":"10.1038/s41590-026-02505-7","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1038/s41590-026-02505-7","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1038/s41590-026-02505-7","tag_type":"modality","value":"Tumor Microenvironment Immunoprofiling","value_numeric":null},{"paper_doi":"10.1038/s41590-026-02505-7","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1038/s41590-026-02505-7","tag_type":"study_design","value":"Comparative Immunoprofiling Study","value_numeric":null},{"paper_doi":"10.1038/s41590-026-02505-7","tag_type":"warning","value":"No explicit sample size (number of human or mouse tumor specimens) was reported in the abstract; a sample_size tag was omitted.","value_numeric":null},{"paper_doi":"10.1038/s41590-026-02505-7","tag_type":"warning","value":"Study design is described as 'systematic immunoprofiling' across 15 mouse models — this is a comparative/observational profiling study, not a clinical trial; level of evidence is estimated accordingly.","value_numeric":null},{"paper_doi":"10.1038/s41590-026-02505-7","tag_type":"warning","value":"The full text of the paper was not accessible — only the abstract was extractable. All structured data is derived solely from the abstract. Specific quantitative findings, cohort sizes, statistical methods, and cancer type breakdowns could not be verified.","value_numeric":null}],"summaries":{"what_studied":"Systematic immunoprofiling of 15 commonly used mouse tumor models compared to human tumors, examining how well murine tumor microenvironments (TMEs) recapitulate human TME composition, chemokine networks, and immune cell frequencies.","key_result":"Most murine TMEs resemble poorly infiltrated human tumors, with heavy macrophage bias; species-specific chemokine expression networks and discoordinated T cell/myeloid subtype frequencies were identified, though a conserved interferon-responsive myeloid–T cell cytotoxicity axis was found to predict clinical outcome across tissue types.","limitations":"Full text body was not extractable from the PDF (only abstract metadata retrieved), limiting verification of specific quantitative results, statistical methods, and patient cohort details. Findings rely on mouse model generalizability to human disease, which is the very limitation being studied.","practice_takeaway":"Clinicians and researchers should be cautious when translating mouse TME findings to human cancer immunotherapy trials, as most mouse models skew toward macrophage-rich, T cell-poor environments unlike many human tumors. The conserved interferon-responsive myeloid–cytotoxic T cell axis may, however, serve as a reliable cross-species biomarker for clinical outcome."}},{"doi":"10.1001/jamaoncol.2026.1036","pmid":"42096237","title":"Tumor-Infiltrating Clonal Hematopoiesis and Pan-Cancer Prognosis in Patients With Solid Tumors","journal_title":"JAMA Oncology","journal_issn":"2374-2437","published_at":"2026-05-07T00:00:00.000Z","url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC13154032/","source_score":26,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-16T13:22:24.323Z","updated_at":"2026-05-16T13:22:24.323Z","tags":[{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"category","value":"Oncology","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"condition","value":"Breast Cancer","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"condition","value":"Clonal Hematopoiesis","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"condition","value":"Endometrial Cancer","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"condition","value":"Solid Tumors","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"modality","value":"Whole-Genome Sequencing","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"sample_size","value":"n=10571","value_numeric":10571},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"study_design","value":"Retrospective Cohort Study","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"warning","value":"Full paper text was not accessible; summary is based solely on the abstract and results excerpt. Details on multivariate model covariates, subgroup sample sizes, and follow-up duration could not be verified.","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"warning","value":"The impact_flag 'practice_changing' reflects the potential clinical utility of TI-CH as a prognostic biomarker, but prospective validation is still needed before routine clinical implementation.","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1036","tag_type":"warning","value":"The study population was 60.83% female, which may reflect enrichment for breast and endometrial cancer; generalizability to other solid tumors or more balanced sex distributions is uncertain.","value_numeric":null}],"summaries":{"what_studied":"This retrospective cohort study used whole-genome sequencing data from 10,571 solid tumor patients in the Genomics England 100,000 Genomes Project (2015–2019) to assess the prevalence of tumor-infiltrating clonal hematopoiesis (TI-CH) — defined by somatic variants in 74 driver genes at 2–30% VAF in tumor tissue — and its association with clinical factors and overall survival (OS).","key_result":"TI-CH was detected in 18.38% of patients (n=1,943); it was linked to older age (OR 1.15) and prior cytotoxic chemotherapy (OR 1.24). TI-CH was independently associated with worse pan-cancer OS (HR 1.13), with the strongest signal in breast cancer (HR 1.95). Gene-level analysis flagged GATA2 variants for pan-cancer mortality (HR 3.00) and TET2 variants for breast cancer mortality (HR 2.92).","limitations":"- Retrospective design limits causal inference between TI-CH and survival outcomes.\n- Full paper text was inaccessible; details on confounding adjustment and subgroup sample sizes are incomplete.\n- TI-CH detection relied on a predefined 74-gene panel and a VAF threshold of 2–30%, which may miss variants outside this range.","practice_takeaway":"Clinicians should be aware that TI-CH — especially GATA2 and TET2 variants — may serve as an adverse prognostic biomarker in solid tumors, particularly breast cancer. Older patients and those receiving cytotoxic chemotherapy are at higher odds of harboring TI-CH, which may warrant prospective integration into tumor sequencing workflows."}},{"doi":"10.1200/jco-25-01546","pmid":"41604598","title":"Efficacy and Safety of Ultra-Low-Dose Immunotherapy in Relapsed Refractory Solid Tumors: Phase III Superiority Randomized Trial (DELII)","journal_title":"Journal of Clinical Oncology","journal_issn":"0732-183X","published_at":"2026-01-28T00:00:00.000Z","url":"https://doi.org/10.1200/jco-25-01546","source_score":99,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-20T13:23:31.296Z","updated_at":"2026-05-20T13:23:31.296Z","tags":[{"paper_doi":"10.1200/jco-25-01546","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1200/jco-25-01546","tag_type":"brand","value":"Opdivo","value_numeric":null},{"paper_doi":"10.1200/jco-25-01546","tag_type":"category","value":"Oncology","value_numeric":null},{"paper_doi":"10.1200/jco-25-01546","tag_type":"condition","value":"Head And Neck Cancer","value_numeric":null},{"paper_doi":"10.1200/jco-25-01546","tag_type":"condition","value":"Lung Cancer","value_numeric":null},{"paper_doi":"10.1200/jco-25-01546","tag_type":"condition","value":"Solid Tumors","value_numeric":null},{"paper_doi":"10.1200/jco-25-01546","tag_type":"generic","value":"docetaxel","value_numeric":null},{"paper_doi":"10.1200/jco-25-01546","tag_type":"generic","value":"nivolumab","value_numeric":null},{"paper_doi":"10.1200/jco-25-01546","tag_type":"generic","value":"paclitaxel","value_numeric":null},{"paper_doi":"10.1200/jco-25-01546","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1200/jco-25-01546","tag_type":"level_of_evidence","value":"1","value_numeric":null},{"paper_doi":"10.1200/jco-25-01546","tag_type":"modality","value":"Chemotherapy","value_numeric":null},{"paper_doi":"10.1200/jco-25-01546","tag_type":"modality","value":"Immune Checkpoint Inhibitor","value_numeric":null},{"paper_doi":"10.1200/jco-25-01546","tag_type":"sample_size","value":"n=500","value_numeric":500},{"paper_doi":"10.1200/jco-25-01546","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1200/jco-25-01546","tag_type":"study_design","value":"Randomized Controlled Trial","value_numeric":null},{"paper_doi":"10.1200/jco-25-01546","tag_type":"warning","value":"No PD-L1 or other predictive biomarker subgroup data were reported in the abstract; the OS benefit may be driven by a biomarker-enriched subset.","value_numeric":null},{"paper_doi":"10.1200/jco-25-01546","tag_type":"warning","value":"The 'impact_flag: practice_changing' designation reflects the Phase III superiority design and statistically significant OS benefit, but the modest absolute gain (~1.2 months) and lack of PFS benefit warrant cautious interpretation.","value_numeric":null},{"paper_doi":"10.1200/jco-25-01546","tag_type":"warning","value":"The paper is published with a 2026-01-28 date but the DOI resolves to a JCO article; the trial appears to be a real Phase III trial (DELII), but clinicians should verify final published data as this may be an ahead-of-print version.","value_numeric":null},{"paper_doi":"10.1200/jco-25-01546","tag_type":"warning","value":"Tumor histology mix (predominantly head & neck and lung) limits applicability to other solid tumor types not well represented in this trial.","value_numeric":null}],"summaries":{"what_studied":"Phase III randomized superiority trial (DELII) comparing ultra-low-dose nivolumab (20 mg IV q2w) vs. standard chemotherapy (docetaxel or paclitaxel) in 500 adults with relapsed/refractory advanced solid tumors (ECOG 0–1, ≥1 prior line), enrolled June 2020–February 2024; primary endpoint was overall survival (OS).","key_result":"Median OS was significantly longer with ultra-low-dose nivolumab vs. chemotherapy (5.88 vs. 4.70 months; HR 0.80 [95% CI 0.66–0.97]; P=.022); 1-year OS 27.3% vs. 16.9%. PFS was similar between arms (2.04 vs. 2.09 months; HR 1.03; P=.77). Grade ≥3 treatment-related adverse events were less frequent with nivolumab (42.5% vs. 60.8%; P<.001), and QoL favored nivolumab.","limitations":"- Heterogeneous tumor types (52% head & neck, 36% lung) limit generalizability to other cancers.\n- No biomarker-stratified analysis (e.g., PD-L1 expression) reported, making it unclear which subgroups drive the OS benefit.\n- Median OS benefit is modest (~1.2 months), and PFS did not differ, raising questions about the mechanism of late survival separation.","practice_takeaway":"Ultra-low-dose nivolumab (20 mg q2w) may be a viable alternative to second-line chemotherapy in pretreated solid tumors, offering a small but significant OS advantage and a better toxicity and QoL profile. Clinicians should consider this option especially in resource-limited settings where standard ICI dosing costs are prohibitive."}},{"doi":"10.1001/jamaoncol.2025.5785","pmid":"41505144","title":"Clonal Hematopoiesis and Cardiovascular Disease Risk After Cancer Therapy in Patients With Solid Tumors","journal_title":"JAMA Oncology","journal_issn":"2374-2437","published_at":"2026-01-08T00:00:00.000Z","url":"https://doi.org/10.1001/jamaoncol.2025.5785","source_score":78,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2026-01-11","doi":"10.1001/jamaoncol.2025.5785","days":"7","issn":"2374-2437","rank":"4","field":"Clinical Medicine","score":"78","category":"Oncology","categories":["Oncology"],"_categories":["Oncology"]},"pubmed":{"doi":"10.1001/jamaoncol.2025.5785","title":"Clonal Hematopoiesis and Cardiovascular Disease Risk After Cancer Therapy in Patients With Solid Tumors.","journal":"JAMA oncology","methods":"","results":"Among 8004 eligible participants (median [IQR] age, 61.9 [52.2-69.9] years; 4385 female individuals [54.8%]) with a primary solid tumor diagnosis, 7438 had no heart failure, 7392 no ischemic CVD, and 6002 no arrhythmia before cancer therapy. Overall, 549 (6.9%) had CHIP. In the propensity score-matched cohort, participants with CHIP had a significantly higher 10-year cumulative incidence of heart failure (20.3%; 95% CI, 16.0%-24.4% vs 14.5%; 95% CI, 13.5%-15.6%; P = .001) and ischemic CVD (25.3%; 95% CI, 20.5%-30.0% vs 18.5%; 95% CI, 17.3%-20.0%; P < .001) compared with those without CHIP. In adjusted Fine-Gray models, CHIP was associated with increased risk of heart failure (subdistribution hazard ratio [sHR], 1.26; 95% CI, 1.02-1.56; P = .03). In an exploratory 24-month landmark analysis, there was a statistically significant interaction between CHIP and intensive chemotherapy (≥7 cycles) on heart failure risk (sHR, 1.02; 95% CI, 1.00-1.04; P = .03).","abstract":"$30","keywords":[],"pubmed_id":"41505144","conclusions":"","publication_date":"2026-01-08T00:00:00"},"crossref":{"DOI":"10.1001/jamaoncol.2025.5785","URL":"https://doi.org/10.1001/jamaoncol.2025.5785","ISSN":["2374-2437"],"link":[{"URL":"https://jamanetwork.com/journals/jamaoncology/articlepdf/2843268/jamaoncology_shyr_2026_oi_250080_1766168135.11316.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["Clonal Hematopoiesis and Cardiovascular Disease Risk After Cancer Therapy in Patients With Solid Tumors"],"author":[{"given":"Derek","family":"Shyr","sequence":"first","affiliation":[{"name":"Heersink School of Medicine, The University of Alabama at Birmingham, Birmingham"},{"name":"Division of Genetic Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Yash","family":"Pershad","sequence":"additional","affiliation":[{"name":"Division of Genetic Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Kun","family":"Zhao","sequence":"additional","affiliation":[{"name":"Division of Genetic Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Ashwin","family":"Kishtagari","sequence":"additional","affiliation":[{"name":"Division of Hematology Oncology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Robert W.","family":"Corty","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Eric","family":"Shinohara","sequence":"additional","affiliation":[{"name":"Department of Radiation Oncology, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"Ben Ho","family":"Park","sequence":"additional","affiliation":[{"name":"Division of Hematology Oncology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee"}]},{"given":"J. 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propensity score–matched analyses showed higher 10-year cumulative incidence with CHIP vs no CHIP for heart failure (20.3% vs 14.5%; P=.001) and ischemic CVD (25.3% vs 18.5%; P<.001). Adjusted Fine–Gray models found increased heart failure risk with CHIP (sHR 1.26; 95% CI, 1.02–1.56; P=.03), and an exploratory 24‑month landmark showed a CHIP×intensive chemotherapy (≥7 cycles) interaction (sHR 1.02; 95% CI, 1.00–1.04; P=.03).","limitations":"Single-center biobank cohort using EHR-linked genomic data limits generalizability. Results are observational despite propensity matching, and the chemotherapy interaction arose from an exploratory landmark analysis.","practice_takeaway":"In adults with solid tumors receiving cancer therapy, CHIP marks higher 10-year risk of heart failure and ischemic CVD. 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Patient populations and detailed timeframes beyond 'past 12 years' are not specified.","practice_takeaway":"T cell engagers are now an established modality with multiple approvals, especially in hematologic cancers, and show emerging activity in solid tumors and autoimmune disease. When using these agents, clinicians should consult this review for targets, dosing, schedules, common side effects, and mitigation strategies."}}],"initialOffset":12,"fetchConfig":{"kind":"tags","tags":[{"tag_type":"condition","value":"Solid Tumors"}]},"breadcrumbItems":[{"name":"Home","href":"/"},{"name":"Research Hub","href":"/hub"},{"name":"Conditions","href":"/hub/tag/condition"},{"name":"Solid Tumors"}],"hrefConfig":{"basePath":"/hub/papers","webViewQueryParams":{"hub_ctx":"tag","hub_tag_type":"condition","hub_tag_value":"Solid Tumors"}}}]]

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