AS WE SEARCH FOR THE CURE, IT IS IMPORTANT TO REMEMBER THAT:
Molecular Biology offers tremendous opportunities to fight cancer. In fact, it is surprising that we seem so early (or late, depending on how you understand this) in the game. The cell can be affected in so many ways that we are late reacting. Using integrated methods and our computer abilities, we should by now be involved in developing patterns of attacks by cancer cell type.
We should define clearly the major drivers by type of cancer, and pick the counter attacks specifically per type of cancer. We should be at the stage where each patient who presents to us has his genotype defined, changes in his membrane receptors described, driver mutations enunciated, status of P53, level of major Cyclins and various cell protections (P-gp, Bcl-2), status and quantitative expression of transcription factors, expression of Metastatic potential (E-Cadherin, Metallo-protease, TGF), histone conformation, level of Endonuclases, status of mitotic speed, types of protein Anchor at cell membranes, and Kinesins (Kif2a,b,c) and so on so forth, all spelled out on his file!
IT IS ONLY WITH THIS LEVEL OF DEFINITION, THAT WE CAN PICK AND CHOOSE AN APPROPRIATE TREATMENT, OR UNDERSTAND THE SHORTCOMINGS OF OUR CURRENT STANDARD TREATMENTS. Computers should also be used to tell us if combination treatments should be used sequentially or concurrently, and at which sequences, order and time our therapeutics should be given.
Molecular Biology, so many "distractions" and stuff that some scientists are spending days on, and may lead to something some day, but as we work in a race against death situation, and people are dying every day, it is time to pause and regroup, look at how to create this panel per patient, and develop computer supported patterns of therapy. And every 2-5 years make a stop, update our computer and reload for the Cure!
A blog about research, awareness, prevention, treatment and survivorship of Breast Cancer and all cancers, including targeted scientific research and a grassroots approach to increase screening for cancer, especially in the low income and under-insured population of El Paso, Texas, with a view to expand this new health care model to many other 'minority' populations across the United States and beyond
Showing posts with label endonuclease. Show all posts
Showing posts with label endonuclease. Show all posts
Saturday, December 29, 2012
Wednesday, December 19, 2012
THIORIDAZINE, A PHENOTHIAZINE WHICH IS AN INHIBITOR OF CALMODULIN WILL HAVE ANTITUMOR EFFECT AS DEMONSTRATED BY CANADIAN RESEARCHERS WHEN THEY DESCRIBED A 50 PERCENT DECREASE OF STEM CELLS. WE AT CRBCM BELIEVE THIS EFFECT IS OF COURSE LINKED TO THE RELEASE OF CALCIUM IN THE CYTOSOL LEADING TO ENDONUCLEASE STIMULATION WITH THE RESULTING ATTACK ON DNA.
THE FACT IS THIS EFFECT WILL BE MORE ON MEMBRANE WHERE CALMODULIN IS MOSTLY LOCATED. THEREFORE LIBERATION OF CALCIUM AFFECTS ELECTRICAL POLARITY AT THE MEMBRANE. TORSADE DE POINTE CAN RESULT AND HAD LED TO THE BANNING OF THIORIDAZINE IN CANADA.
THIORIDAZINE ACTS ALSO AS AN ANTIGROWTH FACTOR IN GENERAL. THIS FACT COULD CONTRIBUTE TO ITS ANTI-CANCER ACTIVITY. IN OUR PREVIOUS NOTES, WE
HAD SUGGESTED ADDING THE ANTI-CALMODULIN TO AVASTIN AS A STRATEGY TO TREAT RECURRENT BRAIN TUMOR.
THE FACT IS THIS EFFECT WILL BE MORE ON MEMBRANE WHERE CALMODULIN IS MOSTLY LOCATED. THEREFORE LIBERATION OF CALCIUM AFFECTS ELECTRICAL POLARITY AT THE MEMBRANE. TORSADE DE POINTE CAN RESULT AND HAD LED TO THE BANNING OF THIORIDAZINE IN CANADA.
THIORIDAZINE ACTS ALSO AS AN ANTIGROWTH FACTOR IN GENERAL. THIS FACT COULD CONTRIBUTE TO ITS ANTI-CANCER ACTIVITY. IN OUR PREVIOUS NOTES, WE
HAD SUGGESTED ADDING THE ANTI-CALMODULIN TO AVASTIN AS A STRATEGY TO TREAT RECURRENT BRAIN TUMOR.
Labels:
anti-growth factor,
antitumor effect,
avastin,
brain tumor,
calmodulin,
cancer,
crbcm,
dna attack,
endonuclease,
phenothiazine,
stem cells,
thioridazine,
torsade de pointe
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