Browse our latest Cancer Biology articles

Cancer-directed treatment using Tumor-Treating Fields spatially modulates the tumor microenvironment at the cellular and molecular levels, decreasing nanotube-based cellular networks of communication while creating a microenvironment more susceptible to immunotherapeutic strategies.

Tumor morphological patterns are linked to distinct transcriptional profiles and may indicate the need for a multi-site tumor sampling in gene expression-based studies.

Deep reinforcement model and experimental evaluations identified a small-molecule CRM1 inhibitor that can selectively ablate extranodal NK/T cell lymphoma cells.

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.