Evidence map›Paper›PMID 33421217›Full record

Observational studyCancer science2021

Pathogenicity assessment of variants for breast cancer susceptibility genes based on BRCAness of tumor sample.

Reiko Yoshida, Taichi Hagio, Tomoko Kaneyasu, Osamu Gotoh, Tomo Osako, Norio Tanaka, Sayuri Amino, Noriko Yaguchi, Eri Nakashima, Dai Kitagawa and 10 more

Open access · goldAbstract readObservational StudyValidation Study
In one paragraph

Observational study in Cancer science, 2021. 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
0.7field-weighted citation impact, top 27% 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, 7 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Observational
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

20 authors at 6 institutions in 2 countries.

Reiko YoshidaDepartment of Oncotherapeutic Medicine, Graduate School of Medicine, Tohoku University, Sendai, Japan.ORCID https://orcid.org/0000-0001-5146-9472
Taichi HagioDivision of Cancer Genomics, Cancer Institute, Japanese Foundation for Cancer Research (JFCR), Tokyo, Japan.
Tomoko KaneyasuDivision of Cancer Genomics, Cancer Institute, Japanese Foundation for Cancer Research (JFCR), Tokyo, Japan.
Osamu GotohDivision of Cancer Genomics, Cancer Institute, Japanese Foundation for Cancer Research (JFCR), Tokyo, Japan.
Tomo OsakoDivision of Pathology, Cancer Institute, JFCR, Tokyo, Japan.ORCID https://orcid.org/0000-0001-9250-4035
Norio TanakaDivision of Cancer Genomics, Cancer Institute, Japanese Foundation for Cancer Research (JFCR), Tokyo, Japan.
Sayuri AminoDivision of Cancer Genomics, Cancer Institute, Japanese Foundation for Cancer Research (JFCR), Tokyo, Japan.
Noriko YaguchiDivision of Cancer Genomics, Cancer Institute, Japanese Foundation for Cancer Research (JFCR), Tokyo, Japan.
Eri NakashimaBreast Oncology Center, CIH, JFCR, Tokyo, Japan.
Dai KitagawaBreast Oncology Center, CIH, JFCR, Tokyo, Japan.
Takayuki UenoBreast Oncology Center, CIH, JFCR, Tokyo, Japan.ORCID https://orcid.org/0000-0002-9080-9377
Shinji OhnoBreast Oncology Center, CIH, JFCR, Tokyo, Japan.
Takeshi NakajimaDepartment of Clinical Genetic Oncology, Cancer Institute Hospital (CIH), JFCR, Tokyo, Japan.
Seigo NakamuraDivision of Breast Surgical Oncology, Showa University School of Medicine, Tokyo, Japan.
Yoshio MikiDivision of Genetic Diagnosis, Cancer Institute, JFCR, Tokyo, Japan.
Toru HirotaDepartment of Cellular and Molecular Imaging of Cancer, Graduate School of Medicine, Tohoku University, Sendai, Japan.
Shunji TakahashiDepartment of Oncotherapeutic Medicine, Graduate School of Medicine, Tohoku University, Sendai, Japan.
Masaaki MatsuuraDivision of Cancer Genomics, Cancer Institute, Japanese Foundation for Cancer Research (JFCR), Tokyo, Japan.
Tetsuo NodaDivision of Cancer Genomics, Cancer Institute, Japanese Foundation for Cancer Research (JFCR), Tokyo, Japan.
Seiichi MoriDivision of Cancer Genomics, Cancer Institute, Japanese Foundation for Cancer Research (JFCR), Tokyo, Japan.
The Cancer Institute Hospital · JPBreast Center · CHTohoku University · JPJapanese Foundation For Cancer Research · JPNational Center for Global Health and Medicine · JPShowa University · JP

Funding

AMED P-CREATE JP 16cm0106503AMED P-CREATE JP 16cm0106511AMED P-CREATE JP 17cm0106503AMED P-CREATE JP 17cm0106511AMED P-CREATE JP 18cm0106503AMED P-CREATE JP 18cm0106511AMED P-CREATE JP 19cm0106503KAKENHI 19K07766
6 · The paper itself

Abstract

Genes involved in the homologous recombination repair pathway-as exemplified by BRCA1, BRCA2, PALB2, ATM, and CHEK2-are frequently associated with hereditary breast and ovarian cancer syndrome. Germline mutations in the loci of these genes with loss of heterozygosity or additional somatic truncation at the WT allele lead to the development of breast cancers with characteristic clinicopathological features and prominent genomic features of homologous recombination deficiency, otherwise referred to as "BRCAness." Although clinical genetic testing for these and other genes has increased the chances of identifying pathogenic variants, there has also been an increase in the prevalence of variants of uncertain significance, which poses a challenge to patient care because of the difficulties associated with making further clinical decisions. To overcome this challenge, we sought to develop a methodology to reclassify the pathogenicity of these unknown variants using statistical modeling of BRCAness. The model was developed with Lasso logistic regression by comparing 116 genomic attributes derived from 37 BRCA1/2 biallelic mutant and 32 homologous recombination-quiescent breast cancer exomes. The model showed 95.8% and 86.7% accuracies in the training cohort and The Cancer Genome Atlas validation cohort, respectively. Through application of the model for variant reclassification of homologous recombination-associated hereditary breast and ovarian cancer causal genes and further assessment with clinicopathological features, we finally identified one likely pathogenic and five likely benign variants. As such, the BRCAness model developed from the tumor exome was robust and provided a reasonable basis for variant reclassification.

Indexed as

Genetic Predisposition to DiseaseHomologous RecombinationModels, GeneticAdultAgedAtaxia Telangiectasia Mutated ProteinsBiomarkers, TumorBRCA1 ProteinBRCA2 ProteinBreastBreast NeoplasmsCheckpoint Kinase 2Datasets as TopicDNA Mutational AnalysisExomeExome SequencingAtaxia Telangiectasia Mutated ProteinsATM protein, humanBiomarkers, TumorBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinBRCA2 protein, humanCheckpoint Kinase 2CHEK2 protein, humanFanconi Anemia Complementation Group N ProteinPALB2 protein, humanBRCAnesshereditary breast and ovarian cancer syndromehomologous recombination deficiencyLasso logistic regressionvariants of uncertain significance

Identifiers

PMID33421217
PMCPMC7935793
OpenAlexW3118863941

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Registered trials

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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.