Evidence map›Paper›PMID 22959031›Full record

ReviewAdvances in pharmacology (San Diego, Calif.)2012

Intratumoral heterogeneity as a therapy resistance mechanism: role of melanoma subpopulations.

Rajasekharan Somasundaram, Jessie Villanueva, Meenhard Herlyn

Open access · greenAbstract readReview
In one paragraph

Review in Advances in pharmacology (San Diego, Calif.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
33.4field-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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Rajasekharan SomasundaramMolecular and Cellular Oncogenesis Program, Melanoma Research Center, The Wistar Institute, Philadelphia, USA.
Jessie Villanueva
Meenhard Herlyn
The Wistar Institute · US

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Luis J Montaner · 1985 to 2026
$75.9M
Targeting the MAP and PI3 Kinase Pathways in MelanomaP01CA114046 · NCI · WISTAR INSTITUTE · PI MURPHY, MAUREEN E. · 2008 to 2023
$37.1M
TUMOR DEVELOPMENT AND PROGRESSION IN HUMAN MELANOCYTESP01CA025874 · NCI · WISTAR INSTITUTE · PI HERLYN, MEENHARD F · 1985 to 2015
$19.0M
NCI NIH HHS CA-010815NCI NIH HHS CA-025874NCI NIH HHS CA-114046NCI NIH HHS P01 CA025874NCI NIH HHS P01 CA114046NCI NIH HHS P30 CA010815
6 · The paper itself

Abstract

Malignant melanoma is an aggressive form of skin cancer whose incidence continues to increase worldwide. Increased exposure to sun, ultraviolet radiation, and the use of tanning beds can increase the risk of melanoma. Early detection of melanomas is the key to successful treatment mainly through surgical excision of the primary tumor lesion. But in advanced stage melanomas, once the disease has spread beyond the primary site to distant organs, the tumors are difficult to treat and quickly develop resistance to most available forms of therapy. The advent of molecular and cellular techniques has led to a better characterization of tumor cells revealing the presence of heterogeneous melanoma subpopulations. The discovery of gene mutations and alterations of cell-signaling pathways in melanomas has led to the development of new targeted drugs that show dramatic response rates in patients. Single-agent therapies generally target one subpopulation of tumor cells while leaving others unharmed. The surviving subpopulations will have the ability to repopulate the original tumors that can continue to progress. Thus, a rational approach to target multiple subpopulations of tumor cells with a combination of drugs instead of single-agent therapy will be necessary for long-lasting inhibition of melanoma lesions. In this context, the recent development of immune checkpoint reagents provides an additional armor that can be used in combination with targeted drugs to expand the presence of melanoma reactive T cells in circulation to prevent tumor recurrence.

Indexed as

Drug Resistance, NeoplasmGenetic HeterogeneityAnimalsAntineoplastic AgentsHumansMelanomaMolecular Targeted TherapyAntineoplastic Agents

Identifiers

PMID22959031
PMCPMC3677516
OpenAlexW1532472884

What OpenQuestion holds

Textmetadata
LicenceTDM
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.