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396 results on '"Sharan, Shyam K."'

1. Mismatch repair protein MLH1 suppresses replicative stress in BRCA2-deficient breast tumors

Author

Sengodan, Satheesh K., Hu, Xiaoju, Peddibhotla, Vaishnavi, Balamurugan, Kuppusamy, Mitrophanov, Alexander Y., McKennett, Lois, Kharat, Suhas S., Sanawar, Rahul, Singh, Vinod Kumar, Albaugh, Mary E., Burkett, Sandra S., Zhao, Yongmei, Tran, Bao, Malys, Tyler, Sterneck, Esta, De, Subhajyoti, and Sharan, Shyam K.

Subjects
United States. National Cancer Institute, Gene mutations, Genes, DNA synthesis, Nucleases, Cancer -- Genetic aspects, RNA, Breast cancer, Health care industry
Abstract

Loss of BRCA2 (breast cancer 2) is lethal for normal cells. Yet it remains poorly understood how, in BRCA2 mutation carriers, cells undergoing loss of heterozygosity overcome the lethality and undergo tissue-specific neoplastic transformation. Here, we identified mismatch repair gene mutL homolog 1 (MLH1) as a genetic interactor of BRCA2 whose overexpression supports the viability of Brca2-null cells. Mechanistically, we showed that MLH1 interacts with Flap endonuclease 1 (FEN1) and competes to process the RNA flaps of Okazaki fragments. Together, they restrained the DNA2 nuclease activity on the reversed forks of lagging strands, leading to replication fork (RF) stability in BRCA2-deficient cells. In these cells, MLH1 also attenuated R-loops, allowing the progression of stable RFs, which suppressed genomic instability and supported cell viability. We demonstrated the significance of their genetic interaction by the lethality of Brca2-mutant mice and inhibition of Brca2-deficient tumor growth in mice by Mlh1 loss. Furthermore, we described estrogen as inducing MLH1 expression through estrogen receptor [alpha] (ER[alpha]), which might explain why the majority of BRCA2 mutation carriers develop ER- positive breast cancer. Taken together, our findings reveal a role of MLH1 in relieving replicative stress and show how it may contribute to the establishment of BRCA2-deficient breast tumors., Introduction Some of the well-established breast and ovarian cancer susceptibility genes, such as breast cancer 1 (BRCA1), BRCA2, and PALB2, encode proteins that play a key role in repairing double-strand [...]

Published
2024
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5. Treatment with novel topoisomerase inhibitors in Ewing sarcoma models reveals heterogeneity of tumor response.

Author

Lee, Unsun, Szabova, Ludmila, Collins, Victor J., Gordon, Melanie, Johnson, Kristine, Householder, Deborah, Jorgensen, Stephanie, Lu, Lucy, Bassel, Laura, Elloumi, Fathi, Peer, Cody J., Nelson, Ariana E., Varriano, Sophia, Varma, Sudhir, Roberts, Ryan D., Ohler, Zoe Weaver, Figg, William D., Sharan, Shyam K., Pommier, Yves, and Heske, Christine M.

Subjects
EWING'S sarcoma, WHOLE genome sequencing, DNA topoisomerase I, INHIBITION of cellular proliferation, RNA sequencing
Abstract

Introduction: The topoisomerase 1 (TOP1) inhibitor irinotecan is a standard-of-care agent for relapsed Ewing sarcoma (EWS), but its efficacy is limited by chemical instability, rapid clearance and reversibility, and dose-limiting toxicities, such as diarrhea. Indenoisoquinolines (IIQs) represent a new class of clinical TOP1 inhibitors designed to address these limitations. Methods: In this study, we evaluated the preclinical efficacy of three IIQs (LMP400, LMP744, and LMP776) in relevant models of EWS. We characterized the pharmacokinetics of IIQs in orthotopic xenograft models of EWS, optimized the dosing regimen through tolerability studies, and tested the efficacy of IIQs in a panel of six molecularly heterogeneous EWS patient-derived xenograft (PDX) models. For each PDX, we conducted whole genome and RNA sequencing, and methylation analysis. Results: We show that IIQs potently inhibit the proliferation of EWS cells in vitro, inducing complete cell growth inhibition at nanomolar concentrations via induction of DNA damage and apoptotic cell death. LMP400 treatment induced ≥30% tumor regression in two of six PDX models, with more durable regression compared to irinotecan treatment in one of these models. RNA sequencing of PDX models identified a candidate predictive biomarker gene signature for LMP400 response. These data, along with pharmacogenomic data on IIQs in sarcoma cell lines, are available at a new interactive public website: https://discover.nci.nih.gov/rsconnect/EwingSarcomaMinerCDB/. Discussion: Our findings suggest that IIQs may be promising new agents for a subset of EWS patients. [ABSTRACT FROM AUTHOR]

Published
2024
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9. The BRCA2 R2645G variant increases DNA binding and induces hyper-recombination.

Author

Alvaro-Aranda, Lucia, Petitalot, Ambre, Djeghmoum, Yasmina, Panigada, Davide, Singh, Jenny Kaur, Ehlén, Åsa, Vugic, Domagoj, Martin, Charlotte, Miron, Simona, Contreras-Perez, Aida, Nhiri, Naima, Boucherit, Virginie, Lafitte, Philippe, Dumoulin, Isaac, Quiles, Francisco, Rouleau, Etienne, Jacquet, Eric, Feliubadaló, Lidia, del Valle, Jesús, and Sharan, Shyam K

Published
2024
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12. Multimodel preclinical platform predicts clinical response of melanoma to immunotherapy

Author

Pérez-Guijarro, Eva, Yang, Howard H., Araya, Romina E., El Meskini, Rajaa, Michael, Helen T., Vodnala, Suman Kumar, Marie, Kerrie L., Smith, Cari, Chin, Sung, Lam, Khiem C., Thorkelsson, Andres, Iacovelli, Anthony J., Kulaga, Alan, Fon, Anyen, Michalowski, Aleksandra M., Hugo, Willy, Lo, Roger S., Restifo, Nicholas P., Sharan, Shyam K., Van Dyke, Terry, Goldszmid, Romina S., Weaver Ohler, Zoe, Lee, Maxwell P., Day, Chi-Ping, and Merlino, Glenn

Published
2020
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16. A novel mouse model of PMS2 founder mutation that causes mismatch repair defect due to aberrant splicing

Author

Biswas, Kajal, Couillard, Martin, Cavallone, Luca, Burkett, Sandra, Stauffer, Stacey, Martin, Betty K., Southon, Eileen, Reid, Susan, Plona, Teri M., Baugher, Ryan N., Mellott, Stephanie D., Pike, Kristen M., Albaugh, Mary E., Maedler-Kron, Chelsea, Hamel, Nancy, Tessarollo, Lino, Marcus, Victoria, Foulkes, William D., and Sharan, Shyam K.

Published
2021
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20. Saturation genome editing of 11 codons and exon 13 of BRCA2 coupled with chemotherapeutic drug response accurately determines pathogenicity of variants

Author

Sahu, Sounak, primary, Sullivan, Teresa L., additional, Mitrophanov, Alexander Y., additional, Galloux, Mélissa, additional, Nousome, Darryl, additional, Southon, Eileen, additional, Caylor, Dylan, additional, Mishra, Arun Prakash, additional, Evans, Christine N., additional, Clapp, Michelle E., additional, Burkett, Sandra, additional, Malys, Tyler, additional, Chari, Raj, additional, Biswas, Kajal, additional, and Sharan, Shyam K., additional

Published
2023
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23. RAD51C deficiency in mice results in early prophase I arrest in males and sister chromatid separation at metaphase II in females

Author

Kuznetsov, Sergey, Pellegrini, Manuela, Shuda, Kristy, Fernandez-Capetillo, Oscar, Liu, Yilun, Martin, Betty K, Burkett, Sandra, Southon, Eileen, Pati, Debananda, Tessarollo, Lino, West, Stephen C, Donovan, Peter J, Nussenzweig, Andre, and Sharan, Shyam K

Subjects
Genetics, Biotechnology, Underpinning research, 1.1 Normal biological development and functioning, Alleles, Animals, Chromatids, Chromosome Aberrations, DNA, Cruciform, DNA-Binding Proteins, Female, Infertility, Male, Meiotic Prophase I, Metaphase, Mice, Models, Genetic, Oocytes, Ovary, Rad51 Recombinase, Recombination, Genetic, Sex Factors, Spermatocytes, Testis, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

RAD51C is a member of the RecA/RAD51 protein family, which is known to play an important role in DNA repair by homologous recombination. In mice, it is essential for viability. Therefore, we have generated a hypomorphic allele of Rad51c in addition to a null allele. A subset of mice expressing the hypomorphic allele is infertile. This infertility is caused by sexually dimorphic defects in meiotic recombination, revealing its two distinct functions. Spermatocytes undergo a developmental arrest during the early stages of meiotic prophase I, providing evidence for the role of RAD51C in early stages of RAD51-mediated recombination. In contrast, oocytes can progress normally to metaphase I after superovulation but display precocious separation of sister chromatids, aneuploidy, and broken chromosomes at metaphase II. These defects suggest a possible late role of RAD51C in meiotic recombination. Based on the marked reduction in Holliday junction (HJ) resolution activity in Rad51c-null mouse embryonic fibroblasts, we propose that this late function may be associated with HJ resolution.

Published
2007

27. Supplementary Figure 1 and Legend from Distinct Biomarker Profiles and TCR Sequence Diversity Characterize the Response to PD-L1 Blockade in a Mouse Melanoma Model

Author

El Meskini, Rajaa, primary, Atkinson, Devon, primary, Kulaga, Alan, primary, Abdelmaksoud, Abdalla, primary, Gumprecht, Michelle, primary, Pate, Nathan, primary, Hayes, Susana, primary, Oberst, Michael, primary, Kaplan, Ian M., primary, Raber, Patrick, primary, Van Dyke, Terry, primary, Sharan, Shyam K., primary, Hollingsworth, Robert, primary, Day, Chi-Ping, primary, Merlino, Glenn, primary, and Weaver Ohler, Zoë, primary

Published
2023
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28. Data from Distinct Biomarker Profiles and TCR Sequence Diversity Characterize the Response to PD-L1 Blockade in a Mouse Melanoma Model

Author

El Meskini, Rajaa, primary, Atkinson, Devon, primary, Kulaga, Alan, primary, Abdelmaksoud, Abdalla, primary, Gumprecht, Michelle, primary, Pate, Nathan, primary, Hayes, Susana, primary, Oberst, Michael, primary, Kaplan, Ian M., primary, Raber, Patrick, primary, Van Dyke, Terry, primary, Sharan, Shyam K., primary, Hollingsworth, Robert, primary, Day, Chi-Ping, primary, Merlino, Glenn, primary, and Weaver Ohler, Zoë, primary

Published
2023
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29. Supplementary Table 2 and Legend from Distinct Biomarker Profiles and TCR Sequence Diversity Characterize the Response to PD-L1 Blockade in a Mouse Melanoma Model

Author

El Meskini, Rajaa, primary, Atkinson, Devon, primary, Kulaga, Alan, primary, Abdelmaksoud, Abdalla, primary, Gumprecht, Michelle, primary, Pate, Nathan, primary, Hayes, Susana, primary, Oberst, Michael, primary, Kaplan, Ian M., primary, Raber, Patrick, primary, Van Dyke, Terry, primary, Sharan, Shyam K., primary, Hollingsworth, Robert, primary, Day, Chi-Ping, primary, Merlino, Glenn, primary, and Weaver Ohler, Zoë, primary

Published
2023
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30. Supplementary Figure 2 and Legend from Distinct Biomarker Profiles and TCR Sequence Diversity Characterize the Response to PD-L1 Blockade in a Mouse Melanoma Model

Author

El Meskini, Rajaa, primary, Atkinson, Devon, primary, Kulaga, Alan, primary, Abdelmaksoud, Abdalla, primary, Gumprecht, Michelle, primary, Pate, Nathan, primary, Hayes, Susana, primary, Oberst, Michael, primary, Kaplan, Ian M., primary, Raber, Patrick, primary, Van Dyke, Terry, primary, Sharan, Shyam K., primary, Hollingsworth, Robert, primary, Day, Chi-Ping, primary, Merlino, Glenn, primary, and Weaver Ohler, Zoë, primary

Published
2023
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31. Supplementary Figure 5 and Legend from Distinct Biomarker Profiles and TCR Sequence Diversity Characterize the Response to PD-L1 Blockade in a Mouse Melanoma Model

Author

El Meskini, Rajaa, primary, Atkinson, Devon, primary, Kulaga, Alan, primary, Abdelmaksoud, Abdalla, primary, Gumprecht, Michelle, primary, Pate, Nathan, primary, Hayes, Susana, primary, Oberst, Michael, primary, Kaplan, Ian M., primary, Raber, Patrick, primary, Van Dyke, Terry, primary, Sharan, Shyam K., primary, Hollingsworth, Robert, primary, Day, Chi-Ping, primary, Merlino, Glenn, primary, and Weaver Ohler, Zoë, primary

Published
2023
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32. Supplementary Figure 3 and Legend from Distinct Biomarker Profiles and TCR Sequence Diversity Characterize the Response to PD-L1 Blockade in a Mouse Melanoma Model

Author

El Meskini, Rajaa, primary, Atkinson, Devon, primary, Kulaga, Alan, primary, Abdelmaksoud, Abdalla, primary, Gumprecht, Michelle, primary, Pate, Nathan, primary, Hayes, Susana, primary, Oberst, Michael, primary, Kaplan, Ian M., primary, Raber, Patrick, primary, Van Dyke, Terry, primary, Sharan, Shyam K., primary, Hollingsworth, Robert, primary, Day, Chi-Ping, primary, Merlino, Glenn, primary, and Weaver Ohler, Zoë, primary

Published
2023
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33. Supplementary Figure 4 and Legend from Distinct Biomarker Profiles and TCR Sequence Diversity Characterize the Response to PD-L1 Blockade in a Mouse Melanoma Model

Author

El Meskini, Rajaa, primary, Atkinson, Devon, primary, Kulaga, Alan, primary, Abdelmaksoud, Abdalla, primary, Gumprecht, Michelle, primary, Pate, Nathan, primary, Hayes, Susana, primary, Oberst, Michael, primary, Kaplan, Ian M., primary, Raber, Patrick, primary, Van Dyke, Terry, primary, Sharan, Shyam K., primary, Hollingsworth, Robert, primary, Day, Chi-Ping, primary, Merlino, Glenn, primary, and Weaver Ohler, Zoë, primary

Published
2023
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34. Supplementary Table 1 and Legend from Distinct Biomarker Profiles and TCR Sequence Diversity Characterize the Response to PD-L1 Blockade in a Mouse Melanoma Model

Author

El Meskini, Rajaa, primary, Atkinson, Devon, primary, Kulaga, Alan, primary, Abdelmaksoud, Abdalla, primary, Gumprecht, Michelle, primary, Pate, Nathan, primary, Hayes, Susana, primary, Oberst, Michael, primary, Kaplan, Ian M., primary, Raber, Patrick, primary, Van Dyke, Terry, primary, Sharan, Shyam K., primary, Hollingsworth, Robert, primary, Day, Chi-Ping, primary, Merlino, Glenn, primary, and Weaver Ohler, Zoë, primary

Published
2023
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35. Characterization of BRCA2 R3052Q variant in mice supports its functional impact as a low-risk variant

Author

Federal Government of the United States, Mishra, Arun Prakash, Hartford, Suzzane, Chittela, Rajani Kant, Sahu, Sounak, Kharat, Suash S., Alvaro-Aranda, Lucia, Contreras-Perez, Aida, Sullivan, Teresa, Martin, Betty K., Albaugh, Mary, Southon, Eileen, Burkett, Sandra, Karim, Baktiar, Carreira, Aura, Tessarollo, Lino, Sharan, Shyam K., Federal Government of the United States, Mishra, Arun Prakash, Hartford, Suzzane, Chittela, Rajani Kant, Sahu, Sounak, Kharat, Suash S., Alvaro-Aranda, Lucia, Contreras-Perez, Aida, Sullivan, Teresa, Martin, Betty K., Albaugh, Mary, Southon, Eileen, Burkett, Sandra, Karim, Baktiar, Carreira, Aura, Tessarollo, Lino, and Sharan, Shyam K.

Abstract

Pathogenic variants in BRCA2 are known to significantly increase the lifetime risk of developing breast and ovarian cancers. Sequencing-based genetic testing has resulted in the identification of thousands of BRCA2 variants that are considered to be variants of uncertain significance (VUS) because the disease risk associated with them is unknown. One such variant is p.Arg3052Gln, which has conflicting interpretations of pathogenicity in the ClinVar variant database. Arginine at position 3052 in BRCA2 plays an important role in stabilizing its C-terminal DNA binding domain. We have generated a knock-in mouse model expressing this variant to examine its role on growth and survival in vivo. Homozygous as well as hemizygous mutant mice are viable, fertile and exhibit no overt phenotype. While we did not observe any hematopoietic defects in adults, we did observe a marked reduction in the in vitro proliferative ability of fetal liver cells that were also hypersensitive to PARP inhibitor, olaparib. In vitro studies performed on embryonic and adult fibroblasts derived from the mutant mice showed significant reduction in radiation induced RAD51 foci formation as well as increased genomic instability after mitomycin C treatment. We observed mis-localization of a fraction of R3052Q BRCA2 protein to the cytoplasm which may explain the observed in vitro phenotypes. Our findings suggest that BRCA2 R3052Q should be considered as a hypomorphic variant.

Published
2023

36. Supplementary Table from The Indenoisoquinoline TOP1 Inhibitors Selectively Target Homologous Recombination-Deficient and Schlafen 11-Positive Cancer Cells and Synergize with Olaparib

Author

Marzi, Laetitia, primary, Szabova, Ludmila, primary, Gordon, Melanie, primary, Weaver Ohler, Zoe, primary, Sharan, Shyam K., primary, Beshiri, Michael L., primary, Etemadi, Moudjib, primary, Murai, Junko, primary, Kelly, Kathleen, primary, and Pommier, Yves, primary

Published
2023
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37. Supplementary Tables from Calibration of Pathogenicity Due to Variant-Induced Leaky Splicing Defects by Using BRCA2 Exon 3 as a Model System

Author

Tubeuf, Hélène, primary, Caputo, Sandrine M., primary, Sullivan, Teresa, primary, Rondeaux, Julie, primary, Krieger, Sophie, primary, Caux-Moncoutier, Virginie, primary, Hauchard, Julie, primary, Castelain, Gaia, primary, Fiévet, Alice, primary, Meulemans, Laëtitia, primary, Révillion, Françoise, primary, Léoné, Mélanie, primary, Boutry-Kryza, Nadia, primary, Delnatte, Capucine, primary, Guillaud-Bataille, Marine, primary, Cleveland, Linda, primary, Reid, Susan, primary, Southon, Eileen, primary, Soukarieh, Omar, primary, Drouet, Aurélie, primary, Di Giacomo, Daniela, primary, Vezain, Myriam, primary, Bonnet-Dorion, Françoise, primary, Bourdon, Violaine, primary, Larbre, Hélène, primary, Muller, Danièle, primary, Pujol, Pascal, primary, Vaz, Fátima, primary, Audebert-Bellanger, Séverine, primary, Colas, Chrystelle, primary, Venat-Bouvet, Laurence, primary, Solano, Angela R., primary, Stoppa-Lyonnet, Dominique, primary, Houdayer, Claude, primary, Frebourg, Thierry, primary, Gaildrat, Pascaline, primary, Sharan, Shyam K., primary, and Martins, Alexandra, primary

Published
2023
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38. Supplementary Figure 2 from The Indenoisoquinoline TOP1 Inhibitors Selectively Target Homologous Recombination-Deficient and Schlafen 11-Positive Cancer Cells and Synergize with Olaparib

Author

Marzi, Laetitia, primary, Szabova, Ludmila, primary, Gordon, Melanie, primary, Weaver Ohler, Zoe, primary, Sharan, Shyam K., primary, Beshiri, Michael L., primary, Etemadi, Moudjib, primary, Murai, Junko, primary, Kelly, Kathleen, primary, and Pommier, Yves, primary

Published
2023
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39. Supplementary Figure 1 from The Indenoisoquinoline TOP1 Inhibitors Selectively Target Homologous Recombination-Deficient and Schlafen 11-Positive Cancer Cells and Synergize with Olaparib

Author

Marzi, Laetitia, primary, Szabova, Ludmila, primary, Gordon, Melanie, primary, Weaver Ohler, Zoe, primary, Sharan, Shyam K., primary, Beshiri, Michael L., primary, Etemadi, Moudjib, primary, Murai, Junko, primary, Kelly, Kathleen, primary, and Pommier, Yves, primary

Published
2023
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40. Data from Calibration of Pathogenicity Due to Variant-Induced Leaky Splicing Defects by Using BRCA2 Exon 3 as a Model System

Author

Tubeuf, Hélène, primary, Caputo, Sandrine M., primary, Sullivan, Teresa, primary, Rondeaux, Julie, primary, Krieger, Sophie, primary, Caux-Moncoutier, Virginie, primary, Hauchard, Julie, primary, Castelain, Gaia, primary, Fiévet, Alice, primary, Meulemans, Laëtitia, primary, Révillion, Françoise, primary, Léoné, Mélanie, primary, Boutry-Kryza, Nadia, primary, Delnatte, Capucine, primary, Guillaud-Bataille, Marine, primary, Cleveland, Linda, primary, Reid, Susan, primary, Southon, Eileen, primary, Soukarieh, Omar, primary, Drouet, Aurélie, primary, Di Giacomo, Daniela, primary, Vezain, Myriam, primary, Bonnet-Dorion, Françoise, primary, Bourdon, Violaine, primary, Larbre, Hélène, primary, Muller, Danièle, primary, Pujol, Pascal, primary, Vaz, Fátima, primary, Audebert-Bellanger, Séverine, primary, Colas, Chrystelle, primary, Venat-Bouvet, Laurence, primary, Solano, Angela R., primary, Stoppa-Lyonnet, Dominique, primary, Houdayer, Claude, primary, Frebourg, Thierry, primary, Gaildrat, Pascaline, primary, Sharan, Shyam K., primary, and Martins, Alexandra, primary

Published
2023
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41. Supplementary Figure 5 from The Indenoisoquinoline TOP1 Inhibitors Selectively Target Homologous Recombination-Deficient and Schlafen 11-Positive Cancer Cells and Synergize with Olaparib

Author

Marzi, Laetitia, primary, Szabova, Ludmila, primary, Gordon, Melanie, primary, Weaver Ohler, Zoe, primary, Sharan, Shyam K., primary, Beshiri, Michael L., primary, Etemadi, Moudjib, primary, Murai, Junko, primary, Kelly, Kathleen, primary, and Pommier, Yves, primary

Published
2023
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42. Supplementary Figure 4 from The Indenoisoquinoline TOP1 Inhibitors Selectively Target Homologous Recombination-Deficient and Schlafen 11-Positive Cancer Cells and Synergize with Olaparib

Author

Marzi, Laetitia, primary, Szabova, Ludmila, primary, Gordon, Melanie, primary, Weaver Ohler, Zoe, primary, Sharan, Shyam K., primary, Beshiri, Michael L., primary, Etemadi, Moudjib, primary, Murai, Junko, primary, Kelly, Kathleen, primary, and Pommier, Yves, primary

Published
2023
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43. Supplementary Data from Calibration of Pathogenicity Due to Variant-Induced Leaky Splicing Defects by Using BRCA2 Exon 3 as a Model System

Author

Tubeuf, Hélène, primary, Caputo, Sandrine M., primary, Sullivan, Teresa, primary, Rondeaux, Julie, primary, Krieger, Sophie, primary, Caux-Moncoutier, Virginie, primary, Hauchard, Julie, primary, Castelain, Gaia, primary, Fiévet, Alice, primary, Meulemans, Laëtitia, primary, Révillion, Françoise, primary, Léoné, Mélanie, primary, Boutry-Kryza, Nadia, primary, Delnatte, Capucine, primary, Guillaud-Bataille, Marine, primary, Cleveland, Linda, primary, Reid, Susan, primary, Southon, Eileen, primary, Soukarieh, Omar, primary, Drouet, Aurélie, primary, Di Giacomo, Daniela, primary, Vezain, Myriam, primary, Bonnet-Dorion, Françoise, primary, Bourdon, Violaine, primary, Larbre, Hélène, primary, Muller, Danièle, primary, Pujol, Pascal, primary, Vaz, Fátima, primary, Audebert-Bellanger, Séverine, primary, Colas, Chrystelle, primary, Venat-Bouvet, Laurence, primary, Solano, Angela R., primary, Stoppa-Lyonnet, Dominique, primary, Houdayer, Claude, primary, Frebourg, Thierry, primary, Gaildrat, Pascaline, primary, Sharan, Shyam K., primary, and Martins, Alexandra, primary

Published
2023
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44. Supplementary Figure 3 from The Indenoisoquinoline TOP1 Inhibitors Selectively Target Homologous Recombination-Deficient and Schlafen 11-Positive Cancer Cells and Synergize with Olaparib

Author

Marzi, Laetitia, primary, Szabova, Ludmila, primary, Gordon, Melanie, primary, Weaver Ohler, Zoe, primary, Sharan, Shyam K., primary, Beshiri, Michael L., primary, Etemadi, Moudjib, primary, Murai, Junko, primary, Kelly, Kathleen, primary, and Pommier, Yves, primary

Published
2023
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