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Loss-of-Function PTPRD Mutations Lead to Increased STAT3 Activation and Sensitivity to STAT3 Inhibition in Head and Neck Cancer.

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PLoS One2015PMID 26267899PMC4534317stubpubmedProvenance
Source
PubMed
Retrieved
Sep 8, 2026
Layer
normalized (units and labels harmonized; values unchanged)
Run
ING-CIVIC-20260908-000001
Published

Abstract

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Linked entities

Linked entities (4)

How each link was made (MeSH, dictionary, registry reference, curation…) and whether it has been validated. Candidate links are not counted in entity statistics.

Validated 4

Curated evidence

Evidence citing this paper (1)

civicProvenance
Source
CIViC — Clinical Interpretation of Variants in Cancer
Dataset
CIViC evidence items
Version
civic-2026-09-08
Retrieved
Sep 8, 2026
Layer
normalized (units and labels harmonized; values unchanged)
Evidence
expert curation
License
CC0 1.0
PMID
26267899
Run
ING-CIVIC-20260908-000001
Open at source
CuratedShowing 1–1 of 1 evidence items · levels, directions and significance as curated at the source; each row links to its CIViC record.
TherapyCancerTypeLevelDirection · significanceRating (1–5)StatusEvidenceSource
PTPRD Mutation1
JSI-124Head and Neck CarcinomaPredictiveDSupports Sensitivity Response3accepted
EID807

In this preclinical study, loss-of-function of PTPRD was mainly caused by mutation in head and neck cancer, as identified in TCGA data. PTPRD mutated cell-lines were more sensitive to STAT3 inhibition… (full text at CIViC)

PMID 26267899 · Peyser et al., 2015 · Open in CIViC

civic