Molecules and Cancer Cells

Now that we know that the cell does not discriminate about what is the category of this molecule invading me as classified by humans, we are ready to suggest some unconventional combinations of chemotherapy drugs:
Nexavar-Metformin for hepatocarcinoma
anti-MEK- calcium channel blocker for K-ras expressing lung cancer
Antibiotic with impact on splicing molecule with the MTOR
(to be continued)

PLATELET DERIVED GROWTH FACTOR, A DEADLY MISNOMER
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By naming this compound PDGF, the scientist who described this cytokine not only picked the wrong name,
but also sent researchers on the wrong path to understanding just how important this growth factor is.  As a result, some people are probably dying because the emphasis brought by the name was not clearly defined.
First of all, PDGF does not come solely from Platelets alone. It is made by a number of cells including Muscle cells, Endothelial cells and even Macrophages.
And when you think of Platelets, Coagulation comes to mind, weakening of platelets and the like.  If this PDGF does this, it is at a strictly minimal or insignificant level.  The effect on Platelets is only mentioned by those who clearly have been fooled and kept looking for rare effects which eventually can be found.  This PDGF works on Mesenchymal cells since creation.  It participates in Embryogenesis, cell survival, proliferation, angiogenesis and differentiation. In adults, its main effect is on Fibroblast and Glial cells.
When you think Platelet, platelet Aggregation, adhesion and so forth.  PDGF kills by Fibrosis in cirrhosis of the liver and Pulmonary hypertension, one of the worse silent killers of our time.  Pulmonary Hypertension is a deadly killer because physicians don't know how to best monitor it.  AND BECAUSE WE CLEARLY DO NOT TREAT IT AGGRESSIVELY.  HOW MANY PHYSICIAN GIVE CIALIS TO THEIR PATIENT FOR PULMONARY HYPERTENSION?   If you raise your hand, you are my hero!
The point is that by misnaming the PDGF, people will assume Aspirin would be the more likely inhibitor.  Think again.  There are almost 20 inhibitors of PDGF listed on the SELLECHEM list.  Believe me it starts with Nexavar and Sutent. Aspirin is not on the list!
HOW MANY PEOPLE THINK OF NEXAVAR IN THEIR TREATMENT OF SCLERODERMA, A DISEASE KNOW TO HAVE PROMINENCE OF PDGF ACTIVITY?    HOW MANY ONCOLOGISTS GIVE GLEEVEC TO TREAT THEIR GLIOBLASTOMA.  (CLUE, AVASTIN IS INDICATED IN REFRACTORY BRAIN DISEASE-YOU THINK AVASTIN-ANGIOGENESIS, THINK NEXAVAR, TELLS SELLECHEM).

In a short study, 11 out of 12 GLIOBLASTOMAS had amplification of PDGF.  This is one of the drivers of GBM.  Forget Platelet, think Mesenchymal derived growth factor, and let us put the right emphasis on this Cytokine!

RENAL CANCER PREVENTION (CHRONIC USE OF DECONGESTANT -AFRIN- COULD DECREASE RENAL CANCER.) and so does a CPAP mask for patients with Sleep Apnea

Renal cell cancer risk is associated to smoking and Obesity (hypertension is a corollary risk we claim).   These 2 conditions lead to Hypoxia generally through sleep Apnea  which in turn leads to a relative increase of Hemoglobin. The rise of Hemoglobin increases the portion of Desaturated hemoglobin. After many years of such exposure desaturated Heme enhances Phosphorylation at Tyr-530 of the SRC leading to its deactivation. In some individuals with the right MEK, suppression pf the SRC could lead to persistent amplification at the MEK which is a versatile activator of almost all signals, but particularly VEGF receptor.  This in turn usually lead to papillary cancers. Amplification of signal transduction started at the MEK (which amplifies almost all major known pathways) will lead to increased ubiquitination and proteasome destruction of the HYPOXIA-inducible factor  (following the Von Hippel-Lindau model.  This will lead to clear cell cancer. Associated desaturated Heme and hypoxia at the mitochondria will participate in the transformation (and possibly the Atypia/clear cell transformation).  The preponderance and center piece role of MEK amplification and subsequent VGEF/PDGF will justify the "bloody" nature of kidney cancers, and vessel involvement in these diseases  (MEK is the driver Mutation in papillary cancers).  IT ALSO EXPLAINS WHY SUTENT, NEXAVAR WORKS.  AND MITOCHONDRIAL DISTURBANCES AND SECONDARY AMPLIFICATION OF AKT, THE MTOR INHIBITORS WORK IN RENAL CANCERS  (MTOR participates more in clear cells)  (proof of concept pending)

In Western society, obesity is increasing, and so is Sleep Apnea.  Also, we live in closed homes (in some regions such as Texas and Louisiana, Mosquitoes are not helping) the level of dust participates in the increased level of allergic Rhinitis/ upper respiratory ailments.  It is not unusual to sleep and wake with closed Nostrils.  In obese individuals, this compounds the hypoxic episodes and worsened and prolonged hypoxia.  And we are back to depression of SRC, activation of MEK---akt, MAPK and so forth.
Keeping your nostrils open at night appears to be a critical strategy in preventing renal cancer, particularly in patients with breathing issues.   Lung cancer may be reduced for non smokers, but I wont touch that speculation, but do remember the role of VEGF in non-smoker lung cancers!

The involvement of PDGF which is by the way affected by Sutent seems to open a window in the frequency of strokes and heart attacks at night!  That's another debate to have...!

MTOR inhibitor in combination with Anti-VGEF/ MEK could have a significant role in non smoker lung cancer.?
Velcade could have a role in VHL prevention ? and in Pheochromocytoma?

Avastin and Mtor inhibitor could treat Leiomysarcoma of the Uterus if you follow this logic!

A FREED CPRIT AND THE NIH COULD HELP!