<i>HRness</i> in Breast and Ovarian Cancers
Ovarian and breast cancers are currently defined by the main pathways involved in the tumorigenesis. The majority are carcinomas, originating from epithelial cells that are in constant division and subjected to cyclical variations of the estrogen stimulus during the female hormonal cycle, therefore...
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MDPI AG
2020-05-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/21/11/3850 |
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| author | Elizabeth Santana dos Santos François Lallemand Ambre Petitalot Sandrine M. Caputo Etienne Rouleau |
| author_facet | Elizabeth Santana dos Santos François Lallemand Ambre Petitalot Sandrine M. Caputo Etienne Rouleau |
| author_sort | Elizabeth Santana dos Santos |
| collection | DOAJ |
| description | Ovarian and breast cancers are currently defined by the main pathways involved in the tumorigenesis. The majority are carcinomas, originating from epithelial cells that are in constant division and subjected to cyclical variations of the estrogen stimulus during the female hormonal cycle, therefore being vulnerable to DNA damage. A portion of breast and ovarian carcinomas arises in the context of DNA repair defects, in which genetic instability is the backdrop for cancer initiation and progression. For these tumors, DNA repair deficiency is now increasingly recognized as a target for therapeutics. In hereditary breast/ovarian cancers (HBOC), tumors with <i>BRCA1/2</i> mutations present an impairment of DNA repair by homologous recombination (HR). For many years, <i>BRCA1/2</i> mutations were only screened on germline DNA, but now they are also searched at the tumor level to personalize treatment. The reason of the inactivation of this pathway remains uncertain for most cases, even in the presence of a HR-deficient signature. Evidence indicates that identifying the mechanism of HR inactivation should improve both genetic counseling and therapeutic response, since they can be useful as new biomarkers of response. |
| first_indexed | 2024-03-10T19:31:31Z |
| format | Article |
| id | doaj.art-5db94afee76043a5b1bdd449ac99fe39 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-10T19:31:31Z |
| publishDate | 2020-05-01 |
| publisher | MDPI AG |
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| series | International Journal of Molecular Sciences |
| spelling | doaj.art-5db94afee76043a5b1bdd449ac99fe392023-11-20T02:05:03ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672020-05-012111385010.3390/ijms21113850<i>HRness</i> in Breast and Ovarian CancersElizabeth Santana dos Santos0François Lallemand1Ambre Petitalot2Sandrine M. Caputo3Etienne Rouleau4Department of Medical Biology and Pathology, Gustave Roussy, Cancer Genetics Laboratory, Gustave Roussy, 94800 Villejuif, FranceDepartment of Genetics, Institut Curie, 75005 Paris, FranceDepartment of Genetics, Institut Curie, 75005 Paris, FranceDepartment of Genetics, Institut Curie, 75005 Paris, FranceDepartment of Medical Biology and Pathology, Gustave Roussy, Cancer Genetics Laboratory, Gustave Roussy, 94800 Villejuif, FranceOvarian and breast cancers are currently defined by the main pathways involved in the tumorigenesis. The majority are carcinomas, originating from epithelial cells that are in constant division and subjected to cyclical variations of the estrogen stimulus during the female hormonal cycle, therefore being vulnerable to DNA damage. A portion of breast and ovarian carcinomas arises in the context of DNA repair defects, in which genetic instability is the backdrop for cancer initiation and progression. For these tumors, DNA repair deficiency is now increasingly recognized as a target for therapeutics. In hereditary breast/ovarian cancers (HBOC), tumors with <i>BRCA1/2</i> mutations present an impairment of DNA repair by homologous recombination (HR). For many years, <i>BRCA1/2</i> mutations were only screened on germline DNA, but now they are also searched at the tumor level to personalize treatment. The reason of the inactivation of this pathway remains uncertain for most cases, even in the presence of a HR-deficient signature. Evidence indicates that identifying the mechanism of HR inactivation should improve both genetic counseling and therapeutic response, since they can be useful as new biomarkers of response.https://www.mdpi.com/1422-0067/21/11/3850homologous recombination deficiencyDNA repairbreast cancer tumorigenesisovarian cancer tumorigenesisBRCA1BRCA2 |
| spellingShingle | Elizabeth Santana dos Santos François Lallemand Ambre Petitalot Sandrine M. Caputo Etienne Rouleau <i>HRness</i> in Breast and Ovarian Cancers International Journal of Molecular Sciences homologous recombination deficiency DNA repair breast cancer tumorigenesis ovarian cancer tumorigenesis BRCA1 BRCA2 |
| title | <i>HRness</i> in Breast and Ovarian Cancers |
| title_full | <i>HRness</i> in Breast and Ovarian Cancers |
| title_fullStr | <i>HRness</i> in Breast and Ovarian Cancers |
| title_full_unstemmed | <i>HRness</i> in Breast and Ovarian Cancers |
| title_short | <i>HRness</i> in Breast and Ovarian Cancers |
| title_sort | i hrness i in breast and ovarian cancers |
| topic | homologous recombination deficiency DNA repair breast cancer tumorigenesis ovarian cancer tumorigenesis BRCA1 BRCA2 |
| url | https://www.mdpi.com/1422-0067/21/11/3850 |
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