Evidence map›Paper›PMID 18728664›Full record

Trial reportBritish journal of cancer2008

Phase II trial of imatinib mesylate in patients with metastatic melanoma.

K B Kim, O Eton, D W Davis, M L Frazier, D J McConkey, A H Diwan, N E Papadopoulos, A Y Bedikian, L H Camacho, M I Ross and 11 more

Registry-linked trialOpen access · hybridAbstract readClinical Trial, Phase II
In one paragraph

Trial report in British journal of cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00027586 (Phase II Trial of Gleevec), which is not on this map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
12.8field-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.

NCT00027586 phase2completednot on this map

Phase II Trial of Gleevec (Imatinib Mesylate, STI-571) in Metastatic Melanoma

TypeinterventionalSponsorM.D. Anderson Cancer CenterRan2001 to 2005Enrolled22ConditionsMelanoma, Skin NeoplasmsArmsImatinib mesylate (STI571)
3 · Its place in the literature

Who cites it

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 215 citations in OpenAlex.

  1. Interventions for melanoma in situ, including lentigo maligna.The Cochrane database of systematic reviews · 2014
    Pooled it
  2. Trial
  3. Trial
  4. Imatinib for melanomas harboring mutationally activated or amplified KIT arising on mucosal, acral, and chronically sun-damaged skin.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2013
    Trial
  5. Trial
  6. Trial
  7. Imatinib mesylate in patients with WHO B3 thymomas and thymic carcinomas.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2009
    Trial
  8. Review
  9. Review
  10. Review
  11. Therapeutic Strategies in BRAF V600 Wild-Type Cutaneous Melanoma.American journal of clinical dermatology · 2024
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Inhibition of KIT Tyrosine Kinase Activity: Two Decades After the First Approval.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2021
    Article
  19. Hypoxia-dependent drivers of melanoma progression.Journal of experimental & clinical cancer research : CR · 2021
    Review
  20. Review

13 more citing papers are in PubMed but not listed here.

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

21 authors at 3 institutions in 1 country.

K B KimDepartment of Melanoma Medical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA.
O Eton
D W Davis
M L Frazier
D J McConkey
A H Diwan
N E Papadopoulos
A Y Bedikian
L H Camacho
M I Ross
J N Cormier
J E Gershenwald
J E Lee
P F Mansfield
L A Billings
C S Ng
C Charnsangavej
M Bar-Eli
M M Johnson
A J Murgo
V G Prieto
The University of Texas MD Anderson Cancer Center · USIncell Corporation (United States) · USNational Institutes of Health · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
NCI NIH HHS CA16672NCI NIH HHS N01 CM-17003NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Metastatic melanoma cells express a number of protein tyrosine kinases (PTKs) that are considered to be targets for imatinib. We conducted a phase II trial of imatinib in patients with metastatic melanoma expressing at least one of these PTKs. Twenty-one patients whose tumours expressed at least one PTK (c-kit, platelet-derived growth factor receptors, c-abl, or abl-related gene) were treated with 400 mg of imatinib twice daily. One patient with metastatic acral lentiginous melanoma, containing the highest c-kit expression among all patients, had dramatic improvement on positron emission tomographic scan at 6 weeks and had a partial response lasting 12.8 months. The responder had a substantial increase in tumour and endothelial cell apoptosis at 2 weeks of treatment. Imatinib was fairly well tolerated: no patient required treatment discontinuation because of toxicity. Fatigue and oedema were the only grade 3 or 4 toxicities that occurred in more than 10% of the patients. Imatinib at the studied dose had minimal clinical efficacy as a single-agent therapy for metastatic melanoma. However, based on the characteristics of the responding tumour in our study, clinical activity of imatinib, specifically in patients with melanoma with certain c-kit aberrations, should be examined.

Indexed as

AdultAgedAged, 80 and overAntineoplastic AgentsBase SequenceBenzamidesDisease ProgressionDNA PrimersFemaleHumansImatinib MesylateMaleMelanomaMiddle AgedPiperazinesPositron-Emission TomographyAntineoplastic AgentsBenzamidesDNA PrimersImatinib MesylatePiperazinesPyrimidines

Identifiers

PMID18728664
PMCPMC2528157
OpenAlexW2019496774

What OpenQuestion holds

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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.