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48 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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5. Validation of a 40-gene expression profile test to predict metastatic risk in localized high-risk cutaneous squamous cell carcinoma

Author

Wysong, Ashley, Newman, Jason G., Covington, Kyle R., Kurley, Sarah J., Ibrahim, Sherrif F., Farberg, Aaron S., Bar, Anna, Cleaver, Nathan J., Somani, Ally-Khan, Panther, David, Brodland, David G., Zitelli, John, Toyohara, Jennifer, Maher, Ian A., Xia, Yang, Bibee, Kristin, Griego, Robert, Rigel, Darrell S., Meldi Plasseraud, Kristen, Estrada, Sarah, Sholl, Lauren Meldi, Johnson, Clare, Cook, Robert W., Schmults, Chrysalyne D., and Arron, Sarah T.

Published
2021
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6. Spliceosome-targeted therapies trigger an antiviral immune response in triple-negative breast cancer

Author

Bowling, Elizabeth A., Wang, Jarey H., Gong, Fade, Wu, William, Neill, Nicholas J., Kim, Ik Sun, Tyagi, Siddhartha, Orellana, Mayra, Kurley, Sarah J., Dominguez-Vidaña, Rocio, Chung, Hsiang-Ching, Hsu, Tiffany Y.-T., Dubrulle, Julien, Saltzman, Alexander B., Li, Heyuan, Meena, Jitendra K., Canlas, Gino M., Chamakuri, Srinivas, Singh, Swarnima, Simon, Lukas M., Olson, Calla M., Dobrolecki, Lacey E., Lewis, Michael T., Zhang, Bing, Golding, Ido, Rosen, Jeffrey M., Young, Damian W., Malovannaya, Anna, Stossi, Fabio, Miles, George, Ellis, Matthew J., Yu, Lihua, Buonamici, Silvia, Lin, Charles Y., Karlin, Kristen L., Zhang, Xiang H.-F., and Westbrook, Thomas F.

Published
2021
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9. Combinatorial inhibition of PTPN12-regulated receptors leads to a broadly effective therapeutic strategy in triple-negative breast cancer

Author

Nair, Amritha, Chung, Hsiang-Ching, Sun, Tingting, Tyagi, Siddhartha, Dobrolecki, Lacey E, Dominguez-Vidana, Rocio, Kurley, Sarah J, Orellana, Mayra, Renwick, Alexander, Henke, David M, Katsonis, Panagiotis, Schmitt, Earlene, Chan, Doug W, Li, Hui, Mao, Sufeng, Petrovic, Ivana, Creighton, Chad J, Gutierrez, Carolina, Dubrulle, Julien, Stossi, Fabio, Tyner, Jeffrey W, Lichtarge, Olivier, Lin, Charles Y, Zhang, Bing, Scott, Kenneth L, Hilsenbeck, Susan G, Sun, Jinpeng, Yu, Xiao, Osborne, C Kent, Schiff, Rachel, Christensen, James G, Shields, David J, Rimawi, Mothaffar F, Ellis, Matthew J, Shaw, Chad A, Lewis, Michael T, and Westbrook, Thomas F

Subjects
Cell receptors -- Health aspects, Esterases -- Health aspects, Gene mutation -- Health aspects, Breast cancer -- Genetic aspects -- Development and progression -- Care and treatment, Gene expression -- Health aspects, Biological sciences, Health
Abstract

Author(s): Amritha Nair [1, 2]; Hsiang-Ching Chung [1, 2, 3]; Tingting Sun [1, 2]; Siddhartha Tyagi [1, 2]; Lacey E Dobrolecki [4]; Rocio Dominguez-Vidana [1, 2, 3]; Sarah J Kurley [...]

Published
2018
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15. The Oncogenic STP Axis Promotes Triple-Negative Breast Cancer via Degradation of the REST Tumor Suppressor

Author

Karlin, Kristen L., Mondal, Gourish, Hartman, Jessica K., Tyagi, Siddhartha, Kurley, Sarah J., Bland, Chris S., Hsu, Tiffany Y.T., Renwick, Alexander, Fang, Justin E., Migliaccio, Ilenia, Callaway, Celetta, Nair, Amritha, Dominguez-Vidana, Rocio, Nguyen, Don X., Osborne, C. Kent, Schiff, Rachel, Yu-Lee, Li-Yuan, Jung, Sung Y., Edwards, Dean P., Hilsenbeck, Susan G., Rosen, Jeffrey M., Zhang, Xiang H.-F., Shaw, Chad A., Couch, Fergus J., and Westbrook, Thomas F.

Published
2014
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16. 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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17. 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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18. 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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19. The spliceosome is a therapeutic vulnerability in MYC-driven cancer

Author

Hsu, Tiffany Y.-T., Simon, Lukas M., Neill, Nicholas J., Marcotte, Richard, Sayad, Azin, Bland, Christopher S., Echeverria, Gloria V., Sun, Tingting, Kurley, Sarah J., Tyagi, Siddhartha, Karlin, Kristen L., Dominguez-Vidaha, Rocio, Hartman, Jessica D., Renwick, Alexander, Scorsone, Kathleen, Bernardi, Ronald J., Skinner, Samuel O., Jain, Antrix, Orellana, Mayra, Lagisetti, Chandraiah, Golding, Ido, Jung, Sung Y., Neilson, Joel R., Zhang, Xiang H.-F., Cooper, Thomas A., Webb, Thomas R., Neel, Benjamin G., Shaw, Chad A., and Westbrook, Thomas F.

Subjects
Gene therapy -- Methods, Cancer -- Care and treatment, Transcription factors, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

MYC (also known as c-MYC) overexpression or hyperactivation is one of the most common drivers of human cancer. Despite intensive study, the MYC oncogene remains recalcitrant to therapeutic inhibition. MYC is a transcription factor, and many of its protumorigenic functions have been attributed to its ability to regulate gene expression programs (1-3). Notably, oncogenic MYC activation has also been shown to increase total RNA and protein production in many tissue and disease contexts (4-7). While such increases in RNA and protein production may endow cancer cells with pro-tumour hallmarks, this increase in synthesis may also generate new or heightened burden on MYC-driven cancer cells to process these macromolecules properly (8). Here we discover that the spliceosome is a new target of oncogenic stress in MYC-driven cancers. We identify BUD31 as a MYC-synthetic lethal gene in human mammary epithelial cells, and demonstrate that BUD31 is a component of the core spliceosome required for its assembly and catalytic activity. Core spliceosomal factors (such as SF3B1 and U2AF1) associated with BUD31 are also required to tolerate oncogenic MYC. Notably, MYC hyperactivation induces an increase in total precursor messenger RNA synthesis, suggesting an increased burden on the core spliceosome to process pre-mRNA. In contrast to normal cells, partial inhibition of the spliceosome in MYC-hyperactivated cells leads to global intron retention, widespread defects in pre-mRNA maturation, and deregulation of many essential cell processes. Notably, genetic or pharmacological inhibition of the spliceosome in vivo impairs survival, tumorigenicity and metastatic proclivity of MYC-dependent breast cancers. Collectively, these data suggest that oncogenic MYC confers a collateral stress on splicing, and that components of the spliceosome may be therapeutic entry points for aggressive MYC-driven cancers., To discover genes and cellular processes required to tolerate oncogenic MYC expression, we previously performed a genome-wide MYC-synthetic lethal screen in human mammary epithelial cells (HMECs) engineered with an inducible [...]

Published
2015

21. 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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22. 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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23. 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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24. MYC-driven accumulation of 2-hydroxyglutarate is associated with breast cancer prognosis

Author

Terunuma, Atsushi, Putluri, Nagireddy, Mishra, Prachi, Mathe, Ewy A., Dorsey, Tiffany H., Yi, Ming, Issaq, Haleem J., Zhou, Ming, Killian, J. Keith, Stevenson, Holly S., Karoly, Edward D., Chan, King, Samanta, Susmita, Prieto, DaRue, Hsu, Tiffany Y.T., Kurley, Sarah J., Putluri, Vasanta, Sonavane, Rajni, Edelman, Daniel C., Wulff, Jacob, Starks, Adrienne M., Yang, Yinmeng, Kittles, Rick A., Yfantis, Harry G., Lee, Dong H., Ioffe, Olga B., Schiff, Rachel, Stephens, Robert M., Meltzer, Paul S., Veenstra, Timothy D., Westbrook, Thomas F., Sreekumar, Arun, and Ambs, Stefan

Subjects
Methylation -- Research, Glutamine -- Research -- Health aspects, Breast cancer -- Prognosis -- Research -- Care and treatment -- Development and progression, Health care industry
Abstract

Metabolic profiling of cancer cells has recently been established as a promising tool for the development of therapies and identification of cancer biomarkers. Here we characterized the metabolomic profile of human breast tumors and uncovered intrinsic metabolite signatures in these tumors using an untargeted discovery approach and validation of key metabolites. The oncometabolite 2-hydroxyglutarate (2HG) accumulated at high levels in a subset of tumors and human breast cancer cell lines. We discovered an association between increased 2HG levels and MYC pathway activation in breast cancer, and further corroborated this relationship using MYC overexpression and knockdown in human mammary epithelial and breast cancer cells. Further analyses revealed globally increased DNA methylation in 2HG-high tumors and identified a tumor subtype with high tissue 2HG and a distinct DNA methylation pattern that was associated with poor prognosis and occurred with higher frequency in African-American patients. Tumors of this subtype had a stem cell-like transcriptional signature and tended to overexpress glutaminase, suggestive of a functional relationship between glutamine and 2HG metabolism in breast cancer. Accordingly, 13C-labeled glutamine was incorporated into 2HG in cells with aberrant 2HG accumulation, whereas pharmacologic and siRNA-mediated glutaminase inhibition reduced 2HG levels. Our findings implicate 2HG as a candidate breast cancer oncometabolite associated with MYC activation and poor prognosis., Introduction Gene expression profiling studies of breast cancer led to the discovery of disease subtypes and expression patterns that are predictive of disease outcome (1-3). Recently, metabolomics emerged as a [...]

Published
2014
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25. Analytical validity of DecisionDx-SCC, a gene expression profile test to identify risk of metastasis in cutaneous squamous cell carcinoma (SCC) patients

Author

Borman, Sherri, primary, Wilkinson, Jeff, additional, Meldi-Sholl, Lauren, additional, Johnson, Clare, additional, Carter, Kelsey, additional, Covington, Kyle R., additional, Fitzgerald, Alison, additional, Kurley, Sarah J., additional, Farberg, Aaron S., additional, Goldberg, Matthew S., additional, Monzon, Federico A., additional, Oelschlager, Kristen, additional, and Cook, Robert W., additional

Published
2021
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26. 25726 Prospective adjuvant therapy trial design using a prognostic 40-gene expression profile (40-GEP) test for high-risk cutaneous squamous cell carcinoma (cSCC) and BWH staging-based risk assessment

Author

Ibrahim, Sherrif F., primary, Arron, Sarah T., additional, Somani, Ally-Khan, additional, Kurley, Sarah J., additional, Covington, Kyle R., additional, Fitzgerald, Alison L., additional, Schmults, Chrysalyne D., additional, and Wysong, Ashley, additional

Published
2021
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27. A Requirement for p120-catenin in the metastasis of invasive ductal breast cancer

Author

Kurley, Sarah J; https://orcid.org/0000-0002-4127-1443, Tischler, Verena; https://orcid.org/0000-0002-6673-8329, Bierie, Brian; https://orcid.org/0000-0001-9367-9507, Novitskiy, Sergey V, Noske, Aurelia; https://orcid.org/0000-0002-0771-3180, Varga, Zsuzsanna; https://orcid.org/0000-0001-6149-4225, Zürrer-Härdi, Ursina; https://orcid.org/0000-0002-6672-8104, Brandt, Simone; https://orcid.org/0000-0002-8558-6674, Carnahan, Robert H; https://orcid.org/0000-0001-5230-1532, Cook, Rebecca S, Muller, William J; https://orcid.org/0000-0001-7690-0695, Richmond, Ann; https://orcid.org/0000-0002-9580-900X, Reynolds, Albert B; https://orcid.org/0000-0002-4514-0491, Kurley, Sarah J; https://orcid.org/0000-0002-4127-1443, Tischler, Verena; https://orcid.org/0000-0002-6673-8329, Bierie, Brian; https://orcid.org/0000-0001-9367-9507, Novitskiy, Sergey V, Noske, Aurelia; https://orcid.org/0000-0002-0771-3180, Varga, Zsuzsanna; https://orcid.org/0000-0001-6149-4225, Zürrer-Härdi, Ursina; https://orcid.org/0000-0002-6672-8104, Brandt, Simone; https://orcid.org/0000-0002-8558-6674, Carnahan, Robert H; https://orcid.org/0000-0001-5230-1532, Cook, Rebecca S, Muller, William J; https://orcid.org/0000-0001-7690-0695, Richmond, Ann; https://orcid.org/0000-0002-9580-900X, and Reynolds, Albert B; https://orcid.org/0000-0002-4514-0491

Abstract

We have examined the effects of targeted p120 KO in a PyMT mouse model of invasive ductal (mammary) cancer (IDC). Mosaic p120 ablation had little effect on primary tumor growth but caused significant pro-metastatic alterations in the tumor microenvironment leading ultimately to a marked increase in the number and size of pulmonary metastases. Surprisingly, although early effects of p120-ablation included decreased cell-cell adhesion and increased invasiveness, cells lacking p120 were almost entirely unable to colonized distant metastatic sites in vivo. The relevance of this observation to human IDC was established by analysis of a large clinical dataset of 1126 IDCs. As reported by others, p120 downregulation in primary IDC predicted worse overall survival. However, as in the mice, distant metastases were almost invariably p120 positive, even in matched cases where the primary tumors were p120 negative. Collectively, our results demonstrate a strong positive role for p120 (and presumably E-cadherin) during metastatic colonization of distant sites. On the other hand, downregulation of p120 in the primary tumor enhanced metastatic dissemination indirectly via pro-metastatic conditioning of the tumor microenvironment.

Published
2021

29. Improved risk stratification in an adjuvant radiation therapy (ART) eligible cutaneous squamous cell carcinoma (cSCC) patient population by integration of the 40-gene expression profile prognostic test (40-GEP).

Author

Koyfman, Shlomo A., primary, Wysong, Ashley, additional, Arron, Sarah, additional, Somani, Ally-Khan B., additional, Siegel, Jennifer, additional, Fitzgerald, Alison, additional, Kurley, Sarah J., additional, Goldberg, Matthew S., additional, Schmults, Chrysalyne, additional, and Newman, Jason, additional

Published
2021
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37. A Requirement for p120-catenin in the metastasis of invasive ductal breast cancer

Author

Kurley, Sarah J., primary, Tischler, Verena, additional, Bierie, Brian, additional, Novitskiy, Sergey V., additional, Noske, Aurelia, additional, Varga, Zsuzsanna, additional, Zürrer-Härdi, Ursina, additional, Brandt, Simone, additional, Carnahan, Robert H., additional, Cook, Rebecca S., additional, Muller, William J., additional, Richmond, Ann, additional, and Reynolds, Albert B., additional

Published
2020
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44. MYC-driven accumulation of 2-hydroxyglutarate is associated with breast cancer prognosis

Author

Terunuma, Atsushi, primary, Putluri, Nagireddy, additional, Mishra, Prachi, additional, Mathé, Ewy A., additional, Dorsey, Tiffany H., additional, Yi, Ming, additional, Wallace, Tiffany A., additional, Issaq, Haleem J., additional, Zhou, Ming, additional, Killian, J. Keith, additional, Stevenson, Holly S., additional, Karoly, Edward D., additional, Chan, King, additional, Samanta, Susmita, additional, Prieto, DaRue, additional, Hsu, Tiffany Y.T., additional, Kurley, Sarah J., additional, Putluri, Vasanta, additional, Sonavane, Rajni, additional, Edelman, Daniel C., additional, Wulff, Jacob, additional, Starks, Adrienne M., additional, Yang, Yinmeng, additional, Kittles, Rick A., additional, Yfantis, Harry G., additional, Lee, Dong H., additional, Ioffe, Olga B., additional, Schiff, Rachel, additional, Stephens, Robert M., additional, Meltzer, Paul S., additional, Veenstra, Timothy D., additional, Westbrook, Thomas F., additional, Sreekumar, Arun, additional, and Ambs, Stefan, additional

Published
2013
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47. A requirement for p120-catenin in the metastasis of invasive ductal breast cancer.

Author

Kurley, Sarah J., Tischler, Verena, Bierie, Brian, Novitskiy, Sergey V., Noske, Aurelia, Varga, Zsuzsanna, Zürrer-Härdi, Ursina, Brandt, Simone, Carnahan, Robert H., Cook, Rebecca S., Muller, William J., Richmond, Ann, and Reynolds, Albert B.

Subjects
*METASTASIS, *BREAST cancer, *METASTATIC breast cancer, *TUMOR growth, *TUMOR microenvironment
Abstract

We report here the effects of targeted p120-catenin (encoded by CTNND1; hereafter denoted p120) knockout (KO) in a PyMT mouse model of invasive ductal (mammary) cancer (IDC). Mosaic p120 ablation had little effect on primary tumor growth but caused significant pro-metastatic alterations in the tumor microenvironment, ultimately leading to a marked increase in the number and size of pulmonary metastases. Surprisingly, although early effects of p120-ablation included decreased cell–cell adhesion and increased invasiveness, cells lacking p120 were almost entirely unable to colonized distant metastatic sites in vivo. The relevance of this observation to human IDC was established by analysis of a large clinical dataset of 1126 IDCs. As reported by others, p120 downregulation in primary IDC predicted worse overall survival. However, as in the mice, distant metastases were almost invariably p120 positive, even in matched cases where the primary tumors were p120 negative. Collectively, our results demonstrate a strong positive role for p120 (and presumably E-cadherin) during metastatic colonization of distant sites. On the other hand, downregulation of p120 in the primary tumor enhanced metastatic dissemination indirectly via pro-metastatic conditioning of the tumor microenvironment. [ABSTRACT FROM AUTHOR]

Published
2021
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48. 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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