A comprehensive survey of genomic alterations in gastric cancer reveals systematic patterns of molecular exclusivity and co-occurrence among distinct therapeutic targets
Open accessAbstract
OBJECTIVE: Gastric cancer is a major gastrointestinal malignancy for which targeted therapies are emerging as treatment options. This study sought to identify the most prevalent molecular targets in gastric cancer and to elucidate systematic patterns of exclusivity and co-occurrence among these targets, through comprehensive genomic analysis of a large panel of gastric cancers. DESIGN: Using high-resolution single nucleotide polymorphism arrays, copy number alterations were profiled in a panel of 233 gastric cancers (193 primary tumours, 40 cell lines) and 98 primary matched gastric non-malignant samples. For selected alterations, their impact on gene expression and clinical outcome were evaluated. RESULTS: 22 recurrent focal alterations (13 amplifications and nine deletions) were identified. These included both known targets (FGFR2, ERBB2) and also novel genes in gastric cancer (KLF5, GATA6). Receptor tyrosine kinase (RTK)/RAS alterations were found to be frequent in gastric cancer. This study also demonstrates, for the first time, that these alterations occur in a mutually exclusive fashion, with KRAS gene amplifications highlighting a clinically relevant but previously underappreciated gastric cancer subgroup. FGFR2-amplified gastric cancers were also shown to be sensitive to dovitinib, an orally bioavailable FGFR/VEGFR targeting agent, potentially representing a subtype-specific therapy for FGFR2-amplified gastric cancers. CONCLUSION: The study demonstrates the existence of five distinct gastric cancer patient subgroups, defined by the signature genomic alterations FGFR2 (9% of tumours), KRAS (9%), EGFR (8%), ERBB2 (7%) and MET (4%). Collectively, these subgroups suggest that at least 37% of gastric cancer patients may be potentially treatable by RTK/RAS directed therapies.
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KRAS, ERBB2, and FGFR2 amplifications are mutually exclusive in stomach cancer.
“Importantly, KRAS, ERBB2, and FGFR2 amplifications are mutually exclusive in stomach cancer (91), with the latter two types of amplification subtypes already representing actionable alterations for precision medicine approaches (92, 93).”
From Expanding the Reach of Precision Oncology by Drugging All <i>KRAS</i> Mutants (2022) · cites this paper as [91]
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- Authors
- Deng, N., Goh, L. K., Wang, H., Das, K., Tao, J., Tan, I. B., Zhang, S., Lee, M., Wu, J., Lim, K. H., Lei, Z., Goh, G., Lim, Q.-Y., Tan, A. L.-K., Sin Poh, D. Y., Riahi, S., Bell, S., Shi, M. M., Linnartz, R., Zhu, F., Yeoh, K. G., Toh, H. C., Yong, W. P., Cheong, H. C., Rha, S. Y., Boussioutas, A., Grabsch, H., Rozen, S., & Tan, P.
- Affiliations
- National University of Singapore (SG)
- Duke-NUS Medical School (SG)
- National Cancer Centre Singapore (SG)
- Singapore General Hospital (SG)
- Nanyang Technological University (SG)
- University of Leeds (GB)
- Novartis (United States) (US)
- National University Health System (SG)
- National University Cancer Institute, Singapore (SG)
- Yonsei University (KR)
- Peter MacCallum Cancer Centre (AU)
- Corresponding author
- Tan, Patrick
- ORCID
- Venue
- Gut
- Publisher
- BMJ
- Published
- 2012-02-07
- Volume
- 61
- Issue
- 5
- Pages
- 673-684
- ISSN
- 0017-5749 (ISSN-L)
- 1468-3288
- PMC
- PMC3322587
- OpenAlex
- W2095605190
- Cited by
- 645
- References
- 79
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- FWCI
- 54.90
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
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- Gut (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- White Rose Research Online (University of Leeds, The University of Sheffield, University of York) (acceptedVersion)
- National University of Singapore (submittedVersion)
- DR-NTU (Nanyang Technological University) (submittedVersion)
- Minerva Access (University of Melbourne) (submittedVersion, cc-by-nc)
- HighWire Press Open Archive (submittedVersion)
- Funders
- American Society of Clinical Oncology
- National University of Singapore
- National Medical Research Council
- Biomedical Research Council
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Gastric Cancer Management and Outcomes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal Tumor Research and Treatment
- Keywords
- gastric cancer, copy number alterations, FGFR2 amplification, KRAS amplification, EGFR, ERBB2, MET, receptor tyrosine kinase, molecular subtypes, dovitinib, targeted therapy, KLF5, GATA6, gene expression
- MeSH terms
- Antineoplastic Agents, Gene Amplification, Genetic Markers, Proto-Oncogene Proteins, Stomach Neoplasms, Proportional Hazards Models, Proto-Oncogene Proteins p21(ras), Gene Deletion, ras Proteins, Erb-b2 Receptor Tyrosine Kinases, Proto-Oncogene Proteins c-met, Oligonucleotide Array Sequence Analysis, Polymorphism, Single Nucleotide, Receptor, Fibroblast Growth Factor, Type 2, Molecular Targeted Therapy, ErbB Receptors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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