Cancer stem cells are cells having a cancer stem cell-like properties, the "self-replicating", and "Multi-cell differentiation" capabilities. These cells are thought to have the potential to form tumors and even develop into cancer. 1994, a molecular biologist at the University of Toronto John Dick experiments, we found that not all of the cancer stem cells are experiencing the same procedure evolved. In particular, only a small part of the self-renewal capacity of leukemic cells can develop into cancer, so John Dick of these can develop into a tumor variant cells called cancer stem cells. CUSABIO has a professional R & D team of Human ferritin ELISA Kit ( http://www.cusabio.com/ELISA_Kit-78429/ ) service synthesis.

In this article, the authors believe that although we often use exclusive model to describe the tumor heterogeneity, but taking into account the impact of genetic diversity and non-genetic factors on tumor heterogeneity, and therefore recommendations can be unified cancer genetics and cancer stem cell model. Here researchers have proposed a new method to integrate cancer stem cells and cancer genetic data, obtained in the past to explain the discovery, and guide future research.

Cancer is a malignant tumor heterogeneity, one important feature of this heterogeneity may be reflected in the level of tumor differentiation and tumor function level, the emergence of heterogeneous antigen expression or biological properties of the cells there are different subsets. This tumor heterogeneity characteristics often bring great difficulties for cancer research and treatment.

Clones previously proposed evolutionary (clonal evolution) model assumes that the tumor originated in normal cells, these cells produce mutations and abnormal progeny, and progeny and mutations, cancer cells form a large number of variation.

The cancer stem cell hypothesis believes that the tumor is triggered and drive a single, abnormal type of adult stem cells. Moreover, normal stem cell function must be activated in several ways, and genes in cancer cells, play a key role in tumor formation. Very few can promote the formation of self-renewing cancer stem cells are difficult to kill, and they can explain why vitality tumors often recur after successful treatment still.

The former model assumes that the microenvironment of continuous selection pressure has led to accumulation of mutations, tumors appeared, the latter indicates that the cancer cells have the same genetic background according to their oncogenic potential, hierarchical organization, cancer stem cells at the top of the hierarchy, with the tumor the ability to start and spread.

A major feature of this model is its behind the obvious way, that is symmetrical division of cancer stem cells to replenish the pool of stem cells, also asymmetric division, resulting in a low carcinogenic daughter cells (non-cancer stem cells).

However, new results emerging research has proposed a new model for carcinogenicity is between the non-cancer stem cells and cancer stem cells in the presence of considerable plasticity, such as non-cancer stem cells can restore the cancer stem cell phenotype. These findings indicate that some tumors may follow the plasticity of cancer stem cell model can be two-way conversion, which is very common, but also an important part of carcinogenicity.

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