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The discovery of oncogenes and tumor suppressor genes firmly established the view that "cancer is fundamentally a disease of genomic alteration" and that the rational approach and is to identify and target critical genetic alterations or particular pathways of tumor cell evolution. The success of Gleevec in the treatment of chronic myelogenous leukemia (CML) provided "proof of principle" and was used to justify the overarching strategy of the National Cancer Institute: identify and target the genetic alterations of cancer. However, there is overwhelming evidence that cancer is actually a hugely diverse, complex, unpredictable, non-linear, stochastic evolutionary process. This conclusion, if true, falsifies much of what is believed to be true of cancer and invalidates most approaches being pursued to develop treatments for cancer patients. However, it also opens up new vistas and therapeutic approaches.[ for more detail read the draft attached below ]
Comments, criticisms, attempted refutations, discussion, debate, and posting of evidence and arguments related to the this topic would be greatly appreciated. Thanks. -- Arny Glazier
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Rafe.Furst |
Latest page update: made by Rafe.Furst
, Jul 28 2008, 1:35 PM EDT
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Keyword tags:
aneuploidy
anticancer drug
cancer
cancer and chaos
cancer and complexity
cancer stem cell
cancer therapy
carcinogenesis
chromosomal aberrations
complexity
Cure Cancer Project
epigenetic alteration
evolution
evolutionary
evolutionary process
genetic alterations
genetic diversity
genetic instability
Human Cancer Genome Project
malignant
metastatic
mutations
mutator phenotype
nonclonal
oncogene
stochastic
The Cancer Genome Atlas
tumor cell
tumor cell evolution
tumor cell heterogeneity
More Info: links to this page
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| Started By | Thread Subject | Replies | Last Post | ||
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| Rafe.Furst | Complex Networks in Genomics and Proteomics | 0 | Feb 19 2008, 2:09 PM EST by Rafe.Furst | ||
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Thread started: Feb 19 2008, 2:09 PM EST
Watch
David, thanks for posting these papers.
In the one titled the same as this thread, I had a question. The gene duplication model is fascinating, and I can see how subnets could be duplicated via aneuploidy. But how is it proposed that rewiring occurs? The only hint is on page 15 where they say "The rewiring steps implement the possible mutations of the replicated gene, which translate into the deletion and addition of interactions, with different probabilities." This is rather vague and speculative, don't you think? |
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complex networks.pdf (Adobe Portable Document Format - 1,542k)
posted by drasnick Feb 16 2008, 5:58 PM EST
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distributed robustness.pdf (Adobe Portable Document Format - 260k)
posted by drasnick Feb 16 2008, 5:57 PM EST
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selection tinkering emergance (Unknown File - 186k)
posted by drasnick Feb 16 2008, 5:56 PM EST
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robustness MCA.pdf (Adobe Portable Document Format - 266k)
posted by drasnick Feb 16 2008, 5:54 PM EST
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Aneuploidy article.doc (Word Document - 84k)
posted by Rafe.Furst Feb 14 2008, 6:08 PM EST
Rasnick article
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