Evidence map›Paper›PMID 27108388›Full record

ArticleNeoplasia (New York, N.Y.)2016

Breast Cancer Heterogeneity Examined by High-Sensitivity Quantification of PIK3CA, KRAS, HRAS, and BRAF Mutations in Normal Breast and Ductal Carcinomas.

Meagan B Myers, Malathi Banda, Karen L McKim, Yiying Wang, Michael J Powell, Barbara L Parsons

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-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

20 citing papers in PubMed, 40 citations in OpenAlex.

  1. CarcSeq detection of lorcaserin-induced clonal expansion of Pik3ca H1047R mutants in rat mammary tissue.Toxicological sciences : an official journal of the Society of Toxicology · 2024
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  9. Adenomyoepithelial tumors of the breast: molecular underpinnings of a rare entity.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 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

6 authors at 2 institutions in 1 country.

Meagan B MyersUS Food and Drug Administration, National Center for Toxicological Research, Division of Genetic and Molecular Toxicology, 3900 NCTR Rd., Jefferson, AR 72079.
Malathi BandaUS Food and Drug Administration, National Center for Toxicological Research, Division of Genetic and Molecular Toxicology, 3900 NCTR Rd., Jefferson, AR 72079.
Karen L McKimUS Food and Drug Administration, National Center for Toxicological Research, Division of Genetic and Molecular Toxicology, 3900 NCTR Rd., Jefferson, AR 72079.
Yiying WangUS Food and Drug Administration, National Center for Toxicological Research, Division of Genetic and Molecular Toxicology, 3900 NCTR Rd., Jefferson, AR 72079.
Michael J PowellDiaCarta, Inc., JOINN Innovation Park, 2600 Hilltop Drive, Richmond, CA 94806.
Barbara L ParsonsUS Food and Drug Administration, National Center for Toxicological Research, Division of Genetic and Molecular Toxicology, 3900 NCTR Rd., Jefferson, AR 72079. Electronic address: barbara.parsons@fda.hhs.gov.
National Center for Toxicological Research · USUnited States Food and Drug Administration · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutant cancer subpopulations have the potential to derail durable patient responses to molecularly targeted cancer therapeutics, yet the prevalence and size of such subpopulations are largely unexplored. We employed the sensitive and quantitative Allele-specific Competitive Blocker PCR approach to characterize mutant cancer subpopulations in ductal carcinomas (DCs), examining five specific hotspot point mutations (PIK3CA H1047R, KRAS G12D, KRAS G12V, HRAS G12D, and BRAF V600E). As an approach to aid interpretation of the DC results, the mutations were also quantified in normal breast tissue. Overall, the mutations were prevalent in normal breast and DCs, with 9/9 DCs having measureable levels of at least three of the five mutations. HRAS G12D was significantly increased in DCs as compared to normal breast. The most frequent point mutation reported in DC by DNA sequencing, PIK3CA H1047R, was detected in all normal breast tissue and DC samples and was present at remarkably high levels (mutant fractions of 1.1 × 10(-3) to 4.6 × 10(-2)) in 4/10 normal breast samples. In normal breast tissue samples, PIK3CA mutation levels were positively correlated with age. However, the PIK3CA H1047R mutant fraction distributions for normal breast tissues and DCs were similar. The results suggest PIK3CA H1047R mutant cells have a selective advantage in breast, contribute to breast cancer susceptibility, and drive tumor progression during breast carcinogenesis, even when present as only a subpopulation of tumor cells.

Indexed as

AdultAgedAged, 80 and overAllelesBreast NeoplasmsCarcinoma, Ductal, BreastCase-Control StudiesCell Transformation, NeoplasticClass I Phosphatidylinositol 3-KinasesDNA Mutational AnalysisFemaleGenetic Predisposition to DiseaseHumansMiddle AgedMutation RatePhosphatidylinositol 3-KinasesClass I Phosphatidylinositol 3-KinasesPhosphatidylinositol 3-KinasesPIK3CA protein, humanProto-Oncogene Proteins B-rafras Proteins

Identifiers

PMID27108388
PMCPMC4840288
OpenAlexW2337521018

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.