Identification of a metabolic-immune signature associated with prognosis in colon cancer and exploration of potential predictive efficacy of immunotherapy response.

The role of metabolic reprogramming of the tumor immune microenvironment in cancer development and immune escape has increasingly attracted attention. However, the predictive value of differences in metabolism-immune microenvironment on the prognosis of colon cancer (CC) and the response to immunotherapy have not been elucidated. The aim of this study was to investigate changes in metabolism and immune profile of CC and to identify a reliable signature for predicting prognosis and therapeutic response.

DYNLL1 accelerates cell cycle via ILF2/CDK4 axis to promote hepatocellular carcinoma development and palbociclib sensitivity.

Background: Disorder of cell cycle represents as a major driver of hepatocarcinogenesis and constitutes an attractive therapeutic target. However, identifying key genes that respond to cell cycle-dependent treatments still facing critical challenges in hepatocellular carcinoma (HCC). Increasing evidence indicates that dynein light chain 1 (DYNLL1) is closely related to cell cycle progression and plays a critical role in tumorigenesis.

Targeting MS4A4A on tumour-associated macrophages restores CD8+ T-cell-mediated antitumour immunity.

Objective: Checkpoint immunotherapy unleashes T-cell control of tumours but is suppressed by immunosuppressive myeloid cells. The transmembrane protein MS4A4A is selectively highly expressed in tumour-associated macrophages (TAMs). Here, we aimed to reveal the role of MS4A4A TAMs in regulating the immune escape of tumour cells and to develop novel therapeutic strategies targeting TAMs to enhance the efficacy of immune checkpoint inhibitor (ICI) in colorectal cancer.