The link between neural stem cells and this aggressive type of cancer is a warning for the scientists to proceed with caution, with new treatments for neurodegenerative diseases such as Alzheimer?s disease, where the hope is to use neural stem cells help the loss of function of nerve regeneration, said Zhu.Over the past six years, some studies have shown that stem cells are the cells involved in a range of cancers, including glioblastoma. But the new study reveals in particular that the GBM begins in neural stem cells, which have a mutation in the p53 gene. These cells then give rise to mutants, rapid multiplication of cells of the cellular differentiation of a class called transit-amplifying progenitor cells.
In mice, neural stem cells that normally live in this segment give rise to more specialized nerve cells that migrate from the niche. The cancer can start with a single genetic mutation in the p53 gene, which makes the stem cells migrate out of the specialized niche as their offspring.
Appear June 2 in Cancer Cell, the team?s results in mice exposed to the UM for the first time: glioblastoma, the type of cancer that affects U. S. Senator Edward Kennedy is diagnosed in about 10,000 Americans each year may originate from neural stem cells located in a brain region known as the subventricular zone or SVZ.
The results found in mice add new knowledge to a sequence of images of how genes go awry to cause brain cancer. Scientists have recently discovered that some genes and cell lines of action are altered in glioblastoma. But so far scientists do not know what type of cell the cancer started, or more precisely as a lack of p53-mediated pathways is working with other mutations to transform cells in brain cancer.
The results in mice can also lead to time for an effective test for early diagnosis for glioblastoma. MU scientists show that the expression of mutated p53 protein is a marker of glioma cells at all stages of the disease.
Many cancer research has focused on the p53 gene, known as the ?guardian of the genome? because it started a wave of another gene that normally fight cancer.
First of all treatments based on these findings may benefit people, scientists will need more studies on animals to verify the results of animals in human studies.
Zhu and his project team to continue the experiments on mice to see if the function of p53 can be restored in tumor cells. They also check whether the inhibition of neural stem cells in the SVZ promise as a potential treatment. Given the plasticity of these tumor cells started, targeting a single path may not be sufficient, said Zhu.
?We found that cells with p53 mutations are very plastic. If treatment blocks a path of action, they can learn other ways to grow,? said Zhu. This explains why the yield of a glioblastoma multiforme in drug-resistant forms.
Sickle cell anemia is characterized by episodic periods of severe pain, resulting in high resource utilization in health care. Although previous studies have described the scope of this use of health services, have generally been limited to select populations of patients with sickle cell disease and therefore limited the generalization and the inability to supply estimates based on population, the authors write.
?Then we asked, mutant p53 has no role in initiation and progression of cancer, if so, we can use as a marker of brain tumor cells in the brain,? said Wang Yuan, the first author of the study and a UM graduate student in Cell and Developmental Biology. The team found that mutant p53 was detected in a minority of highly proliferative neural stem cells from p53-deficient mice two months after the birth and expansion of the mutant p53 expressing cell characteristics people behind transit-amplifying cells initiation of cancer. The evidence supports the idea that mutant p53 may be a useful marker to track glioma cells in all phases.
The finding of a specific area of ??origin could lead to treatments that can improve the median survival rate of 12 disastrous months for this type of brain cancer, said Zhu Yuan, Ph.D., lead author of the study and assistant professor in the Departments of Internal Medicine and Cell and Developmental Biology at the UM Medical School.
University of Michigan, scientists have discovered that a lack of key tumor suppressor gene in the brain leads to the most common form of adult brain cancer. The study, conducted on mice that mimic human cancer, paving the way for more effective treatments and the future of how to diagnose the disease early.
In addition, Wang and Zhu, other authors are Jiong Yang, Zheng Huarui, Gerald J. Tomasek, Zhang Peng, Department of Internal Medicine, UM, Division of Molecular Medicine and Genetics and Department of Cell and Developmental Biology, Paul E. McKeever, Department of Pathology and UM Eva YH. P.
Lee, University of California, Irvine
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