Choon Kiat Ong

Abstract KRAS inhibitors (KRASi) have emerged as promising new cancer therapeutics for KRAS-mutant cancers; however, resistance remains a potential clinical challenge. Here, we show that reactivation of ERK is a hallmark of KRASi-resistant colorectal cancers (CRCs) and further demonstrate that enhancer remodeling rewires cholesterol biosynthesis through the mevalonate (MVA) pathway to confer this resistance.

Letter to the Editor, Angioimmunoblastic T-cell lymphoma (AITL) originates from T follicular helper (TFH) cells and is widely considered to be an aggressive T-cell neoplasm. Cure rates are low, and relapses are common, with a median overall survival of only three years [1,2,3]. In the 2022 World Health Organization classification [4], the term nodal TFH (nTFH) cell lymphomas unites the subtypes of angioimmunoblastic type, follicular type and a not otherwise specified (NOS) category [5].