Pub Date : 2025-12-17DOI: 10.1158/2159-8290.cd-nw2025-0108
ASP3082, a proteolysis targeting chimera that targets mutant KRASG12D, and elironrasib, a tri-complex inhibitor of KRASG12C in the “on” state, showed encouraging efficacy and safety in separate phase I trials.
{"title":"“The RAS Dam Has Broken”","authors":"","doi":"10.1158/2159-8290.cd-nw2025-0108","DOIUrl":"https://doi.org/10.1158/2159-8290.cd-nw2025-0108","url":null,"abstract":"ASP3082, a proteolysis targeting chimera that targets mutant KRASG12D, and elironrasib, a tri-complex inhibitor of KRASG12C in the “on” state, showed encouraging efficacy and safety in separate phase I trials.","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":"11 1","pages":""},"PeriodicalIF":28.2,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145765232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-17DOI: 10.1158/2159-8290.cd-nw2025-0112
Early clinical results show that inside-the-body T-cell engineering can trigger rapid chimeric antigen receptor expression and induce deep responses in patients with relapsed multiple myeloma—without the manufacturing required for conventional adoptive cell therapy. Larger studies are needed, however, to determine how off-the-shelf in vivo approaches compare with existing autologous therapies.
{"title":"In Vivo CAR T Cells Deliver Deep Responses in Myeloma","authors":"","doi":"10.1158/2159-8290.cd-nw2025-0112","DOIUrl":"https://doi.org/10.1158/2159-8290.cd-nw2025-0112","url":null,"abstract":"Early clinical results show that inside-the-body T-cell engineering can trigger rapid chimeric antigen receptor expression and induce deep responses in patients with relapsed multiple myeloma—without the manufacturing required for conventional adoptive cell therapy. Larger studies are needed, however, to determine how off-the-shelf in vivo approaches compare with existing autologous therapies.","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":"152 1","pages":""},"PeriodicalIF":28.2,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145765233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-17DOI: 10.1158/2159-8290.cd-nw2025-0110
In the phase III GIMEMA ALL2820 trial, treatment with ponatinib and blinatumomab led to significantly better response rates and overall survival than a chemotherapy–imatinib regimen for patients with Philadelphia chromosome–positive acute lymphoblastic leukemia. The findings could change the standard of care for the disease.
{"title":"Phase III Data Support Chemo-Free Approach to ALL","authors":"","doi":"10.1158/2159-8290.cd-nw2025-0110","DOIUrl":"https://doi.org/10.1158/2159-8290.cd-nw2025-0110","url":null,"abstract":"In the phase III GIMEMA ALL2820 trial, treatment with ponatinib and blinatumomab led to significantly better response rates and overall survival than a chemotherapy–imatinib regimen for patients with Philadelphia chromosome–positive acute lymphoblastic leukemia. The findings could change the standard of care for the disease.","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":"62 1","pages":""},"PeriodicalIF":28.2,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145765231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-17DOI: 10.1158/2159-8290.cd-nw2025-0111
The addition of the HER2 tyrosine kinase inhibitor tucatinib to trastuzumab and pertuzumab as first-line maintenance therapy significantly increased progression-free survival (PFS) compared to a placebo plus mAb treatment for patients with HER2-positive metastatic breast cancer. The findings position it alongside trastuzumab deruxtecan and palbociclib as agents that have demonstrated impressive PFS improvements in phase III studies.
{"title":"Tucatinib Gives PFS Boost for Metastatic Breast Cancer","authors":"","doi":"10.1158/2159-8290.cd-nw2025-0111","DOIUrl":"https://doi.org/10.1158/2159-8290.cd-nw2025-0111","url":null,"abstract":"The addition of the HER2 tyrosine kinase inhibitor tucatinib to trastuzumab and pertuzumab as first-line maintenance therapy significantly increased progression-free survival (PFS) compared to a placebo plus mAb treatment for patients with HER2-positive metastatic breast cancer. The findings position it alongside trastuzumab deruxtecan and palbociclib as agents that have demonstrated impressive PFS improvements in phase III studies.","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":"4 1","pages":""},"PeriodicalIF":28.2,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145765234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-10DOI: 10.1158/2159-8290.cd-25-0919
Amulya Sreekumar, Eric Blankemeyer, Christopher J. Sterner, Tien-Chi Pan, Dhruv K. Pant, Sarah Acolatse, Hamza Turkistani, George K. Belka, Anupma Nayak, Sean D. Carlin, Charles-Antoine Assenmacher, Mark A. Sellmyer, David A. Mankoff, Lewis A. Chodosh
Recurrent breast cancer accounts for most disease-associated mortality and can develop decades after primary tumor therapy. Recurrences arise from residual tumor cells (RTCs) that can evade therapy in a dormant state, however the mechanisms enforcing dormancy in RTCs are poorly understood. CRISPR-Cas9 screening identified the transcription factors SOX5/6 as functional regulators of tumor recurrence. Loss of SOX5 accelerated recurrence at both local and metastatic sites and promoted dormancy escape in both therapy-associated and microenvironment-induced contexts. Remarkably, SOX5 drove dormant RTCs to adopt a cartilage-dependent bone development program, termed endochondral ossification, that was confirmed by [18F]NaF-PET imaging and reversed in recurrent tumors escaping dormancy. Consistent with findings in mice, osteochondrogenic expression signatures in patients were enriched in residual disease following neoadjuvant therapy, and their enrichment in primary breast cancers predicted improved recurrence-free survival. These findings identify SOX5-dependent mesodermal transdifferentiation as an adaptive mechanism that prevents recurrence by reinforcing tumor cell dormancy.
{"title":"Residual Breast Cancer Cells Co-opt SOX5-driven Endochondral Ossification to Maintain Dormancy","authors":"Amulya Sreekumar, Eric Blankemeyer, Christopher J. Sterner, Tien-Chi Pan, Dhruv K. Pant, Sarah Acolatse, Hamza Turkistani, George K. Belka, Anupma Nayak, Sean D. Carlin, Charles-Antoine Assenmacher, Mark A. Sellmyer, David A. Mankoff, Lewis A. Chodosh","doi":"10.1158/2159-8290.cd-25-0919","DOIUrl":"https://doi.org/10.1158/2159-8290.cd-25-0919","url":null,"abstract":"Recurrent breast cancer accounts for most disease-associated mortality and can develop decades after primary tumor therapy. Recurrences arise from residual tumor cells (RTCs) that can evade therapy in a dormant state, however the mechanisms enforcing dormancy in RTCs are poorly understood. CRISPR-Cas9 screening identified the transcription factors SOX5/6 as functional regulators of tumor recurrence. Loss of SOX5 accelerated recurrence at both local and metastatic sites and promoted dormancy escape in both therapy-associated and microenvironment-induced contexts. Remarkably, SOX5 drove dormant RTCs to adopt a cartilage-dependent bone development program, termed endochondral ossification, that was confirmed by [18F]NaF-PET imaging and reversed in recurrent tumors escaping dormancy. Consistent with findings in mice, osteochondrogenic expression signatures in patients were enriched in residual disease following neoadjuvant therapy, and their enrichment in primary breast cancers predicted improved recurrence-free survival. These findings identify SOX5-dependent mesodermal transdifferentiation as an adaptive mechanism that prevents recurrence by reinforcing tumor cell dormancy.","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":"22 1","pages":""},"PeriodicalIF":28.2,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145717276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-10DOI: 10.1158/2159-8290.cd-25-1493
Meredith S. Shiels, Anika T. Haque, Rena R. Jones, Cari M. Kitahara, John W. Glod, Brigitte C. Widemann, Lindsay M. Morton, Stephen J. Chanock, Sharon A. Savage
We estimated trends in age-standardized childhood and adolescent cancer rates between 2001-2022 using national data from the United States Cancer Statistics database. The incidence of cancer in 0-19-year-olds was 18.2 per 100,000 with rates increasing 0.94%/year between 2001-2016 and then decreasing 0.96%/year during 2016-2022. Lymphoma rates increased 0.49%/year during 2001-2022, while trajectories of other cancers varied over time. Leukemia rates increased by 1.03%/year during 2001-2010 and then plateaued. Rates of central nervous system tumors increased by 0.81%/year during 2001-2014 and then declined 2.10%/year during 2014-2022. Rates of other epithelial neoplasms were stable from 2001-2013, increased in 2013-2016, and were stable during 2016-2022. There were an estimated 1,040 additional childhood cancer diagnoses in 2022 compared with what would have been expected based on 2001 rates. Modifications in cancer classifications, screening practices, and diagnostic technology likely contributed to the observed changes, in addition to the potential contributions of putative risk factors.
{"title":"Trends in Childhood and Adolescent Cancer Incidence Rates in the United States between 2001 and 2022","authors":"Meredith S. Shiels, Anika T. Haque, Rena R. Jones, Cari M. Kitahara, John W. Glod, Brigitte C. Widemann, Lindsay M. Morton, Stephen J. Chanock, Sharon A. Savage","doi":"10.1158/2159-8290.cd-25-1493","DOIUrl":"https://doi.org/10.1158/2159-8290.cd-25-1493","url":null,"abstract":"We estimated trends in age-standardized childhood and adolescent cancer rates between 2001-2022 using national data from the United States Cancer Statistics database. The incidence of cancer in 0-19-year-olds was 18.2 per 100,000 with rates increasing 0.94%/year between 2001-2016 and then decreasing 0.96%/year during 2016-2022. Lymphoma rates increased 0.49%/year during 2001-2022, while trajectories of other cancers varied over time. Leukemia rates increased by 1.03%/year during 2001-2010 and then plateaued. Rates of central nervous system tumors increased by 0.81%/year during 2001-2014 and then declined 2.10%/year during 2014-2022. Rates of other epithelial neoplasms were stable from 2001-2013, increased in 2013-2016, and were stable during 2016-2022. There were an estimated 1,040 additional childhood cancer diagnoses in 2022 compared with what would have been expected based on 2001 rates. Modifications in cancer classifications, screening practices, and diagnostic technology likely contributed to the observed changes, in addition to the potential contributions of putative risk factors.","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":"145 1","pages":""},"PeriodicalIF":28.2,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145717312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-06DOI: 10.1158/2159-8290.CD-25-0556
Ke Wang, Shayan Saniei, Nikita Poddar, Isabella G Martinez, Clifford Chao, Subrina Autar, Persephone Fiore, Saul Carcamo, Meghana Sreenath, Jack H Peplinski, Rhonda E Ries, Anna Huo-Chang Mei, Noshin Azra Rahman, Levan Mekerishvili, Miguel Quijada-Álamo, Grace Freed, Mimi Zhang, Katherine Lachman, Zayna Diaz, Manuel M Gonzalez, Jing Zhang, Giang Pham, Dan Filipescu, Mirela Berisa, Tommaso Balestra, Noelle Wheeler, Julie A Reisz, Angelo D'Alessandro, Daniel J Puleston, Emily Bernstein, Jerry E Chipuk, Mark Wunderlich, Sarah K Tasian, Bridget K Marcellino, Ian A Glass, Christopher M Sturgeon, Dan A Landau, Zhihong Chen, Eirini P Papapetrou, Franco Izzo, Soheil Meshinchi, Dan Hasson, Elvin Wagenblast
Accumulating evidence links pediatric cancers to prenatal transformation events, yet the influence of the developmental stage on oncogenesis remains elusive. We investigated how hematopoietic stem cell developmental stages affect leukemic transformation, disease progression, and therapy response using a novel, humanized model of NUP98::NSD1-driven pediatric acute myeloid leukemia that is particularly aggressive with WT1 comutations. Fetal-derived hematopoietic stem cells readily transform into leukemia, and WT1 mutations further enhance stemness and alter lineage hierarchy. In contrast, stem cells from later developmental stages become progressively resistant to transformation. Single-cell analyses revealed that fetal-origin leukemia stem cells exhibit greater quiescence and reliance on oxidative phosphorylation than their postnatal counterparts. These differences drive distinct therapeutic responses despite identical oncogenic mutations. In patients, onco-fetal transcriptional programs correlate with worse outcomes. By targeting key vulnerabilities of fetal-origin leukemia cells, we identified combination therapies that significantly reduce aggressiveness, highlighting the critical role of ontogeny in pediatric cancer treatment.
Significance: This study signifies the critical consequences of developmental timing in cancer initiation, revealing that identical driver mutations in fetal- versus postnatal-origin leukemias exhibit fundamentally distinct biology and treatment responses. Recognizing these developmental differences opens avenues for personalized therapeutic strategies, improving outcomes for pediatric patients with aggressive disease subtypes in leukemia.
{"title":"Ontogeny Dictates Oncogenic Potential, Lineage Hierarchy, and Therapy Response in Pediatric Leukemia.","authors":"Ke Wang, Shayan Saniei, Nikita Poddar, Isabella G Martinez, Clifford Chao, Subrina Autar, Persephone Fiore, Saul Carcamo, Meghana Sreenath, Jack H Peplinski, Rhonda E Ries, Anna Huo-Chang Mei, Noshin Azra Rahman, Levan Mekerishvili, Miguel Quijada-Álamo, Grace Freed, Mimi Zhang, Katherine Lachman, Zayna Diaz, Manuel M Gonzalez, Jing Zhang, Giang Pham, Dan Filipescu, Mirela Berisa, Tommaso Balestra, Noelle Wheeler, Julie A Reisz, Angelo D'Alessandro, Daniel J Puleston, Emily Bernstein, Jerry E Chipuk, Mark Wunderlich, Sarah K Tasian, Bridget K Marcellino, Ian A Glass, Christopher M Sturgeon, Dan A Landau, Zhihong Chen, Eirini P Papapetrou, Franco Izzo, Soheil Meshinchi, Dan Hasson, Elvin Wagenblast","doi":"10.1158/2159-8290.CD-25-0556","DOIUrl":"10.1158/2159-8290.CD-25-0556","url":null,"abstract":"<p><p>Accumulating evidence links pediatric cancers to prenatal transformation events, yet the influence of the developmental stage on oncogenesis remains elusive. We investigated how hematopoietic stem cell developmental stages affect leukemic transformation, disease progression, and therapy response using a novel, humanized model of NUP98::NSD1-driven pediatric acute myeloid leukemia that is particularly aggressive with WT1 comutations. Fetal-derived hematopoietic stem cells readily transform into leukemia, and WT1 mutations further enhance stemness and alter lineage hierarchy. In contrast, stem cells from later developmental stages become progressively resistant to transformation. Single-cell analyses revealed that fetal-origin leukemia stem cells exhibit greater quiescence and reliance on oxidative phosphorylation than their postnatal counterparts. These differences drive distinct therapeutic responses despite identical oncogenic mutations. In patients, onco-fetal transcriptional programs correlate with worse outcomes. By targeting key vulnerabilities of fetal-origin leukemia cells, we identified combination therapies that significantly reduce aggressiveness, highlighting the critical role of ontogeny in pediatric cancer treatment.</p><p><strong>Significance: </strong>This study signifies the critical consequences of developmental timing in cancer initiation, revealing that identical driver mutations in fetal- versus postnatal-origin leukemias exhibit fundamentally distinct biology and treatment responses. Recognizing these developmental differences opens avenues for personalized therapeutic strategies, improving outcomes for pediatric patients with aggressive disease subtypes in leukemia.</p>","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":" ","pages":"OF1-OF30"},"PeriodicalIF":33.3,"publicationDate":"2025-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145696056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-04DOI: 10.1158/2159-8290.cd-25-1101
Urvi A Shah,Laura Lucia Cogrossi,Juan-Jose Garces,Anna Policastro,Francesca Castro,Andriy Derkach,Teng Fei,Susan DeWolf,Matteo Grioni,Sofia Sisti,Jenna Blaslov,Peter A Adintori,Kinga K Hosszu,Devin McAvoy,Mirae Baichoo,Justin R Cross,Jenny Paredes,Aishwarya Anuraj,Sandeep S Raj,Charlotte Pohl,Paola Zordan,Victoria Zinsmeyer,Ruben J Jesus Faustino Ramos,Marco Lorenzoni,Brianna Gipson,Kylee H Maclachlan,Ana Gradissimo,Leonardo Boiocchi,Nathan Aleynick,Camilla Marchigiani,Sara Pagani,Erica Salehi,Richard P Koche,Ronan Chaligne,Torin Block,Neha Korde,Carlyn R Tan,Malin Hultcrantz,Hani Hassoun,Gunjan L Shah,Michael Scordo,Oscar B Lahoud,David J Chung,Heather J Landau,Jonathan U Peled,Nicola Clementi,Marta Chesi,P Leif Bergsagel,Sham Mailankody,Michael N Pollak,Anita D'Souza,Ola Landgren,Susan Chimonas,Sergio A Giralt,Saad Z Usmani,Neil M Iyengar,Alexander M Lesokhin,Marcel R M van den Brink,Matteo Bellone
Consumption of a western diet and high body mass index (BMI) are risk factors for progression from pre-malignant phenotypes to multiple myeloma, a hematologic cancer. In the NUTRIVENTION trial (NCT04920084), we administered a high-fiber, plant-based diet (meals for 12 weeks, coaching for 24 weeks) to 23 participants with myeloma precursor states and elevated BMI. The intervention was feasible, improved quality of life and modifiable risk factors: metabolic (BMI, insulin resistance), microbiome (diversity, composition), and immune (inflammation, monocyte subsets). Disease-progression trajectory improved (n=2) or was stable. Findings were translated to Vk*MYC mice modeling the myeloma-precursor state, in which a high-fiber diet delayed disease progression through improved metabolism and microbiome composition leading to increased short-chain fatty acid production that reinvigorated anti-tumor immunity and inhibited tumor growth. These effects from fiber consumption were independent of calorie restriction and weight loss. A high-fiber diet is a low-risk intervention that may delay progression to myeloma.
{"title":"A High-Fiber Plant-Based Diet in Myeloma Precursor Disorders - Results from the NUTRIVENTION Clinical Trial and Preclinical Vk*MYC Model.","authors":"Urvi A Shah,Laura Lucia Cogrossi,Juan-Jose Garces,Anna Policastro,Francesca Castro,Andriy Derkach,Teng Fei,Susan DeWolf,Matteo Grioni,Sofia Sisti,Jenna Blaslov,Peter A Adintori,Kinga K Hosszu,Devin McAvoy,Mirae Baichoo,Justin R Cross,Jenny Paredes,Aishwarya Anuraj,Sandeep S Raj,Charlotte Pohl,Paola Zordan,Victoria Zinsmeyer,Ruben J Jesus Faustino Ramos,Marco Lorenzoni,Brianna Gipson,Kylee H Maclachlan,Ana Gradissimo,Leonardo Boiocchi,Nathan Aleynick,Camilla Marchigiani,Sara Pagani,Erica Salehi,Richard P Koche,Ronan Chaligne,Torin Block,Neha Korde,Carlyn R Tan,Malin Hultcrantz,Hani Hassoun,Gunjan L Shah,Michael Scordo,Oscar B Lahoud,David J Chung,Heather J Landau,Jonathan U Peled,Nicola Clementi,Marta Chesi,P Leif Bergsagel,Sham Mailankody,Michael N Pollak,Anita D'Souza,Ola Landgren,Susan Chimonas,Sergio A Giralt,Saad Z Usmani,Neil M Iyengar,Alexander M Lesokhin,Marcel R M van den Brink,Matteo Bellone","doi":"10.1158/2159-8290.cd-25-1101","DOIUrl":"https://doi.org/10.1158/2159-8290.cd-25-1101","url":null,"abstract":"Consumption of a western diet and high body mass index (BMI) are risk factors for progression from pre-malignant phenotypes to multiple myeloma, a hematologic cancer. In the NUTRIVENTION trial (NCT04920084), we administered a high-fiber, plant-based diet (meals for 12 weeks, coaching for 24 weeks) to 23 participants with myeloma precursor states and elevated BMI. The intervention was feasible, improved quality of life and modifiable risk factors: metabolic (BMI, insulin resistance), microbiome (diversity, composition), and immune (inflammation, monocyte subsets). Disease-progression trajectory improved (n=2) or was stable. Findings were translated to Vk*MYC mice modeling the myeloma-precursor state, in which a high-fiber diet delayed disease progression through improved metabolism and microbiome composition leading to increased short-chain fatty acid production that reinvigorated anti-tumor immunity and inhibited tumor growth. These effects from fiber consumption were independent of calorie restriction and weight loss. A high-fiber diet is a low-risk intervention that may delay progression to myeloma.","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":"98 1","pages":""},"PeriodicalIF":28.2,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145664108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-02DOI: 10.1158/2159-8290.cd-25-1784
Nicholas Mai, Nicole Fernandez, Alexander Drilon, Debyani Chakravarty
Summary: This article discusses the specific advances made in precision oncology in 2025, in which we saw the approval of multiple new indications for known precision oncology agents and early promising data for novel agents that target either classical pathways or previously so-called undruggable targets. Additionally, we observed the continued development of antibody–drug conjugates and proteolysis-targeting chimeras, the advent of multiple blood-based methodologies for the early detection of cancer, the identification of nontraditional precision oncology biomarkers, and the growing presence of artificial intelligence technologies to generate precision oncology insights.
{"title":"Precision Oncology: 2025 in Review","authors":"Nicholas Mai, Nicole Fernandez, Alexander Drilon, Debyani Chakravarty","doi":"10.1158/2159-8290.cd-25-1784","DOIUrl":"https://doi.org/10.1158/2159-8290.cd-25-1784","url":null,"abstract":"Summary: This article discusses the specific advances made in precision oncology in 2025, in which we saw the approval of multiple new indications for known precision oncology agents and early promising data for novel agents that target either classical pathways or previously so-called undruggable targets. Additionally, we observed the continued development of antibody–drug conjugates and proteolysis-targeting chimeras, the advent of multiple blood-based methodologies for the early detection of cancer, the identification of nontraditional precision oncology biomarkers, and the growing presence of artificial intelligence technologies to generate precision oncology insights.","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":"6 1","pages":""},"PeriodicalIF":28.2,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145651226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：