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Research in carcinogenesis
Cancer is currently attributed to the mutation of specific genes, which are called oncogenes.
This theory does, however, not explain why: (1) All cancers have individual, clonal karyotypes. (2) Oncogenes are not sufficient to transform normal cells to cancer cells. (3) Carcinogens induce cancers only after exceedingly long latencies of many months to decades. (4) Cancers are karyotypically flexible, whereas conventional mutations are stable. (5) All cancers are immortal, despite karyotypic flexibility.
In view of the ubiquity of 'abnormal' karyotypes in cancers it is tempting to think that the cancer-specific karyotypic abnormality could be normal. In that case carcinogenesis would be a form of speciation.
This speciation theory of carcinogenesis would explain, why cancers have individual karyotypes. It would also explain, why oncogenes are not sufficient to cause cancer. Further it would explain the notorious long latencies from carcinogens to cancer by the very low probalbility of forming a new autonomous karyotype by random karyotypic rearrangements of a precursor - much like in conventional speciation.
But would this theory also explain, why cancers are genomically flexible, and why cancers are immortal?
Currently we are testing the speciation theory of cancer as an explanation for the unique characteristics of cancer, autonomy, individuality, long latency, clonality and the unique karyotypic flexibilty, as follows:
Speciation theory of cancer. Carcinogens, like mutagenic X-rays and non-mutagenic aromatic hydrocarbons, initiate carcinogenesis by inducing random aneuploidy (the loss or gain of chromosomes or segments of chromosomes).
Aneuploidy destabilizes the karyotype by unbalancing 1000s of collaborating genes – particularly the balance-sensitive mitosis genes that segregate, synthesize and repair chromosomes. Thus aneuploidy catalyzes chain reactions of random karyotypic variations automatically.
These chain reactions have two stable endpoints (see graphic):
1) Cell death from lethal karyotypes, and
2) Rare, new autonomous species with new, individual karyotypes – alias cancer cells.
Research in carcinogenesis
Cancer is currently attributed to the mutation of specific genes, which are called oncogenes.
This theory does, however, not explain why: (1) All cancers have individual, clonal karyotypes. (2) Oncogenes are not sufficient to transform normal cells to cancer cells. (3) Carcinogens induce cancers only after exceedingly long latencies of many months to decades. (4) Cancers are karyotypically flexible, whereas conventional mutations are stable. (5) All cancers are immortal, despite karyotypic flexibility.
In view of the ubiquity of 'abnormal' karyotypes in cancers it is tempting to think that the cancer-specific karyotypic abnormality could be normal. In that case carcinogenesis would be a form of speciation.
This speciation theory of carcinogenesis would explain, why cancers have individual karyotypes. It would also explain, why oncogenes are not sufficient to cause cancer. Further it would explain the notorious long latencies from carcinogens to cancer by the very low probalbility of forming a new autonomous karyotype by random karyotypic rearrangements of a precursor - much like in conventional speciation.
But would this theory also explain, why cancers are genomically flexible, and why cancers are immortal?
Currently we are testing the speciation theory of cancer as an explanation for the unique characteristics of cancer, autonomy, individuality, long latency, clonality and the unique karyotypic flexibilty, as follows:
Speciation theory of cancer. Carcinogens, like mutagenic X-rays and non-mutagenic aromatic hydrocarbons, initiate carcinogenesis by inducing random aneuploidy (the loss or gain of chromosomes or segments of chromosomes).
Aneuploidy destabilizes the karyotype by unbalancing 1000s of collaborating genes – particularly the balance-sensitive mitosis genes that segregate, synthesize and repair chromosomes. Thus aneuploidy catalyzes chain reactions of random karyotypic variations automatically.
These chain reactions have two stable endpoints (see graphic):
1) Cell death from lethal karyotypes, and
2) Rare, new autonomous species with new, individual karyotypes – alias cancer cells.
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European Journal of Haematology (2010)
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#Papers: 4
#Citation: 15
H-Index: 2
G-Index: 3
Sociability: 2
Diversity: 0
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