RNASEL (also known as the hereditary prostate cancer 1 gene or HPC1) and because it is a member of a viral family known to CAUSE leukemias and lymphomas in different mammalian species.
...Apparently IF RNASEL is a *mutated* gene.
Interferon, through its effector RNase L (RNASEL), potently inhibits XMRV replication.
But another says RNASEL might be functioning as a tumor SUPPRESSOR:
Several recent studies have suggested that RNase L could have a role in cancer biology and ***evidence of a tumor suppressor function of RNase L *** has emerged from studies on the genetics of hereditary prostate cancer.
RNase L (RNASEL) is part of the body's innate immune defense, namely the antiviral state of the cell.
When a cell is in the antiviral state, it is highly resistant to viral attacks and is also ready to undergo apoptosis upon successful viral infection.
Degradation of all RNA within the cell (which usually occurs with cessation of translation activity caused by protein kinase R is the cell's last stand against a virus before it attempts apoptosis.
RNase L is an ***interferon-induced*** ribonuclease which, upon activation, destroys all RNA within the cell (both cellular and viral).
So...interferon -> RNASEL -> all RNA (ours and viral - including XMRA) within the cell is destroyed. A cell without RNA can't replicate, I would think and thus would be destroyed. Oncogene- turns normal cell into cancer cell.
Tyrosine kinases ***add phosphate groups to the amino acid tyrosine*** in the target protein.
They can cause cancer by *** turning the receptor permanently on***(constitutively), even without signals from outside the cell.
XMRV proteins are also homologous to proteins of the growth factor signalling networks (e.g.***tyrosine kinases FLT3 and TYRO3***) which are relevant to cancer-related growth.
VEGF plays an essential role in induction of: endothelial cell migration and proliferation, microvascular permeability,endothelial cell release of metalloproteinases and interstitial collagenases, and endothelial cell tube formation.
The mechanism of VEGF receptor down-regulation is believed to occur at the ***tyrosine kinase nuclear factor-kappa B (NFκB). ***
NFκB is a nuclear transcription factor that up-regulates COX-2 expression, intracellular adhesion molecule,thrombin, and nitric oxide synthase.
All four factors are associated with vascular instability.
COX-2 drives conversion of AA to a number angiogenic and proinflammatory eicosanoids.
Reciprocal upregulation of urokinase plasminogen activator and its inhibitor, PAI-2, by Borrelia burgdorferi affects bacterial penetration and host-inflammatory response.
CONCLUSIONS: (213)Bi-PAI2 can specifically target pancreatic cancer cells in vitro and inhibit tumor growth in vivo. (213)Bi-PAI2 may be a useful agent for the treatment of post-surgical pancreatic cancer patients with minimum residual disease. PMID: 16475028
Bismuth 213 decays and releases *alpha particles* to destroy cancer.
Plasminogen activator inhibitor type 2 (PAI-2) mRNA and antigen levels are synergistically induced in HT-1080 fibrosarcoma cells when treated with a combination of tumor necrosis factor (TNF) and phorbol 12-myristate 13-acetate (PMA).
PMID: 8824249
Inhibition of protein kinase C completely blocked PMA-stimulated induction of PAI-2 mRNA in both cell types and inhibited the AII-stimulated increase in RASMC by 98.6 +/- 2.8%.
In contrast, protein kinase C inhibition only partially decreased the AII-stimulated PAI-2 expression in RME cells by 68.8 +/- 11.1%, suggesting that a protein kinase C-independent mechanism contributes to a 6.9 +/- 1.5-fold AII induction of PAI-2 expression in endothelial cells.
AII and PMA also stimulated protein tyrosine phosphorylation in RME cells, and the tyrosine kinase inhibitor ***genistein partially blocked their induction of PAI-2 mRNA.***
These findings suggest that AII may regulate plasminogen activation in the vasculature by inducing both PAI-1 and PAI-2 expression. PMID: 7883982
CONCLUSIONS:(213)Bi-PAI2 can specifically target pancreatic cancer cells in vitro and inhibit tumor growth in vivo.
(213)Bi-PAI2 may be a useful agent for the treatment of post-surgical pancreatic cancer patients with minimum residual disease.
While I am NOT (absolutely NOT) recommending smoking, in all fairness this is something you should know:
"In investigations into the health effects of smoking, it was found that tobacco leaves contain small amounts of polonium, which ***emits alpha particles.***
It is theorized that this could be partially responsible for lung cancer among smokers."
Radon...may explain why persons used to go into caves to help with arthritis (intentional exposure to radon which apparently emits alpha particles).
The largest natural contributor to public radiation dose is radon, a naturally occurring, radioactive gas found in soil and rock. If the gas is *inhaled*, some of the radon particles may attach to the inner lining of the lung.
These particles continue to decay, emitting alpha particles which can damage cells in the lung tissue.
The death of Marie Curie at age 66 from leukemia was probably caused by prolonged exposure to high doses of ionizing radiation, but it is not clear if this was due to alpha radiation or X-rays.
Curie worked extensively with radium, which decays into radon,[6] along with other radioactive materials that emit beta and gamma rays.
However, Curie also worked with unshielded X-ray tubes during World War I, and analysis of her skeleton during a reburial showed a relatively low level of radioisotope burden.
Russian dissident Alexander Litvinenko's 2006 murder by radiation poisoning is thought to have been carried out with polonium-210, an alpha emitter.
Wikipedia
Like BREATHING ozone versus being in an ozone sauna (with your head sticking out)to "detox", there appears to be a huge difference.
I do wonder if XMRV/HGRV is a remnant protein. Flagella/root?
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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Marnie
Frequent Contributor (5K+ posts)
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Up for those who are more awake and online in the evenings.
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