Monday, September 16, 2013

THEORY IN CANCER PATHOLOGY

Based on pathology findings in Bladder cancer and the progressive genetic abnormalities proclaimed to be happening in colon cancer it appears that cancer pathology starts with an abnormal persistent stimulation of Receptors (FGFR3, FGF2, EGFR) which eventually under persistent stimulation will be eventually destroyed in an effort to to "desensitize" the cells from further stimulation.  The Receptor destruction however could induce  alterations of glycans covering the surface of receptors but could also cause immediate demise of the cell through  death receptors found in the submenbrane layer of the cell. These Death Receptors are associated with Caspase 3.  As the stimulation persists and some of the stimulation going through will solicit  normal pathways with internalization of the stimuli-Receptor and solicitation of normal pathways such as the RAS leading to transduction of the signal. It also be perceived as stress triggering HSP and the NF-kB / c-JUN. (this pathway can also be stimulated by cytokine altered Receptors)  According to the nature of the stimuli and the nature of the tissue, the HRAS (more epidermal-squamous than Adeno) or KRAS (more adeno then epidermal-squamous) pathway will be engaged.  As aggression at the membrane continue The FAK, the Wnt and NOTCH induce membrane events as well as epigenetic events to escape the stimulation leading to liberation of further cytokines and growth factors  (c-MYC stimulation) that will allow cellular survival and cellular desensitization. But it is not until repair (BRCAs), and regulator/modulators mechanisms failure that the cell becomes engaged in an irreversible proliferative process.  Potentially under the these growth factor the p21,p16, MDM2 etc. are knock down.  When the process reaches the P52,P53 AND Rb1, Malignancy is declared.  (to be edited further) these events could happen concurrently and at various sites.

Stimulation of the MEK /c-MET  Vs  Epidermal...to come

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