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2. Data from Secondary Somatic Mutations Restoring RAD51C and RAD51D Associated with Acquired Resistance to the PARP Inhibitor Rucaparib in High-Grade Ovarian Carcinoma

Author

Kondrashova, Olga, primary, Nguyen, Minh, primary, Shield-Artin, Kristy, primary, Tinker, Anna V., primary, Teng, Nelson N.H., primary, Harrell, Maria I., primary, Kuiper, Michael J., primary, Ho, Gwo-Yaw, primary, Barker, Holly, primary, Jasin, Maria, primary, Prakash, Rohit, primary, Kass, Elizabeth M., primary, Sullivan, Meghan R., primary, Brunette, Gregory J., primary, Bernstein, Kara A., primary, Coleman, Robert L., primary, Floquet, Anne, primary, Friedlander, Michael, primary, Kichenadasse, Ganessan, primary, O'Malley, David M., primary, Oza, Amit, primary, Sun, James, primary, Robillard, Liliane, primary, Maloney, Lara, primary, Bowtell, David, primary, Giordano, Heidi, primary, Wakefield, Matthew J., primary, Kaufmann, Scott H., primary, Simmons, Andrew D., primary, Harding, Thomas C., primary, Raponi, Mitch, primary, McNeish, Iain A., primary, Swisher, Elizabeth M., primary, Lin, Kevin K., primary, and Scott, Clare L., primary

Published
2023
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3. Supplementary Tables and Supplementary Figures 1 through 11 from Secondary Somatic Mutations Restoring RAD51C and RAD51D Associated with Acquired Resistance to the PARP Inhibitor Rucaparib in High-Grade Ovarian Carcinoma

Author

Kondrashova, Olga, primary, Nguyen, Minh, primary, Shield-Artin, Kristy, primary, Tinker, Anna V., primary, Teng, Nelson N.H., primary, Harrell, Maria I., primary, Kuiper, Michael J., primary, Ho, Gwo-Yaw, primary, Barker, Holly, primary, Jasin, Maria, primary, Prakash, Rohit, primary, Kass, Elizabeth M., primary, Sullivan, Meghan R., primary, Brunette, Gregory J., primary, Bernstein, Kara A., primary, Coleman, Robert L., primary, Floquet, Anne, primary, Friedlander, Michael, primary, Kichenadasse, Ganessan, primary, O'Malley, David M., primary, Oza, Amit, primary, Sun, James, primary, Robillard, Liliane, primary, Maloney, Lara, primary, Bowtell, David, primary, Giordano, Heidi, primary, Wakefield, Matthew J., primary, Kaufmann, Scott H., primary, Simmons, Andrew D., primary, Harding, Thomas C., primary, Raponi, Mitch, primary, McNeish, Iain A., primary, Swisher, Elizabeth M., primary, Lin, Kevin K., primary, and Scott, Clare L., primary

Published
2023
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4. Supp Table 1 from Secondary Somatic Mutations Restoring RAD51C and RAD51D Associated with Acquired Resistance to the PARP Inhibitor Rucaparib in High-Grade Ovarian Carcinoma

Author

Kondrashova, Olga, primary, Nguyen, Minh, primary, Shield-Artin, Kristy, primary, Tinker, Anna V., primary, Teng, Nelson N.H., primary, Harrell, Maria I., primary, Kuiper, Michael J., primary, Ho, Gwo-Yaw, primary, Barker, Holly, primary, Jasin, Maria, primary, Prakash, Rohit, primary, Kass, Elizabeth M., primary, Sullivan, Meghan R., primary, Brunette, Gregory J., primary, Bernstein, Kara A., primary, Coleman, Robert L., primary, Floquet, Anne, primary, Friedlander, Michael, primary, Kichenadasse, Ganessan, primary, O'Malley, David M., primary, Oza, Amit, primary, Sun, James, primary, Robillard, Liliane, primary, Maloney, Lara, primary, Bowtell, David, primary, Giordano, Heidi, primary, Wakefield, Matthew J., primary, Kaufmann, Scott H., primary, Simmons, Andrew D., primary, Harding, Thomas C., primary, Raponi, Mitch, primary, McNeish, Iain A., primary, Swisher, Elizabeth M., primary, Lin, Kevin K., primary, and Scott, Clare L., primary

Published
2023
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5. Supp Table 4 from Secondary Somatic Mutations Restoring RAD51C and RAD51D Associated with Acquired Resistance to the PARP Inhibitor Rucaparib in High-Grade Ovarian Carcinoma

Author

Kondrashova, Olga, primary, Nguyen, Minh, primary, Shield-Artin, Kristy, primary, Tinker, Anna V., primary, Teng, Nelson N.H., primary, Harrell, Maria I., primary, Kuiper, Michael J., primary, Ho, Gwo-Yaw, primary, Barker, Holly, primary, Jasin, Maria, primary, Prakash, Rohit, primary, Kass, Elizabeth M., primary, Sullivan, Meghan R., primary, Brunette, Gregory J., primary, Bernstein, Kara A., primary, Coleman, Robert L., primary, Floquet, Anne, primary, Friedlander, Michael, primary, Kichenadasse, Ganessan, primary, O'Malley, David M., primary, Oza, Amit, primary, Sun, James, primary, Robillard, Liliane, primary, Maloney, Lara, primary, Bowtell, David, primary, Giordano, Heidi, primary, Wakefield, Matthew J., primary, Kaufmann, Scott H., primary, Simmons, Andrew D., primary, Harding, Thomas C., primary, Raponi, Mitch, primary, McNeish, Iain A., primary, Swisher, Elizabeth M., primary, Lin, Kevin K., primary, and Scott, Clare L., primary

Published
2023
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6. Supp Video from Secondary Somatic Mutations Restoring RAD51C and RAD51D Associated with Acquired Resistance to the PARP Inhibitor Rucaparib in High-Grade Ovarian Carcinoma

Author

Kondrashova, Olga, primary, Nguyen, Minh, primary, Shield-Artin, Kristy, primary, Tinker, Anna V., primary, Teng, Nelson N.H., primary, Harrell, Maria I., primary, Kuiper, Michael J., primary, Ho, Gwo-Yaw, primary, Barker, Holly, primary, Jasin, Maria, primary, Prakash, Rohit, primary, Kass, Elizabeth M., primary, Sullivan, Meghan R., primary, Brunette, Gregory J., primary, Bernstein, Kara A., primary, Coleman, Robert L., primary, Floquet, Anne, primary, Friedlander, Michael, primary, Kichenadasse, Ganessan, primary, O'Malley, David M., primary, Oza, Amit, primary, Sun, James, primary, Robillard, Liliane, primary, Maloney, Lara, primary, Bowtell, David, primary, Giordano, Heidi, primary, Wakefield, Matthew J., primary, Kaufmann, Scott H., primary, Simmons, Andrew D., primary, Harding, Thomas C., primary, Raponi, Mitch, primary, McNeish, Iain A., primary, Swisher, Elizabeth M., primary, Lin, Kevin K., primary, and Scott, Clare L., primary

Published
2023
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7. Novel insights into RAD51 activity and regulation during homologous recombination and DNA replication (1)

Author

Godin, Stephen K., Sullivan, Meghan R., and Bernstein, Kara A.

Subjects
DNA replication -- Research, Genetic research, Genetic regulation -- Research, Genetic recombination -- Research, Biological sciences
Abstract

Abstract: In this review we focus on new insights that challenge our understanding of homologous recombination (HR) and Rad51 regulation. Recent advances using high-resolution microscopy and single molecule techniques have [...]

Published
2016
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8. Homologous recombination–deficient mutation cluster in tumor suppressor RAD51C identified by comprehensive analysis of cancer variants

Author

Prakash, Rohit, primary, Rawal, Yashpal, additional, Sullivan, Meghan R., additional, Grundy, McKenzie K., additional, Bret, Hélène, additional, Mihalevic, Michael J., additional, Rein, Hayley L., additional, Baird, Jared M., additional, Darrah, Kristie, additional, Zhang, Fang, additional, Wang, Raymond, additional, Traina, Tiffany A., additional, Radke, Marc R., additional, Kaufmann, Scott H., additional, Swisher, Elizabeth M., additional, Guérois, Raphaël, additional, Modesti, Mauro, additional, Sung, Patrick, additional, Jasin, Maria, additional, and Bernstein, Kara A., additional

Published
2022
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10. Distinct pathways of homologous recombination controlled by the SWS1-SWSAP1-SPIDR complex

Author

Prakash, Rohit, primary, Sandoval, Thomas, additional, Morati, Florian, additional, Zagelbaum, Jennifer A, additional, Taylor, Brett, additional, Wang, Raymond, additional, Desclos, Emilie C B, additional, Sullivan, Meghan R, additional, Rein, Hayley L, additional, Bernstein, Kara A, additional, Krawczyk, Przemek M, additional, Gautier, Jean, additional, Modesti, Mauro, additional, Vanoli, Fabio, additional, and Jasin, Maria, additional

Published
2020
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11. Differential Requirements for the RAD51 Paralogs in Genome Repair and Maintenance in Human Cells

Author

Garcin, Edwige B., primary, Gon, Stéphanie, additional, Sullivan, Meghan R., additional, Brunette, Gregory J., additional, Cian, Anne De, additional, Concordet, Jean-Paul, additional, Giovannangeli, Carine, additional, Dirks, Wilhelm G., additional, Eberth, Sonja, additional, Bernstein, Kara A., additional, Prakash, Rohit, additional, Jasin, Maria, additional, and Modesti, Mauro, additional

Published
2019
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12. RAD-ical New Insights into RAD51 Regulation

Author

Sullivan, Meghan R., Bernstein, Kara A., Sullivan, Meghan R., and Bernstein, Kara A.

Abstract

The accurate repair of DNA is critical for genome stability and cancer prevention. DNA double-strand breaks are one of the most toxic lesions; however, they can be repaired using homologous recombination. Homologous recombination is a high-fidelity DNA repair pathway that uses a homologous template for repair. One central HR step is RAD51 nucleoprotein filament formation on the single-stranded DNA ends, which is a step required for the homology search and strand invasion steps of HR. RAD51 filament formation is tightly controlled by many positive and negative regulators, which are collectively termed the RAD51 mediators. The RAD51 mediators function to nucleate, elongate, stabilize, and disassemble RAD51 during repair. In model organisms, RAD51 paralogs are RAD51 mediator proteins that structurally resemble RAD51 and promote its HR activity. New functions for the RAD51 paralogs during replication and in RAD51 filament flexibility have recently been uncovered. Mutations in the human RAD51 paralogs (RAD51B, RAD51C, RAD51D, XRCC2, XRCC3, and SWSAP1) are found in a subset of breast and ovarian cancers. Despite their discovery three decades ago, few advances have been made in understanding the function of the human RAD51 paralogs. Here, we discuss the current perspective on the in vivo and in vitro function of the RAD51 paralogs, and their relationship with cancer in vertebrate models.

Published
2018

15. Secondary Somatic Mutations Restoring RAD51C and RAD51D Associated with Acquired Resistance to the PARP Inhibitor Rucaparib in High-Grade Ovarian Carcinoma

Author

Kondrashova, Olga, primary, Nguyen, Minh, additional, Shield-Artin, Kristy, additional, Tinker, Anna V., additional, Teng, Nelson N.H., additional, Harrell, Maria I., additional, Kuiper, Michael J., additional, Ho, Gwo-Yaw, additional, Barker, Holly, additional, Jasin, Maria, additional, Prakash, Rohit, additional, Kass, Elizabeth M., additional, Sullivan, Meghan R., additional, Brunette, Gregory J., additional, Bernstein, Kara A., additional, Coleman, Robert L., additional, Floquet, Anne, additional, Friedlander, Michael, additional, Kichenadasse, Ganessan, additional, O'Malley, David M., additional, Oza, Amit, additional, Sun, James, additional, Robillard, Liliane, additional, Maloney, Lara, additional, Bowtell, David, additional, Giordano, Heidi, additional, Wakefield, Matthew J., additional, Kaufmann, Scott H., additional, Simmons, Andrew D., additional, Harding, Thomas C., additional, Raponi, Mitch, additional, McNeish, Iain A., additional, Swisher, Elizabeth M., additional, Lin, Kevin K., additional, and Scott, Clare L., additional

Published
2017
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17. The Budding Yeast Ubiquitin Protease Ubp7 Is a Novel Component Involved in S Phase Progression

Author

Boehm, Stefanie, Szakal, Barnabas, Herken, Benjamin W., Sullivan, Meghan R., Mihalevic, Michael J., Kabbinavar, Faiz F., Branzei, Dana, Clark, Nathan L., Bernstein, Kara A., Boehm, Stefanie, Szakal, Barnabas, Herken, Benjamin W., Sullivan, Meghan R., Mihalevic, Michael J., Kabbinavar, Faiz F., Branzei, Dana, Clark, Nathan L., and Bernstein, Kara A.

Abstract

DNAdamage must be repaired in an accurate and timely fashion to preserve genome stability. Cellular mechanisms preventing genome instability are crucial to human health because genome instability is considered a hallmark of cancer. Collectively referred to as the DNA damage response, conserved pathways ensure proper DNA damage recognition and repair. The function of numerous DNA damage response components is fine-tuned by posttranslational modifications, including ubiquitination. This not only involves the enzyme cascade responsible for conjugating ubiquitin to substrates but also requires enzymes that mediate directed removal of ubiquitin. Deubiquitinases remove ubiquitin from substrates to prevent degradation or to mediate signaling functions. The Saccharomyces cerevisiae deubiquitinase Ubp7 has been characterized previously as an endocytic factor. However, here we identify Ubp7 as a novel factor affecting S phase progression after hydroxyurea treatment and demonstrate an evolutionary and genetic interaction of Ubp7 with DNA damage repair pathways of homologous recombination and nucleotide excision repair. We find that deletion of UBP7 sensitizes cells to hydroxyurea and cisplatin and demonstrate that factors that stabilize replication forks are critical under these conditions. Furthermore, ubp7 Delta cells exhibit an S phase progression defect upon checkpoint activation by hydroxyurea treatment. ubp7 Delta mutants are epistatic to factors involved in histone maintenance and modification, and we find that a subset of Ubp7 is chromatin-associated. In summary, our results suggest that Ubp7 contributes to S phase progression by affecting the chromatin state at replication forks, and we propose histone H2B ubiquitination as a potential substrate of Ubp7.

Published
2016

21. Novel insights into RAD51 activity and regulation during homologous recombination and DNA replication1.

Author

Godin, Stephen K., Sullivan, Meghan R., and Bernstein, Kara A.

Subjects
*DNA replication, *GENETIC recombination, *HOMOLOGOUS chromosomes, *CAENORHABDITIS elegans, *DNA damage, *DNA repair
Abstract

In this review we focus on new insights that challenge our understanding of homologous recombination (HR) and Rad51 regulation. Recent advances using high-resolution microscopy and single molecule techniques have broadened our knowledge of Rad51 filament formation and strand invasion at double-strand break (DSB) sites and at replication forks, which are one of most physiologically relevant forms of HR from yeast to humans. Rad51 filament formation and strand invasion is regulated by many mediator proteins such as the Rad51 paralogues and the Shu complex, consisting of a Shu2/SWS1 family member and additional Rad51 paralogues. Importantly, a novel RAD51 paralogue was discovered in Caenorhabditis elegans, and its in vitro characterization has demonstrated a new function for the worm RAD51 paralogues during HR. Conservation of the human RAD51 paralogues function during HR and repair of replicative damage demonstrate how the RAD51 mediators play a critical role in human health and genomic integrity. Together, these new findings provide a framework for understanding RAD51 and its mediators in DNA repair during multiple cellular contexts. [ABSTRACT FROM AUTHOR]

Published
2016
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22. Novel insights into RAD51 activity and regulation during homologous recombination and DNA replication1.

Author

Godin, Stephen K., Sullivan, Meghan R., and Bernstein, Kara A.

Subjects
DNA replication, GENETIC recombination, HOMOLOGOUS chromosomes, CAENORHABDITIS elegans, DNA damage, DNA repair
Abstract

Copyright of Biochemistry & Cell Biology is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2016
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23. Long-term survival of an ovarian cancer patient harboring a RAD51C missense mutation.

Author

Sullivan MR, Prakash R, Rawal Y, Wang W, Sung P, Radke MR, Kaufmann SH, Swisher EM, Bernstein KA, and Jasin M

Subjects
Animals, Binding Sites, Cell Line, DNA-Binding Proteins chemistry, DNA-Binding Proteins metabolism, Drug Resistance, Neoplasm, Female, Gene Knockout Techniques, Germ-Line Mutation, Humans, Insecta, Rad51 Recombinase genetics, Recombination, Genetic, Transcriptome, DNA-Binding Proteins genetics, Mutation, Missense, Ovarian Neoplasms genetics
Abstract

Mutations in homologous recombination (HR) genes predispose to cancer but also sensitize to chemotherapeutics. Although therapy can initially be effective, cancers frequently cease responding, leading to recurrence and poor prognosis. Here we identify a germline mutation in RAD51C , a critical HR factor and known tumor suppressor, in an ovarian cancer patient with exceptionally long, progression-free survival. The RAD51C-T132P mutation is in a highly conserved residue within the nucleotide-binding site and interferes with single-strand DNA binding of the RAD51 paralog complex RAD51B-RAD51C-RAD51D-XRCC2 and association with another RAD51 paralog XRCC3. These biochemical defects lead to highly defective HR and drug sensitivity in tumor cells, ascribing RAD51C-T132P as a deleterious mutation that was likely causal for tumor formation. Conversely, its position within a critical site suggests that it is refractory to secondary mutations that would restore RAD51C gene function and lead to therapy resistance. A need for a greater understanding of the relationship between mutation position and reversion potential of HR genes is underscored, as it may help predict the effectiveness of therapies in patients with HR-deficient cancers., (© 2021 Sullivan et al.; Published by Cold Spring Harbor Laboratory Press.)

Published
2021
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