ReviewFamilial cancer2008
Hereditary breast cancer: pathobiology, clinical translation, and potential for targeted cancer therapeutics.
Review in Familial cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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.
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.
Who cites it
11 citing papers in PubMed, 30 citations in OpenAlex.
- Incidence of contralateral and ipsilateral breast cancers and prognosis in BRCA1/2 pathogenic variant carriers based on the Japanese HBOC Consortium registration.Journal of human genetics · 2021Article
- Proper genomic profiling of (BRCA1-mutated) basal-like breast carcinomas requires prior removal of tumor infiltrating lymphocytes.Molecular oncology · 2015Article
- Are we being overly cautious? A qualitative inquiry into the experiences and perceptions of treatment-focused germline BRCA genetic testing amongst women recently diagnosed with breast cancer.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2012Article
- Genetic risk assessments in individuals at high risk for inherited breast cancer in the breast oncology care setting.Cancer control : journal of the Moffitt Cancer Center · 2012Review
- A Review of Tandem Mass Spectrometry Characterization of Adenosine Diphosphate-Ribosylated Peptides.International journal of mass spectrometry · 2012Article
- Article
- Polymorphic variants in TSC1 and TSC2 and their association with breast cancer phenotypes.Breast cancer research and treatment · 2011Article
- Constitutional methylation of the BRCA1 promoter is specifically associated with BRCA1 mutation-associated pathology in early-onset breast cancer.Cancer prevention research (Philadelphia, Pa.) · 2011Article
- Stemming the tide of cancer for BRCA1/2 mutation carriers.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2008Article
- The Fanconi anaemia/BRCA pathway and cancer susceptibility. Searching for new therapeutic targets.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2008Review
- Genetic counselling and testing for inherited gene mutations in newly diagnosed patients with breast cancer: a review of the existing literature and a proposed research agenda.Breast cancer research : BCR · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BRCA1 and BRCA2 breast cancers have distinct biological features as evidenced by histopathologic, immunohistochemical, gene expression profiling, and array-comparative genomic hybridization data. BRCA1 breast cancers may have a worse prognosis but may, however be amenable to treatment such as chemotherapy for small high-grade, lymph node negative breast cancers. Paradoxically, tamoxifen may provide effective adjuvant and chemopreventive therapy despite the predominantly negative estrogen receptor status of BRCA1 breast cancers. The distinctive biology of BRCA1 and BRCA2 breast cancers bodes well for the development of targeted cancer therapies. Cells with BRCA1 or BRCA2 loss of function are deficient in DNA double strand break repair and are sensitized to poly(ADP-ribose) polymerase (PARP) inhibitors, causing the persistence of DNA lesions which are usually repaired by homologous recombination and ultimately leading to apoptosis. The potentially high efficacy and low toxicity of poly(ADP-ribose) polymerase inhibitors presents an opportunity for targeted cancer therapeutics for BRCA1 and BRCA2 germline mutation carriers. Genotype-tailored chemoprevention may be feasible which could theoretically eliminate single cells that have sustained a second hit, before cancer progression takes place. If targeted cancer therapies emerge, it will become crucially important to identify BRCA carriers at the time of diagnosis for optimal therapy and to identify unaffected carriers for chemoprevention. If so, then to the extent that barriers in the recognition and referral of patients to genetic counseling cannot be surmounted, pathological and genomic methods to identify a BRCA1 or BRCA2 breast cancer profile will gain increasing clinical importance.
Indexed as
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What OpenQuestion holds
Registered trials
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.