CRBCM IS READY FOR CLASS ACTION!
WE ARE COLLECTING NAMES OF COMPANIES NEGLECTED
AND STOPPED FROM PARTICIPATION BY A CPRIT MANAGEMENT NOW UNDER FIRE
AND COMPLETELY BIASED.
WE ARE WAITING FOR OUR LAWYER'S INSTRUCTIONS
Saturday, December 8, 2012
CPRIT Chair wants missing emails found
Following-up on the 2010 grant awarded to the start-up Peloton Therapeutics:
Cancer agency chair wants missing emails found
By Todd Ackerman, Brian Rogers | December 7, 2012 | Updated: December 8, 2012 8:41am
The board chairman of the state cancer agency said on Friday he wants an investigation to locate emails related to an $11 million grant awarded in 2010 without proper review.In a statement, Jimmy Mansour said he will recommend at the Cancer Prevention and Research Institute of Texas board's January meeting that the agency employ forensic experts to find emails about the proposal and process. A new review says emails about the unreviewed grant "are currently unavailable."
"I am determined that the emails be located," wrote Mansour, chairman of CPRIT's oversight committee.
The agency a week ago acknowledged that a commercialization grant to a start-up biotech company in Dallas, Peloton Therapeutics, was never scrutinized by peer review committees set up to evaluate applications. The next day, much of the state's political leadership demanded answers from the agency about what happened.
At an agency meeting Wednesday, executive director Bill Gimson tried to provide some of the answers. Calling the grant's approval the result of a misunderstanding, he attributed the mistake to CPRIT being so young it didn't have all checks and balances in place. The grant was one of the first four commercialization grants awarded by the agency.
Retained 30 days
========================================================
Read the rest in The Houston Chronicle of 12/08/12 under CITY & STATE B2
IF SOMEONE COMES TO YOU, LOOKING GUILTY LIKE HELL, TELLING YOU THAT YOU ONLY BROKE THE COFFEE CUP, WATCH OUT, THE ENTIRE HOUSE MAY HAVE BURNED TO THE GROUND!
SO WHEN CPRIT COMES UP WITH AN INTERNAL REVIEW FINDING, GIVING US A HINT, LOOKS LIKE IT IS TIME TO BRING IN THE FBI ! IS SUCH AN ORGANIZATION READY FOR SCRUTINY? I DON'T THINK SO!
SO WHEN CPRIT COMES UP WITH AN INTERNAL REVIEW FINDING, GIVING US A HINT, LOOKS LIKE IT IS TIME TO BRING IN THE FBI ! IS SUCH AN ORGANIZATION READY FOR SCRUTINY? I DON'T THINK SO!
News from CPRIT
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Nov 29 (9 days ago)
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Email not displaying correctly? View it in your browser.
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Review recommends resubmission of one commercialization grant "CPRIT must have the trust of our fellow Texans that we are not only doing great work but that we are doing everything the right way," said executive director Bill Gimson. "We proactively initiated this comprehensive review to be transparent and ensure good stewardship." CPRIT’s compliance officer learned that CPRIT’s chief commercialization officer had improperly included the Peloton proposal on a commercialization award slate presented to the Institute’s Oversight Committee two years ago. The proposal did not have the required formal recommendation from the commercialization or scientific research peer review committees. Additionally, CPRIT’s investigation revealed that Peloton was unaware CPRIT processes had not been followed and had played no role in placement of the proposal on the award slate. At CPRIT’s request, Peloton has resubmitted its proposal to undergo a commercialization and scientific review pursuant to CPRIT’s formal process. Like all grant reviews, the peer review committee’s recommendation to fund or not fund the proposal will determine whether the application is included on a proposed award slate presented to the Oversight Committee. CPRIT’s compliance officer, in conjunction with CPRIT’s third party grant management provider, confirmed that all other commercialization awards were assigned to and reviewed by a peer review committee pursuant to CPRIT’s established policies. CPRIT is committed to continuing quality improvement in the agency’s processes and procedures. |
So Many Americans have hoped to see work through our work:
"I hope all is well with you at the Coalition for the Reversal of Breast Cancer.
Although we haven’t connected in a while, I wanted to see how things were going with your anticipated new mobile project. Can you share any update with us? Do you need anything to help you with your project?
I would also like to introduce you to our new Sales Manager, Paul Simpson. Paul has over 25 years of customer service and support experience, and is now available to assist you as well.
Please let me know if Paul or I can do anything to help you make your mobile program a complete success for Coalition for the Reversal of Breast Cancer.
Feel free to contact Paul at PSimpson@ArmorMobile.com or 513-923-5627.
Thanks so much for the opportunity to help you “Go Mobile!” We hope to hear from you soon.
Best regards,"
But CPRIT did not get the message from El Paso! Want us to be a UNIVERSITY to put people to work!
We have to find a way so CPRIT does not matter...New leadership is needed at CPRIT. Universities have transformed this in their back pocket. We need to fight to change this EL Paso!
Although we haven’t connected in a while, I wanted to see how things were going with your anticipated new mobile project. Can you share any update with us? Do you need anything to help you with your project?
I would also like to introduce you to our new Sales Manager, Paul Simpson. Paul has over 25 years of customer service and support experience, and is now available to assist you as well.
Please let me know if Paul or I can do anything to help you make your mobile program a complete success for Coalition for the Reversal of Breast Cancer.
Feel free to contact Paul at PSimpson@ArmorMobile.com or 513-923-5627.
Thanks so much for the opportunity to help you “Go Mobile!” We hope to hear from you soon.
Best regards,"
But CPRIT did not get the message from El Paso! Want us to be a UNIVERSITY to put people to work!
We have to find a way so CPRIT does not matter...New leadership is needed at CPRIT. Universities have transformed this in their back pocket. We need to fight to change this EL Paso!
Friday, December 7, 2012
Texas Research Fund Will Re-Review MD Anderson Drug-Discovery Proposal
Reacting to charges of improper procedures, Texas's $3 billion
cancer research fund has agreed to re-review a controversial $20 million
commercialization
award made in March to two Houston institutions. But it's not clear
whether the plan will satisfy the critics, who are asking for a rigorous
scientific
review.
Meanwhile, according to e-mails obtained by a Texas newspaper, a Nobel-prizing scientist who resigned partly over concerns about the grant was pushed to leave after he complained that reviews had become politicized.
The grant from the Cancer Prevention and Research Institute of Texas (CPRIT) provides $20 million in 1 year to be split between Rice University and the University of Texas MD Anderson Cancer Center, which will get the lion's share—up to $18 million—for its Institute for Applied Cancer Science (IACS). CPRIT's chief scientific officer, Alfred Gilman, announced earlier this month that he's resigning in part because he believes IACS, which plans to discover and develop drugs, is a research program "disguise[d]" as commercialization to avoid scientific review. CPRIT's scientific review council shared these concerns.
Other questions about the award process have since come up: Some members of CPRIT's commercialization review council, which approved the incubator grant, have ties to Rice or MD Anderson, for instance. And MD Anderson's portion did not go through the university's provost office, which looks at potential conflicts of interest and might have identified one in this case, because principal investigator Lynda Chin is married to MD Anderson President Ronald DePinho. Critics allege that CPRIT and MD Anderson bypassed normal procedures.
Yesterday, DePinho sent CPRIT a letter that calls the allegations "inaccurate" and "false" but says it is "understandable" why scientists would be concerned "in the absence of all of the facts." The letter says MD Anderson is willing to resubmit its proposal for "further review." But the letter denies that the grant should go through the MD Anderson provost. Because it is a business plan, the proposal will be reviewed by MD Anderson's "business affairs" department, the letter says.
Meanwhile, according to e-mails obtained by a Texas newspaper, a Nobel-prizing scientist who resigned partly over concerns about the grant was pushed to leave after he complained that reviews had become politicized.
The grant from the Cancer Prevention and Research Institute of Texas (CPRIT) provides $20 million in 1 year to be split between Rice University and the University of Texas MD Anderson Cancer Center, which will get the lion's share—up to $18 million—for its Institute for Applied Cancer Science (IACS). CPRIT's chief scientific officer, Alfred Gilman, announced earlier this month that he's resigning in part because he believes IACS, which plans to discover and develop drugs, is a research program "disguise[d]" as commercialization to avoid scientific review. CPRIT's scientific review council shared these concerns.
Other questions about the award process have since come up: Some members of CPRIT's commercialization review council, which approved the incubator grant, have ties to Rice or MD Anderson, for instance. And MD Anderson's portion did not go through the university's provost office, which looks at potential conflicts of interest and might have identified one in this case, because principal investigator Lynda Chin is married to MD Anderson President Ronald DePinho. Critics allege that CPRIT and MD Anderson bypassed normal procedures.
Yesterday, DePinho sent CPRIT a letter that calls the allegations "inaccurate" and "false" but says it is "understandable" why scientists would be concerned "in the absence of all of the facts." The letter says MD Anderson is willing to resubmit its proposal for "further review." But the letter denies that the grant should go through the MD Anderson provost. Because it is a business plan, the proposal will be reviewed by MD Anderson's "business affairs" department, the letter says.
Live Chat: How Close Are We to Birth Control for Men? Thursday 3 p.m. EDT
What's not clear is whether the commercialization reviewers will see the IACS project the same way the scientific critics do. They argue that because IACS has aims such as studying "target biology" and has not identified products or a company, it is not about commercialization but about science. Depending on how soon MD Anderson resubmits its proposal, the commercialization review council could make a decision before the CPRIT board's next meeting in July.
Gilman's concerns over CPRIT's review process led to pressure to leave, according to an online report today from The Dallas Morning News. The article quotes an April e-mail from Gilman to colleagues in which he says Gimson told him to resign because CPRIT's board "has no faith in your ability to do your job." Gilman writes that he responded that "I would not resign, they would need to dismiss me."
More from the article:
The resignation request by Bill Gimson, executive director of the Cancer Prevention and Research Institute of Texas, or CPRIT, came after Gilman wrote a four-page letter in which he warned that "political considerations" should have no place in deciding how CPRIT should award public dollars.
Gilman's email and letters were among hundreds of pages of documents released by CPRIT in response to a public records request by The Dallas Morning News. Reached for comment this morning, Gilman declined to answer questions.
Dozens of emails focus on Gilman's stance that CPRIT's "peer review" system, in which out-of-state scientists review applications to avoid possible conflicts of interest, is under attack from foes, including some members of the agency's Oversight Committee that Gilman referred to as "really evil people."
SABCS: Black Women Less Likely to Undergo Sentinel Lymph Node Biopsy
By Dave Levitan |
December 5, 2012
A large cohort study found that black women with early-stage invasive
breast cancer were significantly less likely than white patients to
undergo the less invasive axillary sentinel lymph node (SLN) biopsy.
Black women also had a higher rate of lymphedema, due largely to that
difference in treatment modalities.
======================================
Caution, read the full report before jumping to conclusion!
http://www.cancernetwork.com/conference-reports/sabcs2012/content/article/10165/2118097
======================================
Caution, read the full report before jumping to conclusion!
http://www.cancernetwork.com/conference-reports/sabcs2012/content/article/10165/2118097
ARSENIC TRIOXIDE COULD SIGNIFICANTLY EXPAND ITS ROLE IN CANCER TREATMENT. AND VITAMIN C AND MICROHYDRIN COULD COME TO THE RESCUE
Cancer cure is through death of the cancer cell. To date, the main way of death for the cancer cell
is through Caspase activation cascade. In most cells, we know how the main way the activation of Caspase occurs. That is Cytochrome C is naturally anchored at the membrane inside the Mitochondria. The Anchor is in fact a chemical bonding or attachment through electrons, like molecules do attach to each other. We believe there, Cytochrome C is attached to a Cardiolipin which is part of the lipids of the membrane. Just imagine another molecule showing up with a free electron, the free electron could attract and pull the one involved in the attachment and break free the Cytochrome C. That Cytochrome C electron no longer attached comes out and activates the Caspase (mostly Caspase 9 which eventually activates members of its family) and there starts the Caspase its work to coagulate DNA and genes start breaking, thus leading to cancer cell death. One of the molecules that produce such disturbing free electrons is Arsenic Trioxide. This delivery of free electrons by arsenic trioxide is not limited to the mitochondria. It occurs through the cytosol (liquid milieu of the cell) disrupting many cellular pathways, delivering global intracellular disruption. ( for those savvy people, do remember that the " breaking" of the anchor could be induced from outside the Mitochondrial membrane through the AKT or Bax effect- this is where Bcl-2 negative effect is the strongest ) arsenic trioxide
This global disruption has been established to treat Acute Promyelocytic Leukemia (APL) (by the way, Chinese researchers lead the way on this one). Frankly speaking, this "Global disruption"can be used in any cancer. The problem is that it can occur in any cell, including our normal cells. Giving caution to the amount you use because of a narrow safety index.
Vitamin C and Microhydrin have also free electron, that is why they can cool down free radicals and therefore are called Anti-Oxydants . The free electrons of these compounds seem to add to those of Arsenic Trioxide to Increase toxicity to the cancer cell. It is worth mentioning that, at the DNA level, these free electron break the strand, triggering our first law (activation of P53 and stoppage of cell cycle).
3 main problems
1. Good and bad pathways are stopped, mitigating the effects of global destruction.
2. (non selectivity) Good and bad cells are killed. This effect is worse in patients with poor reserve of free electron clearing molecules (Gluthatione based, Superoxide based and others). (CAUTION TO EVERYONE)
3. Arsenic is hard to get rid of, and chronic exposure signs will result.
But frankly speaking, you can use this to kill any Cancer. Research will continue at CRBCM no matter what!
Of Note: Use of this information outside of the topic discussed herein, is not endorsed by the CRBCM
is through Caspase activation cascade. In most cells, we know how the main way the activation of Caspase occurs. That is Cytochrome C is naturally anchored at the membrane inside the Mitochondria. The Anchor is in fact a chemical bonding or attachment through electrons, like molecules do attach to each other. We believe there, Cytochrome C is attached to a Cardiolipin which is part of the lipids of the membrane. Just imagine another molecule showing up with a free electron, the free electron could attract and pull the one involved in the attachment and break free the Cytochrome C. That Cytochrome C electron no longer attached comes out and activates the Caspase (mostly Caspase 9 which eventually activates members of its family) and there starts the Caspase its work to coagulate DNA and genes start breaking, thus leading to cancer cell death. One of the molecules that produce such disturbing free electrons is Arsenic Trioxide. This delivery of free electrons by arsenic trioxide is not limited to the mitochondria. It occurs through the cytosol (liquid milieu of the cell) disrupting many cellular pathways, delivering global intracellular disruption. ( for those savvy people, do remember that the " breaking" of the anchor could be induced from outside the Mitochondrial membrane through the AKT or Bax effect- this is where Bcl-2 negative effect is the strongest ) arsenic trioxide
This global disruption has been established to treat Acute Promyelocytic Leukemia (APL) (by the way, Chinese researchers lead the way on this one). Frankly speaking, this "Global disruption"can be used in any cancer. The problem is that it can occur in any cell, including our normal cells. Giving caution to the amount you use because of a narrow safety index.
Vitamin C and Microhydrin have also free electron, that is why they can cool down free radicals and therefore are called Anti-Oxydants . The free electrons of these compounds seem to add to those of Arsenic Trioxide to Increase toxicity to the cancer cell. It is worth mentioning that, at the DNA level, these free electron break the strand, triggering our first law (activation of P53 and stoppage of cell cycle).
3 main problems
1. Good and bad pathways are stopped, mitigating the effects of global destruction.
2. (non selectivity) Good and bad cells are killed. This effect is worse in patients with poor reserve of free electron clearing molecules (Gluthatione based, Superoxide based and others). (CAUTION TO EVERYONE)
3. Arsenic is hard to get rid of, and chronic exposure signs will result.
But frankly speaking, you can use this to kill any Cancer. Research will continue at CRBCM no matter what!
Of Note: Use of this information outside of the topic discussed herein, is not endorsed by the CRBCM
Thursday, December 6, 2012
A CRBCM Satellite has been suggested...
A CRBCM Satellite has been suggested... a facility for well-being is offering to become CRBCM's relay on the Westside of El Paso to make the cancer research, screening and prevention programs and the healthy living interventions accessible to even more El Pasoans.
We will convene with the stakeholders early in January 2013.
We will convene with the stakeholders early in January 2013.
13TH ANNUAL RIO GRANDE TRAUMA CONFERENCE
Enjoying the great updates presented during the 13TH ANNUAL RIO GRANDE TRAUMA CONFERENCE in El Paso, Texas.
Tomorrow it will be a full program of Pediatric Updates.
Tomorrow it will be a full program of Pediatric Updates.
Second project rejected by CPRIT
CPRIT has rejected our second project, this time on "administrative grounds". This is the same project that Bio-Alliance in Houston had promised to pre-review, but in the end had not even taken the trouble to read the Business plan and powerpoint presentation that they had requested from CRBCM.
We have asked permission from CPRIT to post their second rejection letter on our blog because they claim that their rejection letter is "privileged information" and should not be published without prior written consent.
It is important for the public who is reading our blog to know what reasons were given to reject a cancer survivorship center in El Paso! It is interesting to note that this rejection comes as I published the letter to the Senators!
We will submit 2 research projects these coming days. We expect further rejections as CRBCM is or seems to be barred from participation.
This all mis-adventure seems to result from failure from the legislature to tell us their clear intention when CPRIT was created. We know now that University fund raisers seem to have been at the origin and lobbied the State Senate heavily to have this organization created. They have taken it over and distracted the public that this thing is for every one when it is really not. You get lured to it just to find out that in fact you don't belong. If it was for every one, why they have not assigned 99% to university and 1 % to the public to give non university a reasonable chance. They want to give it all to their institutions. It is kind of vicious and disturbing to believe that one would misrepresent a source of funding, hiding the real intention. Make people work hard to submit projects but ultimately reject them because they are not a university. The review process is skewed and secretive. That is why, I am prevented from publishing it. What a twisted world we live in. Frankly speaking the so called review is so biased toward belonging to the university as the main criteria that it is almost laughable. They claim for example that my project will involve humans, and I did not have provide proof of knowing about NCI standards for research on human. The remark is bizarre because I don't know in the USA an Oncologist with 15 years of experience who has not obtain recommended basic NCI standard. I worked for kaiser Permanente, an institution that has its own Hospital and and publications and particpate to national studies, I registered patients to clinical trials, And I did mention this in the project. They basically rush to judgement because CRBCM is new. The gag order is to hide major insufficiencies in the quality of the review at CPRIT now. There are evidences that the guy who rejected the 2nd project did not read it that's all I am saying for now. Another Oncologist called me tonight and asked why I am "wasting my time". " For a principle", I replied. I really trusted this organization and its intention to do good. I am actually surprised of the twisted outcome.
We have asked permission from CPRIT to post their second rejection letter on our blog because they claim that their rejection letter is "privileged information" and should not be published without prior written consent.
It is important for the public who is reading our blog to know what reasons were given to reject a cancer survivorship center in El Paso! It is interesting to note that this rejection comes as I published the letter to the Senators!
We will submit 2 research projects these coming days. We expect further rejections as CRBCM is or seems to be barred from participation.
This all mis-adventure seems to result from failure from the legislature to tell us their clear intention when CPRIT was created. We know now that University fund raisers seem to have been at the origin and lobbied the State Senate heavily to have this organization created. They have taken it over and distracted the public that this thing is for every one when it is really not. You get lured to it just to find out that in fact you don't belong. If it was for every one, why they have not assigned 99% to university and 1 % to the public to give non university a reasonable chance. They want to give it all to their institutions. It is kind of vicious and disturbing to believe that one would misrepresent a source of funding, hiding the real intention. Make people work hard to submit projects but ultimately reject them because they are not a university. The review process is skewed and secretive. That is why, I am prevented from publishing it. What a twisted world we live in. Frankly speaking the so called review is so biased toward belonging to the university as the main criteria that it is almost laughable. They claim for example that my project will involve humans, and I did not have provide proof of knowing about NCI standards for research on human. The remark is bizarre because I don't know in the USA an Oncologist with 15 years of experience who has not obtain recommended basic NCI standard. I worked for kaiser Permanente, an institution that has its own Hospital and and publications and particpate to national studies, I registered patients to clinical trials, And I did mention this in the project. They basically rush to judgement because CRBCM is new. The gag order is to hide major insufficiencies in the quality of the review at CPRIT now. There are evidences that the guy who rejected the 2nd project did not read it that's all I am saying for now. Another Oncologist called me tonight and asked why I am "wasting my time". " For a principle", I replied. I really trusted this organization and its intention to do good. I am actually surprised of the twisted outcome.
Message to Senators Jane Nelson and Jim Keffer
To Senators Jane Nelson and Jim Keffer,
To our representatives,
The Coalition for the Reversal of Breast Cancer Mortality in African American Women (CRBCM), an organization based in El Paso TX, has for mission to fight for the reduction in Breast Cancer Mortality in Minority populations in general, with some focus in death of African American Women from the disease.
Despite the low incidence of breast cancer compared to that in the white race, the mortality from Breast cancer is 40 to 50% higher in minority populations compared to what it should be, based on the low incidence. This incidence-mortality Paradox is due to low screening rates by mammography, late stage of disease at diagnosis, and excessive amount of triple negative Breast cancer, a poor non treatable histology.
Of the estimated 6,000 African American women who have or will die of Breast cancer in the United stated this year, our efforts in prevention and treatment, if effective, could save up to 3,000 of these women yearly, based on current estimates. In El Paso, there will be about 2,600 new cases of cancer in general this year. 350 will be Breast Cancers of which 90 will perish from the disease. We could save up to 45 women per the above estimates yearly in El Paso alone. Our protocol for improved prevention, screening and more efficient treatment of breast cancer in African American and Hispanic women would have a huge impact at the National level, but also in all other countries where these women suffer from that Breast cancer paradox marked by low incidence with high mortality.
Dear Senators,
Your actions and initiatives will save real lives yearly. So it is with dismay that we see CPRIT funds being mismanaged while people are dying. Your strong stance on CPRIT is being applauded in our communities. I should however warn you that the nervousness at CPRIT has a price. And small independent companies or operations that focus on cancer may miss out completely on the opportunity as CPRIT is shifting squarely into becoming an exclusive University funding organization. Universities know this and have started abusing the system as it is now apparent. Indeed, there is a perception at CPRIT that awarding grants to universities is less questionable in the mind of the public, and somehow, Universities and big Biotech companies are more likely to find the cure. If this was true in your mind, you could have called CPRIT "Texas University Funding Source", but you did not. You felt this was a race to the cure. And in a race, remember, the underdogs can sometimes be the first to the finishing line if given a chance. So you did not restrict the grants to universities and biotech companies. CPRIT seems to do this for you and in effect reducing the foot print of the law.
If your initial conception of the law leading to CPRIT was to boost the economy and meet disparity in minority involvement in the program, then the actual awarding process of recurrently funding the same universities over and over again is only making them richer, without meeting these important end points. CPRIT would have a much larger foot print if its leadership allowed it to truly invest in services for prevention, screening and cancer care in low income communities. The positive impact would be immediate on common fellows living today, and it would have a larger reach as it would relate to overall improved health status of communities and intensive job creation.
Also, it is our understanding that CPRIT wanted to come back to the legislature to convey our message regarding the need to increase the proportion of funds allocated to cancer prevention. Under current duress and public criticism, this need will probably not be brought to your attention and prevention is quietly being pushed to the wayside, while the tax dollar is increasingly being used for incubator and commercialization programs. Tertiary prevention programs which include lucrative survivorship centers and programs still have not been developed in satisfactory numbers to satisfy the urgent needs in Texas; such programs would be just as financially viable as the commercialization of new drugs and devices and generate financial revenue for the long term - cancer survivors are every year more numerous, but their needs are being ignored. Remember, services that could be developed under this type of program, are generally reimbursed by the federal government. When fully deployed, it is true that survivorship programs are much more secure revenue generating endeavors than any risky incubator or Biotech start-up company with random and potentially short-lived success.
We, at CRBCM, believe in a cure to cancer. Cure is achievable by causing cancer cell death. And cell death can only be effective following organized natural processes built-in within the cell by nature, leading to coordinated Apoptosis. We believe that there are ways to harness these pathways or cellular metabolic events to maximize cancer cell death. What we need now is proof of concept work in laboratories followed by translation to patients in our clinic. We can't achieve this if we are not allowed to significantly participate. Your help and vision is leading us to the cure, help put aside abuse of power and politics. I agree with you that the cause is much too important to play politics.
The CRBCM has so far submitted 4 research, prevention and survivorship projects to CPRIT. The first one has been rejected not because of its content. But the reviewers insist they do not know the principal investigator or the CRBCM to be certain that we could achieve what we claim. Suffice is to say that I remember participating at the annual American College of physician against John Hopkins residents in Baltimore, that year my presentation and abstract received the first place. I have been doing mostly clinical work. I feel it is time at my age to return to research with sixteen years of sound clinical cancer care experience and background. At CPRIT, they insist that we be affiliated with some University professor to show we are "supervised". This is ignoring that professors have contracts with our competitors for grants. At least 2 El Paso university professors flatly turned our request to collaborate with the CRBCM down because of the obvious conflict it would cause them.
The CRBCM is asking that during your conversation with CPRIT leadership you convey our concerns about the disparity in grant attribution in order to boost the foot print of your initiative and boost the economy in remote Cities such as El Paso. It is after all the 6th largest City in Texas, yet having to date received less than one percent of CPRIT funds for cancer prevention, research and intervention. The race for the cure is on. Let the best win. Skewing the fight does not assure that the underdogs will fail. This is a "just cause" request. Your attention to these issues is called for.
Sincerely yours
Mutombo Kankonde, M.D., M.P.H.
CRBCM
El Paso, Texas
December 6th, 2012.
To our representatives,
The Coalition for the Reversal of Breast Cancer Mortality in African American Women (CRBCM), an organization based in El Paso TX, has for mission to fight for the reduction in Breast Cancer Mortality in Minority populations in general, with some focus in death of African American Women from the disease.
Despite the low incidence of breast cancer compared to that in the white race, the mortality from Breast cancer is 40 to 50% higher in minority populations compared to what it should be, based on the low incidence. This incidence-mortality Paradox is due to low screening rates by mammography, late stage of disease at diagnosis, and excessive amount of triple negative Breast cancer, a poor non treatable histology.
Of the estimated 6,000 African American women who have or will die of Breast cancer in the United stated this year, our efforts in prevention and treatment, if effective, could save up to 3,000 of these women yearly, based on current estimates. In El Paso, there will be about 2,600 new cases of cancer in general this year. 350 will be Breast Cancers of which 90 will perish from the disease. We could save up to 45 women per the above estimates yearly in El Paso alone. Our protocol for improved prevention, screening and more efficient treatment of breast cancer in African American and Hispanic women would have a huge impact at the National level, but also in all other countries where these women suffer from that Breast cancer paradox marked by low incidence with high mortality.
Dear Senators,
Your actions and initiatives will save real lives yearly. So it is with dismay that we see CPRIT funds being mismanaged while people are dying. Your strong stance on CPRIT is being applauded in our communities. I should however warn you that the nervousness at CPRIT has a price. And small independent companies or operations that focus on cancer may miss out completely on the opportunity as CPRIT is shifting squarely into becoming an exclusive University funding organization. Universities know this and have started abusing the system as it is now apparent. Indeed, there is a perception at CPRIT that awarding grants to universities is less questionable in the mind of the public, and somehow, Universities and big Biotech companies are more likely to find the cure. If this was true in your mind, you could have called CPRIT "Texas University Funding Source", but you did not. You felt this was a race to the cure. And in a race, remember, the underdogs can sometimes be the first to the finishing line if given a chance. So you did not restrict the grants to universities and biotech companies. CPRIT seems to do this for you and in effect reducing the foot print of the law.
If your initial conception of the law leading to CPRIT was to boost the economy and meet disparity in minority involvement in the program, then the actual awarding process of recurrently funding the same universities over and over again is only making them richer, without meeting these important end points. CPRIT would have a much larger foot print if its leadership allowed it to truly invest in services for prevention, screening and cancer care in low income communities. The positive impact would be immediate on common fellows living today, and it would have a larger reach as it would relate to overall improved health status of communities and intensive job creation.
Also, it is our understanding that CPRIT wanted to come back to the legislature to convey our message regarding the need to increase the proportion of funds allocated to cancer prevention. Under current duress and public criticism, this need will probably not be brought to your attention and prevention is quietly being pushed to the wayside, while the tax dollar is increasingly being used for incubator and commercialization programs. Tertiary prevention programs which include lucrative survivorship centers and programs still have not been developed in satisfactory numbers to satisfy the urgent needs in Texas; such programs would be just as financially viable as the commercialization of new drugs and devices and generate financial revenue for the long term - cancer survivors are every year more numerous, but their needs are being ignored. Remember, services that could be developed under this type of program, are generally reimbursed by the federal government. When fully deployed, it is true that survivorship programs are much more secure revenue generating endeavors than any risky incubator or Biotech start-up company with random and potentially short-lived success.
We, at CRBCM, believe in a cure to cancer. Cure is achievable by causing cancer cell death. And cell death can only be effective following organized natural processes built-in within the cell by nature, leading to coordinated Apoptosis. We believe that there are ways to harness these pathways or cellular metabolic events to maximize cancer cell death. What we need now is proof of concept work in laboratories followed by translation to patients in our clinic. We can't achieve this if we are not allowed to significantly participate. Your help and vision is leading us to the cure, help put aside abuse of power and politics. I agree with you that the cause is much too important to play politics.
The CRBCM has so far submitted 4 research, prevention and survivorship projects to CPRIT. The first one has been rejected not because of its content. But the reviewers insist they do not know the principal investigator or the CRBCM to be certain that we could achieve what we claim. Suffice is to say that I remember participating at the annual American College of physician against John Hopkins residents in Baltimore, that year my presentation and abstract received the first place. I have been doing mostly clinical work. I feel it is time at my age to return to research with sixteen years of sound clinical cancer care experience and background. At CPRIT, they insist that we be affiliated with some University professor to show we are "supervised". This is ignoring that professors have contracts with our competitors for grants. At least 2 El Paso university professors flatly turned our request to collaborate with the CRBCM down because of the obvious conflict it would cause them.
The CRBCM is asking that during your conversation with CPRIT leadership you convey our concerns about the disparity in grant attribution in order to boost the foot print of your initiative and boost the economy in remote Cities such as El Paso. It is after all the 6th largest City in Texas, yet having to date received less than one percent of CPRIT funds for cancer prevention, research and intervention. The race for the cure is on. Let the best win. Skewing the fight does not assure that the underdogs will fail. This is a "just cause" request. Your attention to these issues is called for.
Sincerely yours
Mutombo Kankonde, M.D., M.P.H.
CRBCM
El Paso, Texas
December 6th, 2012.
What lawmakers are saying
“CPRIT cannot succeed
in its efforts to fight cancer without the public’s trust, and right
now that trust is in serious jeopardy. … Mistakes occur at every agency,
but CPRIT’s mission is too important to be derailed by lapses in
process established by law and by rules to ensure that every dollar
allocated goes through a rigorous review process.” — From a letter
to the Cancer Prevention and Research Institute of Texas by Sen. Jane
Nelson, R-Flower Mound, and Rep. Jim Keffer, R-Eastland=============
FACT:
"Nine members of the agency’s 11-person oversight committee are political appointees, so politically connected people will inevitably seek to use advantage in tapping the fund. It’s up to top state leaders to make sure scientific merit — not connections — is the prevailing criterion for how public money is handed out."
====================
Related
It’s a question that must be asked and answered directly at a meeting Wednesday of the oversight committee of Texas’ cancer-fighting agency. The subject is an $11 million grant to a Dallas biotechnology company whose application was never subject to review by business or science experts.
The lapse has been blamed on the now-resigned chief commercialization officer of the Cancer Prevention and Research Institute of Texas. That official, Jerald “Jerry” Cobbs, “improperly” placed the award to Peloton Therapeutics on the oversight committee’s agenda in 2010, CPRIT disclosed last week.
Questions remain, however, beginning with the role played by CPRIT executive director Bill Gimson. Why hadn’t Gimson ensured that the Peloton grant went up for approval with the required prior review and recommendation? Did the prominence of Peloton officials and financial backers — including UT Southwestern Medical Center department chairs and Nobel Prize winners — have any bearing? How about the financial interest of Dallas philanthropist Peter O’Donnell, a major contributor to Gov. Rick Perry and Lt. Gov. David Dewhurst?
The answers are important to restoring confidence in the 5-year-old agency, and we’re glad key officials are on the case. Two GOP lawmakers who authored legislation to create CPRIT — Sen. Jane Nelson, R-Flower Mound, and Rep. Jim Keffer, R-Eastland — want a written explanation of how the oversight happened and how the agency can prevent a repeat.
They said — and this newspaper agrees — that the work of this unprecedented, voter-approved, $3 billion cancer research fund is too important to be compromised by a loss of public trust. Hints of favoritism and influence-peddling must be addressed.
The departure of CPRIT’s commercialization officer follows the resignation of its chief scientific officer, Nobel laureate Alfred Gilman, and dozens of out-of-state science reviewers. Gilman quit to protest initial approval of a $20 million “incubator” project in Houston that hadn’t been subject to scientific review.
If there’s positive news in all this, it’s that the agency self-reported the flawed Peloton review process in a compliance audit of commercialization awards it had made. The post of compliance officer was created last spring after the furor kicked up by Gilman.
Further, CPRIT said last week that it is tightening up its approval process, and each grant request submitted to the oversight committee will now have detailed documentation of review.
Whether that’s good enough remains to be seen. A state auditor’s report is due in January on CPRIT’s grant-making, and Nelson vows to file legislation to strengthen oversight on the agency.
The magnets for controversy are CPRIT’s 11 commercialization awards, a fraction of the overall 427 grants made over three years. Most are for research and prevention projects.
Nine members of the agency’s 11-person oversight committee are political appointees, so politically connected people will inevitably seek to use advantage in tapping the fund. It’s up to top state leaders to make sure scientific merit — not connections — is the prevailing criterion for how public money is handed out.
==================================================================
DO NOT KILL THE MESSENGER, NONE OF THIS INVOLVES THE CRBCM
WE JUST NEED TO CLARIFY WHAT WE ARE UP AGAINST FOR OUR BLOG VISITORS
WE PLAN TO SUBMIT 6 REPORTS TOTAL TO CPRIT
WE EXPECT 6 NEGATIVE RESPONSE OVER THE COMING YEAR
WE WILL HAVE 6 NEGATIVE "REVIEWS" TO REVIEW FOR THE COMPLETION ON OUR PUBLICATION ON THE "CPRIT EXPERIENCE". THE FIGHT IS ON.
Wednesday, December 5, 2012
CPRIT FUNDING DENIED FOR CRBCM.
And it comes with no surprise. We wanted to publish the review decision but CPRIT forbids us to do so unless we obtain their permission. We have requested promptly the permission and will soon publish an integral copy of the review notes. We believe transparency is good for the reputation of CPRIT. For CRBCM it is critical for our audience to know why we failed. The Audience will understand our argument when we contend that CPRIT is strictly a university source of funding. My CPRIT reviewer clearly suggested that until CRBCM looks like a university with young fellows on board, there is no chance we can win CPRIT money.
We applied for a company formation, but they want us to be a old existing company. It is interesting to note that the comment of the reviewer where less about the the project quality (which by the way was found to be sound) but about the man and institution who submitted it. As if he had investigated me rather than the project. Without knowing him, I could see that his world is a university. He could not imagine any other reality. It is critical that diversification comes to CPRIT review teams, community leaders could see value when our "university professors" fail to recognize what is good for communities. Frankly talking another 100 million to MD Anderson cannot achieve what CRBCM was planning to achieve with 1 million dollars. Our project was aiming to reach 50-70,000 people in El Paso. We will survive and wait on the word for 3 other projects before CPRIT review board. CRBCM representative Victor Poulos will be consulted to guide us in these difficult times.
CRBCM is a Coalition, sometimes "No" is not the answer, will wait to fight another day!
And it comes with no surprise. We wanted to publish the review decision but CPRIT forbids us to do so unless we obtain their permission. We have requested promptly the permission and will soon publish an integral copy of the review notes. We believe transparency is good for the reputation of CPRIT. For CRBCM it is critical for our audience to know why we failed. The Audience will understand our argument when we contend that CPRIT is strictly a university source of funding. My CPRIT reviewer clearly suggested that until CRBCM looks like a university with young fellows on board, there is no chance we can win CPRIT money.
We applied for a company formation, but they want us to be a old existing company. It is interesting to note that the comment of the reviewer where less about the the project quality (which by the way was found to be sound) but about the man and institution who submitted it. As if he had investigated me rather than the project. Without knowing him, I could see that his world is a university. He could not imagine any other reality. It is critical that diversification comes to CPRIT review teams, community leaders could see value when our "university professors" fail to recognize what is good for communities. Frankly talking another 100 million to MD Anderson cannot achieve what CRBCM was planning to achieve with 1 million dollars. Our project was aiming to reach 50-70,000 people in El Paso. We will survive and wait on the word for 3 other projects before CPRIT review board. CRBCM representative Victor Poulos will be consulted to guide us in these difficult times.
CRBCM is a Coalition, sometimes "No" is not the answer, will wait to fight another day!
Tuesday, December 4, 2012
A chance encounter with Kinesis
A chance encounter with KINESIS
Today I met a patient who told me about a BRITISH COMPANY READY TO LAUNCH
"KINESIS" AS WAY TO CONTROL DISEASE. I WAS EXCITED BELIEVING IT HAS SOMETHING TO DO WITH KINESIN THAT WE ARE STUDYING AT CRBCM.
Suffice is to say that we stumbled on a reality within cellular life. In fact, when one speaks about Kinesis,
TAXIS is not far behind! In the presence of certain stimuli, cells will spontaneously move toward these stimuli as if they had a "nose" for them. This is called Taxis. The movement toward the stimulus is coordinated. The cells move deliberately toward the stimulus. For biologists, when the stimulus is not sufficient or weak, the cell will move toward it but with uncoordinated movement they call it KINESIS.
Can we harvest this capacity for cellular migration toward a stimulus for our purpose in cancer fight? CAN WE SEND NATURAL KILLER CELLS TOWARD A CANCER CELL AND /OR VICE VERSA?
IT IS BELIEVED THAT SPERM CELLS RUN TOWARD THE OS OF THE CERVIX BECAUSE OF THE DIFFERENCE IN PH, CAN WE USE OTHER "STIMULI" TO ATTRACT OUR IMMUNE SYSTEM TOWARD LEUKEMIC CELLS? OUR INVESTIGATION IS ON!
ALSO LOOK UP STILL CELL TOLL RECEPTOR AS A STIMULUS FOR INNATE IMMUNE RESPONSE, OR IS IT ANOTHER BALL GAME ALTOGETHER? JOINING THE DISCUSSION!
PUT YOUR NECK OUT LIKE ME!
Today I met a patient who told me about a BRITISH COMPANY READY TO LAUNCH
"KINESIS" AS WAY TO CONTROL DISEASE. I WAS EXCITED BELIEVING IT HAS SOMETHING TO DO WITH KINESIN THAT WE ARE STUDYING AT CRBCM.
Suffice is to say that we stumbled on a reality within cellular life. In fact, when one speaks about Kinesis,
TAXIS is not far behind! In the presence of certain stimuli, cells will spontaneously move toward these stimuli as if they had a "nose" for them. This is called Taxis. The movement toward the stimulus is coordinated. The cells move deliberately toward the stimulus. For biologists, when the stimulus is not sufficient or weak, the cell will move toward it but with uncoordinated movement they call it KINESIS.
Can we harvest this capacity for cellular migration toward a stimulus for our purpose in cancer fight? CAN WE SEND NATURAL KILLER CELLS TOWARD A CANCER CELL AND /OR VICE VERSA?
IT IS BELIEVED THAT SPERM CELLS RUN TOWARD THE OS OF THE CERVIX BECAUSE OF THE DIFFERENCE IN PH, CAN WE USE OTHER "STIMULI" TO ATTRACT OUR IMMUNE SYSTEM TOWARD LEUKEMIC CELLS? OUR INVESTIGATION IS ON!
ALSO LOOK UP STILL CELL TOLL RECEPTOR AS A STIMULUS FOR INNATE IMMUNE RESPONSE, OR IS IT ANOTHER BALL GAME ALTOGETHER? JOINING THE DISCUSSION!
PUT YOUR NECK OUT LIKE ME!
Awaiting the announcement of the latest CPRIT Grant Recipients
Tomorrow is a big day for CANCER:
CPRIT is going to give grants
CPRIT OVERSIGHT COMMITTEE MEETING
Please join us:
Wednesday, December 5, 2012, 1:00 PM
Texas Medical Association, Thompson Auditorium, 1st Floor
401 West 15th Street
Austin, TX 78701
For more information, please call:
(512) 463-3190
For Universities and Biotech companies, it is assured they will get richer...They are laughing straight to the bank.
People with no clout, the common fellow will see another chance escape,
'thank you for participating' but you were not good enough for the game, will be given to us one more time. The world is clearly divided in the Rich and the poor. CRBCM has participated with 4 submissions of research, prevention and intervention proposals to reverse cancer mortality in El Paso and, with the expected findings, beyond the city limits. We were told our work was not good enough by people from Bio-Alliance who are sitting on the board. So we will not be surprised. We still are going to follow this process from the sideline and read about who made it, their thoughts, race and background. What bright and original ideas they submitted to earn the praises.
At CRBCM all we can do is try...the cause is too valuable to quit now...we will keep going that is why we are working hard. For the second week in Houston, we are progressing. Glad to learn from El Paso that new patients are waiting to be seen, thank you Peggy for holding the base!
El Paso, the city we love will also be left with us on the sideline while Houston and Dallas will be awarded a sea of grants. El Paso, keep holding on, tomorrow is still bright we believe, hope is still alive!
CPRIT is going to give grants
Please join us:
Wednesday, December 5, 2012, 1:00 PM
Texas Medical Association, Thompson Auditorium, 1st Floor
401 West 15th Street
Austin, TX 78701
For more information, please call:
(512) 463-3190
For Universities and Biotech companies, it is assured they will get richer...They are laughing straight to the bank.
People with no clout, the common fellow will see another chance escape,
'thank you for participating' but you were not good enough for the game, will be given to us one more time. The world is clearly divided in the Rich and the poor. CRBCM has participated with 4 submissions of research, prevention and intervention proposals to reverse cancer mortality in El Paso and, with the expected findings, beyond the city limits. We were told our work was not good enough by people from Bio-Alliance who are sitting on the board. So we will not be surprised. We still are going to follow this process from the sideline and read about who made it, their thoughts, race and background. What bright and original ideas they submitted to earn the praises.
At CRBCM all we can do is try...the cause is too valuable to quit now...we will keep going that is why we are working hard. For the second week in Houston, we are progressing. Glad to learn from El Paso that new patients are waiting to be seen, thank you Peggy for holding the base!
El Paso, the city we love will also be left with us on the sideline while Houston and Dallas will be awarded a sea of grants. El Paso, keep holding on, tomorrow is still bright we believe, hope is still alive!
New contacts for the CRBCM
Several El Paso Home Health Providers came to visit and are offering to help with networking and informing patients about opportunities to participate in our clinical research studies and in our healthy living program and survivorship program. They all insist on one thing: DON'T GIVE UP! Your intervention is so much needed, even though many patients will initially deny any health issues and say they are doing just "fine".
Early detection of Lung Cancer
LUNG CANCER EARLY DETECTION:
CRBCM IS SEEKING FUNDING FOR A STUDY TO SEE WHETHER CURRENT MOLECULAR TESTING COULD DETECT EARLY LUNG CANCER IN SELECTED GROUPS OF HEAVY SMOKERS. WE PLAN TO SELECT 150 HEAVY SMOKERS (HISTORY OF 60 PACK A YEAR).
OBTAIN SEQUENCIAL SERUM LEVELS OF E-CADHERIN, METALLOPROTEINASE, AND TUMOR GROWTH FACTOR BETA (EVERY 3 MONTHS FOR 1 YEAR). A PET SCAN WILL BE OBTAINED AT DAY 1 AND DAY 365. SELECTED INDIVIDUALS WILL BE OBSERVED FOR 3-5 YEARS THERE AFTER WITH YEARLY CHECK OF MARKERS AFTER THE FIRST YEAR.
ALTHOUGH PET FINDINGS ARE CRITICAL FOR OUR EVALUATION, WHAT WE ARE CONCENTRATING ON IS TO SEE WHETHER THESE "TUMOR MARKERS" FOLLOWED SEQUENTIALLY COULD PREDICT LUNG CANCER IN HEAVY SMOKERS.
IT WOULD BE INTERESTING TO SEE THE LEVELS OF THESE MARKERS ON PATIENTS WITH INCIDENTAL POSITIVE PET FINDINGS. ANOTHER COROLLARY MEASUREMENT WILL SCREEN FOR ANA AND RHEUMATOID FACTOR TO SEE WHETHER COEXISTING AUTOIMMUNE DISEASES AFFECT THE PATTERN OF THESE MARKERS, PARTICULARLY THE TGF.
SHOULD THESE FINDINGS BE SIGNIFICANT, A TRIPLE KIT COULD BE DEVELOPED FOR EARLY DETECTION OF LUNG CANCER.
CRBCM IS SEEKING FUNDING FOR A STUDY TO SEE WHETHER CURRENT MOLECULAR TESTING COULD DETECT EARLY LUNG CANCER IN SELECTED GROUPS OF HEAVY SMOKERS. WE PLAN TO SELECT 150 HEAVY SMOKERS (HISTORY OF 60 PACK A YEAR).
OBTAIN SEQUENCIAL SERUM LEVELS OF E-CADHERIN, METALLOPROTEINASE, AND TUMOR GROWTH FACTOR BETA (EVERY 3 MONTHS FOR 1 YEAR). A PET SCAN WILL BE OBTAINED AT DAY 1 AND DAY 365. SELECTED INDIVIDUALS WILL BE OBSERVED FOR 3-5 YEARS THERE AFTER WITH YEARLY CHECK OF MARKERS AFTER THE FIRST YEAR.
ALTHOUGH PET FINDINGS ARE CRITICAL FOR OUR EVALUATION, WHAT WE ARE CONCENTRATING ON IS TO SEE WHETHER THESE "TUMOR MARKERS" FOLLOWED SEQUENTIALLY COULD PREDICT LUNG CANCER IN HEAVY SMOKERS.
IT WOULD BE INTERESTING TO SEE THE LEVELS OF THESE MARKERS ON PATIENTS WITH INCIDENTAL POSITIVE PET FINDINGS. ANOTHER COROLLARY MEASUREMENT WILL SCREEN FOR ANA AND RHEUMATOID FACTOR TO SEE WHETHER COEXISTING AUTOIMMUNE DISEASES AFFECT THE PATTERN OF THESE MARKERS, PARTICULARLY THE TGF.
SHOULD THESE FINDINGS BE SIGNIFICANT, A TRIPLE KIT COULD BE DEVELOPED FOR EARLY DETECTION OF LUNG CANCER.
Monday, December 3, 2012
New drug released by the FDA
Bio Information: "XL-184 free base (Cabozantinib) is a potent multitargeted VEGFR2, Met, FLT3, Tie2, Kit and Ret inhibitor with IC50 of 0.035, 1.8, 14.4, 14.3 and 4.6 nM for VEGFR2, Met, FLT3, Tie2 and Kit, respectively. In cells XL-184 free base (Cabozantinib) is also very potent, with IC50 under 10 nM for VEGFR2, MET, Kit and FLT3-ITD mechanistic assays. In in vitro angiogenesis assays, XL-184 free base (Cabozantinib) exhibits single-digit nanomolar potency. In mouse xenograft models, XL-184 free base (Cabozantinib), dosed orally, demonstrated dose-dependent inhibition of tumor growth and tumor regression, associated with disruption of the tumor vasculature and extensive tumor cell apoptosis."
for Refractory metastatic Prostate cancer
AN OLD POST UPDATED TO CONTINUE THE STORY...
CLINICAL HYPOTHESIS IN CANCER RESEARCH AND COMMERCIALIZATION:
Of 186,000 Prostate cancers diagnosed each year, only 29,000 patients will die of this disease. In fact 70% of men over 80 years of age may be found with Prostate Cancer. Most will not die of this cancer. This fact has made almost futile the testing for prostate cancer in elderly patients. How does one chose who should be followed closely or treated? In other words how do you know what prostate cancer to observe versus which one to actually treat? In more scientific terms, which are the predictive factors that would prompt us to act versus observe the cancer? To make the matter more confusing, the success of PSA (prostate Specific Antigen) testing has complicated the issue. It has led to over-diagnosis, and experts are now recommending to use PSA findings with caution.
One thing is for sure: the difference between a benign and malignant tumor is that the malignant ones spread and invade our body. This is called "ability to metastasize". It is by invading other organs that cancer causes these organs to fail and finally causing death of the patient. Researchers have now started to look at cancer cells to try to predict which ones will spread and therefore kill the individual.
The Hypothesis:
For a cancer to spread, it has to detach itself from its surroundings and create a way to where it wants to go. Scientists have suggested that wherever a cell is located, it is maintained in place by ADHESION MOLECULES which tie them to the location. To make its move, the cancer cell has to lose these molecules.
This is why E-Cadherin has to be reduced by the cell, so that it can free itself from this environment. The question now is: Is a REDUCTION OF E-CADHERIN A PREDICTOR OF BAD CANCER? IN OTHER WORDS, SHOULD WE BE TESTING FOR THE REDUCTION OF E-CADHERIN IN PROSTATE CANCER TO PREDICT WHICH ONES NEEDS INTERVENTION? This is thought provoking.
P120 and beta- catenins are 2 molecules which could potentially be surrogates of cancer metastasis...who knows for sure!
After it has freed itself, the cancer cell has to move through tissues, it uses enzymes to break through the fibers. Some of these enzymes are called METALLOPROTEINASE. The current question is: SHOULD WE BE MEASURING LEVELS OF METALLOPROTEINASES TO DETECT CANCER CELLS ON THE MOVE?
These questions have been raised, it is time to work.
We could actually improve current means of screening for cancer by checking for reduction of E-Cadherin and increase of metalloproteinase in the tumor or blood if this is possible. Potential for commercialization is high if we can conquer this detection technology. "lets go to work!
TODAY WE ADDED
12/3/2012
METASTASIS AND SEEDING INTO NEW OR INVADED TISSUE.
When the cancer cell reaches the new location, it uses the TGF beta to help its growth and to create exceptional advantage for its growth versus surrounding tissue. This Lead scientists to conclude that TGF beta presence is a sign of resistant disease. When in facts, it is first a late sign of metastasis already COMPLETED, TGF beta seems to be a sign of SEEDING INTO A NEW LOCATION. TGF BETA NOT ONLY STIMULATE GROWTH BUT COULD BE AN INHIBITORY PROTEIN FOR THE HOST DEFENSE AND REJECTION. SAME WAY TUMOR NECROSIS FACTOR COULD BE USED TO INHIBIT SURROUNDING CELLS IN A INFECTION BY FOREIGN HOST.
QUESTION:
SHOULD TGF BETA INCREASE BE THE THE SIGN OF SEEDING VS LATE STEP OF METASTASIS. WE BELIEVE THAT BY THE TIME TGF BETA IS BEING ELEVATED, SEEDING HAS ALREADY OCCURRED.
OCT 14TH WE WROTE THIS ARTICLE
TELL US WHAT YOU THINK...
CLINICAL HYPOTHESIS IN CANCER RESEARCH AND COMMERCIALIZATION:
Of 186,000 Prostate cancers diagnosed each year, only 29,000 patients will die of this disease. In fact 70% of men over 80 years of age may be found with Prostate Cancer. Most will not die of this cancer. This fact has made almost futile the testing for prostate cancer in elderly patients. How does one chose who should be followed closely or treated? In other words how do you know what prostate cancer to observe versus which one to actually treat? In more scientific terms, which are the predictive factors that would prompt us to act versus observe the cancer? To make the matter more confusing, the success of PSA (prostate Specific Antigen) testing has complicated the issue. It has led to over-diagnosis, and experts are now recommending to use PSA findings with caution.
One thing is for sure: the difference between a benign and malignant tumor is that the malignant ones spread and invade our body. This is called "ability to metastasize". It is by invading other organs that cancer causes these organs to fail and finally causing death of the patient. Researchers have now started to look at cancer cells to try to predict which ones will spread and therefore kill the individual.
The Hypothesis:
For a cancer to spread, it has to detach itself from its surroundings and create a way to where it wants to go. Scientists have suggested that wherever a cell is located, it is maintained in place by ADHESION MOLECULES which tie them to the location. To make its move, the cancer cell has to lose these molecules.
This is why E-Cadherin has to be reduced by the cell, so that it can free itself from this environment. The question now is: Is a REDUCTION OF E-CADHERIN A PREDICTOR OF BAD CANCER? IN OTHER WORDS, SHOULD WE BE TESTING FOR THE REDUCTION OF E-CADHERIN IN PROSTATE CANCER TO PREDICT WHICH ONES NEEDS INTERVENTION? This is thought provoking.
P120 and beta- catenins are 2 molecules which could potentially be surrogates of cancer metastasis...who knows for sure!
After it has freed itself, the cancer cell has to move through tissues, it uses enzymes to break through the fibers. Some of these enzymes are called METALLOPROTEINASE. The current question is: SHOULD WE BE MEASURING LEVELS OF METALLOPROTEINASES TO DETECT CANCER CELLS ON THE MOVE?
Matrix metalloproteinases 2 and 9 increase permeability of sheep pleura in vitro
Eleni Apostolidou1*)These questions have been raised, it is time to work.
We could actually improve current means of screening for cancer by checking for reduction of E-Cadherin and increase of metalloproteinase in the tumor or blood if this is possible. Potential for commercialization is high if we can conquer this detection technology. "lets go to work!
TODAY WE ADDED
12/3/2012
METASTASIS AND SEEDING INTO NEW OR INVADED TISSUE.
When the cancer cell reaches the new location, it uses the TGF beta to help its growth and to create exceptional advantage for its growth versus surrounding tissue. This Lead scientists to conclude that TGF beta presence is a sign of resistant disease. When in facts, it is first a late sign of metastasis already COMPLETED, TGF beta seems to be a sign of SEEDING INTO A NEW LOCATION. TGF BETA NOT ONLY STIMULATE GROWTH BUT COULD BE AN INHIBITORY PROTEIN FOR THE HOST DEFENSE AND REJECTION. SAME WAY TUMOR NECROSIS FACTOR COULD BE USED TO INHIBIT SURROUNDING CELLS IN A INFECTION BY FOREIGN HOST.
QUESTION:
SHOULD TGF BETA INCREASE BE THE THE SIGN OF SEEDING VS LATE STEP OF METASTASIS. WE BELIEVE THAT BY THE TIME TGF BETA IS BEING ELEVATED, SEEDING HAS ALREADY OCCURRED.
OCT 14TH WE WROTE THIS ARTICLE
TELL US WHAT YOU THINK...
Sunday, December 2, 2012
Active Sunday for CRBCM!
Activities at CRBCM
good news, our representatives in Greenville, Ohio and Richmond, Indiana have elected to meet and plan strategies for approaching together their respective state representatives. The fight is on and going wide. We have sent them all ammunitions, the 4 projects submitted before CPRIT here in Texas and various contacts in Indiana. (I Used to work at Reid Hospital in Richmond IN after my 14 year tour at Kaiser Permanente MidAtlantic Area). We have urged them to involve Congresswoman Nina Turner and Minority leader Senator Eric H. Kearny in Ohio, all very dynamic leaders for minority populations. Any help we can get to advance our cause will be appreciated!
good news, our representatives in Greenville, Ohio and Richmond, Indiana have elected to meet and plan strategies for approaching together their respective state representatives. The fight is on and going wide. We have sent them all ammunitions, the 4 projects submitted before CPRIT here in Texas and various contacts in Indiana. (I Used to work at Reid Hospital in Richmond IN after my 14 year tour at Kaiser Permanente MidAtlantic Area). We have urged them to involve Congresswoman Nina Turner and Minority leader Senator Eric H. Kearny in Ohio, all very dynamic leaders for minority populations. Any help we can get to advance our cause will be appreciated!
Translational Research Project
Research at CRBCM
The CRBCM has determined that Breast Cancer Mortality in African American is excessive. Of the 6000 African American women who will or have died this year, 3000 could have been saved if leaders paid more attention to this cause.
3 reasons contribute to this excess mortality
1. Poor rates of screening mammograms in these minority population (or low income populations in general).
2. Late stage of disease at diagnosis
3. POOR HISTOLOGY, high rate of triple negative Breast cancer, which can only be managed by adjuvant and palliative chemotherapy. Increasingly however, new target treatments are being tried. (ie.PARP and Histone De-acetylator inhibitors).
The success of chemotherapy, the only option readily available to African American women with triple negative Breast cancer is 20-40% at best. We need further options and further investigation is required.
At CRBCM we believe that the potential contribution of Anti-Kinesin could be even more important, particularly when combined to a Taxane-Cisplatin or related Microtubule disrupting drugs.
The human Genome Project has already determined that the Genome of triple negative Breast Cancer is comparable to that of Ovarian Cancer.This fact re-enforces our choice for Taxane-platinum based combination in this disease.
Another thing we know is that cure happens when the cancer cell is killed. The killing of cells is induced by Caspase release from cellular mitochondria. Caspases are lytic proteins to the extent of achieving death by global disruption of sensitive pathways. To our knowledge one of the determinant inhibitor of Caspase release is the presence of high levels of Bcl-2. Bcl-2 seems to be more effective in mitigating the effect of drugs acting through the Topoisomerase enzyme (etoposide and Adriamycin)
In a cell such as the cancer cell which naturally intend to divide for growth of the cancer, disruption of Microtubule/microfilament, support scaffolding for movement of chromosomes during cell division, appears a stronger argument bypassing the Bcl-2 protection for the release of caspases. In fact, the Mitochondria nearby appear to be located there attached to close-by membranes. Suffice is to say that significant microtubular or Microfilament disruption is not compatible with life. This is why Taxanes (Erubulin and Ixabepilone) are most likely the most powerful drugs in breast cancer. It is also why we believe that the right Anti-kinesin could add significantly to the effect of Taxane-platinum combination in triple negative Breast cancer.
Study Methology
1 We will use 50 tissue sample of 4 different cancers (Breast, Colon, lung and liver) for a total of 200 tissue samples.
2.Using Bcl-2 kits, we will detect and quantify Bcl-2 per tissue and per nature of tissue origin. We can then identify which type of tissue has the highest Bcl-2 at cancerous status.
3.we will expose half of each group of tissue to taxal-Cisplatin ex-vivo. and, using standard kits, will detect and quantify Caspases released.
4. we will expose the other half to a triplet with Taxane-Cisplatin and Antikinesin, and detect and measure quantitatively the level of Caspases released by the tissue
5. Consideration of using Antikinesin alone has been discussed, no one would choose this option given the fact that time and again mono-target therapy have failed to achieve better than 30% because of patient genome heterogeneity.
6. We could also test these tissue response to Etoposide to verify Bcl-2 resistance and therefore appreciate the magnitude of Microtubule disruptions through the Taxane based combinations.
Our conclusions (proof of concept) will relate to:
1. Bcl-2 content by nature of the cancerous tissue. This would predict sensitivity to tested chemotherapy drugs.
2. Verify sensitivity and specificity of Bcl-2 kits
3. Verify sensitivity and specificity of Caspase kits
4.Verify that Taxane-platinum based chemotherapy is better than Etoposide Ex-vivo.
5.Verify that adding Anti-kinesin improves response to therapy
6. By comparing to Etoposide alone by levels of Bcl-2, verify that Taxane based combination do bypass Bcl-2 protection of Mitochondria
7. If differences are corroborated, we can show that response to therapy can be predicted ex-vivo.
It is evident that such a study provide numerous commercial opportunities when it comes to kit development and Antikinesin product selections.
Let's work with this Peggy! add any ideas and suggestions
we ask our readers to send their comments. The fight is on for the cure...
The CRBCM has determined that Breast Cancer Mortality in African American is excessive. Of the 6000 African American women who will or have died this year, 3000 could have been saved if leaders paid more attention to this cause.
3 reasons contribute to this excess mortality
1. Poor rates of screening mammograms in these minority population (or low income populations in general).
2. Late stage of disease at diagnosis
3. POOR HISTOLOGY, high rate of triple negative Breast cancer, which can only be managed by adjuvant and palliative chemotherapy. Increasingly however, new target treatments are being tried. (ie.PARP and Histone De-acetylator inhibitors).
The success of chemotherapy, the only option readily available to African American women with triple negative Breast cancer is 20-40% at best. We need further options and further investigation is required.
At CRBCM we believe that the potential contribution of Anti-Kinesin could be even more important, particularly when combined to a Taxane-Cisplatin or related Microtubule disrupting drugs.
The human Genome Project has already determined that the Genome of triple negative Breast Cancer is comparable to that of Ovarian Cancer.This fact re-enforces our choice for Taxane-platinum based combination in this disease.
Another thing we know is that cure happens when the cancer cell is killed. The killing of cells is induced by Caspase release from cellular mitochondria. Caspases are lytic proteins to the extent of achieving death by global disruption of sensitive pathways. To our knowledge one of the determinant inhibitor of Caspase release is the presence of high levels of Bcl-2. Bcl-2 seems to be more effective in mitigating the effect of drugs acting through the Topoisomerase enzyme (etoposide and Adriamycin)
In a cell such as the cancer cell which naturally intend to divide for growth of the cancer, disruption of Microtubule/microfilament, support scaffolding for movement of chromosomes during cell division, appears a stronger argument bypassing the Bcl-2 protection for the release of caspases. In fact, the Mitochondria nearby appear to be located there attached to close-by membranes. Suffice is to say that significant microtubular or Microfilament disruption is not compatible with life. This is why Taxanes (Erubulin and Ixabepilone) are most likely the most powerful drugs in breast cancer. It is also why we believe that the right Anti-kinesin could add significantly to the effect of Taxane-platinum combination in triple negative Breast cancer.
Study Methology
1 We will use 50 tissue sample of 4 different cancers (Breast, Colon, lung and liver) for a total of 200 tissue samples.
2.Using Bcl-2 kits, we will detect and quantify Bcl-2 per tissue and per nature of tissue origin. We can then identify which type of tissue has the highest Bcl-2 at cancerous status.
3.we will expose half of each group of tissue to taxal-Cisplatin ex-vivo. and, using standard kits, will detect and quantify Caspases released.
4. we will expose the other half to a triplet with Taxane-Cisplatin and Antikinesin, and detect and measure quantitatively the level of Caspases released by the tissue
5. Consideration of using Antikinesin alone has been discussed, no one would choose this option given the fact that time and again mono-target therapy have failed to achieve better than 30% because of patient genome heterogeneity.
6. We could also test these tissue response to Etoposide to verify Bcl-2 resistance and therefore appreciate the magnitude of Microtubule disruptions through the Taxane based combinations.
Our conclusions (proof of concept) will relate to:
1. Bcl-2 content by nature of the cancerous tissue. This would predict sensitivity to tested chemotherapy drugs.
2. Verify sensitivity and specificity of Bcl-2 kits
3. Verify sensitivity and specificity of Caspase kits
4.Verify that Taxane-platinum based chemotherapy is better than Etoposide Ex-vivo.
5.Verify that adding Anti-kinesin improves response to therapy
6. By comparing to Etoposide alone by levels of Bcl-2, verify that Taxane based combination do bypass Bcl-2 protection of Mitochondria
7. If differences are corroborated, we can show that response to therapy can be predicted ex-vivo.
It is evident that such a study provide numerous commercial opportunities when it comes to kit development and Antikinesin product selections.
Let's work with this Peggy! add any ideas and suggestions
we ask our readers to send their comments. The fight is on for the cure...
Saturday, December 1, 2012
Understanding the Laws of Biology
IMPORTANCE OF UNDERSTANDING BIOLOGIC LAWS
With every research performed around the world, scientists learn a little more. It is important that research focuses on a particular molecule and its interactions, specificity and efficacy. Point location research should be understood within a general plan of advances in biomolecular research. To find that, TGF Beta, when produced, will make a cancer grow and therefore make the cancer more resistant to treatment, is nice. It adds to the detailed knowledge. TGF(s) act on membrane receptors, therefore it will harvest the signal pathways to display its might. We know that it will reach or may emanate from some transcription genes. The tract its actions have to follow to affect the cell is full of loopholes and pitfalls. Going after TGF(s) should be part of a planned combination approach. It cannot work in over 30% of the people because of genetic heterogeneity which in itself is nature's protection for host survival.
Here at CRBCM, we understand that to cross the 50% effectiveness, our current treatment strategies must include the activity of the 2nd law well described here. And better yet the first 2 laws. Disruption of gene, and that of Microtubule that will lead to caspase release (Cytochrome c disruption implied). Membrane based effects are only as good as they are able to involve an increased activity of fas and Bax. Short of that, they are 70% ineffective. (You can't discount 30% though)
TGF could present an opportunity for treatment. We made an early allusion to the JUDO. Use the power of the attacker to send him to the floor "in the general direction of his attack". TGF wants to achieve acceleration of growth and cellular multiplication. Disruption of gene and microtubule may in fact be more effective when faster multiplication is achieved? This is risky, but not a crazy a approach. That is also why chemotherapy works only on dividing cells!
Globally, however, TGF and Bcl-2 tend to protect cancer cell. TGF seems to give a growth advantage to cancer cells vis-a-vis surrounding cells. Bcl-2 seems rather to be a protection mechanism from reaching the mitochondrial Caspase, protecting therefore cancer cell from Apoptosis, the cure to cancer.
With this background info, we can now judge any research coming along as to its importance, and see how it fits in the general strategy to achieve the cure we all want.
With every research performed around the world, scientists learn a little more. It is important that research focuses on a particular molecule and its interactions, specificity and efficacy. Point location research should be understood within a general plan of advances in biomolecular research. To find that, TGF Beta, when produced, will make a cancer grow and therefore make the cancer more resistant to treatment, is nice. It adds to the detailed knowledge. TGF(s) act on membrane receptors, therefore it will harvest the signal pathways to display its might. We know that it will reach or may emanate from some transcription genes. The tract its actions have to follow to affect the cell is full of loopholes and pitfalls. Going after TGF(s) should be part of a planned combination approach. It cannot work in over 30% of the people because of genetic heterogeneity which in itself is nature's protection for host survival.
Here at CRBCM, we understand that to cross the 50% effectiveness, our current treatment strategies must include the activity of the 2nd law well described here. And better yet the first 2 laws. Disruption of gene, and that of Microtubule that will lead to caspase release (Cytochrome c disruption implied). Membrane based effects are only as good as they are able to involve an increased activity of fas and Bax. Short of that, they are 70% ineffective. (You can't discount 30% though)
TGF could present an opportunity for treatment. We made an early allusion to the JUDO. Use the power of the attacker to send him to the floor "in the general direction of his attack". TGF wants to achieve acceleration of growth and cellular multiplication. Disruption of gene and microtubule may in fact be more effective when faster multiplication is achieved? This is risky, but not a crazy a approach. That is also why chemotherapy works only on dividing cells!
Globally, however, TGF and Bcl-2 tend to protect cancer cell. TGF seems to give a growth advantage to cancer cells vis-a-vis surrounding cells. Bcl-2 seems rather to be a protection mechanism from reaching the mitochondrial Caspase, protecting therefore cancer cell from Apoptosis, the cure to cancer.
With this background info, we can now judge any research coming along as to its importance, and see how it fits in the general strategy to achieve the cure we all want.
You Flip Flop, Changing all the time.... by Clement Albert on Ubetoo
by Clement AlbertYou Flip Flop, Changing all the time...
BRINGING IT ALL TOGETHER IN A WORLD OF SOUNDS
IF YOU GUESSED WHO IS CLEMENT ALBERT, YOU ARE RIGHT!
WE WILL PROMOTE CURE AND PUBLIC HEALTH
THROUGH MUSIC MEDIA...CRBCM IS EQUIPPED WITH A MUSIC STUDIO!
Friday, November 30, 2012
3rd Law of Nature (continued) & 4th Law of Nature
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.
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.
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.
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