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Mutations in key driver genes of pancreatic cancer: molecularly targeted therapies and other clinical implications
Open accessAbstract
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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In the citing paper
“KRAS and GNAS mutations are known to drive the progression of IPMNs [43].”
From Artificial Intelligence in the Diagnosis and Treatment of Pancreatic Cystic Lesions and Adenocarcinoma (2023) · cites this paper as [43]
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“Pancreatic cancer commonly features mutations in key genes, such as KRAS, p16/CDKN2A, TP53 and SMAD4/DPC4 [3,4,5] (Table 1).”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [5]
In the citing paper
“Co-occurrence of other mutations were common in PDAC”
From Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma (2024) · cites this paper as [47]
In the citing paper
“the disease progression model proposed based on observed co-mutation patterns was early KRAS mutation followed by CDKN2A then loss of TP53 and SMAD447,48”
From Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma (2024) · cites this paper as [47]
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Metadata
- Authors
- Hu, H.-F., Ye, Z., Qin, Y., Xu, X.-W., Yu, X.-J., Zhuo, Q.-F., & Ji, S.-R.
- Affiliations
- Shanghai Medical College of Fudan University (CN)
- ORCID
- Qin, Yi
- Venue
- Acta Pharmacologica Sinica
- Published
- 2021-02-11
- Volume
- 42
- Issue
- 11
- Pages
- 1725-1741
- ISSN
- 0253-9756 (ISSN-L)
- 1671-4083
- 1745-7254
- PMC
- PMC8563973
- OpenAlex
- W3126704571
- Cited by
- 149
- References
- 244
- Citations by year
- 2026: 21 · 2025: 41 · 2024: 50 · 2023: 25 · 2022: 9 · 2021: 3
- FWCI
- 2.70
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Acta Pharmacologica Sinica (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Science Foundation (81625016)
- National Natural Science Foundation of China (81871950 and 81972250, 2019-01-07-00-07-E00057, 81625016, 81871950, 2019-01, 81972250)
- National Science Fund for Distinguished Young Scholars (81625016)
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Surgery › Pancreatitis Pathology and Treatment
- Keywords
- pancreatic ductal adenocarcinoma, driver genes, KRAS mutation, TP53, CDKN2A, SMAD4, BRCA2, oncogene activation, tumor suppressor inactivation, targeted therapy, drug resistance, next-generation sequencing, clinical trials, personalized treatment
- MeSH terms
- Clinical Trials as Topic, Humans, Mutation, Oncogenes, Pancreatic Neoplasms, Biomarkers, Tumor, Tumor Suppressor Protein p53, Proto-Oncogene Proteins p21(ras), Carcinoma, Pancreatic Ductal, Smad4 Protein, Molecular Targeted Therapy, High-Throughput Nucleotide Sequencing
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