Evidence map›Paper›PMID 22315472›Full record

ArticleGut2012

A comprehensive survey of genomic alterations in gastric cancer reveals systematic patterns of molecular exclusivity and co-occurrence among distinct therapeutic targets.

Niantao Deng, Liang Kee Goh, Hannah Wang, Kakoli Das, Jiong Tao, Iain Beehuat Tan, Shenli Zhang, Minghui Lee, Jeanie Wu, Kiat Hon Lim and 19 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Gut, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 363 papers.

0numbers the graph read from it
0cells of the map it votes in
363citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

363 citing papers in PubMed.

  1. Phase II Study of AZD4547 in Patients With Tumors Harboring Aberrations in the FGFR Pathway: Results From the NCI-MATCH Trial (EAY131) Subprotocol W.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2020
    Trial
  2. Efficacy of Combined VEGFR1-3, PDGFα/β, and FGFR1-3 Blockade Using Nintedanib for Esophagogastric Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Trial
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  12. Managing dangerous liaisons: lessons fromJournal of bacteriology · 2026
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303 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

29 authors.

Niantao DengCancer and Stem Cell Biology Program, Duke-NUS Graduate Medical School, 8 College Road, Singapore 169857, Singapore. gmstanp@duke-nus.edu.sg
Liang Kee Goh
Hannah Wang
Kakoli Das
Jiong Tao
Iain Beehuat Tan
Shenli Zhang
Minghui Lee
Jeanie Wu
Kiat Hon Lim
Zhengdeng Lei
Glenn Goh
Qing-Yan Lim
Angie Lay-Keng Tan
Dianne Yu Sin Poh
Sudep Riahi
Sandra Bell
Michael M Shi
Ronald Linnartz
Feng Zhu
Khay Guan Yeoh
Han Chong Toh
Wei Peng Yong
Hyun Cheol Cheong
Sun Young Rha
Alex Boussioutas
Heike Grabsch
Steve Rozen
Patrick Tan

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveGastric 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.

designUsing 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.

results22 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.

conclusionThe 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.

Indexed as

Gene AmplificationGene DeletionPolymorphism, Single NucleotideAntineoplastic AgentsErb-b2 Receptor Tyrosine KinasesErbB ReceptorsGenetic MarkersMolecular Targeted TherapyOligonucleotide Array Sequence AnalysisProportional Hazards ModelsProto-Oncogene ProteinsProto-Oncogene Proteins c-metProto-Oncogene Proteins p21(ras)ras ProteinsReceptor, Fibroblast Growth Factor, Type 2Stomach NeoplasmsAntineoplastic AgentsEGFR protein, humanERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesErbB ReceptorsFGFR2 protein, humanGenetic MarkersKRAS protein, humanMET protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins c-metProto-Oncogene Proteins p21(ras)ras ProteinsReceptor, Fibroblast Growth Factor, Type 2

Identifiers

PMID22315472
PMCPMC3322587

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.