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 usually turn into drug resistant, offers aim, quantitative measures for detecting melanoma and tracking its development, and indicates non-toxic thoughts 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 adjust the process melanoma learn, prevention, prognosis and treatment.
Read Online 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
Example text
If cancer begins as a single cell that eventually progresses to a full blown malignancy, what initiates the deadly sequence? For at least two centuries, the focus has been on external causes. Only in the past two decades, however, have we convinced ourselves that those causes might be united by a common mechanism: the mutation of DNA, the second of our converging themes”. 2. Mutation of DNA “In any poll of modern molecular biologists, you could probably get a rousing majority for the view that carcinogens act by affecting DNA.
1994, Lewin 1994, Lodish et al. 1999, Watson et al. 1987). As a result scientists studying aneuploidy now compare their work to “resurrection” (Brinkley and Goepfert 1998). Even cytogeneticists have disregarded the aneuploidy hypothesis in favor of gene mutation. For example, Nowell wrote in an influential article in Science in 1976, “It is certainly clear that visible alterations in chromosome structure are not essential to the initial change” (Nowell 1976). Twenty years later Mitelman et al. wrote, “We propose that unbalanced primary changes [aneuploidy], in fact, are secondary, the primary being submicroscopic.
According to an editorial in Science in 1999, “Over the following decades, however, [Boveri’s] idea got lost, as researchers concentrated on understanding the specific gene malfunctions that lead to cancer” (Pennisi 1999). The idea got lost so completely that it is now no longer mentioned in the cancer chapters of leading textbooks of biology (Alberts et al. 1994, Lewin 1994, Lodish et al. 1999, Watson et al. 1987). As a result scientists studying aneuploidy now compare their work to “resurrection” (Brinkley and Goepfert 1998).