Whole-exome sequencing of pancreatic cancer defines genetic diversity and therapeutic targets
Open accessAbstract
Pancreatic ductal adenocarcinoma (PDA) has a dismal prognosis and insights into both disease etiology and targeted intervention are needed. A total of 109 micro-dissected PDA cases were subjected to whole-exome sequencing. Microdissection enriches tumour cellularity and enhances mutation calling. Here we show that environmental stress and alterations in DNA repair genes associate with distinct mutation spectra. Copy number alterations target multiple tumour suppressive/oncogenic loci; however, amplification of MYC is uniquely associated with poor outcome and adenosquamous subtype. We identify multiple novel mutated genes in PDA, with select genes harbouring prognostic significance. RBM10 mutations associate with longer survival in spite of histological features of aggressive disease. KRAS mutations are observed in >90% of cases, but codon Q61 alleles are selectively associated with improved survival. Oncogenic BRAF mutations are mutually exclusive with KRAS and define sensitivity to vemurafenib in PDA models. High-frequency alterations in Wnt signalling, chromatin remodelling, Hedgehog signalling, DNA repair and cell cycle processes are observed. Together, these data delineate new genetic diversity of PDA and provide insights into prognostic determinants and therapeutic targets.
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KRAS mutation occurs in about 85% of pancreatic ductal adenocarcinomas.
“Amongst these are four canonical mutations – KRAS (~85%), TP53 (60–70%), CDKN2A (>50%), and SMAD4 (~50%).”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [52]
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- Authors
- Witkiewicz, A. K., McMillan, E. A., Balaji, U., Baek, G., Lin, W.-C., Mansour, J., Mollaee, M., Wagner, K.-U., Koduru, P., Yopp, A., Choti, M. A., Yeo, C. J., McCue, P., White, M. A., & Knudsen, E. S.
- Affiliations
- Harold C. Simmons Comprehensive Cancer Center (US)
- The University of Texas Southwestern Medical Center (US)
- University of Nebraska Medical Center (US)
- Thomas Jefferson University (US)
- Corresponding author
- Witkiewicz, Agnieszka K.
- ORCID
- Venue
- Nature Communications
- Published
- 2015-04-09
- Volume
- 6
- Issue
- 1
- Pages
- 6744-6744
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4403382
- OpenAlex
- W2067826589
- Cited by
- 1,115
- References
- 43
- Citations by year
- 2026: 32 · 2025: 87 · 2024: 60 · 2023: 97 · 2022: 120 · 2021: 144 · 2020: 135 · 2019: 109 · 2018: 122 · 2017: 111 · 2016: 75 · 2015: 21 · 2014: 2
- FWCI
- 47.56
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Cancer Prevention and Research Institute of Texas (P30 CA142543, CA142543, RP140110, 5P30 CA 142543)
- University of Texas Southwestern Medical Center (CA142543, P30CA142543, RP140110)
- National Cancer Institute (P30CA142543)
- National Institute of General Medical Sciences (T32 GM 8203-26, T32GM008203)
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- pancreatic ductal adenocarcinoma, tumor microenvironment, DNA repair genes, mutation spectrum, copy number alterations, MYC amplification, KRAS mutation, BRAF mutation, adenosquamous carcinoma, prognostic factors, therapeutic target, Wnt signaling, Hedgehog signaling, chromatin remodeling, cell cycle alterations
- MeSH terms
- Vemurafenib, Adult, Aged, Aged, 80 and over, Antineoplastic Agents, Cell Cycle, DNA Repair, DNA-Binding Proteins, Female, Gene Amplification, Humans, Indoles, Male, Middle Aged, Nuclear Proteins, Pancreatic Neoplasms, Prognosis, Sulfonamides, Transcription Factors, Genetic Variation, Tumor Suppressor Protein p53, Retinoblastoma Protein, Genes, myc, Proto-Oncogene Proteins p21(ras), RNA-Binding Proteins, Sequence Analysis, DNA, Carcinoma, Adenosquamous, Drug Resistance, Neoplasm, Carcinoma, Pancreatic Ductal, BRCA2 Protein, Proto-Oncogene Proteins B-raf, Kaplan-Meier Estimate, DNA Copy Number Variations, Molecular Targeted Therapy, Exome, Wnt Signaling Pathway
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