Molecular Cancer Therapeutics最新文献

{"title":"Integrin β6-Targeted CAR-T Cells exhibit potent antitumor activity in β6-Positive pancreatic ductal adenocarcinoma and lung adenocarcinoma.","authors":"Lingchao Shi, Le Qin, Shuxin Sun, Kai Yin, Heng Jia, Yongfang Zheng, Yunlin Huang, Georgia Carson, Qiting Wu, Youguo Long, Zhiping Wu, Xing-Yuan Shi, Runhui Zheng, Dajiang Qin, Liqiang Feng, Linping Wu, Jun He, Jiekai Chen, Yao Yao, Peng Li","doi":"10.1158/1535-7163.MCT-25-1246","DOIUrl":"https://doi.org/10.1158/1535-7163.MCT-25-1246","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) and lung adenocarcinoma (LUAD) remain lethal malignancies with limited therapeutic options, highlighting an urgent need for more effective treatments. Integrin αvβ6 (ITGB6) is a receptor preferentially expressed in specific types of tumors, such as PDAC and LUAD, and represents a promising yet largely untapped target for cellular immunotherapy. We aimed to develop and preclinically validate a novel chimeric antigen receptor T-cell (CAR-T) therapy targeting ITGB6 for these aggressive solid tumors. A third-generation anti-ITGB6 CAR was designed and constructed, incorporating both CD28 and TLR2 co-stimulatory domains. TLR2 signaling enhances T-cell expansion, cytokine production, and infiltration into solid tumor. The potency and specificity of anti-ITGB6 CAR-T cells were assessed against a panel of ITGB6-positive PDAC and LUAD cell lines, patient-derived organoids (PDOs), orthotopic models, and patient-derived xenograft (PDX) models. Anti-ITGB6 CAR-T cells demonstrated potent cytotoxicity against ITGB6-positive PDAC and LUAD models in vitro, effectively targeting both cell lines and PDOs. In murine xenograft models, a single dose of anti-ITGB6 CAR-T cells induced significant tumor suppression and prolonged survival, with no evidence of on-target/off-tumor toxicity was observed. Our findings provide compelling preclinical proof-of-concept for anti-ITGB6 CAR-T therapy as a potent and safe investigational strategy against ITGB6-positive solid tumors, supporting its clinical translation for patients with PDAC and LUAD.</p>","PeriodicalId":18791,"journal":{"name":"Molecular Cancer Therapeutics","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148758592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sensitivity of pancreatic adenocarcinoma cells to blockade of post-initiation CDK-dependent Pol II transcription cycle checkpoints.","authors":"Yvonne T Daniel, Benjamin P Martin, Nenad Bartonicek, Ricky W Johnstone, Jennifer R Devlin","doi":"10.1158/1535-7163.MCT-25-1529","DOIUrl":"https://doi.org/10.1158/1535-7163.MCT-25-1529","url":null,"abstract":"<p><p>Pancreatic adenocarcinoma (PDAC) is a leading cause of cancer-related morbidity, with oncogenic KRAS/MAPK/ERK signalling arising from activating KRAS mutations being the key feature of this malignancy. Dysregulation of RNA polymerase II (Pol II)-dependent transcription is a universal hallmark of cancers including PDAC, with aberrant gene expression programs driving tumorigenesis and influencing therapy response. Pol II progression through multiple transcription cycle checkpoints depends on transcriptional cyclin-dependent-kinases (tCDKs), and targeted inhibition of distinct tCDKs has been shown to be a promising anti-cancer strategy. In this study we profile biological and molecular PDAC cell responses to selective blockade of tCDK kinase activity at all Pol II transcription cycle checkpoints, alone and in combination with inhibitors of mutant-KRAS or MEK. We identify post-transcription-initiation checkpoints controlled by CDK9, CDK11, and CDK12/13 as critical for nascent gene expression and cell proliferation in PDAC. However, while dual targeting of tCDK and KRAS/MAPK/ERK networks amplifies transcriptomic phenotypes this resulted in limited cooperative therapeutic impacts.</p>","PeriodicalId":18791,"journal":{"name":"Molecular Cancer Therapeutics","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148761893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dual Targeting of EGFR and HER2 by a Bispecific Antibody-Drug Conjugate Demonstrates Broad Antitumor Activity in Multiple Solid Tumors.","authors":"Xiaojuan Chai, Fu Li, Hongmei Xie, Hanxi Yu, Xiaojing Huang, Yihui Lin, Yuting Lu, Nan Li, Tete Li, Qiangqiang Deng, Weiming He, Wenqiang Zhai, Shu Zhang, Xiaozhen Wang, Haizhou Zhang, Fanglong Yang, Siqin Wang, Lei Jin, John L Xu","doi":"10.1158/1535-7163.MCT-26-0143","DOIUrl":"https://doi.org/10.1158/1535-7163.MCT-26-0143","url":null,"abstract":"<p><p>While HER2-directed antibody-drug conjugates (ADCs), such as ENHERTU® (DS-8201), represent a major therapeutic advance, treatment options for tumors with low HER2 expression remain limited, and acquired resistance continues to pose a significant clinical challenge. Given the frequent co-expression of EGFR and HER2 across multiple tumor types, we hypothesized that dual targeting could improve therapeutic efficacy and overcome resistance mechanisms. This approach may achieve broader tumor coverage, synergistic enhancement of binding and internalization, and concurrent blockade of two key oncogenic pathways. To test this, we developed GenSci139, an EGFR×HER2 bispecific ADC (BsADC). It is conjugated via a novel, proprietary hydrophilic peptide-cleavable linker to a potent topoisomerase I inhibitor payload. In preclinical studies, GenSci139 exhibited remarkable plasma stability and favorable pharmacokinetics, enabling efficient tumor-specific payload delivery. Compared to monospecific ADCs, it demonstrated superior binding affinity and enhanced internalization across a panel of cancer cell lines with diverse EGFR/HER2 expression profiles. In vitro, GenSci139 mediated potent cytotoxic activity and induced a robust bystander-killing effect. Furthermore, its parental bispecific antibody effectively inhibited both EGF-induced signaling and cell proliferation. In vivo, GenSci139 demonstrated superior antitumor efficacy over DS-8201 in multiple cell-line-derived xenograft and patient-derived xenograft models. Mechanistic studies revealed that GenSci139 induced DNA damage, apoptosis, and hallmarks of immunogenic cell death, suggesting potential for synergistic combination with immunotherapies. Collectively, our preclinical data position GenSci139 as a promising novel therapeutic candidate with the potential to address the unmet medical need in a broad spectrum of solid tumors, including those of the lung, breast and stomach.</p>","PeriodicalId":18791,"journal":{"name":"Molecular Cancer Therapeutics","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148684818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microsatellite Instable Cancer Cells Acquire On-target Resistance Mutations to WRN Helicase Inhibitors.","authors":"Faith Fowler, Jessica Gajda, Amirhossein Mafi, Aileen Kelly, Cynthia L Jeffries, Phuong Le, Lei Shi, Mariam George, Nathaniel Elsen, Alla V Korepanova, Sarah M Zerbs, Orville A Pemberton, Xiangdong Xu, Nathan Gesmundo, Wei Qiu, Fei Han, Henry Tang, Sanjay C Panchal, Michael Dart, Jonathan Hickson, Chaohong Sun, Yunsong Tong, Ari J Firestone","doi":"10.1158/1535-7163.MCT-25-0666","DOIUrl":"10.1158/1535-7163.MCT-25-0666","url":null,"abstract":"<p><p>The Werner syndrome helicase (WRN) is a promising target for cancers with microsatellite instability (MSI), leading to the initiation of at least five phase I clinical trials. Acquired resistance is a substantial obstacle to obtaining lasting benefits from targeted therapies in oncology and may be particularly acute in the setting of mismatch repair-deficient (dMMR) tumors, which can sample increased fitness landscapes owing to a higher mutational burden. In this study, we characterized resistance mechanisms using the clinical candidate HRO761 and two novel inhibitors in MSI cell lines and xenograft models. We observed the rapid emergence of resistance both in vitro and in vivo, with sequencing revealing clustered mutations within the WRN helicase domain. Computational structural analyses indicated that these mutations either directly interfere with inhibitor binding or alter the protein conformation required for inhibitor engagement. Notably, although most mutations conferred broad resistance across all three compounds, we identified specific alterations (L528S, C727R, and F730L) that exhibited selectivity between chemical scaffolds. This chemotype-specific resistance profile suggests opportunities for developing next-generation inhibitors that retain activity against resistant variants and for implementing rational treatment strategies with existing inhibitors. Overall, our findings demonstrate that on-target resistance to WRN inhibitors emerges rapidly in dMMR backgrounds but also highlight potential approaches to overcome resistance, supporting the continued development of WRN-targeted therapies for MSI cancers.</p>","PeriodicalId":18791,"journal":{"name":"Molecular Cancer Therapeutics","volume":" ","pages":"1381-1392"},"PeriodicalIF":6.9,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13434289/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146142938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proteolysis Targeting Chimeric-Based Technology in Myeloma and Lymphoma.","authors":"Adrian Bogdan Tigu, Andrei Ivancuta, Ciprian Tomuleasa, Madalina Nistor, David Kegyes, Diana Cenariu, Raluca Munteanu, Anca-Dana Buzoianu, Hermann Einsele, Massimo Federico, Sebastian Kobold, Diana Gulei, Aaron Ciechanover","doi":"10.1158/1535-7163.MCT-25-1148","DOIUrl":"10.1158/1535-7163.MCT-25-1148","url":null,"abstract":"<p><p>Proteolysis-targeting chimeras (PROTAC) leverage the ubiquitin-proteasome system to selectively degrade oncogenic proteins, including those previously seen as undruggable. Recent preclinical studies indicate that PROTACs may represent a novel therapeutic strategy in lymphoma and myeloma. Indeed, preclinically, PROTACs have shown high efficacy and remarkable selectivity, a favorable safety profile, and lower toxicity compared with conventional therapies. Their catalytic, reusable mechanism enables drug dosing and offers the perspective of long-term low-dose treatment. PROTACs have demonstrated their ability to overcome drug resistance by targeting and degrading overexpressed or mutant proteins that are responsible for refractory disease. This review aims to offer a comprehensive evaluation of the currently existing PROTACs that have been tested in lymphoma and myeloma to highlight the need for drug optimization and further translational research that could translate PROTACs to clinical trials.</p>","PeriodicalId":18791,"journal":{"name":"Molecular Cancer Therapeutics","volume":" ","pages":"1264-1280"},"PeriodicalIF":6.9,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13434293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145889557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ISL1: A Novel Neuroendocrine Subtype in Small Cell Lung Cancer Predicts Durable Response to Lurbinectedin.","authors":"Misty D Shields, Katherine G Minton, Hilal Ozakinci, Tianhao Zhou, Olivia C Terry, Paresh Kumar, Reem Akel, Luc Girard, John D Minna, Theresa A Boyle, John M Koomen, Michael Shafique","doi":"10.1158/1535-7163.MCT-25-0663","DOIUrl":"10.1158/1535-7163.MCT-25-0663","url":null,"abstract":"<p><p>Small cell lung cancer (SCLC) is a recalcitrant thoracic malignancy known for acquired chemoresistance, early metastatic spread, and poor overall survival. Lurbinectedin, a DNA minor groove alkylating agent, provides durable efficacy in a minority. Predictive biomarkers for lurbinectedin are needed. Patients with relapsed SCLC who received lurbinectedin (n = 16) were classified by cycles received, including eight durable responders defined as ≥8 cycles (average, 14.75 cycles; median progression-free survival, 9.8 months). Pretreatment specimens were analyzed by immunohistochemistry (IHC) for Schlafen-11 (SLFN11) and tandem mass tag-labeled expression proteomics. Top candidates were confirmed by IHC and functionally validated in SCLC cell lines. SLFN11 failed to predict lurbinectedin response (P = 0.40). Proteomics highlighted a primitive neuroendocrine (NE) pathway [Islet-1 (ISL1), SOX5, SIX1, SIX4]. ISL1 expression significantly correlated with lurbinectedin response (r = 0.65; P = 0.0351). IHC confirmed that lurbinectedin reduced ISL1 after treatment. Lurbinectedin preferentially induced DNA damage in ISL1-\"high\" SCLC (P < 0.0001) without causing NE subtype switching. RNA sequencing showed downregulation of ISL1, RBMS3, ASCL1, SOX5, and SIX1 and upregulation of ATF3. ISL1-\"high\" SCLC demonstrated cellular dependency on ISL1; ISL1 knockdown reduced lurbinectedin sensitivity. L-MYC positively regulated ISL1, whereas ISL1 positively regulated ASCL1 and SOX5. This is the first comprehensive investigation of predictive biomarkers for lurbinectedin. Proteomics identified ISL1 as defining a novel SCLC subtype with enhanced lurbinectedin sensitivity. ISL1 serves as both a predictive biomarker and a functional dependency, as evidenced by its essentiality for cell survival and loss following treatment. Prospective studies using ISL1 as a predictive biomarker for lurbinectedin are planned.</p>","PeriodicalId":18791,"journal":{"name":"Molecular Cancer Therapeutics","volume":" ","pages":"1393-1407"},"PeriodicalIF":6.9,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146046808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In Vivo Analysis of Neuroblastoma Targeting Potential of aGD2-SIRPα Fusion Antibodies for Local CD47 Blockade.","authors":"Fabian Schuurmans, Matthia G M Boros, Renske J E van den Bijgaart, Anja Wittner, Janneke D M Molkenboer-Kuenen, Jasper Lok, Siret Tahk, Karl-Peter Hopfner, Sandra Heskamp, Gosse J Adema","doi":"10.1158/1535-7163.MCT-25-1169","DOIUrl":"10.1158/1535-7163.MCT-25-1169","url":null,"abstract":"<p><p>Anti-GD2 monoclonal antibodies (aGD2 mAbs) are the standard immunotherapy for patients with high-risk neuroblastoma. This treatment has improved 5-year overall survival; however, long-term efficacy still requires improvement. The \"don't eat me\" signal CD47 is upregulated on neuroblastoma tumor cells and inhibits aGD2 mAb effector mechanisms. Although GD2 is restrictively expressed on neuroblastoma tumor cells, CD47 expression is ubiquitous, resulting in an antigen sink and on-target off-tumor-related cytotoxicities. Recently, we developed two aGD2-SIRPα fusion mAbs for the murine and human settings. In vitro, these aGD2-SIRPα fusion mAbs restrict CD47 blockade toward GD2+ neuroblastoma tumor cells. In this study, we explored the tumor-targeting ability of aGD2-SIRPα fusion mAbs in a syngeneic 9464D-Luc-GFP and SK-N-AS xenograft neuroblastoma tumor model. Conventional aCD47 and aSIRPα mAbs encountered a dominant antigen sink in the 9464D-Luc-GFP model. Surprisingly, although aGD2 mAbs preferentially targeted tumors, murine aGD2-mSIRPα fusion mAbs accumulated in similar organs as aCD47 mAbs. Binding analysis of murine aGD2-mSIRPα and human aGD2-hSIRPα fusion mAbs to red blood cells (RBC) revealed strong binding of murine aGD2-mSIRPα to RBCs, whereas their human counterparts showed negligible binding. These data indicate species-specific CD47-SIRPα binding patterns. Utilizing a SK-N-AS xenograft model, we show effective tumor targeting of the human aGD2-hSIRPα fusion mAbs with hSIRPα in a C-terminal configuration. These data provide the first proof of principle for neuroblastoma tumor-targeted blockade of CD47 by aGD2-hSIRPα fusion mAbs in vivo and support the further development of aGD2-hSIRPα mAbs as attractive therapeutics to improve aGD2-based neuroblastoma immunotherapy.</p>","PeriodicalId":18791,"journal":{"name":"Molecular Cancer Therapeutics","volume":" ","pages":"1357-1368"},"PeriodicalIF":6.9,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147513560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction: Mammalian Target of Rapamycin Inhibitors Activate the AKT Kinase in Multiple Myeloma Cells by Up-regulating the Insulin-like Growth Factor Receptor/Insulin Receptor Substrate-1/Phosphatidylinositol 3-Kinase Cascade.","authors":"Yijiang Shi, Huajun Yan, Patrick Frost, Joseph Gera, Alan Lichtenstein","doi":"10.1158/1535-7163.MCT-26-0615","DOIUrl":"10.1158/1535-7163.MCT-26-0615","url":null,"abstract":"","PeriodicalId":18791,"journal":{"name":"Molecular Cancer Therapeutics","volume":"25 8","pages":"1411"},"PeriodicalIF":6.9,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148670092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DSP502 Combines Dual Inhibition of PD-L1 and PVR to Trigger Anticancer Immune Responses.","authors":"Vinicio A Melo Gallegos, Shirley Greenwald, Ami Tamir, Lisa J Jacob, Macarena González Corrales, Lior Tsveyer, Alexandra Aronin, Iris Pecker, Rinat Tabakman, Lucy Ghantous, Liat Tamir, Roy Kahn, Elina Zorde Khvalevsky, Amnon Peled, Ori Wald, Mark Tykocinski, Yaron Pereg, Ayelet Chajut, Edwin Bremer","doi":"10.1158/1535-7163.MCT-25-0102","DOIUrl":"10.1158/1535-7163.MCT-25-0102","url":null,"abstract":"<p><p>PD-1 immune checkpoint inhibition (ICI) is ineffective in most patients with cancer. However, combination therapy can improve response rates, with the checkpoint TIGIT being a particularly interesting candidate as it is expressed on tumor-infiltrating exhausted T and NK cells. TIGIT's primary ligand, PVR, is overexpressed in many cancers, and both TIGIT and PVR correlate with poor prognosis. To therapeutically exploit this, we developed a novel therapeutic termed dual signaling protein 502 (DSP502). DSP502 is composed of the extracellular domains of TIGIT and PD-1, each fused to human IgG1 Fc containing knob-in-hole mutations. DSP502 was designed to simultaneously block PVR/TIGIT and PD-L1/PD-1 by binding to cancer cell-expressed PVR and PD-L1. Moreover, the human IgG1 domain can recruit FcR-positive effector cells to further reactivate anticancer immunity. Treatment with DSP502 potentiated NK cell activation and boosted the anticancer cytotoxicity of peripheral blood mononuclear cells and tumor-infiltrating lymphocytes from patients with non-small cell lung cancer (NSCLC) and metastatic colorectal cancer toward cancer cells expressing both PD-L1 and PVR. Transcriptomic analysis confirmed NSCLC as a potential target, showing co-expression of TIGIT and PD-1 (PDCD1) on a high percentage of exhausted CD8+ T cells. Notably, treatment with DSP502 not only blocked checkpoint signaling but also preserved surface expression of the co-stimulatory PVR ligand, DNAM-1, on T and NK cells. Finally, DSP502 inhibited tumor growth by potentiating antitumor immunity in xenograft ovarian and lung cancer models. Collectively, these findings demonstrate that DSP502, by blocking PVR and PD-L1 pathways, has dual ICI activity and holds potential therapeutic benefits for cancers such as NSCLC.</p>","PeriodicalId":18791,"journal":{"name":"Molecular Cancer Therapeutics","volume":" ","pages":"1246-1263"},"PeriodicalIF":6.9,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146041371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Heat Shock Protein-90 Inhibition Alters Activation of Pancreatic Stellate Cells and Enhances the Efficacy of PD-1 Blockade in Pancreatic Cancer.","authors":"Yuchen Zhang, Michael B Ware, Mohammad Y Zaidi, Amanda N Ruggieri, Brian M Olson, Hannah Komar, Matthew R Farren, Ganji Purnachandra Nagaraju, Chao Zhang, Zhengjia Chen, Juan M Sarmiento, Rafi Ahmed, Shishir K Maithel, Bassel F El-Rayes, Gregory B Lesinski","doi":"10.1158/1535-7163.MCT-26-0614","DOIUrl":"https://doi.org/10.1158/1535-7163.MCT-26-0614","url":null,"abstract":"","PeriodicalId":18791,"journal":{"name":"Molecular Cancer Therapeutics","volume":"25 8","pages":"1409"},"PeriodicalIF":6.9,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148670064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}