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6 results on '"Sahr, Natasha"'

3. Supplementary Table S4 from SLFN11 is Widely Expressed in Pediatric Sarcoma and Induces Variable Sensitization to Replicative Stress Caused By DNA-Damaging Agents

Author

Gartrell, Jessica, primary, Mellado-Largarde, Marcia, primary, Clay, Michael R., primary, Bahrami, Armita, primary, Sahr, Natasha A., primary, Sykes, April, primary, Blankenship, Kaley, primary, Hoffmann, Lauren, primary, Xie, Jia, primary, Cho, Hyekyung P., primary, Twarog, Nathaniel, primary, Connelly, Michele, primary, Yan, Koon-Kiu, primary, Yu, Jiyang, primary, Porter, Shaina N., primary, Pruett-Miller, Shondra M., primary, Neale, Geoffrey, primary, Tinkle, Christopher L., primary, Federico, Sara M., primary, Stewart, Elizabeth A., primary, and Shelat, Anang A., primary

Published
2023
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4. Supplementary Data from SLFN11 is Widely Expressed in Pediatric Sarcoma and Induces Variable Sensitization to Replicative Stress Caused By DNA-Damaging Agents

Author

Gartrell, Jessica, primary, Mellado-Largarde, Marcia, primary, Clay, Michael R., primary, Bahrami, Armita, primary, Sahr, Natasha A., primary, Sykes, April, primary, Blankenship, Kaley, primary, Hoffmann, Lauren, primary, Xie, Jia, primary, Cho, Hyekyung P., primary, Twarog, Nathaniel, primary, Connelly, Michele, primary, Yan, Koon-Kiu, primary, Yu, Jiyang, primary, Porter, Shaina N., primary, Pruett-Miller, Shondra M., primary, Neale, Geoffrey, primary, Tinkle, Christopher L., primary, Federico, Sara M., primary, Stewart, Elizabeth A., primary, and Shelat, Anang A., primary

Published
2023
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5. Supplementary Data from A Phase II Trial of Hu14.18K322A in Combination with Induction Chemotherapy in Children with Newly Diagnosed High-Risk Neuroblastoma

Author

Furman, Wayne L., primary, Federico, Sara M., primary, McCarville, Mary Beth, primary, Shulkin, Barry L., primary, Davidoff, Andrew M., primary, Krasin, Matthew J., primary, Sahr, Natasha, primary, Sykes, April, primary, Wu, Jianrong, primary, Brennan, Rachel C., primary, Bishop, Michael William, primary, Helmig, Sara, primary, Stewart, Elizabeth, primary, Navid, Fariba, primary, Triplett, Brandon, primary, Santana, Victor M., primary, Bahrami, Armita, primary, Anthony, Gwendolyn, primary, Yu, Alice L., primary, Hank, Jacquelyn, primary, Gillies, Stephen D., primary, Sondel, Paul M., primary, Leung, Wing H., primary, and Pappo, Alberto S., primary

Published
2023
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6. SLFN11 is Widely Expressed in Pediatric Sarcoma and Induces Variable Sensitization to Replicative Stress Caused By DNA-Damaging Agents.

Author

Gartrell J, Mellado-Largarde M, Clay MR, Bahrami A, Sahr NA, Sykes A, Blankenship K, Hoffmann L, Xie J, Cho HP, Twarog N, Connelly M, Yan KK, Yu J, Porter SN, Pruett-Miller SM, Neale G, Tinkle CL, Federico SM, Stewart EA, and Shelat AA

Subjects
Adolescent, Adult, Animals, Child, Child, Preschool, Female, Humans, Infant, Infant, Newborn, Male, Mice, Mice, Nude, Young Adult, DNA Damage genetics, Genomics methods, Nuclear Proteins metabolism, Sarcoma, Ewing genetics
Abstract

Pediatric sarcomas represent a heterogeneous group of malignancies that exhibit variable response to DNA-damaging chemotherapy. Schlafen family member 11 protein (SLFN11) increases sensitivity to replicative stress and has been implicated as a potential biomarker to predict sensitivity to DNA-damaging agents (DDA). SLFN11 expression was quantified in 220 children with solid tumors using IHC. Sensitivity to the PARP inhibitor talazoparib (TAL) and the topoisomerase I inhibitor irinotecan (IRN) was assessed in sarcoma cell lines, including SLFN11 knock-out (KO) and overexpression models, and a patient-derived orthotopic xenograft model (PDOX). SLFN11 was expressed in 69% of pediatric sarcoma sampled, including 90% and 100% of Ewing sarcoma and desmoplastic small round-cell tumors, respectively, although the magnitude of expression varied widely. In sarcoma cell lines, protein expression strongly correlated with response to TAL and IRN, with SLFN11 KO resulting in significant loss of sensitivity in vitro and in vivo Surprisingly, retrospective analysis of children with sarcoma found no association between SLFN11 levels and favorable outcome. Subsequently, high SLFN11 expression was confirmed in a PDOX model derived from a patient with recurrent Ewing sarcoma who failed to respond to treatment with TAL + IRN. Selective inhibition of BCL-xL increased sensitivity to TAL + IRN in SLFN11-positive resistant tumor cells. Although SLFN11 appears to drive sensitivity to replicative stress in pediatric sarcomas, its potential to act as a biomarker may be limited to certain tumor backgrounds or contexts. Impaired apoptotic response may be one mechanism of resistance to DDA-induced replicative stress., (©2021 American Association for Cancer Research.)

Published
2021
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