This work identifies MALAT1 as a requisite downstream effector of oncogenic feedforward inflammatory circuits necessary for the development of TET2-mutated CH and fulminant myeloid malignancy. We elucidate a novel mechanism by which MALAT1 "shields" p65 from dephosphorylation to potentiate this circuit and nominate MALAT1 inhibition as a future therapeutic strategy.
RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in TET2-Mutated Clonal Hematopoiesis.
RNA 对 p65 的屏蔽作用是增强 TET2 突变克隆造血中致癌炎症所必需的
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作者：Ben-Crentsil Nana Adjoa, Mohammed Ismail Wazim, Balasis Maria E, Newman Hannah, Quintana Ariel, Binder Moritz, Kruer Traci, Neupane Surendra, Ferrall-Fairbanks Meghan C, Fernandez Jenna, Lasho Terra L, Finke Christy M, Ibrahim Mohammed L, McGraw Kathy L, Wysota Michael, Aldrich Amy L, Ryder Christopher B, Letson Christopher T, Traina Joshua, McLemore Amy F, Droin Nathalie, Shastri Aditi, Yun Seongseok, Solary Eric, Sallman David A, Beg Amer A, Ma Li, Gaspar-Maia Alexandre, Patnaik Mrinal M, Padron Eric
| 期刊： | Cancer Discovery | 影响因子： | 33.300 |
| 时间： | 2024 | 起止号： | 2024 Dec 2; 14(12):2509-2531 |
| doi： | 10.1158/2159-8290.CD-24-0093 | 研究方向： | 肿瘤 |
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