Evidence map›Paper›PMID 38414063›Full record

ReviewCell communication and signaling : CCS2024

KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST.

Shishan Zhou, Omar Abdihamid, Fengbo Tan, Haiyan Zhou, Heli Liu, Zhi Li, Sheng Xiao, Bin Li

Open access · goldAbstract readVideo-Audio MediaReview
In one paragraph

Review in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
15.8field-weighted citation impact, top 1% 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

39 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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

8 authors at 3 institutions in 2 countries.

Shishan ZhouDivision of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, China, Xiangya road 87.
Omar AbdihamidGarissa Cancer Center, Garissa County Referral Hospital, Kismayu road, Garissa town, P.O BOX, 29-70100, Kenya.
Fengbo TanDivision of Surgery, Xiangya Hospital, Central South University, China, Hunan, Changsha.
Haiyan ZhouDivision of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Heli LiuDivision of Surgery, Xiangya Hospital, Central South University, China, Hunan, Changsha.
Zhi LiCenter for Molecular Medicine of Xiangya Hospital, Collaborative Innovation Center for Cancer Medicine, Central South University, Changsha, Hunan, China, 410008.
Sheng XiaoDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, 410008, MA, USA.
Bin LiDivision of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, China, Xiangya road 87#. bincsuxy@csu.edu.cn.
Central South University · CNBrigham and Women's Hospital · USHunan Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastrointestinal stromal tumor (GIST) is the most common sarcoma located in gastrointestinal tract and derived from the interstitial cell of Cajal (ICC) lineage. Both ICC and GIST cells highly rely on KIT signal pathway. Clinically, about 80-90% of treatment-naive GIST patients harbor primary KIT mutations, and special KIT-targeted TKI, imatinib (IM) showing dramatic efficacy but resistance invariably occur, 90% of them was due to the second resistance mutations emerging within the KIT gene. Although there are multiple variants of KIT mutant which did not show complete uniform biologic characteristics, most of them have high KIT expression level. Notably, the high expression level of KIT gene is not correlated to its gene amplification. Recently, accumulating evidences strongly indicated that the gene coding, epigenetic regulation, and pre- or post- protein translation of KIT mutants in GIST were quite different from that of wild type (WT) KIT. In this review, we elucidate the biologic mechanism of KIT variants and update the underlying mechanism of the expression of KIT gene, which are exclusively regulated in GIST, providing a promising yet evidence-based therapeutic landscape and possible target for the conquer of IM resistance. Video Abstract.

Indexed as

Antineoplastic AgentsBiological ProductsGastrointestinal Stromal TumorsDrug Resistance, NeoplasmEpigenesis, GeneticHumansImatinib MesylateMutationProtein Kinase InhibitorsProto-Oncogene Proteins c-kitPyrimidinesAntineoplastic AgentsBiological ProductsImatinib MesylateProtein Kinase InhibitorsProto-Oncogene Proteins c-kitPyrimidinesGastrointestinal stromal tumorImatinib resistanceKIT mutations and expressionTherapeutic targets

Identifiers

PMID38414063
PMCPMC10898159
OpenAlexW4392200477

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.