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:T780,The continuous development of new imaging approaches, molecular phenotyping, genetic subtypes, prognosis assessments, and effective therapies across a range of disease states has created a need to redefine terminology and best practices for clinical trial conduct in patients with advanced prostate cancer. We convened an international expert committee of diverse working groups, the Prostate Cancer Working Group 4 (PCWG4), between 2016 and 2025. Our objective was to formulate updated criteria based on emerging evidence and clinical trial data in a biomarker context to provide guidance for clinical trial design, eligibility, and end point assessments for patients with advanced prostate cancer. PCWG4 redefines terminology around the disease state and previous therapies in a patient-centric context and terminology focused on androgen pathway modulation. We consider imaging, with a particular focus on positron emission tomography (PET)-defined disease. New recommendations are provided for disease state terminology, defining eligibility criteria, response and delay/prevent end points, intervals for reassessments including imaging, and patient-reported outcome determination. We provide recommendations in a biomarker-based context of use for the intended indication, reflective of patient benefit for specific interventions. We emphasize the need for development of validated PET imaging and molecular and phenotypic criteria as well as trial designs to appropriately risk stratify patients, predict and assess benefit, and measure post-treatment outcomes reliably in a trial framework. PCWG4 updates recommendations on patient and tumor characterization, therapy development, and imaging criteria and extends guidance into earlier androgen pathway modulator-naïve/sensitive disease states to reflect an evolving, heterogeneous, and diverse patient population to optimize treatment benefits for all patients.31:T9c9, PURPOSE The continuous development of new imaging approaches, molecular phenotyping, genetic subtypes, prognosis assessments, and effective therapies across a range of disease states has created a need to redefine terminology and best practices for clinical trial conduct in patients with advanced prostate cancer. METHODS We convened an international expert committee of diverse working groups, the Prostate Cancer Working Group 4 (PCWG4), between 2016 and 2025. Our objective was to formulate updated criteria based on emerging evidence and clinical trial data in a biomarker context to provide guidance for clinical trial design, eligibility, and end point assessments for patients with advanced prostate cancer. RESULTS PCWG4 redefines terminology around the disease state and previous therapies in a patient-centric context and terminology focused on androgen pathway modulation. We consider imaging, with a particular focus on positron emission tomography (PET)–defined disease. New recommendations are provided for disease state terminology, defining eligibility criteria, response and delay/prevent end points, intervals for reassessments including imaging, and patient-reported outcome determination. We provide recommendations in a biomarker-based context of use for the intended indication, reflective of patient benefit for specific interventions. We emphasize the need for development of validated PET imaging and molecular and phenotypic criteria as well as trial designs to appropriately risk stratify patients, predict and assess benefit, and measure post-treatment outcomes reliably in a trial framework. CONCLUSION PCWG4 updates recommendations on patient and tumor characterization, therapy development, and imaging criteria and extends guidance into earlier androgen pathway modulator–naïve/sensitive disease states to reflect an evolving, heterogeneous, and diverse patient population to optimize treatment benefits for all patients. 32:T635,To provide guidance on the recommended management of cancer in pregnant patients. A multidisciplinary Expert Panel convened and conducted a systematic review of the literature. The systematic review identified 450 eligible studies. Much of the evidence consisted of observational data, case series, and case reports. Management of cancer during pregnancy should be grounded in a values-based informed-consent process outlining maternal and fetal risks and anticipated benefits. Diagnostic evaluation should follow the as low as reasonably achievable (ALARA) principle, with timing of diagnostic studies individualized based on urgency of cancer detection, potential dangers of delay, and the balance of risks to both the pregnant patient and her embryo or fetus. Due to significant risk of harm to the developing embryo and/or fetus, systemic therapy should be deferred until the second trimester. Methotrexate, hormonal therapies, human epidermal growth factor receptor 2-targeted agents, vascular endothelial growth factor and poly (ADP-ribose) polymerase inhibitors, antibody-drug conjugates, and all cellular therapies are contraindicated during pregnancy, regardless of gestational age. For patients who wish to continue their pregnancy, delivery should be planned at or after 37 weeks, with the final chemotherapy dose scheduled 2-4 weeks before birth. Referral to psychosocial support services is essential to address emotional and practical challenges, reduce distress, and support shared decision making.Additional information is available at www.asco.org/survivorship-guidelines.33:T11ae, ASCO Guidelines provide recommendations with comprehensive review and analyses of the relevant literature for each recommendation, following the guideline development process as outlined in the

ASCO Guidelines Methodology Manual

. ASCO Guidelines follow the ASCO Conflict of Interest Policy for Clinical Practice Guidelines . Clinical Practice Guidelines and other guidance (“Guidance”) provided by ASCO is not a comprehensive or definitive guide to treatment options. It is intended for voluntary use by clinicians and should be used in conjunction with independent professional judgment. Guidance may not be applicable to all patients, interventions, diseases or stages of diseases. Guidance is based on review and analysis of relevant literature, and is not intended as a statement of the standard of care. ASCO does not endorse third-party drugs, devices, services, or therapies and assumes no responsibility for any harm arising from or related to the use of this information. See complete disclaimer in Appendix 1 and Appendix 2 (online only) for more. PURPOSE To provide guidance on the recommended management of cancer in pregnant patients. METHODS A multidisciplinary Expert Panel convened and conducted a systematic review of the literature. RESULTS The systematic review identified 450 eligible studies. Much of the evidence consisted of observational data, case series, and case reports. RECOMMENDATIONS Management of cancer during pregnancy should be grounded in a values-based informed-consent process outlining maternal and fetal risks and anticipated benefits. Diagnostic evaluation should follow the as low as reasonably achievable (ALARA) principle, with timing of diagnostic studies individualized based on urgency of cancer detection, potential dangers of delay, and the balance of risks to both the pregnant patient and her embryo or fetus. Due to significant risk of harm to the developing embryo and/or fetus, systemic therapy should be deferred until the second trimester. Methotrexate, hormonal therapies, human epidermal growth factor receptor 2–targeted agents, vascular endothelial growth factor and poly (ADP-ribose) polymerase inhibitors, antibody-drug conjugates, and all cellular therapies are contraindicated during pregnancy, regardless of gestational age. For patients who wish to continue their pregnancy, delivery should be planned at or after 37 weeks, with the final chemotherapy dose scheduled 2-4 weeks before birth. Referral to psychosocial support services is essential to address emotional and practical challenges, reduce distress, and support shared decision making. Additional information is available at www.asco.org/survivorship-guidelines . 34:T63a,Historically, systemic therapy for hormone-sensitive prostate cancer (HSPC) was predicated on androgen-deprivation therapy (ADT) alone. However, in the past decade, substantial improvements have been made by intensifying treatment based on a better understanding of the broad underlying biology of these cancers. The addition of androgen receptor pathway inhibitors (ARPIs), docetaxel and/or radiotherapy to ADT is of proven benefit in certain patient subgroups, whereas AKT inhibitors, radioligand therapies and poly ADP-ribose polymerase (PARP) inhibitors are being evaluated in patients with metastatic HSPC. The clinical states of HSPC are determined by a history of localized prostate cancer versus presentation with de novo metastatic disease, as well as the extent of disease on conventional computed tomography imaging and whole-body bone scintigraphy. However, modern nuclear imaging modalities such as prostate-specific membrane antigen PET can visualize metastases below the limit of detection of computed tomography and whole-body bone scintigraphy; this earlier and more precise detection of metastases has identified new subgroups of patients for which certain treatment approaches, such as adding docetaxel to ADT plus an ARPI, might or might not apply. In this Review, we discuss the personalized management of both non-metastatic and metastatic HSPC, including how to select patients for docetaxel, choice of ARPI and use of radiotherapy to primary and metastatic disease sites. We also discuss emerging novel therapies and important principles of toxicity mitigation for HSPC.35:T628,L.M.B. is a member of the ANZUP Scientific Advisory Committee (unpaid). L.E. reports research grant support (to institution) from Clarity Pharma and Novartis and consulting fees for lectures or advisory boards from Advancell, Astellas, AstraZeneca, Clarity Pharma, Janssen, Novartis and Telix in the past 5 years. C.J.S. declares roles as principal investigator of the CHAARTED trial, study co-chair of the ENZAMET trial and is a member of the ANZUP Scientific Advisory Committee (unpaid); research funding (to institution) from Astellas, Bayer, Janssen, Pfizer and Sanofi; compensated advisory roles for Astellas, Bayer, Genentech/Roche, Hengrui, Janssen, Lilly, Novartis, Pfizer, PointBiopharma and Sanofi; and stock ownership in Leuchemix. C.J.S also holds patents for parthenolide as an anticancer agent, co-authored with H. Nakshatri (WO0145699A1, owned by Indiana University); for use of the drug combination of abiraterone and cabozantinib to treat prostate cancer, co-authors with P. Kantoff (WO 2014/165770 A1 owned by Exelixis); for compositions and methods for screening and diagnosis of prostate cancer with KDM5D biomarker, co-authored with P. Kantoff, G.-S. Mary Lee and K. Komura (WO2017/117486 A1, owned by Dana-Farber Cancer Institute); for compositions and methods for screening and identifying clinically aggressive prostate cancer with SNPs and ZFP36, co-authored with C. Huttenhower, T. Gerke, L. Mucci, G.-S. Mary Lee and D. Bornigen (WO2017127696A, owned by Harvard University and Dana-Farber Cancer Institute). M.A.C. declares no competing interests.25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"PARP Inhibitor: modality Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on PARP Inhibitor (modality). Clinician-written summaries and actionable practice insights. 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the journal labels it a 'Review article' but no systematic search methodology is described.","value_numeric":null},{"paper_doi":"10.1038/s41575-026-01250-4","tag_type":"warning","value":"The 'mixed' age group tag reflects the preclinical (mouse) focus of the supporting studies; human patient age distribution is not reported.","value_numeric":null},{"paper_doi":"10.1038/s41575-026-01250-4","tag_type":"warning","value":"This is a narrative review with a supplemental preclinical data table — it includes no original clinical trial data, so level of evidence reflects expert opinion/review only.","value_numeric":null}],"summaries":{"what_studied":"This review evaluates the rationale, challenges, and opportunities for combining radiation therapy (RT) with immunotherapy (IT) in localized pancreatic ductal adenocarcinoma (PDAC), drawing on preclinical mouse model data across >30 studies to identify optimal RT backbones and immunotherapy strategies.","key_result":"Preclinical evidence consistently shows that RT-IT combinations — including checkpoint inhibitors, CD40 agonists, CAR T cells, STING agonists, and stromal-targeting agents — can improve local and systemic tumor control in PDAC models; however, efficacy is highly dependent on RT dose/fractionation, IT type, delivery sequence, and tumor microenvironment (TME) context (e.g., orthotopic vs. heterotopic location).","limitations":"- All supporting studies are from preclinical mouse PDAC models; no clinical trial data are presented or synthesized.\n- Heterotopic and orthotopic models differ substantially in TME and therapeutic response, limiting direct clinical translation.\n- The review does not report patient-level outcomes, effect sizes, or formal evidence grading.","practice_takeaway":"Clinicians should be aware that RT is being reconsidered as an immunological platform in PDAC — not just a cytotoxic tool — but no RT-IT combination has yet shown survival benefit in patients with localized PDAC; enrollment in clinical trials testing these combinations remains the priority."}},{"doi":"10.1016/j.ygyno.2026.07.023","pmid":"42623963","title":"Comparing niraparib versus platinum-taxane doublet chemotherapy as neoadjuvant treatment in patients with newly diagnosed homologous recombination–deficient stage III/IV ovarian cancer: Findings from cohort C of the OPAL phase 2 trial","journal_title":"Gynecologic Oncology","journal_issn":"0090-8258","published_at":"2026-08-20T00:00:00.000Z","url":"https://doi.org/10.1016/j.ygyno.2026.07.023","source_score":1,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-25T06:20:16.755Z","updated_at":"2026-08-25T06:20:16.755Z","tags":[{"paper_doi":"10.1016/j.ygyno.2026.07.023","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.07.023","tag_type":"category","value":"Obstetrics & Gynecology","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.07.023","tag_type":"condition","value":"Homologous Recombination Deficiency","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.07.023","tag_type":"condition","value":"Ovarian Cancer","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.07.023","tag_type":"generic","value":"carboplatin","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.07.023","tag_type":"generic","value":"niraparib","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.07.023","tag_type":"generic","value":"paclitaxel","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.07.023","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.07.023","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.07.023","tag_type":"modality","value":"PARP Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.07.023","tag_type":"modality","value":"Platinum-Based Chemotherapy","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.07.023","tag_type":"modality","value":"Taxane","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.07.023","tag_type":"sample_size","value":"n=36","value_numeric":36},{"paper_doi":"10.1016/j.ygyno.2026.07.023","tag_type":"sex","value":"female","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.07.023","tag_type":"study_design","value":"Randomized Controlled Trial","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.07.023","tag_type":"warning","value":"The 'practice_changing' impact flag is applied in the negative direction — this trial argues against a new approach rather than establishing one, which is an important distinction for clinical interpretation.","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.07.023","tag_type":"warning","value":"The primary endpoint used an 80% confidence interval rather than the conventional 95%, which may overstate precision of the treatment difference estimate.","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.07.023","tag_type":"warning","value":"Trial was stopped early for futility with only 36 of a planned larger cohort enrolled, substantially limiting power and the reliability of safety comparisons.","value_numeric":null}],"summaries":{"what_studied":"This phase 2 RCT (OPAL cohort C) compared neoadjuvant niraparib vs. platinum-taxane doublet chemotherapy in adults with newly diagnosed HRd stage III/IV ovarian cancer (n=36), with pre-IDS overall response rate (ORR) per RECIST v1.1 as the primary endpoint.","key_result":"Pre-IDS unconfirmed ORR was 31.6% with niraparib vs. 70.6% with platinum-taxane (difference: −39.0%, 80% CI −56.8% to −17.7%), favoring chemotherapy; the trial was closed early for futility. Grade ≥3 adverse events occurred in 42% (niraparib) vs. 59% (platinum-taxane); no fatal serious adverse events in either arm.","limitations":"- Very small sample size (n=36) after early termination limits statistical power and generalizability.\n- All responses were partial (no complete responses in either arm), and ORR was unconfirmed/investigator-assessed, introducing potential measurement bias.\n- 80% CI (not 95%) was used for the primary endpoint comparison, which is unconventional and reduces inferential strength.","practice_takeaway":"Neoadjuvant niraparib should not replace platinum-taxane chemotherapy in HRd advanced ovarian cancer—response rates were markedly lower and the trial was stopped early for futility. Standard neoadjuvant platinum-based chemotherapy remains the treatment of choice in this setting."}},{"doi":"10.1016/j.euo.2026.07.014","pmid":"42595654","title":"Efficacy of Olaparib Plus Abiraterone for Patients with Metastatic Castration-resistant Prostate Cancer and Single Homologous Recombination Repair Gene Mutations in PROpel","journal_title":"European Urology Oncology","journal_issn":"2588-9311","published_at":"2026-08-13T00:00:00.000Z","url":"https://doi.org/10.1016/j.euo.2026.07.014","source_score":15,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-17T13:33:11.214Z","updated_at":"2026-08-17T13:33:11.214Z","tags":[{"paper_doi":"10.1016/j.euo.2026.07.014","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1016/j.euo.2026.07.014","tag_type":"brand","value":"Lynparza","value_numeric":null},{"paper_doi":"10.1016/j.euo.2026.07.014","tag_type":"brand","value":"Zytiga","value_numeric":null},{"paper_doi":"10.1016/j.euo.2026.07.014","tag_type":"category","value":"Urology & Nephrology","value_numeric":null},{"paper_doi":"10.1016/j.euo.2026.07.014","tag_type":"condition","value":"Metastatic Castration-Resistant Prostate Cancer","value_numeric":null},{"paper_doi":"10.1016/j.euo.2026.07.014","tag_type":"generic","value":"abiraterone","value_numeric":null},{"paper_doi":"10.1016/j.euo.2026.07.014","tag_type":"generic","value":"olaparib","value_numeric":null},{"paper_doi":"10.1016/j.euo.2026.07.014","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1016/j.euo.2026.07.014","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1016/j.euo.2026.07.014","tag_type":"modality","value":"Androgen Receptor Pathway Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.euo.2026.07.014","tag_type":"modality","value":"PARP Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.euo.2026.07.014","tag_type":"sample_size","value":"n=796","value_numeric":796},{"paper_doi":"10.1016/j.euo.2026.07.014","tag_type":"sex","value":"male","value_numeric":null},{"paper_doi":"10.1016/j.euo.2026.07.014","tag_type":"study_design","value":"Randomized Controlled Trial","value_numeric":null},{"paper_doi":"10.1016/j.euo.2026.07.014","tag_type":"warning","value":"Brand name 'Zytiga' is used for abiraterone; prednisone co-administration (standard with abiraterone) is not mentioned in the abstract.","value_numeric":null},{"paper_doi":"10.1016/j.euo.2026.07.014","tag_type":"warning","value":"The level of evidence is tagged as 2 (subgroup analysis of a phase 3 RCT); the primary trial is level 1, but these subgroup findings carry inherent limitations.","value_numeric":null},{"paper_doi":"10.1016/j.euo.2026.07.014","tag_type":"warning","value":"The total sample size (n=796) is inferred from the full PROpel trial; the abstract does not explicitly state the exact N. The HRRm subgroup size is not given as a precise integer.","value_numeric":null}],"summaries":{"what_studied":"This pre-specified subgroup analysis of PROpel (phase 3, double-blind RCT) examined efficacy of olaparib plus abiraterone vs. placebo plus abiraterone as first-line therapy in patients with mCRPC harboring single homologous recombination repair gene mutations (HRRm), determined via tumor tissue and ctDNA assays.","key_result":"Among the 28.4% of patients with an HRRm, BRCA2-mutated patients showed the strongest benefit: rPFS HR 0.20 (95% CI 0.08–0.44) and OS HR 0.20 (95% CI 0.07–0.48). ATM and CDK12 single-gene mutations showed numerically favorable but non-significant rPFS and OS HRs. Overall (biomarker-unselected), olaparib plus abiraterone improved rPFS (HR 0.66; p<0.0001) and median OS by 7.4 months (42.1 vs. ~34.7 mo).","limitations":"- Subgroups for most single HRRm genes other than BRCA2, ATM, and CDK12 had fewer than 5 events per arm, severely limiting interpretation.\n- HRRm status was determined by aggregating two assay platforms (tumor tissue + ctDNA), which may introduce heterogeneity in mutation detection.\n- ATM and CDK12 confidence intervals were wide and crossed 1.0, so benefit in these subgroups remains uncertain.","practice_takeaway":"Olaparib plus abiraterone provides a strong first-line benefit in mCRPC patients with BRCA2 mutations (rPFS and OS HR ~0.20) and should be prioritized in this group. For ATM and CDK12 single-gene mutations, benefit is numerically present but not statistically confirmed, so clinical judgment is needed."}},{"doi":"10.1038/s41568-026-00958-4","pmid":"42521814","title":"The DNA damage response and cancer immunotherapy","journal_title":"Nature Reviews Cancer","journal_issn":"1474-175X","published_at":"2026-07-28T00:00:00.000Z","url":"https://doi.org/10.1038/s41568-026-00958-4","source_score":25,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-08T13:23:34.523Z","updated_at":"2026-08-08T13:23:34.523Z","tags":[{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"brand","value":"Lynparza","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"category","value":"Oncology","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"condition","value":"BRCA-Mutated Cancer","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"condition","value":"Cancer","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"condition","value":"Colorectal Cancer","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"condition","value":"Mismatch Repair-Deficient Cancer","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"condition","value":"Non-Small Cell Lung Cancer","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"condition","value":"Ovarian Cancer","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"condition","value":"Triple-Negative Breast Cancer","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"generic","value":"ceralasertib","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"generic","value":"durvalumab","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"generic","value":"niraparib","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"generic","value":"nivolumab","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"generic","value":"olaparib","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"generic","value":"pembrolizumab","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"generic","value":"rucaparib","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"generic","value":"talazoparib","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"level_of_evidence","value":"7","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"modality","value":"ATM Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"modality","value":"ATR Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"modality","value":"DNA-PK Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"modality","value":"Immune Checkpoint Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"modality","value":"PARP Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"warning","value":"Impact flag 'practice_changing' reflects the established clinical translation of MMR-deficiency testing and PARPi use, both discussed extensively in cited landmark trials rather than new data from this review itself.","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"warning","value":"No sample size tag applied — this is a review article without a primary patient cohort.","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"warning","value":"Some referenced clinical trials listed have completion dates in 2025–2026 and may represent very recent or ongoing work; findings may evolve.","value_numeric":null},{"paper_doi":"10.1038/s41568-026-00958-4","tag_type":"warning","value":"This is a narrative review, not a systematic review or meta-analysis; evidence synthesis reflects author selection and may not be exhaustive.","value_numeric":null}],"summaries":{"what_studied":"This review examines how DNA damage response (DDR) defects and DDR inhibitors potentiate cancer immunotherapy, focusing on the molecular mechanisms linking genomic instability to immune activation — including neoantigen generation and cGAS–STING pathway induction — and evaluates DDR-targeted combination strategies with immune checkpoint blockade (ICB).","key_result":"DDR-deficient tumors (e.g., MMR-deficient, POLE-mutant, BRCA1/2-mutant) generate high neoantigen loads and cytosolic DNA that activates cGAS–STING, triggering type I interferon and immune cell recruitment. MMR deficiency is an established pan-cancer biomarker for ICI response; PARPi + ICB combinations show preclinical and early clinical synergy. Resistance mechanisms include BRCA reversion mutations, TREX1-mediated cGAS suppression, ENPP1-mediated cGAMP hydrolysis, and regulatory T cell activity.","limitations":"This is a narrative review without systematic search methods or meta-analytic synthesis, so it is subject to selection bias in the literature cited. Most combination DDR inhibitor + ICB clinical data are from early-phase or single-arm trials, limiting conclusions about efficacy and generalizability.","practice_takeaway":"Test tumors for MMR deficiency and TMB before initiating immunotherapy, as DDR defects are the strongest predictive biomarkers for ICI benefit across cancer types. Combining PARPi with PD-1/PD-L1 blockade is an active clinical strategy — particularly in BRCA-mutant and HR-deficient cancers — but watch for overlapping toxicity and emerging resistance mechanisms."}},{"doi":"10.1158/1535-7163.mct-26-0182","pmid":"42456172","title":"LIG1 Loss in TP53-mutant Triple Negative Breast Cancer Rewires DNA Repair and Confers Sensitivity to PARP-ATR Inhibitor Combinations","journal_title":"Molecular Cancer Therapeutics","journal_issn":"1535-7163","published_at":"2026-07-15T00:00:00.000Z","url":"https://doi.org/10.1158/1535-7163.mct-26-0182","source_score":50,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-22T13:37:52.203Z","updated_at":"2026-07-22T13:37:52.203Z","tags":[{"paper_doi":"10.1158/1535-7163.mct-26-0182","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1158/1535-7163.mct-26-0182","tag_type":"brand","value":"Lynparza","value_numeric":null},{"paper_doi":"10.1158/1535-7163.mct-26-0182","tag_type":"category","value":"Oncology","value_numeric":null},{"paper_doi":"10.1158/1535-7163.mct-26-0182","tag_type":"condition","value":"Triple Negative Breast Cancer","value_numeric":null},{"paper_doi":"10.1158/1535-7163.mct-26-0182","tag_type":"generic","value":"ceralasertib","value_numeric":null},{"paper_doi":"10.1158/1535-7163.mct-26-0182","tag_type":"generic","value":"olaparib","value_numeric":null},{"paper_doi":"10.1158/1535-7163.mct-26-0182","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1158/1535-7163.mct-26-0182","tag_type":"level_of_evidence","value":"6","value_numeric":null},{"paper_doi":"10.1158/1535-7163.mct-26-0182","tag_type":"modality","value":"ATR Inhibitor","value_numeric":null},{"paper_doi":"10.1158/1535-7163.mct-26-0182","tag_type":"modality","value":"PARP Inhibitor","value_numeric":null},{"paper_doi":"10.1158/1535-7163.mct-26-0182","tag_type":"sex","value":"female","value_numeric":null},{"paper_doi":"10.1158/1535-7163.mct-26-0182","tag_type":"study_design","value":"Preclinical Study","value_numeric":null},{"paper_doi":"10.1158/1535-7163.mct-26-0182","tag_type":"warning","value":"Ceralasertib (AZD6738) brand name is not widely established; tagged under generic name only.","value_numeric":null},{"paper_doi":"10.1158/1535-7163.mct-26-0182","tag_type":"warning","value":"LIG1 loss is not yet an established clinical biomarker; the study proposes it as a stratification factor for future trials rather than current standard practice.","value_numeric":null},{"paper_doi":"10.1158/1535-7163.mct-26-0182","tag_type":"warning","value":"Sample size tag omitted: the paper does not report a total N across models in the abstract; model counts are not quantified.","value_numeric":null},{"paper_doi":"10.1158/1535-7163.mct-26-0182","tag_type":"warning","value":"The 'practice_changing' impact flag is applied cautiously — findings are preclinical only; no patient outcome data are reported. Clinical translation is speculative at this stage.","value_numeric":null}],"summaries":{"what_studied":"This study investigated whether LIG1 (DNA Ligase I) loss in TP53-mutant triple negative breast cancer (TNBC) confers sensitivity to PARP inhibitor (PARPi) and ATR inhibitor (ATRi) combinations, using cell line models, a patient-derived xenograft (PDX), and a patient-derived organoid (PDXO) model.","key_result":"Olaparib + ceralasertib showed synergistic cytotoxicity in LIG1-loss cell lines, significantly reduced tumor volume in a LIG1-low PDX model vs. either monotherapy, and had greater ex vivo cytotoxicity in a LIG1-low PDXO vs. a LIG1-high control; PARPi monotherapy sensitivity in LIG1-loss cells was modest and below that seen in HR-deficient TNBC models.","limitations":"Preclinical study only (cell lines, PDX, PDXO) with no clinical outcome data; findings are based on a limited number of in vivo/ex vivo LIG1-low models; the mechanism linking LIG1 loss to ATRi sensitization is inferred but not fully elucidated.","practice_takeaway":"LIG1 status may serve as a biomarker to select TNBC patients for PARP + ATR inhibitor combination trials. Clinicians should consider LIG1 loss as a potential stratification factor in ongoing DDR-targeted combination studies."}},{"doi":"10.1016/j.eururo.2026.04.014","pmid":"42457456","title":"EAU-EANM-ESTRO-ESUR-ISUP-SIOG Guidelines on Prostate Cancer. Part II—2026 Update: Treatment of Relapsing and Metastatic Prostate Cancer","journal_title":"European Urology","journal_issn":"0302-2838","published_at":"2026-07-15T00:00:00.000Z","url":"https://doi.org/10.1016/j.eururo.2026.04.014","source_score":26,"is_retracted":false,"is_open_access":null,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":false},"created_at":"2026-07-21T13:34:33.976Z","updated_at":"2026-07-21T13:34:33.976Z","tags":[{"paper_doi":"10.1016/j.eururo.2026.04.014","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1016/j.eururo.2026.04.014","tag_type":"category","value":"Urology & Nephrology","value_numeric":null},{"paper_doi":"10.1016/j.eururo.2026.04.014","tag_type":"condition","value":"Castration-Resistant Prostate Cancer","value_numeric":null},{"paper_doi":"10.1016/j.eururo.2026.04.014","tag_type":"condition","value":"Metastatic Hormone-Sensitive Prostate Cancer","value_numeric":null},{"paper_doi":"10.1016/j.eururo.2026.04.014","tag_type":"condition","value":"Prostate Cancer","value_numeric":null},{"paper_doi":"10.1016/j.eururo.2026.04.014","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1016/j.eururo.2026.04.014","tag_type":"level_of_evidence","value":"1","value_numeric":null},{"paper_doi":"10.1016/j.eururo.2026.04.014","tag_type":"modality","value":"Androgen Receptor Pathway Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.eururo.2026.04.014","tag_type":"modality","value":"Metastasis-Directed Therapy","value_numeric":null},{"paper_doi":"10.1016/j.eururo.2026.04.014","tag_type":"modality","value":"PARP Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.eururo.2026.04.014","tag_type":"modality","value":"PSMA-Based Therapy","value_numeric":null},{"paper_doi":"10.1016/j.eururo.2026.04.014","tag_type":"sex","value":"male","value_numeric":null},{"paper_doi":"10.1016/j.eururo.2026.04.014","tag_type":"study_design","value":"Clinical Practice Guideline","value_numeric":null},{"paper_doi":"10.1016/j.eururo.2026.04.014","tag_type":"warning","value":"Cost and reimbursement considerations are explicitly excluded from the recommendations, which may limit direct applicability in resource-constrained settings.","value_numeric":null},{"paper_doi":"10.1016/j.eururo.2026.04.014","tag_type":"warning","value":"No specific sample size is applicable — this is a guidelines document, not a primary study. Level of evidence rated '1' reflects the guideline panel's systematic review process, not a single trial.","value_numeric":null},{"paper_doi":"10.1016/j.eururo.2026.04.014","tag_type":"warning","value":"Specific strength-of-recommendation grades for individual interventions are not detailed in the abstract; the full guideline document should be consulted for granular recommendations.","value_numeric":null}],"summaries":{"what_studied":"The 2026 EAU-EANM-ESTRO-ESUR-ISUP-SIOG guidelines update covers treatment of relapsing, metastatic hormone-sensitive, and castration-resistant prostate cancer (PCa), based on a systematic literature review of evidence published between 2023 and 2025.","key_result":"Updated recommendations endorse risk-stratified salvage therapy for relapsing PCa and an expanded treatment toolkit for metastatic/castration-resistant disease — including ARPIs, PARP inhibitors and their combinations, metastasis-directed therapy, and PSMA-based therapy — each graded by strength of evidence.","limitations":"Recommendations do not account for variations in cost, reimbursement, or resource availability across healthcare systems; the review window is limited to 2023–2025, so very recent data may be excluded.","practice_takeaway":"Use risk stratification to guide salvage therapy after primary PCa treatment, and consider the expanded armamentarium — ARPIs, PARP inhibitors (alone or combined), and PSMA-targeted agents — when managing metastatic or castration-resistant disease. Always weigh local formulary access and reimbursement realities, as the guidelines do not factor these in."}},{"doi":"10.1001/jamaoncol.2026.1924","pmid":"42348196","title":"Long-Term Outcomes in Patients With Recurrent Ovarian Cancer and Exceptional Response to PARP Inhibitors","journal_title":"JAMA Oncology","journal_issn":"2374-2437","published_at":"2026-06-25T00:00:00.000Z","url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC13306488/","source_score":17,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-04T13:26:19.768Z","updated_at":"2026-07-04T13:26:19.768Z","tags":[{"paper_doi":"10.1001/jamaoncol.2026.1924","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1924","tag_type":"category","value":"Oncology","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1924","tag_type":"condition","value":"Acute Myeloid Leukemia","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1924","tag_type":"condition","value":"Myelodysplastic Syndrome","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1924","tag_type":"condition","value":"Ovarian Cancer","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1924","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1924","tag_type":"impact_flag","value":"safety_signal","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1924","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1924","tag_type":"modality","value":"PARP Inhibitor","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1924","tag_type":"sample_size","value":"n=320","value_numeric":320},{"paper_doi":"10.1001/jamaoncol.2026.1924","tag_type":"sex","value":"female","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1924","tag_type":"study_design","value":"Retrospective Cohort Study","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1924","tag_type":"warning","value":"Brand/generic tags for specific PARP inhibitors (e.g., olaparib, niraparib, rucaparib) were not reported in the available text and could not be tagged.","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1924","tag_type":"warning","value":"Full text was inaccessible; all data extracted from the abstract and results section only — OS data, dose-reduction rates, and full subgroup analyses could not be independently verified.","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1924","tag_type":"warning","value":"The '2 (7.5%)' figure for disease progression beyond 5 years appears inconsistent with the surrounding percentages (likely a typo for '2.5%' or similar); clinicians should verify against the published manuscript.","value_numeric":null},{"paper_doi":"10.1001/jamaoncol.2026.1924","tag_type":"warning","value":"The discontinuation comparison (stopped vs. continued PARPi) is not randomized; patients who stopped may have been selected for better prognosis, which could confound the PFS difference.","value_numeric":null}],"summaries":{"what_studied":"This international, multicenter, retrospective cohort study (41 sites, 14 countries) evaluated long-term outcomes — including PFS, overall survival, toxic effects, and MDS/AML risk — in 320 patients with platinum-sensitive recurrent ovarian cancer (PS-ROC) who had an exceptional response (PFS ≥5 years) to maintenance PARP inhibitors, with a median follow-up of 6.8 years.","key_result":"At 10 years, PFS was 78.7% overall; patients who stopped PARP inhibitors without progression (n=85) had a 10-year PFS of 90.1% vs 72.5% for those who continued. Late-onset MDS/AML occurred in only 5 patients (1.6%). Exceptional responders were enriched for BRCA1 RING domain and BRCA2 DNA-binding domain variants.","limitations":"- Retrospective design introduces selection bias; patients who discontinued may differ systematically from those who continued.\n- Full text was inaccessible, so granular subgroup data, OS figures, and dose-reduction details could not be verified beyond the abstract.\n- Genotype-phenotype associations are exploratory and require prospective validation.","practice_takeaway":"For ovarian cancer patients with ≥5 years of disease control on a PARP inhibitor, discontinuation does not appear to compromise long-term outcomes and may be a reasonable option to discuss — particularly given the low but real MDS/AML risk (1.6%) with prolonged use. BRCA variant location (RING or DNA-binding domains) may help identify patients most likely to achieve functional cure."}},{"doi":"10.1016/j.ygyno.2026.06.006","pmid":"42296694","title":"Could chemotherapy response score act as a surrogate marker of response to PARP inhibitor maintenance treatment in patients with advanced ovarian cancer?","journal_title":"Gynecologic Oncology","journal_issn":"0090-8258","published_at":"2026-06-15T00:00:00.000Z","url":"https://doi.org/10.1016/j.ygyno.2026.06.006","source_score":1,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-23T13:25:15.540Z","updated_at":"2026-06-23T13:25:15.540Z","tags":[{"paper_doi":"10.1016/j.ygyno.2026.06.006","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.06.006","tag_type":"category","value":"Obstetrics & Gynecology","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.06.006","tag_type":"condition","value":"Advanced Ovarian Cancer","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.06.006","tag_type":"condition","value":"High-Grade Epithelial Ovarian Cancer","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.06.006","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.06.006","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.06.006","tag_type":"modality","value":"Neoadjuvant Chemotherapy","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.06.006","tag_type":"modality","value":"PARP Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.06.006","tag_type":"sample_size","value":"n=169","value_numeric":169},{"paper_doi":"10.1016/j.ygyno.2026.06.006","tag_type":"sex","value":"female","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.06.006","tag_type":"study_design","value":"Retrospective Cohort Study","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.06.006","tag_type":"warning","value":"BRCA mutation status and HRD testing rates across the cohort are not fully described in the abstract, limiting interpretation of the multivariable analysis.","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.06.006","tag_type":"warning","value":"The DOI and publication date (June 2026) appear to reference a forthcoming or recently published article; full text was not available for review — conclusions are based on the abstract and results sections only.","value_numeric":null},{"paper_doi":"10.1016/j.ygyno.2026.06.006","tag_type":"warning","value":"The 'practice_changing' impact flag is applied cautiously — findings are hypothesis-generating from a single-center retrospective study with a small PARPi-treated subgroup (n=47); prospective validation is needed before changing clinical practice.","value_numeric":null}],"summaries":{"what_studied":"This retrospective cohort study evaluated whether the pathology-based Chemotherapy Response Score (CRS) at interval debulking surgery (IDS) predicts benefit from PARP inhibitor (PARPi) maintenance therapy in 169 patients with high-grade epithelial ovarian cancer who received neoadjuvant chemotherapy followed by IDS between January 2016 and September 2022 at a single academic center.","key_result":"Among patients with CRS 2-3 (moderate/marked response), PARPi maintenance was associated with improved PFS (20 vs. 15 months, p=0.029); no PFS benefit was seen in CRS 1 (minimal/no response) patients (p=0.27). CRS 1 was also linked to lower rates of complete cytoreduction (44.1% vs. 69.3%, p<0.0001) and inferior PFS regardless of PARPi use.","limitations":"- Single-center retrospective design limits generalizability and introduces selection bias.\n- CRS was not reported for 44 of 213 eligible patients, creating potential ascertainment bias.\n- Only 47 patients received PARPi maintenance, limiting statistical power, especially in the CRS 1 subgroup.","practice_takeaway":"Consider CRS at IDS as a practical counseling tool for PARPi maintenance decisions — particularly in BRCA-wildtype patients or settings where HRD testing is unavailable. Patients with CRS 1 may not derive PFS benefit from PARPi maintenance and warrant individualized discussion."}},{"doi":"10.1016/j.ijgc.2026.104774","pmid":null,"title":"Poly(adenosine diphosphate-ribose) polymerase inhibitor maintenance therapy with niraparib in patients with primary advanced or recurrent endometrial cancer receiving dostarlimab plus chemotherapy","journal_title":"International Journal of Gynecological Cancer","journal_issn":"1048-891X","published_at":"2026-06-06T00:00:00.000Z","url":"https://doi.org/10.1016/j.ijgc.2026.104774","source_score":1,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":false,"crossref":true,"unpaywall":true},"created_at":"2026-06-17T13:29:48.036Z","updated_at":"2026-06-17T13:29:48.036Z","tags":[{"paper_doi":"10.1016/j.ijgc.2026.104774","tag_type":"brand","value":"Jemperli","value_numeric":null},{"paper_doi":"10.1016/j.ijgc.2026.104774","tag_type":"brand","value":"Zejula","value_numeric":null},{"paper_doi":"10.1016/j.ijgc.2026.104774","tag_type":"category","value":"Obstetrics & Gynecology","value_numeric":null},{"paper_doi":"10.1016/j.ijgc.2026.104774","tag_type":"condition","value":"Endometrial Cancer","value_numeric":null},{"paper_doi":"10.1016/j.ijgc.2026.104774","tag_type":"generic","value":"dostarlimab","value_numeric":null},{"paper_doi":"10.1016/j.ijgc.2026.104774","tag_type":"generic","value":"niraparib","value_numeric":null},{"paper_doi":"10.1016/j.ijgc.2026.104774","tag_type":"modality","value":"Chemotherapy","value_numeric":null},{"paper_doi":"10.1016/j.ijgc.2026.104774","tag_type":"modality","value":"PARP Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.ijgc.2026.104774","tag_type":"modality","value":"PD-1 Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.ijgc.2026.104774","tag_type":"warning","value":"Study design, level of evidence, sample size, sex, age group, and impact flag cannot be determined from the available metadata alone.","value_numeric":null},{"paper_doi":"10.1016/j.ijgc.2026.104774","tag_type":"warning","value":"The paper was published on June 6, 2026, and only the title, DOI, journal, and publication date were provided — no abstract, methods, results, or conclusions were included. All summary fields requiring study details (key results, sample size, limitations, practice takeaway) have been left null due to insufficient source data.","value_numeric":null}],"summaries":{"what_studied":"This study evaluated niraparib (a PARP inhibitor) as maintenance therapy in patients with primary advanced or recurrent endometrial cancer who received dostarlimab (a PD-1 inhibitor) plus chemotherapy as first-line or subsequent treatment."}},{"doi":"10.1056/nejmoa2604126","pmid":"42223064","title":"PARP and Androgen-Signaling Inhibition plus ADT in Metastatic Prostate Cancer","journal_title":"New England Journal of Medicine","journal_issn":"0028-4793","published_at":"2026-05-30T00:00:00.000Z","url":"https://doi.org/10.1056/nejmoa2604126","source_score":366,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-05T13:22:53.741Z","updated_at":"2026-08-05T13:22:53.741Z","tags":[{"paper_doi":"10.1056/nejmoa2604126","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604126","tag_type":"brand","value":"Talzenna","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604126","tag_type":"brand","value":"Xtandi","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604126","tag_type":"category","value":"Medicine, General & Internal","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604126","tag_type":"condition","value":"Homologous Recombination Repair Gene Alteration","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604126","tag_type":"condition","value":"Metastatic Prostate Cancer","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604126","tag_type":"generic","value":"enzalutamide","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604126","tag_type":"generic","value":"talazoparib","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604126","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604126","tag_type":"level_of_evidence","value":"1","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604126","tag_type":"modality","value":"Androgen Deprivation Therapy","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604126","tag_type":"modality","value":"Androgen Receptor Inhibitor","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604126","tag_type":"modality","value":"PARP Inhibitor","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604126","tag_type":"sample_size","value":"n=599","value_numeric":599},{"paper_doi":"10.1056/nejmoa2604126","tag_type":"sex","value":"male","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604126","tag_type":"study_design","value":"Randomized Controlled Trial","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604126","tag_type":"warning","value":"Overall survival results are from a pre-specified interim analysis and have not crossed the significance threshold; mature OS data are pending.","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604126","tag_type":"warning","value":"The impact_flag 'practice_changing' is applied based on the strong PFS result, but should be interpreted cautiously given immature OS data.","value_numeric":null},{"paper_doi":"10.1056/nejmoa2604126","tag_type":"warning","value":"The trial uses the term 'androgen pathway modulation-sensitive' (APMS) instead of the conventional 'castration-sensitive' or 'hormone-sensitive' — this is an emerging terminology shift that may affect cross-trial comparisons.","value_numeric":null}],"summaries":{"what_studied":"Phase 3 double-blind RCT (TALAPRO-3) evaluating talazoparib (0.5 mg/day) plus enzalutamide (160 mg/day) vs. placebo plus enzalutamide in 599 patients with metastatic androgen pathway modulation-sensitive (APMS) prostate cancer harboring homologous recombination repair (HRR) gene alterations, stratified by disease status, volume, and BRCA mutation status.","key_result":"At 3 years, imaging-based PFS was 77% (talazoparib) vs. 56% (control); HR 0.48 (95% CI 0.36–0.65; P<0.001). Overall survival at 3 years was 78% vs. 72% (HR 0.77; 95% CI 0.56–1.04) — not statistically significant at this interim analysis. Grade ≥3 anemia occurred in 51% of the talazoparib group; serious adverse events in 42% vs. 32%; two treatment-related deaths in the talazoparib arm.","limitations":"- Overall survival data are interim and not yet statistically significant (HR 0.77; 95% CI crosses 1.0), so a survival benefit remains unconfirmed.\n- Trial is restricted to patients with HRR gene alterations, limiting generalizability to unselected metastatic APMS populations.\n- Industry-funded (Pfizer), which may introduce bias risk.","practice_takeaway":"For patients with metastatic hormone-sensitive prostate cancer who harbor HRR gene alterations, adding talazoparib to enzalutamide plus ADT meaningfully reduces the risk of progression or death, but the high rate of grade ≥3 anemia (51%) demands proactive monitoring and dose-management planning. Await mature OS data before fully integrating this regimen into first-line practice."}},{"doi":"10.1158/1541-7786.mcr-25-1068","pmid":"42206981","title":"Mapping the Subtype-Specific PARP1 ADP-ribosylated Proteome in Breast Cancer Cells","journal_title":"Molecular Cancer Research","journal_issn":"1541-7786","published_at":"2026-05-28T00:00:00.000Z","url":"https://doi.org/10.1158/1541-7786.mcr-25-1068","source_score":4,"is_retracted":false,"is_open_access":null,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":false},"created_at":"2026-06-08T13:46:45.120Z","updated_at":"2026-06-08T13:46:45.120Z","tags":[{"paper_doi":"10.1158/1541-7786.mcr-25-1068","tag_type":"category","value":"Oncology","value_numeric":null},{"paper_doi":"10.1158/1541-7786.mcr-25-1068","tag_type":"condition","value":"Breast Cancer","value_numeric":null},{"paper_doi":"10.1158/1541-7786.mcr-25-1068","tag_type":"condition","value":"Triple Negative Breast Cancer","value_numeric":null},{"paper_doi":"10.1158/1541-7786.mcr-25-1068","tag_type":"generic","value":"olaparib","value_numeric":null},{"paper_doi":"10.1158/1541-7786.mcr-25-1068","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1158/1541-7786.mcr-25-1068","tag_type":"level_of_evidence","value":"6","value_numeric":null},{"paper_doi":"10.1158/1541-7786.mcr-25-1068","tag_type":"modality","value":"Chemical Genetics / Mass Spectrometry","value_numeric":null},{"paper_doi":"10.1158/1541-7786.mcr-25-1068","tag_type":"modality","value":"PARP Inhibitor","value_numeric":null},{"paper_doi":"10.1158/1541-7786.mcr-25-1068","tag_type":"sample_size","value":"n=6","value_numeric":6},{"paper_doi":"10.1158/1541-7786.mcr-25-1068","tag_type":"study_design","value":"Translational/Exploratory Laboratory Study","value_numeric":null},{"paper_doi":"10.1158/1541-7786.mcr-25-1068","tag_type":"warning","value":"The sample size tag (n=6) refers to cell lines, not patients — no human subject data was involved. Level of evidence is assigned as 6 (cell line/in vitro study). No specific PARP inhibitor drug is named in the abstract; 'olaparib' tag is inferred from the PARP inhibitor class context and may not be the exact agent referenced. Age group and sex tags are omitted as these apply to cell lines, not a defined patient population.","value_numeric":null}],"summaries":{"what_studied":"This study mapped the PARP1-mediated ADP-ribosylated (ADPRylated) proteome across six human breast cancer cell lines — representing luminal and basal/triple-negative subtypes — using an NAD⁺ analog-sensitive PARP1 chemical genetics approach paired with mass spectrometry, under basal (non-DNA-damage) growth conditions.","key_result":"Thousands of PARP1 substrates and hundreds of Glu/Asp ADPRylation sites were identified; luminal-specific substrates were enriched in chromatin and transcriptional regulators, while basal-specific substrates linked to translation and RNA processing. TFAP2A, selectively ADPRylated in luminal cells, showed altered promoter occupancy when PARP1 catalytic activity was inhibited.","limitations":"Findings are derived entirely from cell line models, limiting direct translational relevance to human tumors. Only basal (unstressed) growth conditions were studied, so DNA-damage-induced ADPRylation landscapes are not captured. Functional validation was performed for only one transcription factor (TFAP2A) as proof-of-concept.","practice_takeaway":"This proteome-wide dataset reveals that PARP1 shapes subtype-specific transcriptional programs in breast cancer beyond DNA repair, suggesting that subtype identity may influence PARP inhibitor sensitivity. Clinicians should be aware that PARP inhibitor effects may extend to gene regulation in a breast cancer subtype-dependent manner."}},{"doi":"10.1007/s12282-026-01867-y","pmid":"42176176","title":"Real-world uptake of gBRCA testing as a companion diagnostic for olaparib in patients with high-risk HER2-negative early breast cancer in Japan: a cross-sectional multicenter study (BRCAwareness)","journal_title":"Breast Cancer","journal_issn":"1340-6868","published_at":"2026-05-23T00:00:00.000Z","url":"https://doi.org/10.1007/s12282-026-01867-y","source_score":4,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-29T13:23:05.679Z","updated_at":"2026-05-29T13:23:05.679Z","tags":[{"paper_doi":"10.1007/s12282-026-01867-y","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1007/s12282-026-01867-y","tag_type":"brand","value":"Lynparza","value_numeric":null},{"paper_doi":"10.1007/s12282-026-01867-y","tag_type":"category","value":"Obstetrics & Gynecology","value_numeric":null},{"paper_doi":"10.1007/s12282-026-01867-y","tag_type":"condition","value":"Early Breast Cancer","value_numeric":null},{"paper_doi":"10.1007/s12282-026-01867-y","tag_type":"condition","value":"HER2-Negative Breast Cancer","value_numeric":null},{"paper_doi":"10.1007/s12282-026-01867-y","tag_type":"condition","value":"Hereditary Breast and Ovarian Cancer","value_numeric":null},{"paper_doi":"10.1007/s12282-026-01867-y","tag_type":"generic","value":"olaparib","value_numeric":null},{"paper_doi":"10.1007/s12282-026-01867-y","tag_type":"impact_flag","value":"safety_signal","value_numeric":null},{"paper_doi":"10.1007/s12282-026-01867-y","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1007/s12282-026-01867-y","tag_type":"modality","value":"Germline Genetic Testing","value_numeric":null},{"paper_doi":"10.1007/s12282-026-01867-y","tag_type":"modality","value":"PARP Inhibitor","value_numeric":null},{"paper_doi":"10.1007/s12282-026-01867-y","tag_type":"sample_size","value":"n=691","value_numeric":691},{"paper_doi":"10.1007/s12282-026-01867-y","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1007/s12282-026-01867-y","tag_type":"study_design","value":"Cross-Sectional Multicenter Study","value_numeric":null},{"paper_doi":"10.1007/s12282-026-01867-y","tag_type":"warning","value":"Sample represents 46 facilities likely enriched for genetics infrastructure; true national testing rates in Japan may be lower than 63.2%.","value_numeric":null},{"paper_doi":"10.1007/s12282-026-01867-y","tag_type":"warning","value":"Study funded by AstraZeneca and MSD, the co-developers of olaparib; sponsor reviewed the protocol and manuscript, which may introduce reporting bias despite no claimed role in data analysis.","value_numeric":null},{"paper_doi":"10.1007/s12282-026-01867-y","tag_type":"warning","value":"The 'safety_signal' impact flag is applied here to flag a significant care gap (underuse of companion diagnostic), not a drug safety concern in the traditional sense.","value_numeric":null}],"summaries":{"what_studied":"Real-world uptake of germline BRCA1/2 (gBRCA) testing as a companion diagnostic for adjuvant olaparib in 691 patients with high-risk HER2-negative early breast cancer who had curative surgery in 2023 across 46 facilities in Japan, using OlympiA trial eligibility criteria.","key_result":"Testing rate was 63.2% (95% CI 59.5–66.9%), well below the anticipated 88%. Among 254 untested patients, 66% were never informed — mostly due to physician oversight (57%) or physician-perceived ineligibility (40%). Of 437 tested patients, 42 (9.6%) carried gBRCA pathogenic variants; 32 of those 42 received adjuvant olaparib. Women aged ≥65 years (OR 3.33), those with major comorbidities (OR 16.67), postmenopausal status (OR 2.44), upfront surgery (OR 1.94), no family history of HBOC-related cancer (OR 3.57), and no bilateral/multiple primary cancers (OR 2.16) were significantly less likely to be tested.","limitations":"- Participating sites skewed toward centers with breast specialists and genetic counselors, likely **overestimating** real-world testing rates nationwide.\n- Reasons for olaparib non-initiation in 10 gBRCA PV carriers were not systematically collected.\n- Patient-reported barriers to testing were derived from chart review, not direct patient surveys, risking undercapture of psychological or financial concerns.","practice_takeaway":"Only 6 in 10 eligible patients received gBRCA testing — and the biggest gap was physician failure to recognize or offer it, not patient refusal. Clinicians should proactively flag all patients who meet OlympiA high-risk criteria for gBRCA testing, paying special attention to older, postmenopausal, or comorbid patients who may be wrongly passed over."}},{"doi":"10.1097/ju.0000000000005131","pmid":"42171515","title":"First-Line Systemic Treatments of Metastatic Hormone-Sensitive Prostate Cancer: Updated Systematic Review and Network Meta-Analysis","journal_title":"Journal of Urology","journal_issn":"0022-5347","published_at":"2026-05-22T00:00:00.000Z","url":"https://doi.org/10.1097/ju.0000000000005131","source_score":8,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-14T13:24:59.421Z","updated_at":"2026-08-14T13:24:59.421Z","tags":[{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"brand","value":"Erleada","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"brand","value":"Nubeqa","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"brand","value":"Pluvicto","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"brand","value":"Xtandi","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"brand","value":"Zytiga","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"category","value":"Urology & Nephrology","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"condition","value":"Metastatic Hormone-Sensitive Prostate Cancer","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"generic","value":"abiraterone","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"generic","value":"apalutamide","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"generic","value":"capivasertib","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"generic","value":"darolutamide","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"generic","value":"docetaxel","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"generic","value":"enzalutamide","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"generic","value":"lutetium-177 PSMA-617","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"generic","value":"niraparib","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"level_of_evidence","value":"1","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"modality","value":"AKT Inhibitor","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"modality","value":"Androgen Deprivation Therapy","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"modality","value":"Androgen Receptor Pathway Inhibitor","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"modality","value":"PARP Inhibitor","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"modality","value":"Radioligand Therapy","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"modality","value":"Taxane Chemotherapy","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"sample_size","value":"n=18689","value_numeric":18689},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"sex","value":"male","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"study_design","value":"Network Meta-Analysis","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"warning","value":"Biomarker-driven trials (AMPLITUDE, CAPItello-281, PSMAddition) were excluded from the NMA due to selected populations and evaluated qualitatively only; OS results are immature for all three.","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"warning","value":"PARPi+ARPI+ADT OS data were not available for inclusion in the NMA; OS benefit for this triplet remains unknown.","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"warning","value":"Several included trials had open-label designs, introducing risk of bias in investigator-assessed progression endpoints.","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"warning","value":"The impact_flag 'practice_changing' reflects the high-certainty subgroup finding for docetaxel triplet in high-volume disease and the emerging biomarker-driven data; the all-comer analysis does not confirm a practice change for unselected patients.","value_numeric":null},{"paper_doi":"10.1097/ju.0000000000005131","tag_type":"warning","value":"The NMA grouped all ARPIs (abiraterone, apalutamide, darolutamide, enzalutamide, orteronel, rezvilutamide) as a single class to preserve network connectivity; class-level effects may mask agent-specific differences.","value_numeric":null}],"summaries":{"what_studied":"This updated systematic review and network meta-analysis (NMA) compared the efficacy and safety of first-line systemic combination therapies for metastatic hormone-sensitive prostate cancer (mHSPC) across 23 RCTs (n=18,689), searched through March 2026. Outcomes included progression-free survival (PFS), overall survival (OS), and severe adverse events (AEs), with a separate systematic review of biomarker-driven trials (AMPLITUDE, CAPItello-281, PSMAddition).","key_result":"No triplet regimen showed a statistically significant OS benefit over ARPI+ADT in all-comers. However, **docetaxel+ARPI+ADT** significantly improved OS in high-volume disease (HR 0.76, 95% CI 0.61–0.95; high certainty). For PFS, docetaxel+ARPI+ADT (HR 0.66, 95% CI 0.43–1.01; moderate certainty) and PARPi+ARPI+ADT (HR 0.55, 95% CI 0.23–1.34; low certainty) showed clinically relevant but non-significant trends vs. ARPI+ADT. In biomarker-selected populations: niraparib+abiraterone improved rPFS in HRR-mutated mHSPC (HR 0.63); capivasertib+abiraterone improved rPFS in PTEN-deficient mHSPC (HR 0.81); Lu-177-PSMA+ARPI+ADT improved rPFS in PSMA-positive mHSPC (HR 0.72); OS data remain immature for all three.","limitations":"- Direct head-to-head comparisons between key triplet regimens were unavailable, requiring reliance on indirect NMA contrasts with interstudy heterogeneity.\n- Combining radiographic and clinical PFS endpoints introduced heterogeneity; earlier trials used conventional imaging vs. more sensitive modalities in recent trials, risking stage migration bias.\n- PARPi-, PSMA-, and AKT-based evidence comes from single trials with immature OS data and small phase II samples, yielding low or very low certainty.","practice_takeaway":"For patients with **high-volume mHSPC**, docetaxel+ARPI+ADT offers a proven OS benefit (HR 0.76; high certainty) and should be preferred. For patients with specific biomarkers (HRR mutation, PTEN loss, or PSMA-positive disease), targeted intensification with PARPi, AKT inhibitor, or radioligand therapy respectively shows rPFS benefit—but OS data are still maturing, so treatment decisions must weigh distinct toxicity profiles against uncertain long-term gains."}},{"doi":"10.1097/01.ju.0001191680.76138.83.06","pmid":null,"title":"PD23-06 RADIOGRAPHIC PROGRESSION-FREE SURVIVAL AS A MEANINGFUL ENDPOINT IN METASTATIC CASTRATION-RESISTANT PROSTATE CANCER (MCRPC): THE TALAPRO-2 RANDOMIZED CLINICAL TRIAL","journal_title":"Journal of Urology","journal_issn":"0022-5347","published_at":"2026-04-27T00:00:00.000Z","url":"https://doi.org/10.1097/01.ju.0001191680.76138.83.06","source_score":7,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":false,"crossref":true,"unpaywall":true},"created_at":"2026-05-08T13:23:52.857Z","updated_at":"2026-05-08T13:23:52.857Z","tags":[{"paper_doi":"10.1097/01.ju.0001191680.76138.83.06","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1097/01.ju.0001191680.76138.83.06","tag_type":"brand","value":"Talzenna","value_numeric":null},{"paper_doi":"10.1097/01.ju.0001191680.76138.83.06","tag_type":"brand","value":"Xtandi","value_numeric":null},{"paper_doi":"10.1097/01.ju.0001191680.76138.83.06","tag_type":"category","value":"Urology & Nephrology","value_numeric":null},{"paper_doi":"10.1097/01.ju.0001191680.76138.83.06","tag_type":"condition","value":"Metastatic Castration-Resistant Prostate Cancer","value_numeric":null},{"paper_doi":"10.1097/01.ju.0001191680.76138.83.06","tag_type":"generic","value":"enzalutamide","value_numeric":null},{"paper_doi":"10.1097/01.ju.0001191680.76138.83.06","tag_type":"generic","value":"talazoparib","value_numeric":null},{"paper_doi":"10.1097/01.ju.0001191680.76138.83.06","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1097/01.ju.0001191680.76138.83.06","tag_type":"level_of_evidence","value":"1","value_numeric":null},{"paper_doi":"10.1097/01.ju.0001191680.76138.83.06","tag_type":"modality","value":"Androgen Receptor Signaling Inhibitor","value_numeric":null},{"paper_doi":"10.1097/01.ju.0001191680.76138.83.06","tag_type":"modality","value":"PARP Inhibitor","value_numeric":null},{"paper_doi":"10.1097/01.ju.0001191680.76138.83.06","tag_type":"sex","value":"male","value_numeric":null},{"paper_doi":"10.1097/01.ju.0001191680.76138.83.06","tag_type":"study_design","value":"Randomized Controlled Trial","value_numeric":null},{"paper_doi":"10.1097/01.ju.0001191680.76138.83.06","tag_type":"warning","value":"Sample size tag omitted as total N was not reported in the available abstract text.","value_numeric":null},{"paper_doi":"10.1097/01.ju.0001191680.76138.83.06","tag_type":"warning","value":"The impact_flag 'practice_changing' is assigned based on the known significance of TALAPRO-2 in the mCRPC landscape, but confirmation from the full publication is advised.","value_numeric":null},{"paper_doi":"10.1097/01.ju.0001191680.76138.83.06","tag_type":"warning","value":"The paper is available only as a conference abstract (PD23-06 from a AUA meeting proceeding); full text data including specific hazard ratios, median rPFS values, and patient numbers were not provided, so quantitative details in the summary are limited.","value_numeric":null}],"summaries":{"what_studied":"The TALAPRO-2 randomized clinical trial evaluated radiographic progression-free survival (rPFS) as a meaningful clinical endpoint in patients with metastatic castration-resistant prostate cancer (mCRPC), assessing the treatment effect of talazoparib combined with enzalutamide.","key_result":"The trial supported rPFS as a meaningful endpoint in mCRPC, with the talazoparib plus enzalutamide combination demonstrating a statistically significant improvement in rPFS compared to placebo plus enzalutamide; specific hazard ratios and median survival numbers are not available in the provided abstract.","limitations":"Full numerical results and subgroup data are not available from the abstract alone, limiting precise quantitative interpretation. The clinical meaningfulness of rPFS as a surrogate for overall survival in mCRPC remains an ongoing debate in the field.","practice_takeaway":"Clinicians treating mCRPC can consider rPFS a meaningful endpoint when evaluating combination regimens like talazoparib plus enzalutamide. The TALAPRO-2 data support use of this endpoint to guide treatment decisions, particularly in patients with homologous recombination repair (HRR) gene alterations."}},{"doi":"10.1200/jco-25-02834","pmid":"41744290","title":"Trial Design and Objectives for Patients With Prostate Cancer: Recommendations From the Prostate Cancer Working Group 4","journal_title":"Journal of Clinical Oncology","journal_issn":"0732-183X","published_at":"2026-02-26T00:00:00.000Z","url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC13132095/","source_score":61,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2026-05-02","doi":"10.1200/jco-25-02834","days":"14","issn":"0732-183X","rank":"9","field":"Clinical Medicine","score":"61","category":"Oncology","categories":["Oncology"],"_categories":["Oncology"]},"pubmed":{"doi":"10.1200/JCO-25-02834","title":"Trial Design and Objectives for Patients With Prostate Cancer: Recommendations From the Prostate Cancer Working Group 4.","journal":"Journal of clinical oncology : official journal of the American Society of Clinical Oncology","methods":"","results":"PCWG4 redefines terminology around the disease state and previous therapies in a patient-centric context and terminology focused on androgen pathway modulation. We consider imaging, with a particular focus on positron emission tomography (PET)-defined disease. New recommendations are provided for disease state terminology, defining eligibility criteria, response and delay/prevent end points, intervals for reassessments including imaging, and patient-reported outcome determination. We provide recommendations in a biomarker-based context of use for the intended indication, reflective of patient benefit for specific interventions. We emphasize the need for development of validated PET imaging and molecular and phenotypic criteria as well as trial designs to appropriately risk stratify patients, predict and assess benefit, and measure post-treatment outcomes reliably in a trial framework.","abstract":"$30","keywords":[],"pubmed_id":"41744290","conclusions":"PCWG4 updates recommendations on patient and tumor characterization, therapy development, and imaging criteria and extends guidance into earlier androgen pathway modulator-naïve/sensitive disease states to reflect an evolving, heterogeneous, and diverse patient population to optimize treatment benefits for all patients.","publication_date":"2026-02-26T00:00:00"},"crossref":{"DOI":"10.1200/jco-25-02834","URL":"https://doi.org/10.1200/jco-25-02834","ISSN":["0732-183X","1527-7755"],"link":[{"URL":"https://ascopubs.org/doi/pdfdirect/10.1200/JCO-25-02834","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":"1249-1265","type":"journal-article","issue":"13","score":1,"title":["Trial Design and Objectives for Patients With Prostate Cancer: Recommendations From the Prostate Cancer Working Group 4"],"author":[{"given":"Andrew J.","family":"Armstrong","sequence":"first","affiliation":[{"name":"Department of Medicine, Duke Cancer Institute Center for Prostate and Urologic Cancer, Duke University, Durham, NC"}]},{"given":"Michael J.","family":"Morris","sequence":"additional","affiliation":[{"name":"Memorial Sloan Kettering Cancer Center, New York, NY"}]},{"given":"Wassim","family":"Abida","sequence":"additional","affiliation":[{"name":"Memorial Sloan Kettering Cancer Center, New York, NY"}]},{"given":"Rahul R.","family":"Aggarwal","sequence":"additional","affiliation":[{"name":"San Francisco Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA"}]},{"given":"Emmanuel S.","family":"Antonarakis","sequence":"additional","affiliation":[{"name":"Masonic Cancer Center, University of Minnesota, Minneapolis, MN"}]},{"given":"Gerhardt","family":"Attard","sequence":"additional","affiliation":[{"name":"University College London Cancer Institute, London, United Kingdom"}]},{"given":"Himisha","family":"Beltran","sequence":"additional","affiliation":[{"name":"Dana Farber Cancer Institute, Boston, MA"}]},{"given":"Alan","family":"Bryce","sequence":"additional","affiliation":[{"name":"City of Hope Cancer Center, Goodyear, AZ"}]},{"given":"Michael A.","family":"Carducci","sequence":"additional","affiliation":[{"name":"Sidney Kimmel Cancer Center, Johns Hopkins University, Baltimore, MD"}]},{"given":"Heather H.","family":"Cheng","sequence":"additional","affiliation":[{"name":"University of Washington and Fred Hutchinson Cancer Center, Seattle, WA"}]},{"given":"Delphine L.","family":"Chen","sequence":"additional","affiliation":[{"name":"University of Washington and Fred Hutchinson Cancer Center, Seattle, WA"}]},{"given":"Kim N.","family":"Chi","sequence":"additional","affiliation":[{"name":"BC Cancer Agency, Vancouver, BC, Canada"}]},{"given":"Daniel S.","family":"Childs","sequence":"additional","affiliation":[{"name":"Department of Oncology, Mayo Clinic, Rochester, MN"}]},{"given":"William","family":"Dahut","sequence":"additional","affiliation":[{"name":"American Cancer Society, Atlanta, GA"}]},{"given":"Louise","family":"Emmett","sequence":"additional","affiliation":[{"name":"Department of Theranostics and Nuclear Medicine, St Vincent's Hospital, Sydney, Australia"}]},{"given":"Karim","family":"Fizazi","sequence":"additional","affiliation":[{"name":"Department of Cancer Medicine, Centre Oscar Lambret, Institut Gustave Roussy, University of Paris Saclay, Villejuif, France"}]},{"given":"Andrei","family":"Gafita","sequence":"additional","affiliation":[{"name":"Department of Radiology and Radiological Sciences, Johns Hopkins Theranostics Center, Johns Hopkins University, Baltimore, MD"}]},{"given":"Daniel J.","family":"George","sequence":"additional","affiliation":[{"name":"Department of Medicine, Duke Cancer Institute Center for Prostate and Urologic Cancer, Duke University, Durham, NC"}]},{"given":"Ken","family":"Hermann","sequence":"additional","affiliation":[{"name":"Universitätsklinikum Essen, Essen, Germany"}]},{"given":"Michael S.","family":"Hofman","sequence":"additional","affiliation":[{"name":"Peter MacCallum Cancer Centre, Melbourne, VIC, Australia"},{"name":"University of Melbourne, Parkville, VIC, Australia"}]},{"given":"Thomas","family":"Hope","sequence":"additional","affiliation":[{"name":"University of California, San Francisco, San Francisco, CA"}]},{"given":"Maha","family":"Hussain","sequence":"additional","affiliation":[{"name":"Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL"}]},{"given":"W. Kevin","family":"Kelly","sequence":"additional","affiliation":[{"name":"Sidney Kimmel School of Medicine at Thomas Jefferson University, Philadelphia, PA"}]},{"given":"Elizabeth","family":"Kessler","sequence":"additional","affiliation":[{"name":"University of Colorado School of Medicine, Aurora, CO"}]},{"given":"Phillip H.","family":"Kuo","sequence":"additional","affiliation":[{"name":"Department of Radiology, City of Hope National Medical Center, Duarte, CA"}]},{"given":"Joshua","family":"Lang","sequence":"additional","affiliation":[{"name":"University of Wisconsin Carbone Cancer Center, University of Wisconsin, Madison, WI"}]},{"given":"Glenn","family":"Liu","sequence":"additional","affiliation":[{"name":"University of Wisconsin Carbone Cancer Center, University of Wisconsin, Madison, WI"}]},{"given":"Catherine H.","family":"Marshall","sequence":"additional","affiliation":[{"name":"Sidney Kimmel Cancer Center, Johns Hopkins University, Baltimore, MD"}]},{"given":"Alicia K.","family":"Morgans","sequence":"additional","affiliation":[{"name":"Dana Farber Cancer Institute, Boston, MA"}]},{"given":"Rana R.","family":"McKay","sequence":"additional","affiliation":[{"name":"University of California San Diego, San Diego, CA"}]},{"given":"David","family":"Nanus","sequence":"additional","affiliation":[{"name":"Weill Cornell Medicine, New York, NY"},{"name":"Weill Cornell Medicine-NewYork Presbyterian Hospital, New York, NY"}]},{"given":"Peter","family":"Nelson","sequence":"additional","affiliation":[{"name":"Fred Hutchinson Cancer Center, Seattle, WA"}]},{"given":"Channing","family":"Paller","sequence":"additional","affiliation":[{"name":"Sidney Kimmel Cancer Center, Johns Hopkins University, Baltimore, MD"}]},{"given":"Zachery R.","family":"Reichert","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Michigan, Ann Arbor, MI"}]},{"given":"Charles J.","family":"Ryan","sequence":"additional","affiliation":[{"name":"Memorial Sloan Kettering Cancer Center, New York, NY"}]},{"given":"A. 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