Selective Requirement of PI3K/PDK1 Signaling for Kras Oncogene-Driven Pancreatic Cell Plasticity and Cancer
Stefan Eser, Nina Reiff, et al.
Read it. It tells you that not only the implications of a stimulation of one molecule change with the tissue because of tissue specific genetic silencing , but also changes can occur on different RAS family member (NRas or Hras) leading to different meaning in terms of consequence for the cell.
Another discrimination level is that many types of stimulation can induce the same pathway. C-JUN can be induced by radiation, chemical, hypoxia or infection. Any thing that is considered stressful, including lack of extracellular stimulation. This last point is very important in the Central nervous system where pre-synaptic stimulation is critical for post synaptic neurons. Lack of stimulation induces an inflammatory process in both the neuron and the glial cell. In the glial cell, the myelin sheath is scarily attacked or no longer formed.
The duplicity phenomena occurs particularly at the cellular membrane where many receptors would be stimulated by several stimulants and vice versa (many stimulants for same receptor). Only the cell and its tissue type know what to give out!
*New study concurs that mammogram should be done every 2 years and after 50 years of age. That only those women with dense breasts should start at 40 years of age and annually. The controversy dance is fueled once again and I don't blame anyone! We have seen cases of course which did not fit these prescription. Why change things that work.
Showing posts with label glial cells. Show all posts
Showing posts with label glial cells. Show all posts
Tuesday, March 19, 2013
Tuesday, February 12, 2013
PLATELET DERIVED GROWTH FACTOR, A DEADLY MISNOMER
====================================================
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!
====================================================
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!
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