3rd Law of Nature (continued)
At CRBCM we believe in the cure to cancer.
We believe that the path to cure lies in our ability to harvest natural forces and tendencies in existence in the cell, and turn these to cell death. We call these natural tendencies, laws of nature. If nature wants you to grow, you will grow. If nature wants you to die, you will die. If nature wants you to resist, you will resist. So far we have shown that nature has put in place some mechanisms to control major functions of cell life. If there is a mistake in the genes whether caused or random, nature will stop the cycle of cell life to allow correction (1st law). If however the Nuclear material and supporting scaffolding (the microtubule/microfilament complex) are irreparably compromised, cell destruction through the caspase is pretty much assured ( 2nd law) . The 3rd law (nature prefers what is good for it) leads to differentiation. A cancer cell will make its own growth factors to allow its own growth and to give it unique advantage for growth compared to surrounding cells. HOW DO YOU USE THIS GREEDY BEHAVIOR TO OUR ADVANTAGE? IN JUDO, YOU USE THE FORCE OF THE ATTACKER TO PROJECT HIM IN THE GENERAL DIRECTION OF THE ATTACK. Meaning you could use the machinery put in place by the cancer cell to produce killer proteins. Viruses do that in the host by incorporating their genome in the host. Are we at the stage where we can incorporate non sense mutation, silent mutation, transversion or other silencing frame shifts into the promoter of the unique growth factor to the cancer cell? CAN WE USE VIRUS TO SELECTIVELY INFECT CANCER CELLS AND ELECTIVELY SILENCE PROMOTER GENES OF TGF(S)? We are delving into this now...
4TH LAW: CANCER CELLS COULD BE EFFECTIVELY KILLED BY OUR IMMUNE SYSTEM IF PERCEIVED AS FOREIGN. AND WE KNOW THE ROLE OF TOLL CELL RECEPTORS IN THE INNATE IMMUNITY. WHAT CAN WE DO THERE? We will spend some time here, too...
THESE QUESTIONS WILL BE FURTHER INVESTIGATED IN THE NEXT FEW DAYS.
WE ARE LOOKING IN THE SUPEROXIDE (SOD) AND OTHER INTERVENTIONS TO FIGHT CANCER.
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
Friday, November 30, 2012
The 3rd Law of Nature
The 3rd LAW OF NATURE is still to come:
Harvesting the power of tissue differentiation or silencing as a way to control cancer cells.
Cancer cure is achieved by death of the cancer cell. But remission is just as powerful. Rendering a cancer "innocuous", something you can live with, something our immune system can control, is just as critical an objective. WHEN YOU CAN'T KILL IT, CONTROL IT AS LONG AS POSSIBLE. FRANKLY THE MEDIAN SURVIVAL MAY NOT BE DIFFERENT, ALTHOUGH THE QUALITY OF LIFE MAY BE DIFFERENT...OR NOT! CAN WE TALK THE LANGUAGE OF THE CELL, AND ASK IT TO BE SILENT?!
WE WILL DELVE INTO THIS IN THE COMING DAYS!
Harvesting the power of tissue differentiation or silencing as a way to control cancer cells.
Cancer cure is achieved by death of the cancer cell. But remission is just as powerful. Rendering a cancer "innocuous", something you can live with, something our immune system can control, is just as critical an objective. WHEN YOU CAN'T KILL IT, CONTROL IT AS LONG AS POSSIBLE. FRANKLY THE MEDIAN SURVIVAL MAY NOT BE DIFFERENT, ALTHOUGH THE QUALITY OF LIFE MAY BE DIFFERENT...OR NOT! CAN WE TALK THE LANGUAGE OF THE CELL, AND ASK IT TO BE SILENT?!
WE WILL DELVE INTO THIS IN THE COMING DAYS!
Apoptosomes
Apoptosomes: engines for caspase activation.
Source
The Walter and Eliza Hall Institute of Medical Research, Melbourne, 3050, Victoria, Australia. adams@wehi.edu.auAbstract
"Activation of the caspases that initiate apoptosis typically requires cognate scaffold proteins, including CED-4 in Caenorhabditis elegans, Apaf-1 in mammals and Dark in Drosophila. Each scaffold protein oligomerizes procaspases into a complex called the apoptosome, but the regulation and biological roles of the scaffolds differ. Whereas CED-4 is restrained by the Bcl-2 homologue CED-9, Apaf-1 is inhibited by its WD40 repeat region, until it is activated by cytochrome c, derived from damaged mitochondria. Although Dark also has a WD40 region, its activation does not seem to involve cytochrome c. CED-4 is essential for apoptosis in the worm and Dark for many apoptotic responses in the fly, but the Apaf-1/caspase-9 system probably amplifies rather than initiates the mammalian caspase cascade."(end of abstract)
=====================================================================
This research further confirms the path of the second law driving the forces down the cascade of events
starting with Microfilament/Microtubule disturbance or destruction. The author clearly feels that once the
Apaf-1/Caspase-9 system is initiated, it amplifies its action leading to apoptosis. Mention of the Bcl-2 (or other molecules comparable) is critical because it is the main barrier to full display toward apoptosis. Last point :the Caspases are also a family of enzymes/protein based structure/meaning the potency to achieve Apoptosis varies.
Apaf-1 is Apoptotic Protease-activating Factor-1, a key factor in the cascade to Apoptosis. I should also stress that this factor is more concentrated in liver, spleen, kidney and brain. Tissues where primary tumors are the toughest to treat. Therefore, targeting this enzyme for activation could drive up Apoptotic cascade or cell death.
Of note, people in full inflammatory process with increased TNF have a mitigated result when it comes to Apoptosis because TNF also stimulate NF-kB which has anti-apoptotic trends. Unless it chooses to go down the path of death-domain signaling way (Fas) or stimulate MAPK pathway which is more pro-apoptotic. ARE PEOPLE WITH AUTOIMMUNE DISEASE POOR RESPONDERS TO TAXOL BASED CHEMOTHERAPY BECAUSE OF THIS? SHOULD WE BE TESTING ANA AND LEVEL OF TNF (Tumor Necrosis Factor) TO GAGE RESPONSE TO THERAPY?
Thursday, November 29, 2012
Great minds meet: Italy is connected
Glad to discover that Dr. Stefania Erra in a public hospital in Casale Monferrato, province of Alessandria. Casale Monferrato, Italy is also actively researching how to fight the Triple negative invasive ductal carcinoma of the breast which is, as she points out, "a
particularly aggressive type of cancer with a bleak prognosis, which is
resistant to traditional chemotherapy treatments and which—for the time
being—is unresponsive to current molecular therapies. Additionally, this
neoplasm is predominantly diagnosed in pre-menopausal women."
CRBCM today: Further evidence of 2nd law of nature
Further evidences of 2nd law of nature/CRBCM
If you compromise Cell divison, the cell will need to be destroyed
one thing is for sure. DNA Breakage and mistakes or mismatches lead to cell cycle arrest (First law). What is interesting is that the second law is very much linked to this. Once the repair occurs, a number of peri microtubular reactions need to occur to relieve that arrest and allow continuation of the mitosis. This is the connection to the second law.
Also as we are further looking into this matter, we are finding further evidence that there is an intricate connection between Microtubule and Mitochondria. Even the location of Mitochondria is not random and seems linked to the integrity of the filamentous connection. We are learning about Nuage and Mitochondrial Cement. The further we look, the more we can now ascertain the existence of the 2nd law.
We are also learning, that not all the antikinesin are the same. Some are not as important, affecting peripheral molecules, but some involve the location of the "consensus sequence", and may be more important.
We also are learning that Cyclin ubiquitination and therefore destruction could be exacerbated by perimicrotubular disturbances. Is this the mechanism of bypassing BCL-2 resistance? More light is needed.
We will let you know what we find at CRBCM.
If you compromise Cell divison, the cell will need to be destroyed
one thing is for sure. DNA Breakage and mistakes or mismatches lead to cell cycle arrest (First law). What is interesting is that the second law is very much linked to this. Once the repair occurs, a number of peri microtubular reactions need to occur to relieve that arrest and allow continuation of the mitosis. This is the connection to the second law.
Also as we are further looking into this matter, we are finding further evidence that there is an intricate connection between Microtubule and Mitochondria. Even the location of Mitochondria is not random and seems linked to the integrity of the filamentous connection. We are learning about Nuage and Mitochondrial Cement. The further we look, the more we can now ascertain the existence of the 2nd law.
We are also learning, that not all the antikinesin are the same. Some are not as important, affecting peripheral molecules, but some involve the location of the "consensus sequence", and may be more important.
We also are learning that Cyclin ubiquitination and therefore destruction could be exacerbated by perimicrotubular disturbances. Is this the mechanism of bypassing BCL-2 resistance? More light is needed.
We will let you know what we find at CRBCM.
Wednesday, November 28, 2012
CRBCM is expanding
CRBCM EXPANSION
Volunteers and viewers of our blog intend to start CRBCM activities in Ohio and Indiana.
We are sending plan of activities and various suggestions of implementation. We are holding President Obama's pledge to help these states deal with the economic crisis and create jobs. We will dispatch our plan for expansion to our representatives Amy McCullough (Dayton, OH) and Mariane Alberts & Stephanie Hart (Richmond, IN). My daughter Kyle will organize in Maryland ( I still own a house in Brandywine MD). Her help is appreciated!
Work there will be the creation of Survivorship Centers. We have secured the attention of prominent Senators from both states to help with minority causes. Breast cancer needs to be faced with strength of science and determination from our volunteers.
We believe success is reachable as our Clinic (Greater East Cancer Center) is getting greater footing in El Paso. Slow Progress is best for footing on solid ground. A retiring Oncologist wants to meet to give us a look for progress. Thank you for the call...light is clear at the end of the implementation tunnel.
OF NOTE:
Volunteers and viewers of our blog intend to start CRBCM activities in Ohio and Indiana.
We are sending plan of activities and various suggestions of implementation. We are holding President Obama's pledge to help these states deal with the economic crisis and create jobs. We will dispatch our plan for expansion to our representatives Amy McCullough (Dayton, OH) and Mariane Alberts & Stephanie Hart (Richmond, IN). My daughter Kyle will organize in Maryland ( I still own a house in Brandywine MD). Her help is appreciated!
Work there will be the creation of Survivorship Centers. We have secured the attention of prominent Senators from both states to help with minority causes. Breast cancer needs to be faced with strength of science and determination from our volunteers.
We believe success is reachable as our Clinic (Greater East Cancer Center) is getting greater footing in El Paso. Slow Progress is best for footing on solid ground. A retiring Oncologist wants to meet to give us a look for progress. Thank you for the call...light is clear at the end of the implementation tunnel.
OF NOTE:
1 | Trastuzumab emtansine for HER2-positive advanced breast cancer. |
PARP Inhibitors
PARP
Day 2 went very well in Houston
made it on time
in the meantime received positive news from El Paso
can apply for faculty time in clinic at University Medical Center
will be an honor if it gets through'
willing to cover at another Hospital over coming holidays to broaden my share of patients
while veterans physicians take it easy...will use any opportunity to shine.
Now Back to PARP inhibitor, (Poly ADP Ribose Polymerase), they are powerful drugs which follow our first law, they break DNA or cause failure to repair DNA mistakes. Therefore cause automatic activation of intact P53 to induce automatic cell division Arrest. In other words, they act like Cisplatin and therefore will have a role in Ovarian cancer and by inference, will have a role in basal cell like Breast cancer (or triple negative Breast cancer). Again, their limitation depend on preservation of P53 and all other molecules of that cascade. They will also be limited by how fast the cell makes its repair.
Remember the 2nd law is the break of Microtubules/Microfilaments that leads to direct Caspase release, more powerful law. This implies that a combination of PARP with Taxane (or Ixabepilone or Erubilin)will be the next non platinum combination of significance.
Following this logic, we predict an expanded role to Arsenic trioxyde. But fear of its use resides in its cardiac toxicity. But it acts like a Multikinase inhibitor because it interferes with so many cascades in the signal transduction. Its limitation could also be that it may not lend itself to combination therapy because of "assumed" risk to the host.
Day 2 went very well in Houston
made it on time
in the meantime received positive news from El Paso
can apply for faculty time in clinic at University Medical Center
will be an honor if it gets through'
willing to cover at another Hospital over coming holidays to broaden my share of patients
while veterans physicians take it easy...will use any opportunity to shine.
Now Back to PARP inhibitor, (Poly ADP Ribose Polymerase), they are powerful drugs which follow our first law, they break DNA or cause failure to repair DNA mistakes. Therefore cause automatic activation of intact P53 to induce automatic cell division Arrest. In other words, they act like Cisplatin and therefore will have a role in Ovarian cancer and by inference, will have a role in basal cell like Breast cancer (or triple negative Breast cancer). Again, their limitation depend on preservation of P53 and all other molecules of that cascade. They will also be limited by how fast the cell makes its repair.
Remember the 2nd law is the break of Microtubules/Microfilaments that leads to direct Caspase release, more powerful law. This implies that a combination of PARP with Taxane (or Ixabepilone or Erubilin)will be the next non platinum combination of significance.
Following this logic, we predict an expanded role to Arsenic trioxyde. But fear of its use resides in its cardiac toxicity. But it acts like a Multikinase inhibitor because it interferes with so many cascades in the signal transduction. Its limitation could also be that it may not lend itself to combination therapy because of "assumed" risk to the host.
Monday, November 26, 2012
More Field Work in Houston
I am back in Houston,
ready to embrace its heavy "Rush hour"congestion!
Never seen this much congestion in a town,
too much power concentrated in one City I guess,
somebody got to do the work, spread it around, El Paso can take a little pressure out of this town. Expand there, please! We need to be put to work in El Paso.
Got to go, 8 consults planned and long trips through the "Houston congestion"awaiting!
ready to embrace its heavy "Rush hour"congestion!
Never seen this much congestion in a town,
too much power concentrated in one City I guess,
somebody got to do the work, spread it around, El Paso can take a little pressure out of this town. Expand there, please! We need to be put to work in El Paso.
Got to go, 8 consults planned and long trips through the "Houston congestion"awaiting!
Following-up on the 2nd Law discussed previously
Follow-up on the 2nd law discussed yesterday.
It is not by mistake that the 2 new drugs active in breast cancer, triple negative, target microtubules.
Indeed, both Erubilin and Ixabepilone target Microtubules.
I just took the test on Hope S. Rugo's presentation following the logic, passed the test without problem. So:
SHOULD WE USE CASPASE RELEASE IN LABORATORY AS PROOF OF CHEMOTHERAPY EFFECTIVENESS ON A STANDARD BASE (ROUTINELY), ON FRESHLY OBTAINED TISSUE, THAT IS!
Nature seems to tell us that when there is an error in the gene, we can repair this, but when the Microfilaments are destroyed, Mitosis is compromised and the cells' destiny is to die! This is where the power of Vinorelbine comes from...Vinorelbine-Cisplatin is used as standard therapy for lung cancer, particularly in other parts of the world!
DISCUSSION ON PARP INHIBITOR TO FOLLOW...
It is not by mistake that the 2 new drugs active in breast cancer, triple negative, target microtubules.
Indeed, both Erubilin and Ixabepilone target Microtubules.
I just took the test on Hope S. Rugo's presentation following the logic, passed the test without problem. So:
SHOULD WE USE CASPASE RELEASE IN LABORATORY AS PROOF OF CHEMOTHERAPY EFFECTIVENESS ON A STANDARD BASE (ROUTINELY), ON FRESHLY OBTAINED TISSUE, THAT IS!
Nature seems to tell us that when there is an error in the gene, we can repair this, but when the Microfilaments are destroyed, Mitosis is compromised and the cells' destiny is to die! This is where the power of Vinorelbine comes from...Vinorelbine-Cisplatin is used as standard therapy for lung cancer, particularly in other parts of the world!
DISCUSSION ON PARP INHIBITOR TO FOLLOW...
Sunday, November 25, 2012
SEARCHING FOR A CANCER CURE
At CRBCM we believe that CPRIT is our necessary path to Victory over Cancer.
We also know we will not get its help this time around, not because we do not deserve the help but frankly because it is distracted. Science is an objective thing. It is a race. You have the right move, the right stuff, you win, no matter where you come from. It is the Olympics without steroids.
We at CRBCM have understood one thing, in the race for the cure, harnessing the force and laws of nature has an unparalleled advantage. Forcing a cell to die can be done by telling and convincing it to die. Or blasting it and crossing our fingers and hoping it will die. Chemotherapy did this mostly the second way but its success was partial. Chemotherapy only works when it manages to finally talk the language. Indeed, some chemotherapy manages to reach the syllables of the cellular language of death.
Sorting through the maze of messages, 2 powerful set of syllables come out:
1. That if it fails to repair broken DNA and therefore does not perform GENE REPAIR, this fact will automatically activate your P53 leading to an automatic stop of the cell into its cycle division. There is no loophole to this principle unless the P53 is abnormal. Knowing this is powerful. Now we understand why Cisplatin (and to some extent Gemcitabine) is a powerful drug because it disrupts the DNA structure. We also understand that cells with rapid repair of DNA, will brush it off, literally.
2.with further proof of principle, we believe that there is a second automatic message or syllables.
Destruction of Microfilaments (and therefore secondarily Microtubules in general) during cell division, leads to an automatic release of Caspase from the Mitochondria no matter what (and this is what includes the BCL-2 protection). It is in this law that resides the strength of Taxanes. Medication that works even in resistant diseases such as Melanoma where Abraxane has a role. Taxanes' limitations appear to be in the type of microtubules attacked. Medication that attacks Microfilament of the type involved in cell divison, where the Centromere is attached, appears to send a more determinant trigger to Caspase release. This is where our interest comes in the Anti-kinesin. We believe and predict that an effective anti-kinesin drug in combination with Taxane and Cisplatin/gemzar based combination, will harness best this law. They will prove to be effective in cure because they will be effective in both treatment and maintenance settings. This is also why the combination of Gemzar and Taxol has proven to be the strongest non platinum combination.
Following this principle, we believe now at CRBCM, that target therapy not following the laws of nature will have only 20-30% response rate, meaning effective in only the cells that lack loophole mechanisms. (this also means because of phenotype heterogeneity, 70-85% of cells have potentially intrinsic loophole to any signal transduction target stimulation or blockage).
Lets keep our eyes on the ball, do not invest in stuff they are throwing at you! More to come...
At CRBCM we believe that CPRIT is our necessary path to Victory over Cancer.
We also know we will not get its help this time around, not because we do not deserve the help but frankly because it is distracted. Science is an objective thing. It is a race. You have the right move, the right stuff, you win, no matter where you come from. It is the Olympics without steroids.
We at CRBCM have understood one thing, in the race for the cure, harnessing the force and laws of nature has an unparalleled advantage. Forcing a cell to die can be done by telling and convincing it to die. Or blasting it and crossing our fingers and hoping it will die. Chemotherapy did this mostly the second way but its success was partial. Chemotherapy only works when it manages to finally talk the language. Indeed, some chemotherapy manages to reach the syllables of the cellular language of death.
Sorting through the maze of messages, 2 powerful set of syllables come out:
1. That if it fails to repair broken DNA and therefore does not perform GENE REPAIR, this fact will automatically activate your P53 leading to an automatic stop of the cell into its cycle division. There is no loophole to this principle unless the P53 is abnormal. Knowing this is powerful. Now we understand why Cisplatin (and to some extent Gemcitabine) is a powerful drug because it disrupts the DNA structure. We also understand that cells with rapid repair of DNA, will brush it off, literally.
2.with further proof of principle, we believe that there is a second automatic message or syllables.
Destruction of Microfilaments (and therefore secondarily Microtubules in general) during cell division, leads to an automatic release of Caspase from the Mitochondria no matter what (and this is what includes the BCL-2 protection). It is in this law that resides the strength of Taxanes. Medication that works even in resistant diseases such as Melanoma where Abraxane has a role. Taxanes' limitations appear to be in the type of microtubules attacked. Medication that attacks Microfilament of the type involved in cell divison, where the Centromere is attached, appears to send a more determinant trigger to Caspase release. This is where our interest comes in the Anti-kinesin. We believe and predict that an effective anti-kinesin drug in combination with Taxane and Cisplatin/gemzar based combination, will harness best this law. They will prove to be effective in cure because they will be effective in both treatment and maintenance settings. This is also why the combination of Gemzar and Taxol has proven to be the strongest non platinum combination.
Following this principle, we believe now at CRBCM, that target therapy not following the laws of nature will have only 20-30% response rate, meaning effective in only the cells that lack loophole mechanisms. (this also means because of phenotype heterogeneity, 70-85% of cells have potentially intrinsic loophole to any signal transduction target stimulation or blockage).
Lets keep our eyes on the ball, do not invest in stuff they are throwing at you! More to come...
Labels:
abraxane,
anti-kinesin,
caspase,
cell division,
centromere,
cisplatin,
cprit,
crbcm,
cycle division,
gemcitabine,
gemzar,
gene repair,
microfilaments,
microtubules,
P53,
taxane,
taxol
Googlish misadventures...
Life at CRBCM
Big money did it again,
trying to steal by corrupting search engines,
frankly it is frustrating, and Google has been bought...
This morning I woke up trying to look up Adriamycin on google
I asked for ADRIAMYCIN PACKAGE INSERT,
I got Neulasta, went to the next item on the list, I got Votrien.
I understand that people need to push new medications, but corrupting search engines is not the way.
Now I am upset against Google which must have been paid to allow such a thing
and I am upset against the drug companies which are trying to make it hard for me to use Google as a search engine.
There are in life things you don't do even if you can afford them,
one of them is to assume people are imbeciles and you can just twist their mind
and Big money has a way to try politics where it does not belong.
If you are smart, remember the word BACKFIRE when you are making your plan next time!
If Google goes this way, we need another search engine!
Did not plan to start this way my day!
Big money did it again,
trying to steal by corrupting search engines,
frankly it is frustrating, and Google has been bought...
This morning I woke up trying to look up Adriamycin on google
I asked for ADRIAMYCIN PACKAGE INSERT,
I got Neulasta, went to the next item on the list, I got Votrien.
I understand that people need to push new medications, but corrupting search engines is not the way.
Now I am upset against Google which must have been paid to allow such a thing
and I am upset against the drug companies which are trying to make it hard for me to use Google as a search engine.
There are in life things you don't do even if you can afford them,
one of them is to assume people are imbeciles and you can just twist their mind
and Big money has a way to try politics where it does not belong.
If you are smart, remember the word BACKFIRE when you are making your plan next time!
If Google goes this way, we need another search engine!
Did not plan to start this way my day!
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.
Friday, November 23, 2012
CRBCM /Greater East Cancer Center.
Nice to stay busy with some new patients, thanks to you referring Doctors.
But time to go back to Houston to complete other contractual field work agreements, and gather further resources which will allow us to live another day! When you are a Coalition, expect long fights and anything that allows you to go the distance needs full and careful completion. Some, because of their circumstances, born with Silver Spoon, get an easy ride. Some of us rise slowly and surely when circumstances are right! Some leaders get there easy, some leaders are born because life circumstances place them there...No matter how you get there, making a difference is what counts! But you got to live another day! Something is putting me back in Houston for 1 month, I got to go there and find it or find why!
As promised in my recent Blog, we are still looking into use of Inhibitors of Ion Pumps in membranes to kill cancer cells. We know that in Cholera, a similar disruption kills the host. Cells must also be susceptible. We also spoke of using the opportunity offered by cell cycle check points as a place for intervention. Our work is cut out. We will submit our comments on this while in Houston. In the last word on Lysosome, the proton pump was discussed. PLEASE READ IT, WE WELCOME YOUR COMMENTS!
Nice to stay busy with some new patients, thanks to you referring Doctors.
But time to go back to Houston to complete other contractual field work agreements, and gather further resources which will allow us to live another day! When you are a Coalition, expect long fights and anything that allows you to go the distance needs full and careful completion. Some, because of their circumstances, born with Silver Spoon, get an easy ride. Some of us rise slowly and surely when circumstances are right! Some leaders get there easy, some leaders are born because life circumstances place them there...No matter how you get there, making a difference is what counts! But you got to live another day! Something is putting me back in Houston for 1 month, I got to go there and find it or find why!
As promised in my recent Blog, we are still looking into use of Inhibitors of Ion Pumps in membranes to kill cancer cells. We know that in Cholera, a similar disruption kills the host. Cells must also be susceptible. We also spoke of using the opportunity offered by cell cycle check points as a place for intervention. Our work is cut out. We will submit our comments on this while in Houston. In the last word on Lysosome, the proton pump was discussed. PLEASE READ IT, WE WELCOME YOUR COMMENTS!
Thursday, November 22, 2012
Reflections at the CRBCM
Rubric -Reflections at CRBCM,
Value of the truth...
One of the things I learned quickly in life is NOT TO LIE NO MATTER WHAT.
I grew up at my older brother's house who paid for everything in my life since my father became incapacitated from a stroke. My brother was a lawyer. Lying to him was hard. debunking lies was a profession for him.
"Trying to lie to me is the last crime I can tolerate because it is equivalent to telling me I am an IMBECILE,"
and you did not want to be on the the bad side of that table.
On our recent blog we spoke of how important it is to stay truthful because the sanity of our conscience depends on it. We suggested that because the truth always wins, our life needs to be wrapped in it to stand the test of time. We went on to suggest that because the truth can be slow to surface, we need to stick to it because when it does surface, we could control the outcome of the argument being made.
Critics of our theme did not wait to point to many weaknesses of the "truth". one of the major argument is that the TRUTH CAN BE WRONG. It can easily be non properly used, it can be bent and easily suppressed long enough to become irrelevant. It can be obfuscated to oblivion!
But no matter the cynical argument, no matter the fact that people have gotten away with perjury, just fear the moment when people realize you are a phony. That at the end of the day you deserve what comes to you. That you have been pulling their legs all along. You will feel the pain of a traitor and the ire of those you deceive. You will be watching your back!
Value of the truth...
One of the things I learned quickly in life is NOT TO LIE NO MATTER WHAT.
I grew up at my older brother's house who paid for everything in my life since my father became incapacitated from a stroke. My brother was a lawyer. Lying to him was hard. debunking lies was a profession for him.
"Trying to lie to me is the last crime I can tolerate because it is equivalent to telling me I am an IMBECILE,"
and you did not want to be on the the bad side of that table.
On our recent blog we spoke of how important it is to stay truthful because the sanity of our conscience depends on it. We suggested that because the truth always wins, our life needs to be wrapped in it to stand the test of time. We went on to suggest that because the truth can be slow to surface, we need to stick to it because when it does surface, we could control the outcome of the argument being made.
Critics of our theme did not wait to point to many weaknesses of the "truth". one of the major argument is that the TRUTH CAN BE WRONG. It can easily be non properly used, it can be bent and easily suppressed long enough to become irrelevant. It can be obfuscated to oblivion!
But no matter the cynical argument, no matter the fact that people have gotten away with perjury, just fear the moment when people realize you are a phony. That at the end of the day you deserve what comes to you. That you have been pulling their legs all along. You will feel the pain of a traitor and the ire of those you deceive. You will be watching your back!
Lysosome
Hypothesis for cancer research
In the cell there is a small body covered by a membrane called Lysosome.
This body is full of enzymes capable of causing death to the cell should the enzyme (Acid hydrolase) get released in the intracellular solution. Acid Hydrolase and related enzymes are powerfully destructive but they only act in a very acid environment. When they come out mistakenly, the neutral state of the Cytosol (intracellular solution where all the organelles of the cell are floating) paralyzes these enzymes. The reason why the inside of the lysosome can stay very Acid to allow the function of these enzymes is linked to the existence in the lysosomal membranes of proton pumps forcing hydrogen ions into the lysosome. Scientists are looking at paralyzing these proton pumps in cancer cells in order to disturb selectively lysosomal function of targeted cancer cells. Just changing the Ph of the cell to a more Acidic environment could kill the cell by affecting the many metabolic reactions that only occur effectively at neutral Ph.
Also in this structure (lysosome) there are other targets such the mannose Monophosphate receptors which, if successfully paralyzed, could also induce various lysosomal disturbances. Weakening cancer cells could cure one from cancer. The struggle continues.
In the cell there is a small body covered by a membrane called Lysosome.
This body is full of enzymes capable of causing death to the cell should the enzyme (Acid hydrolase) get released in the intracellular solution. Acid Hydrolase and related enzymes are powerfully destructive but they only act in a very acid environment. When they come out mistakenly, the neutral state of the Cytosol (intracellular solution where all the organelles of the cell are floating) paralyzes these enzymes. The reason why the inside of the lysosome can stay very Acid to allow the function of these enzymes is linked to the existence in the lysosomal membranes of proton pumps forcing hydrogen ions into the lysosome. Scientists are looking at paralyzing these proton pumps in cancer cells in order to disturb selectively lysosomal function of targeted cancer cells. Just changing the Ph of the cell to a more Acidic environment could kill the cell by affecting the many metabolic reactions that only occur effectively at neutral Ph.
Also in this structure (lysosome) there are other targets such the mannose Monophosphate receptors which, if successfully paralyzed, could also induce various lysosomal disturbances. Weakening cancer cells could cure one from cancer. The struggle continues.
Wednesday, November 21, 2012
Cancer Survivorship Program for El Paso
CRBCM met tonight with CIMA Hospice Administrator Michele Diaz Aboud,
discussed referral to Hospice but also looked at how some Hospice services could be integrated
in an overall Survivorship program. We also discussed the level of government reimbursement by Medicare (and in some cases Medicaid). We will be working with their support on future grant applications. We concluded by discussing some of the ideas about improvement in Navigation of patient diagnosed with Cancer, and policy recommendations. In attendance was Cynthia McWilliams of the same organization. Great meeting!
discussed referral to Hospice but also looked at how some Hospice services could be integrated
in an overall Survivorship program. We also discussed the level of government reimbursement by Medicare (and in some cases Medicaid). We will be working with their support on future grant applications. We concluded by discussing some of the ideas about improvement in Navigation of patient diagnosed with Cancer, and policy recommendations. In attendance was Cynthia McWilliams of the same organization. Great meeting!
Tuesday, November 20, 2012
Veterans of El Paso
Meeting Today with Chaplain Lovett of the VA in EL Paso. The Chaplain has been in the Navy, and is currently in charge of the Home visits for Veterans in EL Paso. We discuss strategies and opportunities in approaching veterans with a Health intervention. We will have further contacts to sharpen our Messages.
The Meeting occurred at the CRBCM office this morning. We are an official provider of care for the VA. Our office has engaged the VA office in El Paso for direct care to our veterans. We have advertized aggressively in VA journal and newspaper, results are now showing slowly with interest by the VA staff. The CRBCM and the Greater East Cancer Center will continue to push for further integration in the VA programs.
The Meeting occurred at the CRBCM office this morning. We are an official provider of care for the VA. Our office has engaged the VA office in El Paso for direct care to our veterans. We have advertized aggressively in VA journal and newspaper, results are now showing slowly with interest by the VA staff. The CRBCM and the Greater East Cancer Center will continue to push for further integration in the VA programs.
CRBCM Audience as of Nov.20th, 2012
Country/Pageviews as of Nov 20,2012
United States: 1870,
Russia: 36,
United Kingdom: 21,
Sweden: 20,
Germany: 15,
France: 13,
Latvia: 10,
Ukraine: 9,
India: 4,
China: 3
Over 2000 hits, the truth is in the pudding!
we will not deceive our readers.
Will tell the truth in our position and path to progress.
We know we can't be right all the time, but we will say where we are, what our understanding is, and where we are going. Thank you to our reviewers!
United States: 1870,
Russia: 36,
United Kingdom: 21,
Sweden: 20,
Germany: 15,
France: 13,
Latvia: 10,
Ukraine: 9,
India: 4,
China: 3
Over 2000 hits, the truth is in the pudding!
we will not deceive our readers.
Will tell the truth in our position and path to progress.
We know we can't be right all the time, but we will say where we are, what our understanding is, and where we are going. Thank you to our reviewers!
Music & Well-being, a fruitful combination!
Activities at CRBCM
The CRBCM has invested heavily in Music equipment for Health Promotion songs to energize the mass into participating in health education programs. We had a 3 hours working session with J. Jarret, a member of the powerful Zion Baptist church of El Paso. Through Music, we intend to reach the youth and promote health in a vehicle sensitive to the Hispanic culture and community.
Through Music, we want to send empowering health messages, energize the people to embrace health issues and recommendations, convey a way to join the action. Guitarist John Bashengezi is ready to add the last touch, an overwhelming Spanish guitar sound to conclude your excitement. Working for the masses asks us to use media loved by the locals, and Music, the world language, is ripe and right for this mission!
For Samples, go to "ubetoo.com/clementalbert" and we will be posting sample songs recorded with Jackie Jarret soon!
(This Music Activity is part of a comprehensive Health plan submitted for possible funding to organizations such as CPRIT, NIH, NCI and local chapters of the NCS and the Susan G Komen)
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!
Managing the loopholes in the cell cycle
Cure to cancer is within reach and is within the management of LOOPHOLES.
Cancer cells have within their pathways, redundancy that protects these pathways to maintain life of the malignant cell. You close one door, just to see another one open up to ensure that the life of the cancer cell is maintained. So, unless you hit a critical pathway with no escape routes, the treatment result will be partial and temporary. To succeed we need to hit several targets in total and and sometimes sequentially to impose on the cell to choose the path to its natural death (apoptosis). So most treatments which are limited to one or only a few targets prove partially and temporary effective.
This is why building an electronic Cell and being able to put in all the pathways and observe where they lead to, what doors open and which ones are closed or closing, which are critical and which lead to apoptosis (natural cell death) is crucial. Which sequence of shut down leads to sure cell death?
Right now we are at the step where we are learning about shutting or opening one door and evaluating the sequence of events that follow. But with our model in hand, we can be more comprehensive in our approach. The model will help determine effects on cancer cells by shutting several doors at once, "closing Loopholes" as Tax people would love to say.
This approach with target therapy has led to breaking resistance to certain types of cancers that were notoriously resistant. Today, we are starting to have response rates in Melanoma. We have double or triple longevity in Chronic Myeloid Leukemia, GIST, Myeloma etc...Just wait to see what we will get once we manage to give Multistage Multitarget Therapies (MMT). Cure is within the management of Loopholes!
Saturday, November 17, 2012
The CRBCM has completed a 3 week field work
for its client. Successful completion of this work has earned the CRBCM further work in Houston. Texas. We will be back here in Houston November 26th, 2012. In the meantime, This coming week, we will continue clinic work in El Paso as Greater East Cancer Center continue to increase slowly its share of patients. This is hard work to ensure we survive the struggle and fight another day!
News from Washington is positive. We just may make it with a new contract in January.
We will continue to update our reader with new proposal for research as we study new opportunities offered by weakness in the Sodium-Potassion Ion pump in cancer cells and cell division check points (details to follow).
Get to catch that flight to El Paso!
Friday, November 16, 2012
Targeting Triple-Negative Breast Cancer Cells With the Histone Deacetylase Inhibitor Panobinostat
Targeting Triple-Negative Breast Cancer Cells With the Histone Deacetylase Inhibitor Panobinostat
Chandra R Tate, Lyndsay V Rhodes, H Chris Segar, Jennifer L Driver, F Nell Pounder Matthew E Burow, Bridgette M Collins-Burow
Jul 27, 2012 Authors & Disclosures
Breast Cancer Res. 2012;14(3):R79 © 2012 BioMed Central, Ltd.
This article catches the Attention of the CRBCM. Thank you Medscape Alert!
Wednesday, November 14, 2012
CLINICAL RESEARCH AND COMMERCIALIZATION FOR OUR CPRIT SUBMISSION.
Our suggestion of a CPRIT submission formulated on Oct 14th (see our posts) has excited our readers
we felt compelled to dig deeper in this story. We basically suggested that in Prostate Cancer, the incidence was much higher as opposed to a relative low mortality. We went on to say that this paradox begs scientists to find ways of discriminating which Prostate Cancer should be considered dangerous for our patient to compel us to aggressively treat the patient. We suggested that a cancer that is spreading needs to be treated because only metastasis ( spread of the cancer) can kill the patient. How to tell which cancer will spread? We submitted that cancer cells before they spread, needed to lose their attachments to other cells by decreasing their Membrane Adhesion Molecules. One of the Adhesion Molecule of interest was E-Cadherin. We therefore suggested that in all cancers of the prostate, dosing the amount of Adhesion molecule was a way to predict its potential for spreading. If we make it simple to quantify E-Cadherin, a kit can be commercialized to determine quickly the spread of disease. We also suggested that cancer cells to penetrate tissues and leading to organ failure and killing the host, must create its road through cellular tissues. It needs to secrete enzymes called Metalloproteases (2,9) to break through. We suggested that a high level of these Metalloproteases in the biopsy tissue could predict a moving cancer. A Kit to detect Metalloproteases could be commercialized to help Doctors take medical decisions for the benefit of patients. All this, if proven in our intended research could advance medical practice.
There is further discussion to have about this:
1. Could Blocking Metalloprotease gene stop the spread of disease?
2. Could restoring E-Cadherin level or function stop the spread of disease?
Scientist from California believe that activating P120 could restore E-Cadherin function efficiently enough to restore or correct deficiency of E-cadherin function. Should we use this approach to slow down cancer.
The story of E-Cadherin is just beginning. We know that cancer in fact spread very early. In small cell lung cancers, Doctors perform a bone marrow biopsy to see that even in early stage, the cancer has already invaded away from the lung. This is true also in Breast cancer where even in stage I (the first stage of Breast cancer) the Bone marrow could already be invaded. The meaning of this distant invasion has been interpreted with controversy. But even in these cases, it portend a bad prognosis. Worse prognosis then that of patient with negative Bone Marrow finding. DOES E-CADHERIN REDUCTION CORRELATES WITH POSITIVE INVASION OF THE BONE MARROW? COULD WE SPARE PATIENTS A BONE MARROW PROCEDURE IF THE E-CADHERIN IS LOW. These are some of the question that have a bearing on clinical matter and would impact today practice as we move forward.
The level of E-Cadherin has broad implications. In Colon cancers, particularly in the Familial Adenomatous Polyposis (FAP), The E-cadherin level could predict not only evolution to cancer state of the Polyposis but also and again predict metastasis. He even beg to suggest that it could have prognosis implication. The decrease of E-cadherin has profound consequence on the amount the Beta-catenin that E-cadherin can not longer "sequester". Whether this will lead to increase the Cyclin D level down the line could be assumed and therefore sustain life of cancer cell. It is also worth mentioning that in the sequence of gene Mutation leading to Colorectal cancer, the loss of 5q (ADENOMA PHASE)which seems to correspond to the phase where Beta- Catenin is important is the earliest stage in the sequence of transformation. This fact correspond to the "good Prognosis" of these cancer....COULD E-CADHERIN REDUCTION BE AN EARLY SIGN OF COLORECTAL CANCER METASTASIS? OR SHOULD THIS MODEL BE CHALLENGED?
Assuming we find a Molecule A which, when it is incorporated by the cell, it opens up and adopt a conformational change increasing phosphorylation of Beta-Catenin leading it to proteasomic destruction, could that decrease Cyclin D formation and induce Apoptosis? What would be the impact if that incorporation was selective to cancer cells? These are the challenges we face!
Through genetic intervention, could we restore the wnt-signalling pathways to prevent FAP and prevent removal of the Colon in FAP? Remember this, 80-85% of sporadic colorectal cancers have disturbance in the wnt pathways, what we are talking about could impact the majority of Colorectal cncers (second leading cause of cancer death in the United States)
Does the wide spread use of Calcium based product for Osteoporosis prevention correspond to decrease of Colorectal cancer in the terminal colon. Calcium is critical in the function of membrane receptors.
The cure is achievable, let get it!
Our suggestion of a CPRIT submission formulated on Oct 14th (see our posts) has excited our readers
we felt compelled to dig deeper in this story. We basically suggested that in Prostate Cancer, the incidence was much higher as opposed to a relative low mortality. We went on to say that this paradox begs scientists to find ways of discriminating which Prostate Cancer should be considered dangerous for our patient to compel us to aggressively treat the patient. We suggested that a cancer that is spreading needs to be treated because only metastasis ( spread of the cancer) can kill the patient. How to tell which cancer will spread? We submitted that cancer cells before they spread, needed to lose their attachments to other cells by decreasing their Membrane Adhesion Molecules. One of the Adhesion Molecule of interest was E-Cadherin. We therefore suggested that in all cancers of the prostate, dosing the amount of Adhesion molecule was a way to predict its potential for spreading. If we make it simple to quantify E-Cadherin, a kit can be commercialized to determine quickly the spread of disease. We also suggested that cancer cells to penetrate tissues and leading to organ failure and killing the host, must create its road through cellular tissues. It needs to secrete enzymes called Metalloproteases (2,9) to break through. We suggested that a high level of these Metalloproteases in the biopsy tissue could predict a moving cancer. A Kit to detect Metalloproteases could be commercialized to help Doctors take medical decisions for the benefit of patients. All this, if proven in our intended research could advance medical practice.
There is further discussion to have about this:
1. Could Blocking Metalloprotease gene stop the spread of disease?
2. Could restoring E-Cadherin level or function stop the spread of disease?
Scientist from California believe that activating P120 could restore E-Cadherin function efficiently enough to restore or correct deficiency of E-cadherin function. Should we use this approach to slow down cancer.
The story of E-Cadherin is just beginning. We know that cancer in fact spread very early. In small cell lung cancers, Doctors perform a bone marrow biopsy to see that even in early stage, the cancer has already invaded away from the lung. This is true also in Breast cancer where even in stage I (the first stage of Breast cancer) the Bone marrow could already be invaded. The meaning of this distant invasion has been interpreted with controversy. But even in these cases, it portend a bad prognosis. Worse prognosis then that of patient with negative Bone Marrow finding. DOES E-CADHERIN REDUCTION CORRELATES WITH POSITIVE INVASION OF THE BONE MARROW? COULD WE SPARE PATIENTS A BONE MARROW PROCEDURE IF THE E-CADHERIN IS LOW. These are some of the question that have a bearing on clinical matter and would impact today practice as we move forward.
The level of E-Cadherin has broad implications. In Colon cancers, particularly in the Familial Adenomatous Polyposis (FAP), The E-cadherin level could predict not only evolution to cancer state of the Polyposis but also and again predict metastasis. He even beg to suggest that it could have prognosis implication. The decrease of E-cadherin has profound consequence on the amount the Beta-catenin that E-cadherin can not longer "sequester". Whether this will lead to increase the Cyclin D level down the line could be assumed and therefore sustain life of cancer cell. It is also worth mentioning that in the sequence of gene Mutation leading to Colorectal cancer, the loss of 5q (ADENOMA PHASE)which seems to correspond to the phase where Beta- Catenin is important is the earliest stage in the sequence of transformation. This fact correspond to the "good Prognosis" of these cancer....COULD E-CADHERIN REDUCTION BE AN EARLY SIGN OF COLORECTAL CANCER METASTASIS? OR SHOULD THIS MODEL BE CHALLENGED?
Assuming we find a Molecule A which, when it is incorporated by the cell, it opens up and adopt a conformational change increasing phosphorylation of Beta-Catenin leading it to proteasomic destruction, could that decrease Cyclin D formation and induce Apoptosis? What would be the impact if that incorporation was selective to cancer cells? These are the challenges we face!
Through genetic intervention, could we restore the wnt-signalling pathways to prevent FAP and prevent removal of the Colon in FAP? Remember this, 80-85% of sporadic colorectal cancers have disturbance in the wnt pathways, what we are talking about could impact the majority of Colorectal cncers (second leading cause of cancer death in the United States)
Does the wide spread use of Calcium based product for Osteoporosis prevention correspond to decrease of Colorectal cancer in the terminal colon. Calcium is critical in the function of membrane receptors.
The cure is achievable, let get it!
CPRIT Leadership gives answers ...
CPRIT leadership is responding to the Houston Chronicle’s criticism in the Editorial of Nov.1st, 2012. We appreciate their answer and do support the
current leadership. We will also wait to
see how they will meet the need to address minority disparities. We support the leadership position and wait
to see what will result from their efforts to reorganize.
-----------------------I appreciate the Houston Chronicle's affirmation in its Nov. 1 editorial of the Cancer Prevention and Research Institute of Texas' core mission and goals, and the need to continue improving the agency's administration and effectiveness ("Fighting for life; Our state's anti-cancer agency needs aggressive treatment: Its leaders should resign," Page B8). As executive director of CPRIT, I have a solemn responsibility to uphold the original statute by ensuring taxpayer money is being used only for research, development and prevention projects that will have the strongest impact on defeating cancer.
The Chronicle makes a sound case for a deliberative process and for avoiding any precipitous actions that would defeat CPRIT's mission. At the same time, the newspaper calls for an immediate resignation and across-the-board replacement of CPRIT's leadership. Such an "off-with-their-heads" approach cuts against and undermines the notion of careful consideration and deliberation. As the editorial says, the subject matter is too important for political solutions.
Part of the mandate to CPRIT, in the constitutional amendment approved by an overwhelming majority of voters five years ago, is to fund research and development (R&D) of groundbreaking discoveries in cancer drugs, devices and diagnostics. The amendment specifically calls on CPRIT "to develop therapies, protocols, medical pharmaceuticals or procedures for the cure or substantial mitigation of all types of cancer." That language directly translates into activities that are carried out in the commercial arena.
While research is vitally important in making the discoveries, developing those discoveries for use by cancer patients is equally important if not more so. Without the "D" in "R&D," many amazing scientific discoveries will sit in a laboratory. That does not help cancer patients.
The disagreement that has fueled the Chronicle's coverage is one between basic science labs, well funded by the National Institute of Health and the National Cancer Institute, and activities that are focused on treating patients - such as clinical trials and drug development. Tension of this type is healthy and this is exactly where Texas stands to make a difference - getting lifesaving treatments to cancer patients faster, cheaper and more effectively. I am especially concerned when a former CPRIT basic science peer review chair refers to the process of developing discoveries to make them available to cancer patients as "hucksterism." This type of thinking and lack of vision is perhaps one of the reasons why it is so difficult to get new cancer drugs into practice. CPRIT's mission isn't just to foot the bills for research, but to push that research out of the labs and into clinical trials and into the hands of doctors and patients as safely and quickly as possible.
I was surprised that the editorial questioned my request that four company applications, currently under peer review, undergo additional scrutiny by our scientific reviewers - especially without calling the institute for reaction. Rather than "a major intrusion into scientific review," it is my responsibility to ensure that taxpayer dollars are invested wisely. New information on all four companies was received after the scientific reviewers had given their scores. The request for re-evaluation was to make sure that all the reviewers, science and commercial, had access to the same information to evaluate the projects fairly. That's the least that companies, many with lifesaving projects, can expect - a fair process.
The vetting of commercial projects is different than that of scientific projects. Scientific reviewers many times are not familiar with this type of back-and-forth review because of differences in the culture of academic peer review and business investment. Academic reviewers are used to proposals structured like NIH grant proposals, in which all data are disclosed up front, rather than as a due diligence process geared toward investment. All four of these companies are still undergoing the peer review process.
The public appointees that make up CPRIT's Oversight Committee volunteer enormous amounts of their time. Many have been touched by cancer first hand. They are all committed to public service and receive no personal gain for their work. Any attempt to attribute other motives to Oversight Committee members is completely unfounded. Charles Tate is appointed by the board as the chairman of the Economic Development and Commercialization Subcommittee. Tate, one of the longest serving board members and previously inaccurately identified as a venture capitalist by the Chronicle, is tireless and selfless in the fight against cancer. That same altruistic motivation holds true for Jimmy Mansour, chairman of the Oversight Committee. Mansour was instrumental in the establishment of the institute and is driven by a sincere passion to serve, as are all of the members.
It is important that these citizen Oversight Committee members represent the people of Texas. We are investing billions of dollars and the self interests of a science-oriented board would invite conflict. The temptation would be too great to substitute its judgment for that of the peer reviewers. The Legislature was very careful in writing this legislation. It ensures that the science and business value of grants are reviewed and recommended by experts in the field of cancer. The Oversight Committee is required to accept those recommendations or overturn them with a supermajority vote. To date, every grant recommended by the peer reviewers and brought before the Oversight Committee has been funded.
The editorial goes on to state that "(Albert) Gilman resigned over the rushed approval (since revoked) of an $18 million 'commercialization' grant … " Again this is not accurate. Gilman's own resignation letter of May 8 to me states: "The purpose of this letter is to indicate my intention to resign from CPRIT, effective (with your permission) on October 12, 2012. At that time I will have worked for CPRIT for over three years - I believe longer than originally anticipated." CPRIT employees have always committed themselves to the cause of curing cancer. All left other jobs to come to the institute because of their hearts. Many are cancer survivors themselves. They realize what one drug, one device or one diagnostic can do. They know the importance of getting these products into practice. And most importantly, they know that each dollar CPRIT invests, and each minute of CPRIT's 10 years we expend, means lives saved. Everyone associated with CPRIT strives daily to do the right thing.
I am honored to work with both the Oversight Committee and the staff at CPRIT. They give their blood, sweat and tears to a mission of hope for millions of Texans. We all serve with passion. I've seen that passion before, serving for many years at the Centers for Disease Control and Prevention (CDC), most recently as the agency's chief operating officer. I also spent time in Iraq in early 2008, a duty for which I volunteered, leading a team to improve health and prevent cholera in the province that includes the city of Tikrit - all in the pursuit of having a positive impact on people's lives.
The teams I have had the privilege to lead, both in this country and in Iraq, truly fall into the category of heroes. The Oversight Committee, employees of CPRIT, cancer patients, cancer survivors and their families are the true heroes in this story.
Because I take this responsibility and recent criticisms of the institute very seriously, my top priority has been to address the concerns and continue to move CPRIT forward. I look forward to working with the CPRIT Oversight Committee, state leaders, the Legislature, academic and nonacademic institutions and the private medical community to consider and reach consensus on the best course to maximize the effectiveness of CPRIT.
Gimson is executive director of the Cancer Prevention and Research Institute of Texas.
Tuesday, November 13, 2012
Reflections at CRBCM
Reflections at CRBCM.
Life has a way to complicate things
and people who dwell in politics do not know when to stop.
Science is strong when it is full of objectivity,
let the people who know how to do things, work free of politics.
It does not matter how big you are, if you are always wrong, you will become irrelevant to history,
will be brushed aside because the world will realize who you really are...
let people with the vision lead the way because human adventure will have to sustain itself through unwelcome noise and unfriendly misadventure. The vision remains the best protector of the adventure and of the place where the adventure tries to reach. Don't get distracted, if a door is closed, keep looking for one that will open. For as long as there is hope, the vision is possible. Just find a way to survive a little longer, until your door opens, until the opposition comes to its senses, until your voice is heard, until the critics realize you are not going away, until their bet fails, until they become irrelevant to the race. Because it will happen without failing. The truth always wins over falsification. Politicians always get entangled in their own games. Unless they speak the truth, they will keep on cheating until they unravel. Give them time to realize it! If you conspire behind closed door, believe me, over time, those with you could one day change allegiance given shifting conditions of life, and whatever perfidy will come to light. You will lose control of the consequences and outcome. History did not bring you to your position to fail, win by acting on your conscience and do things to improve the human condition, not reign by division and creating enemies. I am saddened to meet people who proclaim as true the lies they have been fed, spreading division and blunt racism. Racism is the resort of those with no argument and intrinsic value. There is no wrong in being proud of yourself as long as you do not impose those values on people who cannot see your positions and change to satisfy you. Imposing an unfair burden on others is never right. Level the field and give to a chance to all. That is the American way!
Life has a way to complicate things
and people who dwell in politics do not know when to stop.
Science is strong when it is full of objectivity,
let the people who know how to do things, work free of politics.
It does not matter how big you are, if you are always wrong, you will become irrelevant to history,
will be brushed aside because the world will realize who you really are...
let people with the vision lead the way because human adventure will have to sustain itself through unwelcome noise and unfriendly misadventure. The vision remains the best protector of the adventure and of the place where the adventure tries to reach. Don't get distracted, if a door is closed, keep looking for one that will open. For as long as there is hope, the vision is possible. Just find a way to survive a little longer, until your door opens, until the opposition comes to its senses, until your voice is heard, until the critics realize you are not going away, until their bet fails, until they become irrelevant to the race. Because it will happen without failing. The truth always wins over falsification. Politicians always get entangled in their own games. Unless they speak the truth, they will keep on cheating until they unravel. Give them time to realize it! If you conspire behind closed door, believe me, over time, those with you could one day change allegiance given shifting conditions of life, and whatever perfidy will come to light. You will lose control of the consequences and outcome. History did not bring you to your position to fail, win by acting on your conscience and do things to improve the human condition, not reign by division and creating enemies. I am saddened to meet people who proclaim as true the lies they have been fed, spreading division and blunt racism. Racism is the resort of those with no argument and intrinsic value. There is no wrong in being proud of yourself as long as you do not impose those values on people who cannot see your positions and change to satisfy you. Imposing an unfair burden on others is never right. Level the field and give to a chance to all. That is the American way!
Volunteers keep knocking at our door...
It is encouraging to see the number of men and women passionate about their involvement in medicine and public health. Together, we can fight disease and prompt our patients into action to achieve a healthier lifestyle .
More HYPOTHESIS FOR CANCER RESEARCH
Given what we know now, could intermittent use of Cipro and laxative (5 days every 6-8weeks) be the most effective prevention against Colorectal cancer? The CRBCM is reviewing data to make this assumption. There is sufficient scientific data to suggest this is true and a larger clinical trial is warranted to assess this hypothesis.
Through the work of others, we now know that Ciprofloxacin has anti-topoisomerase activity. That is comparable in its mechanism to some powerful chemotherapy drug. But compared to chemotherapy drugs, it has been used for longer periods safely. It is not innocuous, nothing is, however, it has been used broadly and side effects denounced to date may all be reversible. The major concern of such broad use of an antibiotic will be potential hematologic toxicity and bacterial resistance. This is to be balanced against prevention of a deadly disease (colorectal cancer). Intermittent use could address some of these concerns.
Development of other safer mild anti-topoisomerase could result to avoid CIPRO use, and preserve it in our Antibiotic armamentarium.
It is now known that certain bacteria produce chemical molecules such as nitrates that affect the colonic epithelium. And that the progression to Colon cancer is an evolutionary process, possibly this evolution to cancer cells is driven by chronic continuous irritation. Cleaning intermittently the colon has been assumed to be good as it provides an interruption in these irritations. It would make sense if the laxative follows the Cipro.
ADDING AN ANTI-PROSTAGLANDIN MAY HAVE ADDITIONAL EFFECT.
Given the fact that this may be controversial, it would make sense to have a broader discussion before implementing this idea. Tell me what you think!
Monday, November 12, 2012
Reflections at the CRBCM
Doing the right thing no matter what because you have a conscience to live with, and because the joy of winning through politics are generally short lived, the truth will catch up with you soon enough. You will have to cave in. Acting in the wrong direction because you can, you will have a day of reckoning because you will not know when to stop. You will cross the line one day and get burned. When you win because you can is not enough, you will continue to believe the wrong is right until you hit the wall, and you will end up backtracking and have to apologize or disappear in disgrace. If your aim is to profiteer no matter what, do realize that if you choose a cynical way of winning, you lose control of the nature of the outcome and its consequences. That is when the truth will come to claim its place, you may end up in a harder place than when you first started gambling. Remember real life is not to be lived like a poker game where you have to win no matter what, life is to be lived with as much closeness to the truth as possible because you have a conscience, and because we all have to account soon or later!
Sunday, November 11, 2012
Looking into the role of Ciprofloxacin in cancer cell apoptosis
Colorectal cancer (CRC) is the second most commonly diagnosed cancer and
the second leading cause of cancer mortality in the United States among
cancers that affect both men and women.
Screening lowers colorectal cancer (CRC) incidence and mortality. CRC is preventable through the removal of premalignant polyps and is curable if diagnosed early. Increased CRC screening and reduced CRC incidence and mortality are among the Healthy People 2020 objectives.
What if CRC could be prevented, at least to a certain degree?
Here an interesting finding that will need further research and require validation in the endeavor to prevent cancer, CRC being a priority target:
Pulm Pharmacol Ther. 2010 Oct;23(5):373-5. Epub 2010 Mar 6.
"Ciprofloxacin can significantly affect eukaryotic cells including human cancer cells. Its bactericidal action relay on inhibition of topoisomerase II, enzyme responsible for alterations in 3D structure of DNA during replication, transcription and chromatin condensation. Thanks to that, ciprofloxacin can induce cell cycle arrest and apoptosis of cancer cells."
The stakes are high. Lives can be saved. The cost to society for premature death from CRC are too high - we need to become even more proactive than with screening alone.
The medical and societal costs of CRC are substantial. Estimated direct medical costs for CRC care in 2010 were $14 billion, with projected costs of up to $20 billion by 2020 (13). In 2006, estimated lost productivity costs for persons who died from CRC were $15.3 billion (14). This equals $288,468 of lost productivity per CRC death in 2006 (14). Screening costs per person vary by test. The lifetime (age 50--80 years) average per person cost of screening ranges from $71 per person for guaiac-based FOBT to $1,397 per person for colonoscopy (15).
Screening lowers colorectal cancer (CRC) incidence and mortality. CRC is preventable through the removal of premalignant polyps and is curable if diagnosed early. Increased CRC screening and reduced CRC incidence and mortality are among the Healthy People 2020 objectives.
What if CRC could be prevented, at least to a certain degree?
Here an interesting finding that will need further research and require validation in the endeavor to prevent cancer, CRC being a priority target:
Pulm Pharmacol Ther. 2010 Oct;23(5):373-5. Epub 2010 Mar 6.
"Ciprofloxacin can significantly affect eukaryotic cells including human cancer cells. Its bactericidal action relay on inhibition of topoisomerase II, enzyme responsible for alterations in 3D structure of DNA during replication, transcription and chromatin condensation. Thanks to that, ciprofloxacin can induce cell cycle arrest and apoptosis of cancer cells."
The stakes are high. Lives can be saved. The cost to society for premature death from CRC are too high - we need to become even more proactive than with screening alone.
The medical and societal costs of CRC are substantial. Estimated direct medical costs for CRC care in 2010 were $14 billion, with projected costs of up to $20 billion by 2020 (13). In 2006, estimated lost productivity costs for persons who died from CRC were $15.3 billion (14). This equals $288,468 of lost productivity per CRC death in 2006 (14). Screening costs per person vary by test. The lifetime (age 50--80 years) average per person cost of screening ranges from $71 per person for guaiac-based FOBT to $1,397 per person for colonoscopy (15).
Comprehensive Health Intervention Program to Reverse Breast Cancer Mortality in El Paso, TX
We started the application process for a 3-year CPRIT Company Formation Award for our "Comprehensive Health Intervention Program to Reverse Breast Cancer Mortality in El Paso, TX":
CP130064, Application Abstract
This
Comprehensive Health Intervention Program to Reverse Breast Cancer Mortality
fills the need for a global breast cancer research, prevention,treatment and
survivorship program for the underserved and underinsured Hispanic and
African-American population on the greater Eastside of the city and county of
El Paso.Primary goal is the reversal of breast cancer mortality.However,other
health issues are expected to be discovered, we anticipate to find Diabetes
Mellitus II, High blood pressure, Anemia, Obesity, Metabolic Syndrome and cancers
of other sites than the Breast. Patients will be referred to nearest available
care for those conditions and invited to join our cancer prevention program for
free. Monitoring of their weight,education about healthy diet, physical activity
and the benefit of screening will be offered to them. Laboratory research
collaboration with Dr.Kirken, chair of the Dept of Biology, UTEP, to understand
the specificity of the basal cell type breast cancer (a more aggressive cancer
seen in minority populations), six molecular targets and the role of e-Cadherine
and Metalloproteases.Mobile applications as developed by CPRIT grantee will
help monitor patients' efforts and send critical updates on prevention,
treatment schedule, track and encourage their healthy lifestyle efforts such as
weight control, healthy diet and regular physical activity.The Survivorship
Center will offer all standard medical services and a welcoming environment for
patients in treatment.
CP130064, Executive Summary
The
Coalition for the Reversal of Breast Cancer Mortality in African American Women
is a Coalition 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.
The
CRBCM’s reason for existence is to combat the famous “Breast Cancer Mortality
Paradox” that has been known to exist for years. The paradox states that the
incidence of Breast Cancer in minority populations (African American and
Hispanic populations) is lower when compared with that in White women. However,
their mortality rate is 40% to 70% higher than in White women.
This
projects includes the Provision of Services to Patients and the Creation of
Infrastructure for a Permanent and Comprehensive Cancer Center on the East side
of El Paso to serve this population now and in the future in its needs for the
best cancer treatments, most cost efficient medical and psycho-social care in a
culturally appropriate setting where patients feel welcome and cared about like
members of a large family to which they will stay linked as survivors in order
to maintain the benefits of lifestyle changes including weight management,
healthy diet, physical activity and regular follow-ups and screenings in their
cancer care.
This
project is unique as it to feed latest research findings as quickly as possible
into research intervention programs in order to benefit patients in an easily
accessible and understandable grassroots approach. The long-term benefits of a
healthy lifestyle and education to raise awareness of risk factors together
with a clear understanding of the benefits of appropriate screening routines
will, hopefully, allow to improve the overall health of the El Paso population.
The
cost/fee per patient care model is a dynamic one where all stakeholders push
for efficiency and appropriateness of interventions and avoid wastage of
precious resources wherever possible.
The
use of mobile technology to communicate with the patient community in an active
and regular way seems to be the future of an efficient and beneficial health
care model. These technologies can also easily be tailored to language and
socio-cultural specific sets of population and therefore increase the positive
impact on public health of all these educational and improved healthy lifestyle
behavior efforts.
CP130064 / Coalition for the Reversal of Breast Cancer
Mortality in African American Women
Texas, CPRIT and and the Governor, enough with ignoring EL PASO.
Women from El Paso have to starve themselves in front of the White House
to attract attention in a state that can give 3 billions to a club of people who practice
blatant selective attribution of public money. It is not that we did not try...we have projects submitted
to various organizations that are supposed to be fair! We are hitting an intangible wall.
Those who have been admitted, such as BRC/BioAlliance of Houston are trying to keep us out of the race!
We will continue to fight...Funding to BioAlliance needs further investigation...
Until our voices are heard and funding is sent to El Paso projects, we will not rest.
Women from El Paso have to starve themselves in front of the White House
to attract attention in a state that can give 3 billions to a club of people who practice
blatant selective attribution of public money. It is not that we did not try...we have projects submitted
to various organizations that are supposed to be fair! We are hitting an intangible wall.
Those who have been admitted, such as BRC/BioAlliance of Houston are trying to keep us out of the race!
We will continue to fight...Funding to BioAlliance needs further investigation...
Until our voices are heard and funding is sent to El Paso projects, we will not rest.
Reminder as needs still huge: Border Women Strike for Visibility
By Ambreen Ali
Nov. 16, 2010 – 10:46 a.m.
The Obamas had visitors waiting for them when they returned from their Asia trip this week.Eight women from El Paso, Texas, have been holding daily vigils outside the White House since Nov. 8 in an effort to get government funding for their community.
They have also been on a hunger strike since that date, relying on water and a mixture of water, sugar and salt to restore electrolytes.
It’s a drastic step for what they say is a desperate situation — unemployment and poverty levels that are among the highest in the country.
“We’re basically invisible,” Lorena Andrade, one of the activists. “We had to come here to make ourselves visible.”
The group called La Mujer Obrera, or The Working Woman, wants Congress and the White House to fund a commission that would direct development funds to the border community.
One model could be the Appalachian Regional Commission, set up by President John F. Kennedy in 1964. The women hope President Barack Obama or the first lady will consider a trip to the region such as the one that inspired Kennedy to create the panel.
They delivered a letter to Michelle Obama on Monday, appealing to her woman to woman.
“We are not victims,” they wrote. “We are rebuilding our communities with dignified courage. As women, we know we have and are exercising, the right to determine our own destiny.”
El Paso’s Rep. Silvestre Reyes, a Democrat, helped set up a government commission for the region’s development, but it remains unfunded.
La Mujer Obrera has three demands: for the government to organize a summit of federal agencies to discuss border needs, set aside money for the border commission, and promise to include local women in the decision making.
They have already laid out those demands in meetings with the Departments of Agriculture, Treasury, and Housing and Urban Development. They expect to meet with the State Department later this week.
The women say they want to be home for Thanksgiving, but they are willing to stay if their demands are not met.
“We get a lot of support and acknowledgment but we want something in writing,” Rubi Orozco, a spokeswoman for the group, said. “We have left before with that kind of pat on the head, and it doesn’t materialize into anything.”
Orozco said there was an irony in border residents having such few resources when so much money is spent on border security.
“The region gets loads of money but it goes to the fence and security,” she said, adding that the jobs for those projects rarely go to locals.
Many of the women active with the group are former garment workers who lost their jobs when the factories in their area moved to Mexico.
Today, they have refurbished those factories into day care centers and shops to sell imported artisan handiwork from Mexico.
“This is another definition to border security,” Cindy Alford, also with the group, said. “Genuine border security has to include sustainable communities.”http://www.congress.org/news/border-women-strike-for-visibility/
Hypothesis for Cancer Research: Mucinous Cancer
One of the bad types of gastroenterologic cancers such as Gastric and Colon cancers is the one known as Mucinous Cancer. Basically, this cancer produces a Mucin assumed to be a viscous liquid surrounding the cell. This tumor spreads early and deeply. At the time it is found, most of the time, the cancer is in advanced stage. Researchers have explained this phenomenon by stating that this Mucin contains many ingredients suppressive to immunity (including Cytokines), and soluble Molecules (such as Prostaglandin E2) that may down regulate local immunity against the cancer. It may also have those metalloproteases that we discussed in our earlier post for research suggestions on Oct, 14, 2012
Prostaglandins in general respond to anti inflammatory agents.
CAN WE MEASURE THE LEVEL OF TISSUE PROSTAGLANDINS IN MUCINOUS CANCERS AS A PREDICTOR OF ANTI-INFLAMMATORY (ASPIRIN) MAINTENANCE THERAPY POST PRIMARY TREATMENT TO DECREASE RATE OF METASTASIS IN COLON AND GASTRIC CANCERS?
CAN ANTI-MUCIN (AFTER WE KNOW THE REAL CONTENT FOR SPECIFIC CANCER TISSUE) PROVIDE AN INCREASE OF ANTIBODY BINDING TO CANCER CELLS?
TREG CELLS are cells involved in tolerance of our own cells. They work to stop us from killing our own cells. ARE THEY INCREASED IN CANCERS TO DECREASE CELLULAR IMMUNITY AGAINST CANCERS?
CANCER CELLS SEEMS TO HAVE A SELF GROWTH HORMONE WHICH IS SECRETED IN ITS IMMEDIATE SURROUNDING. THIS HORMONE ACTS THROUGH RECEPTORS ON THE EXTERNAL MEMBRANE OF THE CELL. THE PROFILE OF RECEPTORS ON CANCER MEMBRANES IS DEFINITELY DIFFERENT FROM THE NORMAL CELL. WHY CAN'T WE PRACTICE "PROFILING" BY INVENTORYING ALL THE RECEPTORS (OR CRITICAL RECEPTORS)?
RECEPTORS ARE MADE BY GENES MOSTLY, WE CAN CONTROL THESE THROUGH OUR KNOWLEDGE OF GENETICS. IF WE KNOW RECEPTORS EXCLUSIVE TO CANCER CELLS,
CAN WE DEVELOP ANTIBODY TO THESE RECEPTORS?
Prostaglandins in general respond to anti inflammatory agents.
CAN WE MEASURE THE LEVEL OF TISSUE PROSTAGLANDINS IN MUCINOUS CANCERS AS A PREDICTOR OF ANTI-INFLAMMATORY (ASPIRIN) MAINTENANCE THERAPY POST PRIMARY TREATMENT TO DECREASE RATE OF METASTASIS IN COLON AND GASTRIC CANCERS?
CAN ANTI-MUCIN (AFTER WE KNOW THE REAL CONTENT FOR SPECIFIC CANCER TISSUE) PROVIDE AN INCREASE OF ANTIBODY BINDING TO CANCER CELLS?
TREG CELLS are cells involved in tolerance of our own cells. They work to stop us from killing our own cells. ARE THEY INCREASED IN CANCERS TO DECREASE CELLULAR IMMUNITY AGAINST CANCERS?
CANCER CELLS SEEMS TO HAVE A SELF GROWTH HORMONE WHICH IS SECRETED IN ITS IMMEDIATE SURROUNDING. THIS HORMONE ACTS THROUGH RECEPTORS ON THE EXTERNAL MEMBRANE OF THE CELL. THE PROFILE OF RECEPTORS ON CANCER MEMBRANES IS DEFINITELY DIFFERENT FROM THE NORMAL CELL. WHY CAN'T WE PRACTICE "PROFILING" BY INVENTORYING ALL THE RECEPTORS (OR CRITICAL RECEPTORS)?
RECEPTORS ARE MADE BY GENES MOSTLY, WE CAN CONTROL THESE THROUGH OUR KNOWLEDGE OF GENETICS. IF WE KNOW RECEPTORS EXCLUSIVE TO CANCER CELLS,
CAN WE DEVELOP ANTIBODY TO THESE RECEPTORS?
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