CancerHubs: a systematic data mining and elaboration approach for identifying novel cancer-related protein interaction hubs.

Conventional approaches to predict protein involvement in cancer often rely on defining either aberrant mutations at the single-gene level or correlating/anti-correlating transcript levels with patient survival. These approaches are typically conducted independently and focus on one protein at a time, overlooking nucleotide substitutions outside of coding regions or mutational co-occurrences in genes within the same interaction network. Here, we present CancerHubs, a method that integrates unbiased mutational data, clinical outcome predictions and interactomics to define novel cancer-related protein hubs.

Dissecting the Puzzling Roles of FAM46C: A Multifaceted Pan-Cancer Tumour Suppressor with Increasing Clinical Relevance.

FAM46C is a well-established tumour suppressor with a role that is not completely defined or universally accepted. Although FAM46C expression is down-modulated in several tumours, significant mutations in the gene are only found in multiple myeloma (MM). Consequently, its tumour suppressor activity has primarily been studied in the MM context.

FAM46C Is an Interferon-Stimulated Gene That Inhibits Lentiviral Particle Production by Modulating Autophagy.

FAM46C is a multiple myeloma (MM) tumor suppressor whose function is only starting to be elucidated. We recently showed that in MM cells FAM46C triggers apoptosis by inhibiting autophagy and altering intracellular trafficking and protein secretion. To date, both a physiological characterization of FAM46C role and an assessment of FAM46C-induced phenotypes outside of MM are lacking.