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Yoko Katsuki Laboratory of DNA Damage Signaling, Department of Late Effects Studies, Radiation Biology Center, Kyoto University, Yoshidakonoecho, Sakyo-ku, Kyoto, Japan

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Minoru Takata Laboratory of DNA Damage Signaling, Department of Late Effects Studies, Radiation Biology Center, Kyoto University, Yoshidakonoecho, Sakyo-ku, Kyoto, Japan

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to be ‘caretakers’, and they function in homologous recombination (HR) repair, thereby protecting our genome from carcinogenic alterations. Furthermore, cancer genome sequences have revealed an unexpectedly high frequency of HR gene mutations in

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-16-0221
Volume/Issue:
Volume 23: Issue 10
Free access
Olga Lakiza Endocrine and Neuroendocrine Surgery Research Program, Division of General Surgery and Surgical Oncology, Department of Surgery, University of Chicago Medicine, Chicago, Illinois, USA

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Julian Lutze Committee on Cancer Biology, University of Chicago, Chicago, Illinois, USA

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Alyx Vogle Endocrine and Neuroendocrine Surgery Research Program, Division of General Surgery and Surgical Oncology, Department of Surgery, University of Chicago Medicine, Chicago, Illinois, USA

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Jelani Williams Endocrine and Neuroendocrine Surgery Research Program, Division of General Surgery and Surgical Oncology, Department of Surgery, University of Chicago Medicine, Chicago, Illinois, USA

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Abde Abukdheir Division of Hematology, Oncology, and Cell Therapy, Department of Internal Medicine, Rush University Medical Center, Chicago, Illinois, USA

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Paul Miller Endocrine and Neuroendocrine Surgery Research Program, Division of General Surgery and Surgical Oncology, Department of Surgery, University of Chicago Medicine, Chicago, Illinois, USA

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Chih-Yi ‘Andy’ Liao Division of Hematology and Oncology, Department of Internal Medicine, University of Chicago, Chicago, Illinois, USA

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Sean P Pitroda Department of Radiation Oncology and Cellular Biology, University of Chicago, Chicago, Illinois, USA

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Carlos Martinez Department of Radiation Oncology and Cellular Biology, University of Chicago, Chicago, Illinois, USA

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Andrea Olivas Department of Pathology, University of Chicago, Chicago, Illinois, USA

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Namrata Setia Department of Pathology, University of Chicago, Chicago, Illinois, USA

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Stephen J Kron Committee on Cancer Biology, University of Chicago, Chicago, Illinois, USA
Department of Molecular Genetics and Cell Biology, University of Chicago, Chicago, Illinois, USA

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Ralph R Weichselbaum Department of Radiation Oncology and Cellular Biology, University of Chicago, Chicago, Illinois, USA
Ludwig Center for Metastasis Research, University of Chicago, Chicago, Illinois, USA

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Xavier M Keutgen Endocrine and Neuroendocrine Surgery Research Program, Division of General Surgery and Surgical Oncology, Department of Surgery, University of Chicago Medicine, Chicago, Illinois, USA

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( Lord & Ashworth 2017 ). Here, poly (ADP-ribose) polymerase (PARP) inhibitors are selectively toxic to cells with homologous recombination (HR) DSB repair defects. In breast cancer, tumors with mutations in BRCA1 or BRCA2 display synthetic lethality with

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-21-0247
Volume/Issue:
Volume 29: Issue 4
Restricted access
Diana Lim Department of Pathology, National University Health System, Singapore, Singapore

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Joanne Ngeow Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore
Cancer Genetics Service, Division of Medical Oncology, National Cancer Centre, Singapore, Singapore

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recruitment of patients for some of these trials has been based on molecular and phenotypic evidence of defects in DNA repair, in particular homologous recombination (HR) repair, such as those with germ line BRCA mutations, or included tumor types known to

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-16-0116
Volume/Issue:
Volume 23: Issue 6
Free access
Amélie Fradet-Turcotte Laval University Cancer Research Center, CHU de Québec Research Center - Université Laval, Hôtel-Dieu de Québec, Oncology Axis, Quebec City, Canada

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Justine Sitz Laval University Cancer Research Center, CHU de Québec Research Center - Université Laval, Hôtel-Dieu de Québec, Oncology Axis, Quebec City, Canada

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Damien Grapton Lady Davis Institute for Medical Research, Segal Cancer Centre, Jewish General Hospital, Montreal, Canada

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Alexandre Orthwein Lady Davis Institute for Medical Research, Segal Cancer Centre, Jewish General Hospital, Montreal, Canada
Department of Oncology, McGill University, Montreal, Canada

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genome integrity. In that regard, BRCA2 plays an essential role in several DNA repair pathways, including DSB repair by homologous recombination (HR) and DNA crosslink repair by the FA pathway. The BRCA2 gene was identified in 1995 ( Wooster et al

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-16-0297
Volume/Issue:
Volume 23: Issue 10
Free access
Nely Díaz-Mejía Vall d’Hebron Institute of Oncology (VHIO) and Vall d’Hebron University Hospital, Barcelona, Spain

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David García-Illescas Vall d’Hebron Institute of Oncology (VHIO) and Vall d’Hebron University Hospital, Barcelona, Spain

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Rafael Morales-Barrera Vall d’Hebron Institute of Oncology (VHIO) and Vall d’Hebron University Hospital, Barcelona, Spain

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Cristina Suarez Vall d’Hebron Institute of Oncology (VHIO) and Vall d’Hebron University Hospital, Barcelona, Spain

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Jacques Planas Vall d’Hebron Institute of Oncology (VHIO) and Vall d’Hebron University Hospital, Barcelona, Spain

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Xavier Maldonado Vall d’Hebron Institute of Oncology (VHIO) and Vall d’Hebron University Hospital, Barcelona, Spain

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Joan Carles Vall d’Hebron Institute of Oncology (VHIO) and Vall d’Hebron University Hospital, Barcelona, Spain

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Joaquin Mateo Vall d’Hebron Institute of Oncology (VHIO) and Vall d’Hebron University Hospital, Barcelona, Spain

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-strand break repair genes are common in prostate cancer, and their prevalence increases in advanced disease states. These mutations would lead to a relative impairment of error-free homologous recombination-mediated repair, so the cell will preferentially rely

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-21-0133
Volume/Issue:
Volume 28: Issue 8
Free access
Bo Chen Department of Breast Cancer, Cancer Center, Guangdong Provincial People’s Hospital and Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China

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Guochun Zhang Department of Breast Cancer, Cancer Center, Guangdong Provincial People’s Hospital and Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China

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Guangnan Wei Department of Breast Cancer, Cancer Center, Guangdong Provincial People’s Hospital and Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China

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Yulei Wang Department of Breast Cancer, Cancer Center, Guangdong Provincial People’s Hospital and Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China
School of Medicine, South China University of Technology, Guangzhou, Guangdong, China

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Liping Guo Department of Breast Cancer, Cancer Center, Guangdong Provincial People’s Hospital and Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China
The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, China

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Jiali Lin Department of Breast Cancer, Cancer Center, Guangdong Provincial People’s Hospital and Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China
The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, China

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Kai Li Department of Breast Cancer, Cancer Center, Guangdong Provincial People’s Hospital and Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China

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Hsiaopei Mok Department of Breast Cancer, Cancer Center, Guangdong Provincial People’s Hospital and Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China

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Li Cao Department of Breast Cancer, Cancer Center, Guangdong Provincial People’s Hospital and Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China

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Chongyang Ren Department of Breast Cancer, Cancer Center, Guangdong Provincial People’s Hospital and Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China

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Lingzhu Wen Department of Breast Cancer, Cancer Center, Guangdong Provincial People’s Hospital and Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China

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Minghan Jia Department of Breast Cancer, Cancer Center, Guangdong Provincial People’s Hospital and Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China

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Cheukfai Li Department of Breast Cancer, Cancer Center, Guangdong Provincial People’s Hospital and Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China

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Ting Hou Burning Rock Biotech, Guangzhou, Guangdong, China

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Han Han-Zhang Burning Rock Biotech, Guangzhou, Guangdong, China

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Jing Liu Burning Rock Biotech, Guangzhou, Guangdong, China

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Charles M Balch Department of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA

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Ning Liao Department of Breast Cancer, Cancer Center, Guangdong Provincial People’s Hospital and Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China

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pathways that are distinct between the two groups. Our results demonstrate that the major signaling pathways affected in HR+/HER2+ tumors were homologous recombination ( Fig. 2A , 37.5% vs 11.6%, P  = 0.004), TGF-beta ( Fig. 2B , 35.9% vs 11.6%, P  = 0

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-19-0414
Volume/Issue:
Volume 27: Issue 3
Restricted access
Louis de Mestier Department of Gastroenterology and Pancreatology, Beaujon Hospital, Paris 7 University, APHP, Clichy, France

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Jean-Baptiste Danset Department of Hepato-Gastroenterology, European Georges-Pompidou Hospital, APHP, Paris, France

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Cindy Neuzillet Department of Digestive Oncology, Beaujon Hospital, Paris 7 University, APHP, Clichy, France

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Vinciane Rebours Department of Gastroenterology and Pancreatology, Beaujon Hospital, Paris 7 University, APHP, Clichy, France

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Jérôme Cros Department of Pathology, Beaujon Hospital, Paris 7 University, APHP, Clichy, France

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Nadem Soufir Department of Genetics, Bichat Hospital, Paris 7 University, APHP, Clichy, France

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Pascal Hammel Department of Digestive Oncology, Beaujon Hospital, Paris 7 University, APHP, Clichy, France

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radicals generated by the cellular metabolism, ultraviolet light, radiation and chemicals. Homologous recombination (HR) is a high-fidelity repair system of double-strand DNA breaks and DNA cross-linking damages induced by DNA-damaging agents. The BRCA1 and

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-16-0269
Volume/Issue:
Volume 23: Issue 10
Free access
Cathy B Moelans Department of Pathology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands

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Joep de Ligt Department of Biomedical Genetics, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands

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Petra van der Groep Department of Pathology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
Department of Internal Medicine, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands

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Pjotr Prins Department of Biomedical Genetics, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands

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Nicolle J M Besselink Department of Biomedical Genetics, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
Center for Personalized Cancer Treatment, Rotterdam, The Netherlands

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Marlous Hoogstraat Department of Biomedical Genetics, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands

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Natalie D ter Hoeve Department of Pathology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands

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Miangela M Lacle Department of Pathology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands

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Robert Kornegoor Department of Pathology, Gelre Ziekenhuizen, Appeldoorn, The Netherlands

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Carmen C van der Pol Cancer Center, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands

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Wendy W J de Leng Department of Pathology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands

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Ellis Barbé Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands

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Bert van der Vegt Department of Pathology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands

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John Martens Department of Medical Oncology, Daniel den Hoed Cancer Center, Erasmus University Medical Center, Rotterdam, The Netherlands

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Peter Bult Department of Pathology, Radboud University Medical Center, Nijmegen, The Netherlands

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Vincent T H B M Smit Department of Pathology, LUMC, Leiden, The Netherlands

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Marco J Koudijs Department of Biomedical Genetics, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
Center for Personalized Cancer Treatment, Rotterdam, The Netherlands

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Isaac J Nijman Department of Biomedical Genetics, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
Center for Personalized Cancer Treatment, Rotterdam, The Netherlands

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Emile E Voest Center for Personalized Cancer Treatment, Rotterdam, The Netherlands
Department of Medical Oncology, The Netherlands Cancer Institute, Amsterdam, The Netherlands

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Pier Selenica Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Britta Weigelt Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Jorge S Reis-Filho Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Elsken van der Wall Cancer Center, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands

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Edwin Cuppen Department of Biomedical Genetics, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
Cancer Genomics.nl, Center for Molecular Medicine, UMC Utrecht, Utrecht, The Netherlands

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Paul J van Diest Department of Pathology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands

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and/or TCGA. Mutational signature analysis revealed that 24% of MBCs have a dominant signature 3 associated with defective homologous recombination DNA repair, whereas only 13% of TCGA FBCs demonstrated a dominant signature 3 ( Fig. 3 ). In

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-19-0278
Volume/Issue:
Volume 26: Issue 10
Free access
F J DeMayo
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J P Lydon
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O M Conneely
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B W O'Malley
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Abstract

The ability to modify the genome by homologous recombination in embryonic stem cells has proven to be a powerful tool in evaluating the role specific genes play in normal development and during the progression of specific diseases. This technology has already provided valuable information in understanding the roles of specific genes in the development of the mammary gland and the interaction of specific genes in the development of mammary cancer. This paper discusses some of the current findings that knockout technology has made with regards to mammary development and discusses some of the limitations of this technology.

Endocrine-Related Cancer (1997) 4 85-92

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Research Article
DOI:
https://doi.org/10.1677/erc.0.0401085
Volume/Issue:
Volume 4: Issue 1
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Deborah J Marsh Hormones and Cancer Group, Kolling Institute of Medical Research, Royal North Shore Hospital, University of Sydney, St Leonards, Sydney, New South Wales 2065, Australia

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been shown to have critical cellular functions. An example of this is monoubiquitination of the Fanconi Anemia protein FANCD2 in response to DNA damage that promotes homologous recombination repair of DNA double strand breaks ( Nakanishi et al . 2005

Article Type:
Editorial
DOI:
https://doi.org/10.1530/ERC-14-0585
Volume/Issue:
Volume 22: Issue 1
Free access