Anil Belur Nagaraj
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Anil Belur Nagaraj has a total of 43 co-authors. Here are the top co-authors by number of shared publications:
- Amal Yussuf
Ambry Genetics, Aliso Viejo, CA
6 shared publications - Carolyn A. Lumby
Mayo Clinic, Rochester, Minnesota
6 shared publications - Celine M. Vachon
Department of Quantitative Health Sciences, Mayo Clinic, Rochester, MN 55905, USA
6 shared publications - Christopher A. Haiman
Department of Preventive Medicine, Keck School of Medicine of USC, Los Angeles, USA
6 shared publications - Chunling Hu
Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, USA
6 shared publications - Elizabeth Chao
Department of Clinical Diagnostics, Ambry Genetics, Aliso Viejo, USA
6 shared publications
Latest Publications
- Open Access
- 24 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Materials, Figure S1-S4, Table S1-S9 from Functional and Clinical Characterization of Variants of Uncertain Significance Identifies a Hotspot for Inactivating Missense Variants in RAD51C
Supplementary Materials, References, Tables and Figures
- 24 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Materials, Figure S1-S4, Table S1-S9 from Functional and Clinical Characterization of Variants of Uncertain Significance Identifies a Hotspot for Inactivating Missense Variants in RAD51C
Supplementary Materials, References, Tables and Figures
- Open Access
- 16 September 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Materials, Figure S1-S4, Table S1-S9 from Functional and clinical characterization of variants of uncertain significance identifies a hotspot for inactivating missense variants in RAD51C
Supplementary Materials, References, Tables and Figures
- 16 September 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Materials, Figure S1-S4, Table S1-S9 from Functional and clinical characterization of variants of uncertain significance identifies a hotspot for inactivating missense variants in RAD51C
Supplementary Materials, References, Tables and Figures
- Open Access
- 16 September 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Materials, Figure S1-S4, Table S1-S9 from Functional and clinical characterization of variants of uncertain significance identifies a hotspot for inactivating missense variants in RAD51C
Supplementary Materials, References, Tables and Figures
- 16 September 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Materials, Figure S1-S4, Table S1-S9 from Functional and clinical characterization of variants of uncertain significance identifies a hotspot for inactivating missense variants in RAD51C
Supplementary Materials, References, Tables and Figures
- Open Access
- 1 August 2023
- Published by American Association for Cancer Research (AACR)
Supplementary Materials, Figure S1-S4, Table S1-S9 from Functional and Clinical Characterization of Variants of Uncertain Significance Identifies a Hotspot for Inactivating Missense Variants in RAD51C
Supplementary Materials, References, Tables and Figures
- 1 August 2023
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Materials, Figure S1-S4, Table S1-S9 from Functional and Clinical Characterization of Variants of Uncertain Significance Identifies a Hotspot for Inactivating Missense Variants in RAD51C
Supplementary Materials, References, Tables and Figures
- Open Access
- 1 August 2023
- Published by American Association for Cancer Research (AACR)
Supplementary Materials, Figure S1-S4, Table S1-S9 from Functional and Clinical Characterization of Variants of Uncertain Significance Identifies a Hotspot for Inactivating Missense Variants in RAD51C
Supplementary Materials, References, Tables and Figures
- 1 August 2023
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Materials, Figure S1-S4, Table S1-S9 from Functional and Clinical Characterization of Variants of Uncertain Significance Identifies a Hotspot for Inactivating Missense Variants in RAD51C
Supplementary Materials, References, Tables and Figures
- Open Access
- 30 May 2023
- Published by American Association for Cancer Research (AACR) in Cancer Research
- Vol. 83 (15) , 2557-2571
Functional and Clinical Characterization of Variants of Uncertain Significance Identifies a Hotspot for Inactivating Missense Variants in RAD51C
Pathogenic protein-truncating variants of RAD51C, which plays an integral role in promoting DNA damage repair, increase the risk of breast and ovarian cancer. A large number of RAD51C missense variants of uncertain significance (VUS) have been identified, but the effects of the majority of these variants on RAD51C function and cancer predisposition have not been established. Here, analysis of 173 missense variants by a homology-directed repair (HDR) assay in reconstituted RAD51C−/− cells identified 30 nonfunctional (deleterious) variants, including 18 in a hotspot within the ATP-binding region. The deleterious variants conferred sensitivity to cisplatin and olaparib and disrupted formation of RAD51C/XRCC3 and RAD51B/RAD51C/RAD51D/XRCC2 complexes. Computational analysis indicated the deleterious variant effects were consistent with structural effects on ATP-binding to RAD51C. A subset of the variants displayed similar effects on RAD51C activity in reconstituted human RAD51C-depleted cancer cells. Case–control association studies of deleterious variants in women with breast and ovarian cancer and noncancer controls showed associations with moderate breast cancer risk [OR, 3.92; 95% confidence interval (95% CI), 2.18–7.59] and high ovarian cancer risk (OR, 14.8; 95% CI, 7.71–30.36), similar to protein-truncating variants. This functional data supports the clinical classification of inactivating RAD51C missense variants as pathogenic or likely pathogenic, which may improve the clinical management of variant carriers. Significance: Functional analysis of the impact of a large number of missense variants on RAD51C function provides insight into RAD51C activity and information for classification of the cancer relevance of RAD51C variants.
- 30 May 2023
- Published by American Association for Cancer Research (AACR) in Cancer Research
- Vol. 83 (15) , 2557-2571
Open AccessFunctional and Clinical Characterization of Variants of Uncertain Significance Identifies a Hotspot for Inactivating Missense Variants in RAD51C
Pathogenic protein-truncating variants of RAD51C, which plays an integral role in promoting DNA damage repair, increase the risk of breast and ovarian cancer. A large number of RAD51C missense variants of uncertain significance (VUS) have been identified, but the effects of the majority of these variants on RAD51C function and cancer predisposition have not been established. Here, analysis of 173 missense variants by a homology-directed repair (HDR) assay in reconstituted RAD51C−/− cells identified 30 nonfunctional (deleterious) variants, including 18 in a hotspot within the ATP-binding region. The deleterious variants conferred sensitivity to cisplatin and olaparib and disrupted formation of RAD51C/XRCC3 and RAD51B/RAD51C/RAD51D/XRCC2 complexes. Computational analysis indicated the deleterious variant effects were consistent with structural effects on ATP-binding to RAD51C. A subset of the variants displayed similar effects on RAD51C activity in reconstituted human RAD51C-depleted cancer cells. Case–control association studies of deleterious variants in women with breast and ovarian cancer and noncancer controls showed associations with moderate breast cancer risk [OR, 3.92; 95% confidence interval (95% CI), 2.18–7.59] and high ovarian cancer risk (OR, 14.8; 95% CI, 7.71–30.36), similar to protein-truncating variants. This functional data supports the clinical classification of inactivating RAD51C missense variants as pathogenic or likely pathogenic, which may improve the clinical management of variant carriers. Significance: Functional analysis of the impact of a large number of missense variants on RAD51C function provides insight into RAD51C activity and information for classification of the cancer relevance of RAD51C variants.