Loss of SYNCRIP unleashes APOBEC-driven mutagenesis, tumor heterogeneity, and AR-targeted therapy resistance in prostate cancer

Tumor mutational burden and heterogeneity has been suggested to fuel resistance to many targeted therapies. The cytosine deaminase APOBEC proteins have been implicated in the mutational signatures of more than 70% of human cancers. However, the mechanism underlying how cancer cells hijack the APOBEC...

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Detalles Bibliográficos
Autores principales: Li, Xiaoling, Wang, Yunguan, Deng, Su, Zhu, Guanghui, Wang, Choushi, Johnson, Nickolas A., Zhang, Zeda, Tirado, Carla Rodriguez, Xu, Yaru, Metang, Lauren A., Gonzalez, Julisa, Mukherji, Atreyi, Ye, Jianfeng, Yang, Yuqiu, Peng, Wei, Tang, Yitao, Hofstad, Mia, Xie, Zhiqun, Yoon, Heewon, Chen, Liping, Liu, Xihui, Chen, Sujun, Zhu, Hong, Strand, Douglas, Liang, Han, Raj, Ganesh, He, Housheng Hansen, Mendell, Joshua T., Li, Bo, Wang, Tao, Mu, Ping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2023
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10530398/
https://www.ncbi.nlm.nih.gov/pubmed/37478850
http://dx.doi.org/10.1016/j.ccell.2023.06.010

Internet

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10530398/
https://www.ncbi.nlm.nih.gov/pubmed/37478850
http://dx.doi.org/10.1016/j.ccell.2023.06.010

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