ReviewClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2008
The Fanconi anaemia/BRCA pathway and cancer susceptibility. Searching for new therapeutic targets.
Review in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Apoptosis-modulatory miR-361-3p as a novel treatment target in endocrine-responsive and endocrine-resistant breast cancer.The Journal of endocrinology · 2023Article
- Fanconi Anemia Pathway Genes Advance Cervical CancerFrontiers in cell and developmental biology · 2021Article
- Clonal hematopoietic mutations linked to platelet traits and the risk of thrombosis or bleeding.Haematologica · 2020Review
- The antitumorigenic roles of BRCA1-BARD1 in DNA repair and replication.Nature reviews. Molecular cell biology · 2020Review
- Constitutional Mosaic Epimutations - a hidden cause of cancer?Cell stress · 2019Review
- Resistance to cis- and carboplatin initiated by epigenetic changes in ovarian cancer patients.Cancer drug resistance (Alhambra, Calif.) · 2019Review
- 'BRCAness' and its implications for platinum action in gynecologic cancer.Anticancer research · 2014Review
- Fanconi anaemia: from a monogenic disease to sporadic cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2011Review
- Classical and Novel Prognostic Markers for Breast Cancer and their Clinical Significance.Clinical Medicine Insights. Oncology · 2010Article
- Evolutionary genomics of human intellectual disability.Evolutionary applications · 2010Article
- Cisplatin-induced DNA damage activates replication checkpoint signaling components that differentially affect tumor cell survival.Molecular pharmacology · 2009Article
- Hereditary breast cancer: new genetic developments, new therapeutic avenues.Human genetics · 2008Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer is one of the most frequent cancers in the world. The majority of cases are sporadic but around 15% show some type of familial aggregation and about 5% exhibit a clear hereditary pattern. Common and rare low- moderate-penetrance genes, and high-penetrance genes are thought to explain the genetic susceptibility to the disease. Only around 20% of the inherited risk to breast cancer is explained by germline mutations in the known high-penetrance susceptibility genes BRCA1 and BRCA2. Mutations in genes such as TP53 and PTEN have also been linked with high risk for breast cancer within specific cancer syndromes and rare germline variants in genes such as CHEK2 and ATM have been found to confer modest risk to breast cancer. However, we can say that less than 30% of familial risk of breast cancer is due to known genes. Identification in 2002 of the Fanconi anaemia (FA) gene FANCD1 as BRCA2 and recent studies indicating that heterozygous mutations in FANCN/PALB2 and FANCJ/ BRIP1 predispose to breast cancer have emphasised an important connection between the FA and BRCA pathway. Here we review the emerging DNA-damage response network consisting of FA and BRCA proteins, summarise what is currently known about the direct involvement of these molecules in breast cancer susceptibility and discuss the prospect offered by this pathway in order to identify more breast cancer related genes. We finally present the current stage of therapeutic options specifically targeting the FA/BRCA pathway and summarise the challenges this field encounters.
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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.