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.
Showing posts with label brain tumor. Show all posts
Showing posts with label brain tumor. Show all posts
Wednesday, December 19, 2012
Saturday, November 24, 2012
Sons of the Sevenless
SONS OF THE SEVENLESS/Hypothesis for cancer Research
As we move forward here at CRBCM, we are increasingy fond of one line of molecules;
first because of their name, and because we believe that their inhibitors could be the answer to the resistance
to some of the medications already in our armamentarium, namely Avastin, Imatinib and Herceptin. We believe that the Sons of The Sevenless which are regulator molecules switching on RAS would break resistance to Tyrosine Kinase resistance. Sons of the Sevenless, what a name! But don't you remember they say: "KILL THE SWITCH" AND DARK WILL COME. THE SWITCH IS THE SONS OF THE SEVENLESS...BASAL CELL CANCER OF THE BREAST, THE CRBCM IS AFTER YOU...SINCE THE SUGGESTION THAT BASAL CELL CANCER OF THE BREAST IS LIKE OVARIAN CANCER BY ITS GENOME. MARK MY WORD: KILLING THE SONS OF THE SEVENLESS OR KILLING THE SWITCH IS THE KEY TO TREATMENT.
ADDING TAXANE (or better yet an Anti-Kinesin) AFTER KILLING THE SWITCH (SONS OF THE SEVENLESS) WILL TURN ON THE MITOCHONDRIAL CASPASE BY AN INHERENT REFLEX MECHANISM WHICH WILL BYPASS BCL-2. THAT'S HOW YOU LEAD TO CANCER CURE!
OH BY THE WAY, ADDING STELAZINE TO AVASTIN MAY JUST DO THE TRICK FOR RECURRENT BRAIN TUMORS TOO. IT IS AN ANTI-CALMODULIN AFTER ALL!
RESEARCH IS ON AT CRBCM.
As we move forward here at CRBCM, we are increasingy fond of one line of molecules;
first because of their name, and because we believe that their inhibitors could be the answer to the resistance
to some of the medications already in our armamentarium, namely Avastin, Imatinib and Herceptin. We believe that the Sons of The Sevenless which are regulator molecules switching on RAS would break resistance to Tyrosine Kinase resistance. Sons of the Sevenless, what a name! But don't you remember they say: "KILL THE SWITCH" AND DARK WILL COME. THE SWITCH IS THE SONS OF THE SEVENLESS...BASAL CELL CANCER OF THE BREAST, THE CRBCM IS AFTER YOU...SINCE THE SUGGESTION THAT BASAL CELL CANCER OF THE BREAST IS LIKE OVARIAN CANCER BY ITS GENOME. MARK MY WORD: KILLING THE SONS OF THE SEVENLESS OR KILLING THE SWITCH IS THE KEY TO TREATMENT.
ADDING TAXANE (or better yet an Anti-Kinesin) AFTER KILLING THE SWITCH (SONS OF THE SEVENLESS) WILL TURN ON THE MITOCHONDRIAL CASPASE BY AN INHERENT REFLEX MECHANISM WHICH WILL BYPASS BCL-2. THAT'S HOW YOU LEAD TO CANCER CURE!
OH BY THE WAY, ADDING STELAZINE TO AVASTIN MAY JUST DO THE TRICK FOR RECURRENT BRAIN TUMORS TOO. IT IS AN ANTI-CALMODULIN AFTER ALL!
RESEARCH IS ON AT CRBCM.
Sunday, November 18, 2012
Quantia / Brain tumors and methylated C-MET
Nice presentation on Quantia.
They presented a case of a "disruptive Doctor" who was reported by staff as being "late", "not responsive to call" and "being rude to staff". Pretty much led me to agree with them. But through due process, heard the Dr's response to these accusations, I was able to give him some slack and another chance. Often we rush to condemnation without knowledge of other people's values and perspective. The key to finding the truth is due diligence! The lack of institutional due diligence led to misconstruction and mistakes!
We also attended a talk on Brain tumor, one of the resistant cancers, about importance of finding methylated C-MET as it gives a positive prognosis, responsiveness to treatment, and high pseudo-progression rate on MRI. This all is relevant to our Targeting therapy. An interesting observation to make is that, in cancers that are resistant, the response rate is consistently hovering around 15-30%. This is seen with Avastin in Brain cancers and Ipilimumab in Melanoma. This is pointing to the fact that we still have not reached the main target to apoptosis, or that we need sequential additional hits, or have not closed a loophole! We need to go back to the drawing board!
We also attended a talk on Brain tumor, one of the resistant cancers, about importance of finding methylated C-MET as it gives a positive prognosis, responsiveness to treatment, and high pseudo-progression rate on MRI. This all is relevant to our Targeting therapy. An interesting observation to make is that, in cancers that are resistant, the response rate is consistently hovering around 15-30%. This is seen with Avastin in Brain cancers and Ipilimumab in Melanoma. This is pointing to the fact that we still have not reached the main target to apoptosis, or that we need sequential additional hits, or have not closed a loophole! We need to go back to the drawing board!
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