Cancer stem cells in hepatocellular carcinomas.

Abstract

There are currently two major schools of thought or theories that explain the formation of tumours. According to the classical stochastic theory or clonal-evolution model of carcinogenesis, it is believed that a cancer cell develops as a random process (stoʊˈkaestɪk in Greek, means “guessing” indicating randomness) and thus any cell in the body can undergo the required harmful changes in DNA sequences that culminate in the formation of cancer1. Eventually there is a clonal-selection of cells such that a clonal population of cells forms the cancer. The other model is the cancer stem cell (CSC) or tumour initiating cell (TIC) theory. The cancer stem cells model proposes that tumours are made of a heterogenous cells comprising a small population of cancer stem cells and a bulk of non-cancer stem cells. These cancer stem cells have properties of self-renewal and differentiation. In this model of cancer biology, the presence of residual CSC gives rise to tumour relapse1,2,3. This is also true for the local intra-organ or distant metastasis, where the CSC in tumour emboli may act as a hidden reservoir of cancer cells and give rise to distant relapse and metastasis1,2. Since these cells posses distinct charecteristics and comprise a very small percentage (1-3%) of the total tumour burden1,2 and drive tumour development and tumour sustenance, it is logical to believe that identification and subsequent targeted therapy would go a long way in treating malignancies3.