We usually see that cancer progression is increased till death of a patient. Sometimes, this progression becomes fast after chemotherapy. As a result, patient dies due to synergistic effect of the cancer biomarkers. How could we explain this silent aggression of cancer? what is the mechanism behind this and what kind of experiment can monitor and reveal this complex condition of any cancer?
Thank you.
Good questions. However, harder to address these questions because each tumor within a patient could be very different genetically and phenotypically. Therefore, generalization may be wrong. Broadly speaking, chemotherapy kills cancer cells (and non-cancer cells), resulting in lot of dead cells that can initiate systemic inflammation. Further, the therapy also induces senescence. Again, this results in senescent cells that secrete pro-inflammatory cytokines. Together, these two cellular processes contribute to various phenotypes (side effects) that are observed in cancer patients undergoing chemotherapy. Increased inflammation (localized and systemic) contributes to observed aggressiveness of cancer and alterations of bio-markers.
Alright Prof Divakaer. What kind of experiment we should conduct to explain this mechanism?
Why some cancers (not all) becomes aggressive after chemotherapy? Think of blebbishield emergency program. This program sets in after commencement of apoptosis but saves cancer stem cells from death. So, after therapy the cells that underwent apoptosis but yet survived are cancer stem cells, which can make the progression faster. All papers related to this are in my researchgate page. https://www.researchgate.net/profile/Goodwin_Jinesh
To design experiments to test this program, After induction of apoptosis check for complete degradation of full-length proteins of VEGFR2, p70S6K and N-Myc, c-IAP2 (use the antibody listed in my paper, Mitochondrial Oligomers.....). Complete degradation of these indicates proper apoptosis and if there are full length proteins left behind (VEGFR2, p70S6K, N-Myc and c-IAP2), then the cells can survive after apoptosis. PKC-zeta is another marker (See Novel PKC-z to p47 interaction paper).
Very good work Goodwin. My interest is bit complex to address the tumorigenesis inhibition strategies.
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