Cytostatic and cancer
Researchers from New York found that hematopoietic stem cells in the tumor suppressor p53 expression levels will increase, when a cell chemotherapy or radiation therapy, if this or a MEF cells lacking p53 gene is called, then the cell will not only from stationary, but also more vulnerable to attack. The research for the study of stationary that has very little understanding of biological processes is significant, still helps maintain hematopoietic stem cells in the dormant, so the cells will not grow or divide, this study now identifies maintain cytostatic genetic pathway, whereby bone marrow cells may be able to avoid the side effects of conventional cancer treatment-induced.
When a cell is damaged in cancer treatment DNA, p53 started to play its role: either initiating cells "death signal", or let it stop growing, so that repair DNA, so to ensure the integrity of the cells, but p53 in blood formation process also has other effects. The researchers hope to understand whether p53, as well as increasing its target gene expression level would still lead to cell, as well as resistance to chemotherapeutic.
In addition, the researchers also found a new target of two p53 proteins: Necdin and Gfi-1, these two tumor suppressor genes also regulate cell stationary. Researchers reduce hematopoietic stem cells (deletion MEF) in Necdin and Gfi-1 expression levels, these cells will lose quiescent state, indicating that these p53 target function involved in the regulation of HSCs stationary.