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!

Ponatinib in CML

FDA Approvals > Medscape Medical News

FDA Approves Ponatinib for Rare Leukemias

Zosia Chustecka

Disclosures Dec 14, 2012

Editors' Recommendations

• Ponatinib Works in CML When Nothing Else Is Effective
• Ponatinib 'Best of the Bunch' in Ph-Positive Leukemia?
• Acute Leukemia News & Perspectives

Drug & Reference Information

• Chronic Myelogenous Leukemia
• Pediatric Hematopoietic Stem Cell Transplantation
• Immunotherapeutic Targeting in Children

Ponatinib ( Iclusig, Araid) was approved today by the US Food and Drug Administration (FDA) for use in patients with 2 leukemias that have stopped responding to other therapies, and offers new hope for these subgroups of patients. The approval comes 2 months earlier than expected.
Ponatinib is approved for use in patients with chronic myeloid leukemia (CML) and also Philadelphia chromosome–positive (Ph+) acute lymphoblastic leukemia (Ph+ ALL) who have relapsed or are refractory to other therapies. Many of these patients, but not all, have developed a T3151 mutation, which makes the disease resistant to the standard treatment with tyrosine kinase inhibitors (TKIs) such as imatinib ( Gleevec).
"The approval of ponatinib is important because it provides a treatment option to patients with CML who are not responding to other drugs, particularly those with the T3151 mutation who have few therapeutic options," said Richard Pazdur, MD,