Evidence map›Paper›PMID 28632504›Full record

ReviewAdvances in anatomic pathology2017

What is New in Gastrointestinal Stromal Tumor?

Inga-Marie Schaefer, Adrián Mariño-Enríquez, Jonathan A Fletcher

Open access · greenAbstract readReview
In one paragraph

Review in Advances in anatomic pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
6.3field-weighted citation impact, top 3% of its field
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

59 citing papers in PubMed, 108 citations in OpenAlex.

  1. Phase II Study of Ponatinib in Advanced Gastrointestinal Stromal Tumors: Efficacy, Safety, and Impact of Liquid Biopsy and Other Biomarkers.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Trial
  2. Review
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  10. Gastrointestinal stromal tumors: Clinicopathological features and outcome-Real-world experience.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2025
    Article
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  12. Article
  13. Article
  14. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Inga-Marie SchaeferDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Adrián Mariño-Enríquez
Jonathan A Fletcher
Brigham and Women's Hospital · USHarvard University · US

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Tasleem J Padamsee · 1985 to 2026
$132.3M
Tissue and Pathology ResourcesP50CA127003 · NCI · DANA-FARBER CANCER INST · PI EL-BARDEESY, NABEEL, SELLERS, WILLIAM R · 2007 to 2023
$33.2M
Tissue and Pathology ResourcesU54CA168512 · NCI · SARC · PI BAKER, LAURENCE HOWARD, POLLOCK, RAPHAEL E. · 2012 to 2016
$11.0M
NCI NIH HHS P30 CA016058NCI NIH HHS P50 CA127003NCI NIH HHS U54 CA168512
6 · The paper itself

Abstract

The classification "gastrointestinal stromal tumor" (GIST) became commonplace in the 1990s and since that time various advances have characterized the GIST lineage of origin, tyrosine kinase mutations, and mechanisms of response and resistance to targeted therapies. In addition to tyrosine kinase mutations and their constitutive activation of downstream signaling pathways, GISTs acquire a sequence of chromosomal aberrations. These include deletions of chromosomes 14q, 22q, 1p, and 15q, which harbor putative tumor suppressor genes required for stepwise progression from microscopic, preclinical forms of GIST (microGIST) to clinically relevant tumors with malignant potential. Recent advances extend our understanding of GIST biology beyond that of the oncogenic KIT/PDGFRA tyrosine kinases and beyond mechanisms of KIT/PDGFRA-inhibitor treatment response and resistance. These advances have characterized ETV1 as an essential interstitial cell of Cajal-GIST transcription factor in oncogenic KIT signaling pathways, and have characterized the biologically distinct subgroup of succinate dehydrogenase deficient GIST, which are particularly common in young adults. Also, recent discoveries of MAX and dystrophin genomic inactivation have expanded our understanding of GIST development and progression, showing that MAX inactivation is an early event fostering cell cycle activity, whereas dystrophin inactivation promotes invasion and metastasis.

Indexed as

Chromosome AberrationsGastrointestinal Stromal TumorsHumansMutationNeoplasm InvasivenessSignal TransductionTranscription FactorsTranscription Factors

Identifiers

PMID28632504
PMCPMC5608028
OpenAlexW2662622861

What OpenQuestion holds

Textmetadata
LicenceTDM
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.