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Your search keyword '"Kurley, Sarah J"' showing total 19 results
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19 results on '"Kurley, Sarah J"'

4. 31-Gene Expression Profile Testing in Cutaneous Melanoma and Survival Outcomes in a Population-Based Analysis: A SEER Collaboration

Author

Bailey, Christine N., Martin, Brian J., Petkov, Valentina I., Schussler, Nicola C., Stevens, Jennifer L., Bentler, Suzanne, Cress, Rosemary D., Doherty, Jennifer A., Durbin, Eric B., Gomez, Scarlett L., Gonsalves, Lou, Hernandez, Brenda Y., Liu, Lihua, Morawski, Boz[Combining Dot Above]ena M., Schymura, Maria J., Schwartz, Stephen M., Ward, Kevin C., Wiggins, Charles, Wu, Xiao-Cheng, Goldberg, Matthew S., Siegel, Jennifer J., Cook, Robert W., Covington, Kyle R., and Kurley, Sarah J.

Published
2023
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10. Real-World Evidence Shows Clinicians Appropriately Use the Prognostic 40-Gene Expression Profile (40-GEP) Test for High-Risk Cutaneous Squamous Cell Carcinoma (cSCC) Patients

Author

Hooper, Perry B., primary, Farberg, Aaron S., additional, Fitzgerald, Alison L., additional, Siegel, Jennifer J., additional, Rackley, Briana B., additional, Prasai, Anesh, additional, Kurley, Sarah J., additional, Goldberg, Matthew S., additional, and Litchman, Graham H., additional

Published
2022
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11. Human WDR5 promotes breast cancer growth and metastasis via KMT2-independent translation regulation

Author

Cai, Wesley L, primary, Chen, Jocelyn Fang-Yi, primary, Chen, Huacui, additional, Wingrove, Emily, additional, Kurley, Sarah J, additional, Chan, Lok Hei, additional, Zhang, Meiling, additional, Arnal-Estape, Anna, additional, Zhao, Minghui, additional, Balabaki, Amer, additional, Li, Wenxue, additional, Yu, Xufen, additional, Krop, Ethan D, additional, Dou, Yali, additional, Liu, Yansheng, additional, Jin, Jian, additional, Westbrook, Thomas F, additional, Nguyen, Don X, additional, and Yan, Qin, additional

Published
2022
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12. Author response: Human WDR5 promotes breast cancer growth and metastasis via KMT2-independent translation regulation

Author

Cai, Wesley L, primary, Chen, Jocelyn Fang-Yi, primary, Chen, Huacui, additional, Wingrove, Emily, additional, Kurley, Sarah J, additional, Chan, Lok Hei, additional, Zhang, Meiling, additional, Arnal-Estape, Anna, additional, Zhao, Minghui, additional, Balabaki, Amer, additional, Li, Wenxue, additional, Yu, Xufen, additional, Krop, Ethan D, additional, Dou, Yali, additional, Liu, Yansheng, additional, Jin, Jian, additional, Westbrook, Thomas F, additional, Nguyen, Don X, additional, and Yan, Qin, additional

Published
2022
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14. Enhanced metastatic risk assessment in cutaneous squamous cell carcinoma with the 40-gene expression profile test

Author

Ibrahim, Sherrif F, primary, Kasprzak, Julia M, additional, Hall, Mary A, additional, Fitzgerald, Alison L, additional, Siegel, Jennifer J, additional, Kurley, Sarah J, additional, Covington, Kyle R, additional, Goldberg, Matthew S, additional, Farberg, Aaron S, additional, Trotter, Shannon C, additional, Reed, Kenneth, additional, Brodland, David G, additional, Koyfman, Shlomo A, additional, Somani, Ally-Khan, additional, Arron, Sarah T, additional, and Wysong, Ashley, additional

Published
2022
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15. Using a 31-Gene Expression Profile Test to Stratify Patients with Stage I–II Cutaneous Melanoma According to Recurrence Risk: Update to a Prospective, Multicenter Study

Author

Podlipnik, Sebastian, primary, Boada, Aram, additional, López-Estebaranz, Jose L., additional, Martín-González, Manuel M., additional, Redondo, Pedro, additional, Martin, Brian, additional, Quick, Ann P., additional, Bailey, Christine N., additional, Kurley, Sarah J., additional, Cook, Robert W., additional, and Puig, Susana, additional

Published
2022
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16. Gene expression profiling for metastatic risk in head and neck cutaneous squamous cell carcinoma

Author

Arron, Sarah T., primary, Wysong, Ashley, additional, Hall, Mary A., additional, Bailey, Christine N., additional, Covington, Kyle R., additional, Kurley, Sarah J., additional, Goldberg, Matthew S., additional, Kasprzak, Julia M., additional, Somani, Ally‐Khan, additional, Ibrahim, Sherrif F., additional, Brodland, David G., additional, Cleaver, Nathan J., additional, Maher, Ian A., additional, Xia, Yang, additional, Koyfman, Shlomo A., additional, and Newman, Jason G., additional

Published
2022
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19. MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer.

Author

Meena JK, Wang JH, Neill NJ, Keough D, Putluri N, Katsonis P, Koire AM, Lee H, Bowling EA, Tyagi S, Orellana M, Dominguez-Vidaña R, Li H, Eagle K, Danan C, Chung HC, Yang AD, Wu W, Kurley SJ, Ho BM, Zoeller JR, Olson CM, Meerbrey KL, Lichtarge O, Sreekumar A, Dacso CC, Guddat LW, Rejman D, Hocková D, Janeba Z, Simon LM, Lin CY, Pillon MC, and Westbrook TF

Subjects
Animals, Female, Humans, Mice, Cell Line, Tumor, Gene Expression Regulation, Neoplastic, Breast Neoplasms metabolism, Breast Neoplasms genetics, Breast Neoplasms pathology, Proto-Oncogene Proteins c-myc metabolism, Proto-Oncogene Proteins c-myc genetics, Ribonucleotides metabolism, RNA Stability
Abstract

Upregulation of MYC is a hallmark of cancer, wherein MYC drives oncogenic gene expression and elevates total RNA synthesis across cancer cell transcriptomes. Although this transcriptional anabolism fuels cancer growth and survival, the consequences and metabolic stresses induced by excess cellular RNA are poorly understood. Herein, we discover that RNA degradation and downstream ribonucleotide catabolism is a novel mechanism of MYC-induced cancer cell death. Combining genetics and metabolomics, we find that MYC increases RNA decay through the cytoplasmic exosome, resulting in the accumulation of cytotoxic RNA catabolites and reactive oxygen species. Notably, tumor-derived exosome mutations abrogate MYC-induced cell death, suggesting excess RNA decay may be toxic to human cancers. In agreement, purine salvage acts as a compensatory pathway that mitigates MYC-induced ribonucleotide catabolism, and inhibitors of purine salvage impair MYC+ tumor progression. Together, these data suggest that MYC-induced RNA decay is an oncogenic stress that can be exploited therapeutically. Significance: MYC is the most common oncogenic driver of poor-prognosis cancers but has been recalcitrant to therapeutic inhibition. We discovered a new vulnerability in MYC+ cancer where MYC induces cell death through excess RNA decay. Therapeutics that exacerbate downstream ribonucleotide catabolism provide a therapeutically tractable approach to TNBC (Triple-negative Breast Cancer) and other MYC-driven cancers., (©2024 The Authors; Published by the American Association for Cancer Research.)

Published
2024
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