Increased genetic liability to colorectal cancer is associated with altered levels of circulating metabolites, including fatty acids, up to 40 years before average age of diagnosis.

Integrated molecular analysis demonstrated that colorectal cancer can be classified into four molecular subtypes (proliferative, immunomodulatory, immunosuppressed, and immune-excluded subtypes), providing valuable insight into the intricate relationship between tumor microenvironment heterogeneity and various clinical phenotypes.

The gluconeogenic enzyme PCK1 and pyrimidine nucleotide biosynthetic enzyme DHODH drive hypoxic pyrimidine nucleotide biosynthesis and liver metastatic colonization in colorectal cancer, which is therapeutically exploitable by DHODH pharmacologic inhibition.

Based on the proteomics results, T1 CRC LNM prediction models were built using machine learning, the functional differences and biomarkers between LNM-negative and LNM-positive patients were revealed.

Only about half of women 50–64 years old are up-to-date for both cervical and colorectal cancer screening.

The physician involving the woman as much as she wants in her health care is significantly associated with up-to-date dual cervical and colorectal cancer screening compared to being up to date in only cervical cancer screening.

GrimAge acceleration may increase the risk of colorectal cancer.

Assessments using chemogenetic and pharmacological approaches reveal that modulation of the activities of oxytocin neurons in the hypothalamus of the central nervous system could inhibit colorectal cancer progression in mice.

A transcriptional coactivator turns into a repressor at specific genes in colorectal cancer cells.

Non-coding mutations in microsatellite-instable (MSI) colorectal tumors are prevalent and activate cancer-specific enhancers, thereby disrupting gene expression control.