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Cellular Phones and Brain Cancer

Neoplastic transformation appears to be a multistep process in which the normal controls of cell proliferation and cell-cell interaction are lost, thus transforming a normal cell into a brain cancer cell with a cellular phone, causing brain cancer or brain tumor. This tumorigenic process involves an interplay between at least two classes of genes: oncogenes and tumor suppressor genes in some relation to cellular phone radiation. Oncogenes are abnormally activated versions of cellular genes that promote cell proliferation and growth associated with cellular phone electromagnetic radiation. 

Activated oncogenes thereby result in an exaggerated impulse for a cell to grow and divide. Tumor-suppressor genes, on the other hand, are normal genes that act to inhibit cell proliferation and growth. The inactivation of these genes results in tumor formation or progression. The most common scenario for inactivation of both copies of a tumor suppressor gene is mutation of one allelic copy, followed by loss of all or part of the chromosome.

As a consequence, the identification of consistent regions of chromosomal loss in specific tumor types suggests a tumor-suppressor gene in that chromosomal region related to cellular phone electromagnetic radiation. These basic themes of oncogene activation and tumor-suppressor gene inactivation coupled with chromosomal homozygosity underlie the current molecular understanding of human tumor formation and cellular phone electromagnetic radiation.

DIFFUSE, FIBRILLARY BRAIN CANCER

Diffuse, fibrillary astrocytomas are the most common type of primary brain tumor in adults. These tumors are classified histopathologically into three grades of malignancy brain cancer or tumor caused by microwaves or cell phone radiation.

The p53 gene, a tumor-suppressor gene located on chromosome 17p, has an integral role in a number of cellular processes, including cell cycle arrest, response to DNA damage, apoptosis, angiogenesis, and differentiation; as a result, p53 has been called the guardian of the genome. The p53 gene is involved in the early stages of astrocytoma tumorigenesis. For instance, p53 mutations and allelic loss of chromosome 17p are observed in approximately one-third of all three grades of adult astrocytomas, suggesting that inactivation of p53 is important in the formation of the grade II tumors. Moreover, high-grade astrocytomas with homogeneous p53 mutations evolve clonally from subpopulations of similarly mutated cells present in initially low-grade tumors. 

Such mutation studies are complemented by functional studies that have recapitulated the role of the p53 inactivation in the early stages of astrocytoma formation. For instance, cortical astrocytes from mice without functional p53 appear immortalized when grown in vitro and rapidly acquire a transformed phenotype. Cortical astrocytes from mice with one functional copy of p53 behave more like wild-type astrocytes and only show signs of immortalization and transformation after they have lost the one functional p53 copy. Those cells without functional p53 become markedly aneuploid, confirming prior work showing that p53 loss results in genomic instability cellular phone electromagnetic radiation and that astrocytomas with mutant p53 are often aneuploid.

Many growth factors and their receptors are overexpressed in astrocytomas, including platelet-derived growth factor (PDGF), fibroblast growth factors (FGFs), and vascular endothelial growth factor (VEGF). For example, PDGF ligands and receptors are expressed approximately equally in all grades of astrocytoma, suggesting that such overexpression is also important in the initial stages of astrocytoma formation. Tumors often overexpress cognate PDGF ligands and receptors in an autocrine stimulatory fashion. The mechanisms for PDGF overexpression in most cases have not been elucidated, although rare astrocytomas display amplification of the PDGF alpha-receptor gene.