Browse our latest Cancer Biology articles

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.

Theoretical modeling reveals how stochastic optimal cancer immune evasion via antigen downregulation gives rise to diverse post-escape cancer antigenic profiles in a manner dependent on the immune microenvironment.

Deficiencies of several DNA damage response genes can be predicted by their association with genome-wide mutation patterns.

Targeted therapies induce an aberrant fucosylation of complex tumor secretomes stimulating the expansion of minority drug-resistant clones and promoting therapy resistance.

New role of P2Y₂-αV integrin interactions in ATP-driven pancreatic cancer cell invasion provides a potential anti-metastatic target for pancreatic cancer.

Transferred mitochondria do not always regulate cell behavior by simply restoring mitochondrial function, but rather, transferred mitochondria are dysfunctional, initiating downstream signaling and proliferation in response to reactive oxygen species.