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Tumours often become resistant to treatment, but how this occurs is poorly understood. An analysis of how the protein Rb affects tumour growth and the response to therapy might cast light on the problem. Assessing how the protein Rb affects cancer reveals possible drug targets., Author(s): Seth M. Rubin, Julien Sage Author Affiliations: Manipulating the tumour-suppressor protein Rb in lung cancer reveals possible drug targets The development of cancer invariably involves cellular proteins that have [...]

The tumour-suppressor protein PTEN is mostly found in the cell cytoplasm, tethered to endosome vesicles. This localization regulates the enzyme's activity towards specific lipids and influences its control of cell [...]

The Deleted in colorectal cancer (DCC) gene was identified as a potential tumour-suppressor gene on human chromosome 18q, although it has not been conclusively implicated as the colorectal tumour-suppressor gene. Investigations indicate that DCC is an axonal chemoattractant netrin-1 receptor. The effects of inactivation of the mouse homologue of DCC are similar to those in netrin-1-deficient mice.

Analysis of the genomic sequences of the 1A1-3B gene and the BRCA1 gene, which mediates the early onset of familial breast and ovarian cancer, reveals that the 5' end of both the genes are separated by a distance of 295 base pairs. BRCA1 exon 1 is centromeric to the 1A1-3B gene and the sequence between the first exons of both the genes reveal potential CAT boxes, which are crucial for the expression of the gene. The decrease of BRCA1 expression is associated with increased 1A1-3B expression.