Evidence map›Paper›PMID 24341335›Full record

ArticleBMC cancer2013

PIK3CA, HRAS and PTEN in human papillomavirus positive oropharyngeal squamous cell carcinoma.

Simion I Chiosea, Jennifer R Grandis, Vivian W Y Lui, Brenda Diergaarde, Jessica H Maxwell, Robert L Ferris, Seungwon W Kim, Alyssa Luvison, Megan Miller, Marina N Nikiforova

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
6.5field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Pooled it
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  3. Erlotinib, erlotinib-sulindac versus placebo: a randomized, double-blind, placebo-controlled window trial in operable head and neck cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014
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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

10 authors at 1 institution in 1 country.

Simion I ChioseaDepartment of Pathology, University of Pittsburgh, 200 Lothrop St, Pittsburgh, PA 15213, USA. chioseasi@upmc.edu.
Jennifer R Grandis
Vivian W Y Lui
Brenda Diergaarde
Jessica H Maxwell
Robert L Ferris
Seungwon W Kim
Alyssa Luvison
Megan Miller
Marina N Nikiforova
University of Pittsburgh · US

Funding

WILD TYPE P53-BASED ADJUVANT IMMUNOTHERAPY FOR SCCHNP50CA097190 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHRISTOPHER J. BAKKENIST · 2004 to 2026
$49.6M
PI3K Pathway Mutations in Head and Neck CancerR01DE023685 · NIDCR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GRANDIS, JENNIFER RUBIN, JOHNSON, DANIEL E · 2014 to 2023
$5.1M
GRPR Signaling in SCCHN: Integration with EGFRR01CA098372 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GRANDIS, JENNIFER RUBIN · 2004 to 2017
$3.8M
NCI NIH HHS P50 CA097190NCI NIH HHS P50CA97190NCI NIH HHS R01 CA098372NIDCR NIH HHS R01 DE023685
6 · The paper itself

Abstract

backgroundRecent genomic evidence suggests frequent phosphatidylinositide 3-kinase (PI3K) pathway activation in human papillomavirus (HPV) positive oropharyngeal squamous cell carcinoma. Mutations/amplification of the gene encoding p110α catalytic subunit of phosphoinositide 3-kinase (PIK3CA), loss of phosphatase and tensin homolog (PTEN) and HRAS mutations are known to activate PI3K pathway. METHODS AND

resultsPIK3CA mutations were identified by Sanger sequencing in 23 of 75 (31%) HPV-positive oropharyngeal carcinomas, including exon 9 (p.E545K [n = 10] and p.E542K [n = 5]) or exon 20 (p.H1047Y, n = 2) mutations. Five rare and one novel (p.R537Q) PIK3CA mutations were identified. HRAS mutation (p.Q61L) was detected in 1 of 62 tested cases. PIK3CA amplification by fluorescence in situ hybridization (FISH) was identified in 4 cases (4/21, 20%), while PTEN loss was seen in 7 (7/21, 33%) cases (chromosome 10 monosomy [n = 4], homozygous deletion [n = 3]).

conclusionsOverall, genetic alterations that likely lead to PI3K pathway activation were identified in 34 of 75 cases (45%) and did not correlate with disease specific survival. These findings offer a molecular rationale for therapeutic targeting of PI3K pathway in patients with HPV-positive oropharyngeal carcinoma.

Indexed as

PapillomaviridaeAdultAgedCarcinoma, Squamous CellClass I Phosphatidylinositol 3-KinasesExonsFemaleHumansMaleMiddle AgedMutationNeoplasm StagingOropharyngeal NeoplasmsPapillomavirus InfectionsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins p21(ras)Class I Phosphatidylinositol 3-KinasesHRAS protein, humanPhosphatidylinositol 3-KinasesPIK3CA protein, humanProto-Oncogene Proteins p21(ras)PTEN Phosphohydrolase

Identifiers

PMID24341335
PMCPMC3878565
OpenAlexW2162816379

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.