Browse our latest Cancer Biology articles

Epigenetic regulator MLL3 is mutated and lost in human hepatocellular carcinoma due to its ability to activate a well-defined tumor suppressor and cell death in transformed cells.

Analysis of the tumor microenvironment reveals that pancreatic tumors experience metabolic stress caused by immune cell degradation of the amino acid arginine, and that pancreatic cancers cope by synthesizing arginine to provide access this amino acid despite low tumor availability.

Deletion of Arginase 1 in myeloid cells delays tumor formation in pancreatic cancer.

Targeting CD73 not only enhances anti-tumor immunity but also disrupts tumor cell metabolism and hinders poly ADP ribose polymerase (PARP) activity, thus unveiling novel opportunities for combination cancer treatments.

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.

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.

A physiological mathematical model of chronic myeloid leukemia, validated by experiments in transgenic mice and clinical data, identifies mechanisms underlying the response to tyrosine kinase inhibitor therapy, predicts biomarkers of primary resistance, and suggests new strategies to improve treatment outcomes.

ERK3 controls actin cytoskeleton.

Replication stress-indepedent synthetic lethality can be triggered in BRCA2-deficient cells by exploiting M phase defects.

Fifteen continuous high-grade serous ovarian carcinoma patient-derived organoids are characterized by transcriptomic, genomic, and drug sensitivity assays to reveal that they comprise communities of clonal populations and represent models of different causes of chromosomal instability and degrees of genome complexity.