Removal of the genetics of a glioma


From the remaining residue of the successful surgery for glioma the removal of the disease part of the brain due to the fact that this can be utilized in the lab to find out the correct genetics the correct epi-genetics The correct sequence is events that lead to the proliferation of the glioma and the effect that it should constitute a growth in the brain the correct genetics the correct sequences the removal of those glioma causation agents and the subsequent repair by stem cell integration as well as self assembly and polymerization after genetic surgery removing the cause and purpose of the glioma.

 

preventable?
Levin VA1.
Author information
1Neuro-Oncology Unit 431, University of Texas, M.D. Anderson Cancer Center, Houston 77230-1402, USA.
Abstract
Gliomas are a family of primary central nervous system tumors of variable malignancy that are derived from supporting glia (astrocytes, oligodendrocytes, ependymal cells) or their progenitors/stem cells. There are two potential strategies to prevention: preventing gliomas from forming and preventing lower-grade gliomas from developing into higher-grade gliomas. Each would lower time-dependent mortality. Each also depends on an understanding of what causes gliomas so that these factors can be modulated. In this presentation, I will discuss primary prevention, chemoprevention, and screening. I will first focus on the known chromosomal, genetic, and protein changes associated with the different histologic varieties of glioma and the environmental, hereditary, and infectious/viral factors that may promote glioma development and malignant progression. I will discuss a number of clinical scenarios that eventuate from the known genetic patterns of these tumors and the changes in genetic patterns that reflect malignant progression. The basic thinking is that if one could prevent specific gene mutations and/or deletions or gains of specific chromosomes that lead to the development of low-grade (WHO 2) gliomas, then theoretically this would reduce the occurrence of high-grade (WHO 3 and 4) gliomas and hence the almost certain death that now is the fate of most patients with these tumors. In the case of de novo WHO 3 and 4 tumors, being able to prevent or counter specific gene mutations and/or the deletion of specific chromosomes would in itself reduce the occurrence of these gliomas and increase survival. Alternatively, a curative treatment for low-grade glioma that prevents these chromosomal/gene changes would prevent some glioblastomas (WHO 4) from forming and would have the same desired effect on survival. Obviously, for the latter to be achieved, we must also be able to diagnose and treat low-grade gliomas earlier.

 

So will be preventable status would be incurred after the surgery to in sure that the gliomas do not regrow the preventable techniques would be incurred of a chromosome level of genetic level to ensure that the genetics would be safe and secure in the future for the plug to stop the proliferation of the glioma

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3047463/

Steroids are commonly administered for the control of edema, mass effect, and side effects from therapy to patients with malignant glioma who are receiving radiotherapy and chemotherapy. Here, we report that therapeutic concentrations of dexamethasone (DEX) attenuate cytotoxicity and growth inhibition of human malignant glioma cells induced by exposure to several chemotherapeutics, including ACNU, VM-26, vincristine, cytarabine, metho-trexate, and adriamycin. DEX-mediated cytoprotection is not linked to DEX effects on glioma cell proliferation. However, the cytoprotective effects of DEX appeared to be more prominent in cell lines with wild-type p53 status (n = 2) than in p53 mutant cell lines (n = 3). Further, DEX-mediated rescue from chemotherapy does not directly involve Bcl-2 family proteins since DEX failed to change the expression of Bcl-2 or Bax proteins and since bcl-2 gene transfer-mediated cytoprotection was not redundant with the effects of DEX. DEX thus appears to control a common, bcl-2-independent death pathway in glioma cells that is not limited to specific drug actions. Chemotherapy is usually given as an elective, adjuvant treatment to glioma patients in stable condition who can tolerate steroid withdrawal. To maximize therapeutic I efficacy, steroids should be withdrawn from glioma patients prior to chemotherapy.

© 1997 by the American Academy of Neurology

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About garyskeete

ASHWORTH MEDICINE-Professional Medical Assisting, Doctor of Science,Legal Assistant Diploma BSc Criminal Justice
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