Tumour progression is not only dictated by events within tumour cells, but also by whether the surrounding niche is permissive to growth at all stages of disease.
Mitochondria undertake multiple critical functions in a cell.
In recent years the ubiquitin–proteasome system has been identified as essential for maintaining a crucial balance between cell growth and death, the progression of human malignancies, and the development of drug resistance in cancer cells.
Cancer stem cells (CSCs) are cells with properties that are similar to those described for tissue stem cells: self renewal and asymmetric division resulting in the generation of daughter cells destined to differentiate, enabling the regeneration of a tissue.
The DNA damage response pathways can activate cell cycle checkpoints (which can involve p53) to arrest the cell either transiently or permanently (senescence) or they can activate specific DNA repair pathways in response to certain types of DNA damage.
In 1979 the discovery of p53 was reported. The gene encoding p53 (TP53) was initially believed to be an oncogene but 10 years later it was correctly characterized as a tumour suppressor, which led to a steep rise in p53 research.
Genetically engineered mouse models of cancer have taught us much about how cancer develops.
Stem cells have been identified and characterized in several mammalian tissues.
Tumour formation and progression occur through a range of defects that develop both within and outside the cancer cell.
ancer arises from the stepwise accumulation of genetic changes that confer upon an incipient neoplastic cell the properties of unlimited, self-sufficient growth and resistance to normal homeostatic regulatory mechanisms.