Evidence map›Paper›PMID 16731599›Full record

ReviewJournal of clinical pathology2006

An update on molecular genetics of gastrointestinal stromal tumours.

L Tornillo, L M Terracciano

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Journal of clinical pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01227746 (A Retrospective Study of C-kit Mutation Status in Asian Patients With Advanced Gastro-intestinal Stromal Tumors), which is not on this map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
9.1field-weighted citation impact, top 2% 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.

NCT01227746 unknown statusnot on this mapstarted 2011, after this paper: background citation

A Retrospective Study of C-kit Mutation Status in Asian Patients With Advanced Gastro-intestinal Stromal Tumors (GIST) Treated With Imatinib.

TypeobservationalSponsorNational University Hospital, SingaporeRan2011 to 2014ConditionsAsian Patients With Advanced Gastro-intestinal Stromal Tumors (GIST) Treated With ImatinibArmsTumor biopsies
3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 107 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Tumor-targetingHeliyon · 2018
    Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. PI3K-targeted therapy can be evaded by gene amplification along the MYC-eukaryotic translation initiation factor 4E (eIF4E) axis.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  17. Article
  18. Article
  19. Article
  20. Loss of RKIP expression is associated with poor survival in GISTs.Virchows Archiv : an international journal of pathology · 2009
    Article
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

2 authors at 1 institution in 1 country.

L TornilloInstitute of Pathology, University of Basel, Basel, Switzerland. tornillol@uhbs.ch
L M Terracciano
University of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastrointestinal stromal tumours (GISTs) are the most common primary mesenchymal tumours of the gastrointestinal tract. Most of them show activating mutations of the genes coding for KIT or platelet-derived growth factor receptor alpha (PDGFRalpha), two receptor tyrosine kinases (RTKs). The RTK inhibitor Imatinib (Gleevec, Novartis, Switzerland), induces regression of the tumour. The level of response to treatment, together with other clinicopathological parameters is related to the type and site of the activating mutation, thus suggesting that these tumours should be classified according to the molecular context. This is confirmed also by the phenomenon of the resistance to treatment, which arises because of different mechanisms (second mutation, amplification, activation of other RTKs) and can be fought only by specific RTK inhibitors, that are at present under development. RTK activation involves an homogeneous transduction pathway whose components (MAPK, AKT, PI3K, mTOR and RAS) are possible targets of new molecular treatment. A new paradigm of classification integrating the classic pathological criteria with the molecular changes will permit personalised prognosis and treatment.

Indexed as

AdolescentAdultAntineoplastic AgentsBenzamidesChildDrug Resistance, NeoplasmGastrointestinal Stromal TumorsHumansImatinib MesylateMiddle AgedMutationNeoplasm ProteinsPiperazinesProto-Oncogene Proteins c-kitPyrimidinesReceptor, Platelet-Derived Growth Factor alphaAntineoplastic AgentsBenzamidesImatinib MesylateNeoplasm ProteinsPiperazinesProto-Oncogene Proteins c-kitPyrimidinesReceptor, Platelet-Derived Growth Factor alpha

Identifiers

PMID16731599
PMCPMC1860404
OpenAlexW1980758734

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.