Evidence map›Paper›PMID 26001532›Full record

ArticleHuman genetics2015

The somatic autosomal mutation matrix in cancer genomes.

Nuri A Temiz, Duncan E Donohue, Albino Bacolla, Karen M Vasquez, David N Cooper, Uma Mudunuri, Joseph Ivanic, Regina Z Cer, Ming Yi, Robert M Stephens and 2 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Human genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 6 institutions in 2 countries.

Nuri A TemizIn Silico Research Centers of Excellence, Advanced Biomedical Computing Center, Information Systems Program, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc., P.O. Box B, Frederick, MD, 21702, USA.
Duncan E Donohue
Albino Bacolla
Karen M Vasquez
David N Cooper
Uma Mudunuri
Joseph Ivanic
Regina Z Cer
Ming Yi
Robert M Stephens
Jack R Collins
Brian T Luke
Frederick National Laboratory for Cancer Research · USLeidos (United States) · USThe University of Texas at Austin · USCardiff University · GBNaval Medical Research Command · USUniversity of Minnesota System · US

Funding

REPAIR OF GENOME DESTABILIZING DNA STRUCTURESR01CA093729 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Karen M Vasquez · 2002 to 2026
$8.2M
CCR NIH HHS HHSN261200800001CNCI NIH HHS CA093729NCI NIH HHS HHSN261200800001ENCI NIH HHS R01 CA093729
6 · The paper itself

Abstract

DNA damage in somatic cells originates from both environmental and endogenous sources, giving rise to mutations through multiple mechanisms. When these mutations affect the function of critical genes, cancer may ensue. Although identifying genomic subsets of mutated genes may inform therapeutic options, a systematic survey of tumor mutational spectra is required to improve our understanding of the underlying mechanisms of mutagenesis involved in cancer etiology. Recent studies have presented genome-wide sets of somatic mutations as a 96-element vector, a procedure that only captures the immediate neighbors of the mutated nucleotide. Herein, we present a 32 × 12 mutation matrix that captures the nucleotide pattern two nucleotides upstream and downstream of the mutation. A somatic autosomal mutation matrix (SAMM) was constructed from tumor-specific mutations derived from each of 909 individual cancer genomes harboring a total of 10,681,843 single-base substitutions. In addition, mechanistic template mutation matrices (MTMMs) representing oxidative DNA damage, ultraviolet-induced DNA damage, (5m)CpG deamination, and APOBEC-mediated cytosine mutation, are presented. MTMMs were mapped to the individual tumor SAMMs to determine the maximum contribution of each mutational mechanism to the overall mutation pattern. A Manhattan distance across all SAMM elements between any two tumor genomes was used to determine their relative distance. Employing this metric, 89.5% of all tumor genomes were found to have a nearest neighbor from the same tissue of origin. When a distance-dependent 6-nearest neighbor classifier was used, 10.4% of the SAMMs had an Undetermined tissue of origin, and 92.2% of the remaining SAMMs were assigned to the correct tissue of origin. [corrected]. Thus, although tumors from different tissues may have similar mutation patterns, their SAMMs often display signatures that are characteristic of specific tissues.

Indexed as

Databases, GeneticDNA DamageGenome, HumanMutation, MissenseDNA, NeoplasmFemaleHumansMaleNeoplasmsDNA, Neoplasm

Identifiers

PMID26001532
PMCPMC4495249
OpenAlexW1748752296

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.