By David Rasnick
Exploring the chromosomal imbalance (aneuploidy) thought of melanoma, this quantity describes how melanoma is initiated and why development takes years to a long time. It clarifies why melanoma cells frequently develop into drug resistant, presents goal, quantitative measures for detecting melanoma and tracking its development, and indicates non-toxic suggestions of melanoma remedy and prevention. The publication posits that the autocatalyzed development of aneuploidy is carcinogenesis. The readability and unifying simplicity of the speculation of chromosomal imbalance has the capability to essentially modify the process melanoma study, prevention, analysis and treatment.
Read or Download The Chromosomal Imbalance Theory of Cancer: The Autocatalyzed Progression of Aneuploidy is Carcinogenesis PDF
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Additional info for The Chromosomal Imbalance Theory of Cancer: The Autocatalyzed Progression of Aneuploidy is Carcinogenesis
The tsunami of 11,000 gene mutations per cancer cell reported by Stoler et al. obliterated the idea of a manageable number of targets (Stoler et al. 1999). indd 21 30-09-2011 13:43:03 3 Genesis of “The Enemy Within”? We now believe that we know the ‘why for these happenings,’ and it takes a remarkable form. Two sorts of genes govern the proliferation of our cells: proto-oncogenes, which serve as accelerators to activate the genes of the cell; and tumor suppressor genes, which serve as brakes to retard the growth of cells.
Point out, “numerous questions remain about how mutations in DNA lead to the acquisition of these traits” (Anderson et al. 2011). Bishop correctly stated, every tumor represents the outcome of an individual experiment in cellular evolution, fueled by a genetic instability and overseen by relentless selection for advantageous cellular properties, which is consistent with virtually all theories of cancer, including aneuploidy. He forthrightly acknowledged the paradox that at least half of all known carcinogens are not mutagenic.
1984) because it is genomically unstable (with a modal number of 68 chromosomes instead of the euploid number of 40 for the mouse) (American Type Culture Collection 1992) and can spontaneously transform into cancer cells within days (Rubin and Xu 1989). The unrecognized (or disregarded) significance of the preneoplastic nature of the highly aneuploid 3T3 cells has misdirected decades of cancer research. In one set of highly regarded experiments using the 3T3 cells, Ed Scolnick working at the NIH fused the cellular prototype of the Harvey sarcoma virus transforming gene, ras, to a promoter from the virus, and thus created in the test tube something close to an artificial transforming retrovirus (Chang et al.