ReviewOncotarget2017
Genetic progression in gastrointestinal stromal tumors: mechanisms and molecular interventions.
Review in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Prognostic Significance of Circulating Tumor DNA Mutations in Gastrointestinal Stromal Tumors: A Systematic Review and Meta-analysis Based on Time-To-Event Data.Journal of gastrointestinal cancer · 2025Pooled it
- Clinical impact of primary and secondary KIT mutations on the efficacy of molecular-targeted therapies in gastrointestinal stromal tumors.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2025Article
- Pathologic diagnosis and molecular features of gastrointestinal stromal tumors: a mini-review.Frontiers in oncology · 2024Review
- Biological and therapeutic implications of RKIP in Gastrointestinal Stromal Tumor (GIST): an integrated transcriptomic and proteomic analysis.Cancer cell international · 2023Article
- Molecular Mechanisms of Gastrointestinal Stromal Tumors and Their Impact on Systemic Therapy Decision.Cancers · 2023Review
- c-Kit Receptors as a Therapeutic Target in Cancer: Current Insights.OncoTargets and therapy · 2023Review
- Modeling tissue-specific breakpoint proximity of structural variations from whole-genomes to identify cancer drivers.Nature communications · 2022Article
- Clinical Activity of Ripretinib in Patients with Advanced Gastrointestinal Stromal Tumor Harboring HeterogeneousClinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- Prevalence and significance of M541L single nucleotide polymorphism in the central European cohort of gastrointestinal stromal tumor patients.Journal of cancer research and clinical oncology · 2021Article
- Article
- Gastrointestinal Stromal Tumors (GISTs): Novel Therapeutic Strategies with Immunotherapy and Small Molecules.International journal of molecular sciences · 2021Review
- RETRACTED: Synthetic Makaluvamine Analogs Decrease c-Kit Expression and Are Cytotoxic to Neuroendocrine Tumor Cells.Molecules (Basel, Switzerland) · 2020Article
- The Role of miR-375-3p and miR-200b-3p in Gastrointestinal Stromal Tumors.International journal of molecular sciences · 2020Article
- Imatinib, sunitinib and pazopanib: From flat-fixed dosing towards a pharmacokinetically guided personalized dose.British journal of clinical pharmacology · 2020Review
- Racial Disparity in Incidence and Survival for Gastrointestinal Stromal Tumors (GISTs): an Analysis of SEER Database.Journal of racial and ethnic health disparities · 2019Article
- Clinicopathological characteristics and prognosis of primary appendiceal stromal tumors.World journal of surgical oncology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastrointestinal stromal tumors (GISTs) are the most common sarcomas in humans. Constitutively activating mutations in the KIT or PDGFRA receptor tyrosine kinases are the initiating oncogenic events. Most metastatic GISTs respond dramatically to therapies with KIT/PDGFRA inhibitors. Asymptomatic and mitotically-inactive KIT/PDGFRA-mutant "microGISTs" are found in one third of adults, but most of these small tumors never progress to malignancy, underscoring that a progression of oncogenic mutations is required. Recent studies have identified key genomic abnormalities in GIST progression. Novel insights into the genetic progression of GISTs are shedding new light on therapeutic innovations.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.