Browse our latest Cancer Biology articles

SF3B1-K700E, a gene mutaiton found recurrently mutated in pancreatic cancer, increases malignancy in an autochthonous mouse model of pancreatic cancer and induces resistance against TGF-β-induced apoptosis in vitro by missplicing of MAP3K7.

A certain type of primary cancer may cause another second primary cancer which would be of clinical importance to make a personalized screening plan for certain primary cancer patients.

The archetypal tumor promoter PMA, which promotes cancer without mutating the DNA, increases Wnt signaling by activating macropinocytosis and membrane trafficking in Xenopus embryos and tumor cells.

Loss of membrane-bound ICAM-1, overexpression of soluble ICAM-1 or ILKAP activity in tumor cells induce resistance to antigen-specific cytotoxic T-cell-mediated killing independently from regulating antigen presentation, PD-L1 expression, IFN-γ, or TNF-α responsiveness.

Morphological profiling of untreated HCT116 cells using Cell Painting reveals a signature of bortezomib resistance, providing a proof-of-concept for the unbiased analysis of drug resistance.

A new type of mRNAs-loaded CD133⁺ vesicles, named intercellsome, mediate cell-cell communications to compensate intracellular proliferative signal deficit, representing a previously unrecognized mechanism of cell proliferation under stress.

SPOT-MAS (screening for the presence of tumor by methylation and size) is an affordable and effective multi-cancer early detection test analyzing multiple features of circulating tumor DNA.

TNFAIP2 was found to interact with IQGAP1 and Integrin β4, which activates RAC1 through TNFAIP2 and IQGAP1 and confers DNA damage-related drug resistance in triple-negative breast cancer.