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    CANCER:

    Pancreatic Ductal Adenocarcinoma

    Related cancers:
    1d
    SRC at the Crossroads of KRAS Inhibitor Resistance: Mechanisms and Therapeutic Opportunities. (PubMed, Cancer Lett)
    We also critically examine the shortcomings of early-generation SRC inhibitors in solid tumors and highlight emerging therapeutic avenues such as next-generation inhibitors, proteolysis-targeting chimera (PROTAC) degraders, and biomarker-guided combination strategies. By connecting molecular insights with preclinical and clinical findings, this review positions SRC as a therapeutically actionable vulnerability in KRAS-driven cancers and outlines a translational framework for overcoming drug resistance.
    Review • Journal
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    KRAS (KRAS proto-oncogene GTPase)
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    KRAS mutation • KRAS G12C
    1d
    Extracellular vesicles from obese visceral adipose promote pancreatic cancer development and resistance to immune checkpoint blockade therapy. (PubMed, Cell Metab)
    Animal experiments indicate that Ctsa knockdown effectively enhances ICB efficacy on PDAC. Our study uncovers a VAT-EV CTSA-pseudouridine-mast cell axis connecting obesity and cancer, which holds promise for developing new therapeutic strategies for obesity-related cancers.
    Journal • Checkpoint inhibition
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    CD8 (cluster of differentiation 8) • RNASET2 (Ribonuclease T2)
    1d
    The CHPT-pSTAT3-SLC7A11 signaling axis controls progression and ferroptosis susceptibility of pancreatic cancer. (PubMed, Transl Oncol)
    The CHPT1-pSTAT3-SLC7A11 axis governs ferroptosis-dependent chemoresistance in PDAC. Dual targeting of CHPT1 and ferroptosis pathways represents a promising strategy to overcome GEM resistance, highlighting metabolic-kinase crosstalk as a therapeutic vulnerability.
    Journal
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    PTPN1 (Protein Tyrosine Phosphatase Non-Receptor Type 1) • SLC7A11 (Solute Carrier Family 7 Member 11)
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    gemcitabine • erastin
    1d
    Decoding the role of mesothelin in tumor dynamics and targeted treatment innovations. (PubMed, Mol Biomed)
    We also summarize ongoing therapeutic strategies targeting MSLN and discuss how TME-driven resistance mechanisms are shaping the next generation of MSLN-directed therapies. By integrating molecular insights with translational perspectives, this work provides a comprehensive overview of MSLN biology and its emerging therapeutic relevance in cancer.
    Review • Journal
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    MSLN (Mesothelin) • MRC1 (Mannose Receptor C-Type 1) • MMP7 (Matrix metallopeptidase 7)
    2d
    A Study of Blood Based Biomarkers for Pancreas Adenocarcinoma (clinicaltrials.gov)
    P=N/A, N=700, Recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Oct 2025 --> Oct 2026 | Trial primary completion date: Oct 2025 --> Oct 2026
    Trial completion date • Trial primary completion date
    3d
    A targeted combination therapy achieves effective pancreatic cancer regression and prevents tumor resistance. (PubMed, Proc Natl Acad Sci U S A)
    Likewise, a combination of selective inhibitors of KRAS (RMC-6236/daraxonrasib), EGFR family (afatinib), and STAT3 (SD36) induced the complete regression of orthotopic PDAC tumors with no evidence of tumor resistance for over 200 d posttreatment...Of importance, this combination therapy was well tolerated. In sum, these results should guide the development of new clinical trials that may benefit PDAC patients.
    Journal
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    EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53)
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    TP53 mutation • KRAS mutation
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    Gilotrif (afatinib) • MRTX1133 • daraxonrasib (RMC-6236)
    3d
    Serum MicroRNA-196, -200 and -423 Improve Diagnostics and Differentiate Pancreatic Ductal Adenocarcinoma From Chronic Pancreatitis. (PubMed, Physiol Res)
    Panel of six miRNAs could be used as reliable marker in differentiating PDAC from chronic pancreatitis with the most impressive difference in miR-196 and miR-423. Key words microRNA " Pancreatic ductal adenocarcinoma " Chronic pancreatitis " Biomarker " CA19-9.
    Journal
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    MIR21 (MicroRNA 21) • CA 19-9 (Cancer antigen 19-9) • MIR423 (MicroRNA 423)
    3d
    Mitochondrial-targeted photodynamic therapy combined with TGF-β inhibition potentiates anti-PD-1 therapy in pancreatic ductal adenocarcinoma. (PubMed, J Nanobiotechnology)
    To address these challenges, we develop a liposomal nanodrug that co-encapsulates a mitochondrial-targeted photosensitizer (MP) and a TGF-β receptor inhibitor (LY2109761) to synergize PDT with PD-1 checkpoint blockade...In murine PDAC models, this dual-action strategy transforms the immune-cold TME into an immune-inflamed phenotype, sensitizing tumors to PD-1 therapy and leading to pronounced tumor regression and prolonged survival. Our findings present a promising nanodrug-based approach to remodel the fibrotic and immunosuppressive TME of PDAC and enhance immunotherapeutic outcomes.
    Journal
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    TGFB1 (Transforming Growth Factor Beta 1)
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    LY2109761
    3d
    NIRADO: Basket Trial Exploring the Efficacy and Safety of the Combination of Niraparib and Dostarlimab (clinicaltrials.gov)
    P2, N=51, Terminated, Gustave Roussy, Cancer Campus, Grand Paris | Trial completion date: Dec 2027 --> Feb 2025 | Suspended --> Terminated; Abandon of the partner, GSK
    Trial completion date • Trial termination • Pan tumor • Platinum sensitive
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    HER-2 (Human epidermal growth factor receptor 2) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • ARID1A (AT-rich interaction domain 1A) • PBRM1 (Polybromo 1) • CDK12 (Cyclin dependent kinase 12) • CHEK2 (Checkpoint kinase 2) • RAD51 (RAD51 Homolog A) • FANCA (FA Complementation Group A) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • RAD51C (RAD51 paralog C) • RAD51D (RAD51 paralog D) • ARID2 (AT-Rich Interaction Domain 2) • BARD1 (BRCA1 Associated RING Domain 1) • NBN (Nibrin Nijmegen Breakage Syndrome 1 (Nibrin)) • RAD54L (DNA Repair And Recombination Protein RAD54) • DRD (DNA Repair Deficiency)
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    HER-2 positive • HER-2 amplification • DDR • CDK12 mutation • CHEK2 mutation • BRIP1 mutation • RAD51C mutation • RAD51D mutation • BARD1 mutation
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    Zejula (niraparib) • Jemperli (dostarlimab-gxly)
    3d
    RASH3D19 mediates RAS activation through a positive feedback loop in KRAS-mutant cancer. (PubMed, Nat Cell Biol)
    Genetic deletion of RASH3D19 in mutant KRAS-expressing cancer cells exhibits growth retardation in vitro, in vivo and sensitized pancreatic ductal adenocarcinoma and colorectal cancer cells, organoids and xenografts to mutant KRAS inhibitors, suppressing feedback reactivation of RAS pathways. Therapeutic targeting of RASH3D19 is expected to lead to tumour debulking and alleviating resistance to KRAS inhibitors in mutant KRAS-expressing cancers.
    Journal
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    EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • ETS1 (ETS Proto-Oncogene 1) • SH3D19 (SH3 Domain Containing 19) • GAB1 (GRB2 Associated Binding Protein 1) • MIR222 (MicroRNA 222)
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    KRAS mutation
    4d
    NQO1 as a predictor of response to adjuvant GemCap treatment for pancreatic cancer. (PubMed, J Natl Cancer Inst)
    High tumor NQO1 predicts better outcome following GemCap therapy.
    Journal
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    NQO1 (NAD(P)H dehydrogenase, quinone 1)
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    gemcitabine • 5-fluorouracil • capecitabine
    4d
    Oncolytic Newcastle-disease-virus-mediated CD47 blockade in preclinical melanoma and pancreatic cancer models. (PubMed, Mol Ther Oncol)
    Although NDV-mediated CD47 blockade resulted in increased numbers of PD-1+ CD8 T cells, synergy between NDV, CD47, and PD-L1 blockade was limited. Together these data highlight the importance of considering tumor-intrinsic factors when combining cancer immunotherapies for improved outcomes.
    Preclinical • Journal • PD(L)-1 Biomarker • IO biomarker
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    CD8 (cluster of differentiation 8) • CD47 (CD47 Molecule) • SIRPA (Signal Regulatory Protein Alpha)