Evidence map›Paper›PMID 22511720›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Pleckstrin homology domain-interacting protein (PHIP) as a marker and mediator of melanoma metastasis.

David De Semir, Mehdi Nosrati, Vladimir Bezrookove, Altaf A Dar, Scot Federman, Geraldine Bienvenu, Suraj Venna, Javier Rangel, Joan Climent, Tanja M Meyer Tamgüney and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
1.5field-weighted citation impact, top 19% 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

36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 57 citations in OpenAlex.

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  17. PHIP drives glioblastoma motility and invasion by regulating the focal adhesion complex.Proceedings of the National Academy of Sciences of the United States of America · 2020
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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

19 authors at 5 institutions in 2 countries.

David De SemirAuerback Melanoma Research Laboratory and Melanoma Center, University of California, San Francisco, CA 94115, USA.
Mehdi Nosrati
Vladimir Bezrookove
Altaf A Dar
Scot Federman
Geraldine Bienvenu
Suraj Venna
Javier Rangel
Joan Climent
Tanja M Meyer Tamgüney
Suresh Thummala
Schuyler Tong
Stanley P L Leong
Chris Haqq
Paul Billings
James R Miller
Richard W Sagebiel
Robert Debs
Mohammed Kashani-Sabet
Melanoma Institute Australia · AUCalifornia Pacific Medical Center · USUCSF Helen Diller Family Comprehensive Cancer Center · USCrossLife Technologies (United States) · USUniversity of California, San Francisco · US

Funding

Validation of Genomic Targets in MelanomaR01CA114337 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KASHANI-SABET, MOHAMMED · 2005 to 2015
$3.2M
Molecular Classification of Primary Cutaneous MelanomaR01CA122947 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KASHANI-SABET, MOHAMMED · 2007 to 2011
$1.5M
NCI NIH HHS CA109171NCI NIH HHS CA114337NCI NIH HHS CA122947NCI NIH HHS R01 CA114337NCI NIH HHS R01 CA122947
6 · The paper itself

Abstract

Although melanomas with mutant v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) can now be effectively targeted, there is no molecular target for most melanomas expressing wild-type BRAF. Here, we show that the activation of Pleckstrin homology domain-interacting protein (PHIP), promotes melanoma metastasis, can be used to classify a subset of primary melanomas, and is a prognostic biomarker for melanoma. Systemic, plasmid-based shRNA targeting of Phip inhibited the metastatic progression of melanoma, whereas stable suppression of Phip in melanoma cell lines suppressed metastatic potential and prolonged the survival of tumor-bearing mice. The human PHIP gene resides on 6q14.1, and although 6q loss has been observed in melanoma, the PHIP locus was preserved in melanoma cell lines and patient samples, and its overexpression was an independent adverse predictor of survival in melanoma patients. In addition, a high proportion of PHIP-overexpressing melanomas harbored increased PHIP copy number. PHIP-overexpressing melanomas include tumors with wild-type BRAF, neuroblastoma RAS viral (v-ras) oncogene homolog, and phosphatase and tensin homolog, demonstrating PHIP activation in triple-negative melanoma. These results describe previously unreported roles for PHIP in predicting and promoting melanoma metastasis, and in the molecular classification of melanoma.

Indexed as

AnimalsBase SequenceBiomarkers, TumorCell Line, TumorFemaleHumansIntracellular Signaling Peptides and ProteinsMelanomaMelanoma, ExperimentalMiceMice, Inbred C57BLMice, NudeNerve Tissue ProteinsRNA, Small InterferingSignal TransductionBiomarkers, TumorIntracellular Signaling Peptides and ProteinsNerve Tissue ProteinsPHIP protein, humanPhip protein, mouseRNA, Small Interfering

Identifiers

PMID22511720
PMCPMC3344978
OpenAlexW2009631794

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.