Browse our latest Cancer Biology articles

Why does cancer develop in situations where the immune system is perfectly capable of eliminating it?

BRD9 provides the first actionable therapeutic target in synovial sarcoma tumours that is both biochemically and functionally linked to the SS18-SSX fusion protein which drives disease development.

Global transcriptome analysis reveals that the transcription factor SOX4 can promote breast tumor development via tumor angiogenesis by promoting paracrine signalling through endothelin-1.

A new, high-throughput in vivo MHC-I peptide minigene library platform shows that the naive immune system cannot eliminate cells presenting immunogenic antigens found at low frequencies within a growing tumor.

A multi-transcriptional CDKs inhibitor suppresses MYC and induces regression of ovarian tumors, indicating that targeting CDK7, 12, 13 with THZ1 may be an effective approach for treating MYC-dependent malignancies.

The identification of key determinants of LSC “stemness” and LSC differentiation that is reversible through an epigenetic mechanism may have considerable implications in understanding leukemia and designing effective therapies.

Ectopic expression of Dnmt3b leads to wide-spread CpG island hypermethylation that is largely defined by chromatin state and has some distinct features when compared to the cancer methylome.

Major secondary tumor suppressors in kidney cancer are required to maintain the activity of a tumor suppressive transcription factor after the loss of the primary tumor suppressor VHL.

During tumorigenesis loss of p53 not only abrogates cell cycle arrest and apoptosis, but also suppresses the induction of replication-stress-induced DNA double-stranded breaks.

The mRNA of the apoptosis inducing death ligand CD95L/FasL kills cancer cells through RNAi after conversion into small RNAs that are loaded into the RNA-induced Silencing Complex.