Evidence map›Paper›PMID 18953432›Full record

ArticleNeoplasia (New York, N.Y.)2008

p16INK4a expression and absence of activated B-RAF are independent predictors of chemosensitivity in melanoma tumors.

Stuart J Gallagher, John F Thompson, James Indsto, Lyndee L Scurr, Margaret Lett, Bo-Fu Gao, Ruth Dunleavey, Graham J Mann, Richard F Kefford, Helen Rizos

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. The relationship between promoter methylation of p16 gene and bladder cancer risk: a meta-analysis.International journal of clinical and experimental medicine · 2015
    Article
  6. Article
  7. Article
  8. Tumor genetic analyses of patients with metastatic melanoma treated with the BRAF inhibitor dabrafenib (GSK2118436).Clinical cancer research : an official journal of the American Association for Cancer Research · 2013
    Article
  9. Current and future trials of targeted therapies in cutaneous melanoma.Advances in experimental medicine and biology · 2013
    Review
  10. Future directions in treatment of brain metastases.Surgical neurology international · 2013
    Article
  11. Review
  12. Article
  13. Review
  14. The War on Cancer rages on.Neoplasia (New York, N.Y.) · 2009
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Neoplasia: the second decade.Neoplasia (New York, N.Y.) · 2008
    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

10 authors at 4 institutions in 1 country.

Stuart J GallagherWestmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Westmead NSW 2145, Australia.
John F Thompson
James Indsto
Lyndee L Scurr
Margaret Lett
Bo-Fu Gao
Ruth Dunleavey
Graham J Mann
Richard F Kefford
Helen Rizos
Westmead Institute · AURoyal Prince Alfred Hospital · AUThe University of Sydney · AUWestmead Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastatic cutaneous melanoma is highly resistant to cytotoxic drugs, and this contributes to poor prognosis. In vivo studies on the chemosensitivity of metastatic melanoma are rare and hampered by poor response rates to systemic chemotherapeutics. Patients who undergo isolated limb infusion (ILI) with cytotoxic drugs show high response rates and are, therefore, a good cohort for studying chemosensitivity in vivo. We used tumors from patients who underwent ILI to study the role of melanoma tumor-suppressor genes and oncogenes on melanoma chemosensitivity. Prospectively acquired tumors from 30 patients who subsequently underwent ILI with melphalan and actinomycin-D for metastatic melanoma were investigated for mRNA expression levels of p14(ARF), p16(INK4a), and MITFm. The mutation status of B-RAF, N-RAS, and PTEN were also determined. A high percentage of tumors had activating mutations in either B-RAF (15/30) or N-RAS (10/30) and only two tumors carried altered PTEN. High expression of p16(INK4a) and absence of an activating B-RAF mutation independently predicted response to treatment. Further, inducible expression of p16(INK4a) sensitized a melanoma cell line to death induced by melphalan or actinomycin-D. This study shows that high expression of p16(INK4a) or the absence of activated B-RAF correlates with in vivo response of melanoma to cytotoxic drugs.

Indexed as

Genes, p16AgedAged, 80 and overAntineoplastic AgentsApoptosisCell CycleCyclin-Dependent Kinase Inhibitor p16DactinomycinFemaleGene Expression Regulation, NeoplasticGenes, rasHumansMaleMelanomaMelphalanMicrophthalmia-Associated Transcription FactorAntineoplastic AgentsBRAF protein, humanCyclin-Dependent Kinase Inhibitor p16DactinomycinMelphalanMicrophthalmia-Associated Transcription FactorMITF protein, humanProto-Oncogene Proteins B-rafPTEN PhosphohydrolasePTEN protein, humanTumor Suppressor Protein p14ARF

Identifiers

PMID18953432
PMCPMC2570599
OpenAlexW1486941471

What OpenQuestion holds

Textmetadata
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.