Article
Mutant p53 promotes clonal hematopoiesis by generating a chronic inflammatory microenvironment.
The Journal of clinical investigation - 2 Feb 2026
Chen Sisi, Barajas Sergio, Vemula Sasidhar, Yang Yuxia, Simpson Ed, Gao Hongyu, Li Rudong, Behzadnia Farzaneh, Nabinger Sarah C, Schmitz David A, Chen Hongxia, Cai Wenjie, Xiao Shiyu, Luo Ruyue, Amin Mohammed Abdullahel, Capitano Maegan L, Ropa James P, Fahey Aidan, Zhou Shuyi, Mays Tiffany M, Sotelo Magdalena, Pan Hao, Hu Sophie K, Veranga Sophia, Ali Moiez, Shumilina Maria, Kapur Reuben, Ren Kehan, Jia Yuzhi, Liu Huiping, Khan Irum, Abaza Yasmin, Altman Jessica K, Eklund Elizabeth A, Godley Lucy A, Zhang Christine R, Ji Peng, Masters Seth L, Croker Ben A, Boswell H Scott, Sandusky George E, Gao Zhonghua, Mayo Lindsey D, Savage Sharon A, Halene Stephanie, Dou Yali, Platanias Leonidas C, Sukhanova Madina, Liu Yunlong, Abdel-Wahab Omar, Liu Yan
Abstract excerpt
Older individuals with somatic TP53 mutations manifest clonal hematopoiesis (CH) and are at high risk of developing myeloid neoplasms. However, the underlying mechanisms are not fully understood. Here, we show that inflammatory stress confers a competitive advantage to p53 mutant hematopoietic stem and progenitor cells (HSPCs) by activating the NLRP1 inflammasome and increasing the secretion of pro-inflammatory...
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