Evidence map›Paper›PMID 19679016›Full record

ReviewCurrent oncology reports2009

Inside life of melanoma cell signaling, molecular insights, and therapeutic targets.

Jeffrey A Sosman, Kim A Margolin

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current oncology reports, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

2 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. 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

2 authors at 1 institution in 1 country.

Jeffrey A SosmanDivision of Hematology/Oncology, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, 777 Preston Research Building, 2220 Pierce Avenue, Nashville, TN 37232, USA. Jeff.sosman@vanderbilt.edu
Kim A Margolin
Vanderbilt University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melanoma is one of the fastest growing tumor types in the United States. Immunotherapy and chemotherapy benefit only a few patients with metastatic disease. Therapy targeting a signaling pathway critical to the cancer's growth can provide dramatic benefit in several other malignancies and may be a valuable strategy for advanced melanoma, if drugs with a favorable therapeutic index are effective against essential molecular pathways. One such target is the V600E "gain-of-function" BRAF mutation found in 60% of melanomas; other mutations or molecular alterations cooperate with V600E BRAF, particularly those that cause loss of function of PTEN, upstream of Akt and mammalian target of rapamycin. Rapid development of new agents, a better understanding of the target pathways and mechanisms of resistance, and carefully designed strategies to optimize combinations and sequences of these agents, potentially with chemotherapy or immunotherapy, may ultimately have the potential to overcome the previously insurmountable obstacle of therapy resistance in melanoma.

Indexed as

Antineoplastic AgentsHumansMelanomaModels, BiologicalMutationProtein KinasesProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionTOR Serine-Threonine KinasesAntineoplastic AgentsBRAF protein, humanMTOR protein, humanProtein KinasesProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanTOR Serine-Threonine Kinases

Identifiers

PMID19679016
OpenAlexW2046841902

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.