Evidence map›Paper›PMID 27536319›Full record

ArticleFrontiers in genetics2016

Gene Coexpression Analyses Differentiate Networks Associated with Diverse Cancers Harboring TP53 Missense or Null Mutations.

Kathleen Oros Klein, Karim Oualkacha, Marie-Hélène Lafond, Sahir Bhatnagar, Patricia N Tonin, Celia M T Greenwood

Open access · goldAbstract read
In one paragraph

Article in Frontiers in genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
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  10. Differential gene regulatory networks in development and disease.Cellular and molecular life sciences : CMLS · 2018
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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

6 authors at 3 institutions in 1 country.

Kathleen Oros KleinLady Davis Research Institute, Jewish General Hospital Montreal, QC, Canada.
Karim OualkachaDépartement de Mathématiques, Université du Québec à Montréal Montreal, QC, Canada.
Marie-Hélène LafondDépartement de Mathématiques, Université du Québec à Montréal Montreal, QC, Canada.
Sahir BhatnagarLady Davis Research Institute, Jewish General HospitalMontreal, QC, Canada; Department of Epidemiology, Biostatistics and Occupational Health, McGill UniversityMontreal, QC, Canada.
Patricia N ToninCancer Research Program, The Research Institute of the McGill University Health CentreMontreal, QC, Canada; Departments of Medicine and Human Genetics, McGill UniversityMontreal, QC, Canada.
Celia M T GreenwoodLady Davis Research Institute, Jewish General HospitalMontreal, QC, Canada; Department of Epidemiology, Biostatistics and Occupational Health, McGill UniversityMontreal, QC, Canada; Departments of Oncology and Human Genetics, McGill UniversityMontreal, QC, Canada.
McGill University · CAUniversité du Québec à Montréal · CAJewish General Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In a variety of solid cancers, missense mutations in the well-established TP53 tumor suppressor gene may lead to the presence of a partially-functioning protein molecule, whereas mutations affecting the protein encoding reading frame, often referred to as null mutations, result in the absence of p53 protein. Both types of mutations have been observed in the same cancer type. As the resulting tumor biology may be quite different between these two groups, we used RNA-sequencing data from The Cancer Genome Atlas (TCGA) from four different cancers with poor prognosis, namely ovarian, breast, lung and skin cancers, to compare the patterns of coexpression of genes in tumors grouped according to their TP53 missense or null mutation status. We used Weighted Gene Coexpression Network analysis (WGCNA) and a new test statistic built on differences between groups in the measures of gene connectivity. For each cancer, our analysis identified a set of genes showing differential coexpression patterns between the TP53 missense- and null mutation-carrying groups that was robust to the choice of the tuning parameter in WGCNA. After comparing these sets of genes across the four cancers, one gene (KIR3DL2) consistently showed differential coexpression patterns between the null and missense groups. KIR3DL2 is known to play an important role in regulating the immune response, which is consistent with our observation that this gene's strongly-correlated partners implicated many immune-related pathways. Examining mutation-type-related changes in correlations between sets of genes may provide new insight into tumor biology.

Indexed as

breast cancerimmune pathwaysKIR3DL2lung cancermelanomaovarian cancerTP53weighted gene expression network

Identifiers

PMID27536319
PMCPMC4971393
OpenAlexW2505703352

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.