ReviewActa pharmacologica Sinica2021
Mutations in key driver genes of pancreatic cancer: molecularly targeted therapies and other clinical implications.
Review in Acta pharmacologica Sinica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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Who cites it
98 citing papers in PubMed, 145 citations in OpenAlex.
- Simultaneous quantitative detection of multiple low-frequency variants by high-dynamic-range capillary electrophoresis.Molecular therapy. Nucleic acids · 2026Article
- Targeted Therapy in Pancreatic Ductal Adenocarcinoma: Current Advances and Challenges.Current oncology (Toronto, Ont.) · 2026Review
- Improving pancreatic adenocarcinoma prognosis models through ligand receptor interactions and histopathological integration.Journal of translational medicine · 2026Article
- Review
- An integrative mutational and network analysis of pancreatic cancer reveals key genes, and signalling pathways.Functional & integrative genomics · 2026Article
- Pancreatic ductal adenocarcinoma: integrating molecular insights for targeted interventions.Signal transduction and targeted therapy · 2026Review
- Personalized signaling pathway analysis of gastrointestinal tumors for patient stratification and drug target evaluation using clinically derived core biopsies.NPJ precision oncology · 2026Article
- Combination of PARP and KRASNature communications · 2026Article
- Antimetastatic effects of MRTX1133 KRAS G12D specific inhibitor in a liver metastatic model of pancreatic ductal adenocarcinoma.Scientific reports · 2026Article
- A Combinatorial Effect of Immune Checkpoint Inhibitors and CD40 Agonistic Antibody in Murine Pancreatic Cancer Model.Cancer science · 2026Article
- Blockade of CC chemokine receptor 2 suppresses pancreatic cancer progression through the interaction with macrophages in the tumor microenvironment.Scientific reports · 2025Article
- Identifying gene expression signatures of oncolytic virus response in patient-derived pancreatic ductal adenocarcinoma organoids.Molecular therapy. Oncology · 2025Article
- Gastrointestinal cancer: molecular pathogenesis and targeted therapy.Molecular biomedicine · 2025Review
- Nationwide Real-World Usage of Blood-Based (Liquid) Biomarker Testing in Japan.Cancer science · 2025Article
- Emerging therapeutic advancements in pancreatic cancer: a contemporary review.Discover oncology · 2025Review
- P53 Function Status Correlates With Overall Survival in Patients With Resected Pancreatic Cancer.Journal of surgical oncology · 2025Article
- Review
- Somatic Mutation Detection in Tumor Tissue and Matched Cell-Free DNA Using PCR-Based Methods in Pancreatic Cancer Patients Undergoing Upfront Resection.International journal of molecular sciences · 2025Article
- PR55α subunit of protein phosphatase 2A supports KRASOncogene · 2025Article
- Identification of multiple genomic alterations and prediction of neoantigens from circulating tumor cells at the single-cell level.Nature communications · 2025Article
38 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers, with a minimal difference between its incidence rate and mortality rate. Advances in oncology over the past several decades have dramatically improved the overall survival of patients with multiple cancers due to the implementation of new techniques in early diagnosis, therapeutic drugs, and personalized therapy. However, pancreatic cancers remain recalcitrant, with a 5-year relative survival rate of <9%. The lack of measures for early diagnosis, strong resistance to chemotherapy, ineffective adjuvant chemotherapy and the unavailability of molecularly targeted therapy are responsible for the high mortality rate of this notorious disease. Genetically, PDAC progresses as a complex result of the activation of oncogenes and inactivation of tumor suppressors. Although next-generation sequencing has identified numerous new genetic alterations, their clinical implications remain unknown. Classically, oncogenic mutations in genes such as KRAS and loss-of-function mutations in tumor suppressors, such as TP53, CDNK2A, DPC4/SMAD4, and BRCA2, are frequently observed in PDAC. Currently, research on these key driver genes is still the main focus. Therefore, studies assessing the functions of these genes and their potential clinical implications are of paramount importance. In this review, we summarize the biological function of key driver genes and pharmaceutical targets in PDAC. In addition, we conclude the results of molecularly targeted therapies in clinical trials and discuss how to utilize these genetic alterations in further clinical practice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.