Evidence map›Paper›PMID 37067535›Full record

ArticleCancer science2023

The pathogenic role of the BRCA2 c.7847C>T (p.Ser2616Phe) variant in breast and ovarian cancer predisposition.

Kazuki Yamazawa, Kokichi Sugano, Kohji Tanakaya, Satomi Inoue, Haruka Murakami, Moeko Nakashima, Masataka Adachi, Shinya Oki, Takeshi Makabe, Hiroshi Yamashita and 12 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Comprehensive evidence for the pathogenicity of theJournal of medical genetics · 2026
    Article
  3. Article
  4. Article
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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

22 authors at 8 institutions in 1 country.

Kazuki YamazawaDepartment of Medical Genetics, National Hospital Organization Tokyo Medical Center, Tokyo, Japan.ORCID https://orcid.org/0000-0003-4895-2759
Kokichi SuganoDepartment of Genetic Medicine, Sasaki Foundation, Kyoundo Hospital, Tokyo, Japan.
Kohji TanakayaDepartment of Surgery, National Hospital Organization Iwakuni Clinical Center, Iwakuni, Japan.
Satomi InoueDepartment of Medical Genetics, National Hospital Organization Tokyo Medical Center, Tokyo, Japan.
Haruka MurakamiDepartment of Medical Genetics, National Hospital Organization Tokyo Medical Center, Tokyo, Japan.
Moeko NakashimaDepartment of Medical Genetics, National Hospital Organization Tokyo Medical Center, Tokyo, Japan.
Masataka AdachiDepartment of Medical Genetics, National Hospital Organization Tokyo Medical Center, Tokyo, Japan.
Shinya OkiDepartment of Medical Genetics, National Hospital Organization Tokyo Medical Center, Tokyo, Japan.
Takeshi MakabeDepartment of Medical Genetics, National Hospital Organization Tokyo Medical Center, Tokyo, Japan.
Hiroshi YamashitaDepartment of Obstetrics and Gynecology, National Hospital Organization Tokyo Medical Center, Tokyo, Japan.
Arisa UekiDivision of Clinical Genetic Oncology, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Ayako SasaokaDepartment of Nursing, National Hospital Organization Tokyo Medical Center, Tokyo, Japan.
Ayako NakashojiDepartment of Breast Surgery, National Hospital Organization Tokyo Medical Center, Tokyo, Japan.
Takayuki KinoshitaDepartment of Breast Surgery, National Hospital Organization Tokyo Medical Center, Tokyo, Japan.
Tatsuo MatsunagaDepartment of Medical Genetics, National Hospital Organization Tokyo Medical Center, Tokyo, Japan.
Masami AraiDepartment of Clinical Genetics, Graduate School of Medicine, Juntendo University, Tokyo, Japan.
Seigo NakamuraDivision of Breast Surgical Oncology, Department of Surgery, Showa University School of Medicine, Tokyo, Japan.
Hiroaki MiyataDepartment of Health Policy and Management, Keio University School of Medicine, Tokyo, Japan.
Masachika IkegamiDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo, Japan.
Hiroyuki ManoDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo, Japan.ORCID https://orcid.org/0000-0003-4645-0181
Shinji KohsakaDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo, Japan.ORCID https://orcid.org/0000-0001-8651-6136
Akira MatsuiDepartment of Breast Surgery, National Hospital Organization Tokyo Medical Center, Tokyo, Japan.
Tokyo Medical Center · JPIwakuni Medical Center · JPJapanese Foundation For Cancer Research · JPJuntendo University · JPKeio University · JPSasaki Institute · JPShowa University · JPTokyo Metropolitan Komagome Hospital · JP

Funding

Japan Agency for Medical Research and Development JP22ck0106536Japan Agency for Medical Research and Development JP22kk0305018Japan Society for the Promotion of Science 19H03628Japan Society for the Promotion of Science 20K19082Japan Society for the Promotion of Science 21K19751
6 · The paper itself

Abstract

Substantial numbers of variants of unknown significance (VUSs) have been identified in BRCA1/2 through genetic testing, which poses a significant clinical challenge because the contribution of these VUSs to cancer predisposition has not yet been determined. Here, we report 10 Japanese patients from seven families with breast or ovarian cancer harboring the BRCA2 c.7847C>T (p.Ser2616Phe) variant that was interpreted as a VUS. This variant recurs only in families from Japan and has not been reported in the global general population databases. A Japanese patient with Fanconi anemia with compound heterozygous variants c.7847C>T (p.Ser2616Phe) and c.475+1G>A in BRCA2 was reported. In silico predictions and quantitative cosegregation analysis suggest a high probability of pathogenicity. The clinical features of the variant carriers were not specific to, but were consistent with, those of patients with hereditary breast and ovarian cancer. A validated functional assay, called the mixed-all-nominated-in-one-BRCA (MANO-B) method and the accurate BRCA companion diagnostic (ABCD) test, demonstrated the deleterious effects of the variant. Altogether, following the American College of Medical Genetics and Genomics and the Association for Molecular Pathology (ACMG/AMP) guidelines, this variant satisfied the "PS3," "PM2," "PM3," and "PP3" criteria. We thus conclude that the BRCA2 c.7847C>T (p.Ser2616Phe) variant is a "likely pathogenic" variant that is specifically observed in the Japanese population, leading to a breast and ovarian cancer predisposition.

Indexed as

Breast NeoplasmsOvarian NeoplasmsBRCA1 ProteinBRCA2 ProteinFemaleGenetic Predisposition to DiseaseGenetic TestingHumansNeoplasm Recurrence, LocalPedigreeBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinBRCA2 protein, humanBRCA2 genegenetic testinghereditary breast and ovarian cancer syndromemutationpedigree

Identifiers

PMID37067535
PMCPMC10323079
OpenAlexW4366083467

What OpenQuestion holds

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LicenceCC BY-NC
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.