Showing posts with label cancer. Show all posts
Showing posts with label cancer. Show all posts

Monday, November 4, 2013

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State of Texas Seal
CPRIT’s Oversight Committee met November 1 for the first time since February beginning a new era for the agency – one with a higher level of transparency, improved processes and strengthened accountability to the taxpayers of Texas. As I reported to the Oversight Committee, in addition to provisions in SB 149 which modified CPRIT’s enabling legislation, the agency has taken action to implement all 41 of the State Auditor’s January 2013 recommendations.

We accomplished a number of important items at the meeting that will allow CPRIT’s work to move forward. We also began our commitment to transparency by holding the meeting at the State Capitol and streaming the meeting live over the web – a first for CPRIT. Within days, we’ll post a video of the proceedings to our website as well. Major actions of the Oversight Committee include:
  • Adopting new bylaws for how the Oversight Committee will operate as a governing body, including an updated code of conduct. These bylaws indicate the Oversight Committee commitment to operating with the highest level of integrity;
  • Posting revised administrative rules to the Texas Register for public comment. The rules expanded from 40 to over 120 pages, and implement many of the State Auditor’s recommendations as well as other process and accountability improvements;
  • Restarting our grantmaking process, including the approval of Scientific Review Council appointees. This action allows CPRIT to resume review of grants and enable healthcare and medical professionals to apply for new grants. We expect additional steps at the next Oversight Committee meeting scheduled for November 22, 2013. At that session, I anticipate discussion about research and prevention program priorities, and a number of other actions important to our continuing operations.
I want to express my gratitude to the members of the 83rd Legislature and their staffs, state leadership offices and CPRIT staff for getting us to November 1. The new Oversight Committee came to the meeting well-prepared and eager to resume the important responsibilities assigned to CPRIT by the citizens of Texas.

It’s nice to be back at work!

Regards,

Wayne R. Roberts
Interim Executive Director
Cancer Prevention & Research Institute of Texas
P.O. Box 12097
Austin, Texas 78711

Marching on toward future therapies in Cancer Medicine

Most cancers result from a disturbance of our genes.  The disturbance could be functional or simply a change in the nature of genes called Mutations.  Mutations that are deleterious are those that stop or otherwise alter the fundamental function of the gene.  Genes can initiate, regulate, facilitate or simply hook to other genes.  Hooking (Adapter) to other genes has a strong impact because it can change the direction of the pathways, or give a gene the powers of the gene it is now hooked onto!  There are those who simply allow hooking to membranes as in Anchor genes that sometimes allow trans-membrane transport, sometime just providing a substrate from other reactions to occur. 
Hooks can also connect several molecules (Homeobox).

Suffice is to say that if a gene is broken, let's introduce a new gene.

The challenge is: how do we get a new gene in there?
Here we are looking at Nanotechnology to achieve this challenge!

Tuesday, October 29, 2013

Progress in Genome studies: case in point the DIGITAL PCR.

If what they promise is real, we are entering an important phase where not only we can count mutations,  but can also try to determine levels of gene amplifications  that are secondary, versus those that are in response or a consequence of upstream genes normally amplified or amplified because they are mutated!

" Next-generation sequencing technology has transformed cancer genomics, but faces the challenge of genome and transcriptome heterogeneity inherent to any tumor sample. One strategy for capturing the complex landscape of mutational processes, clonal evolution/amplification and tissue invasion is the application of digital PCR, which enables the identification and precise quantitation of individual mutations - including those present at a very low frequency."(Biomedcentral)

This new technology will open new evaluations of gene quantities as to their meaning and trigger!  It will allow also to detect levels of suppression of a normal gene when it is found in an unexpected amount.  We know for example that in many lung cancers PTEN is suppressed.  Whether  this is a primary happening or secondary can be further debated.  In Ovarian cancer DAB2 is suppressed. ("The down-regulation of DAB2 may play an important role in ovarian carcinogenesis. This gene was initially named DOC2 (for Differentially expressed in Ovarian Cancer) and is distinct from the DOC2A and DOC2B genes (for double C2-like domains, alpha and beta).[3]

 Most of these suppressions are the result of an amplification of an upstream gene or an overexpression of an inhibitory protein.  When it comes to DAB2, it is important to report that this gives the cancerous process some teeth and bad prognosis.  Indeed, the suppression of DOC2 gives the tumor ways of escaping proliferation control by the cancerous cell by activating E3 (removing by unbiquitilation of the inhibitor of the inhibitor of E3).  This new technology will allow direct quantification of the 2 inhibitors or the E3 for that matter.  It may also clarify how Velcade works in relation to the 3 compounds!

Thursday, May 2, 2013

The MEANING OF THE MDHonors AWARD for CRBCM.

MEANING OF THE MDHonors AWARD for CRBCM.

The CRBCM would like to thank MDHonors for the Research award given to our Coalition and young clinic (Greater East cancer Center of El Paso Texas).  This award will allow to build our institution's primary steps into the research power house we intend to become.  It will formalize in practical terms (working on a tangible research project) some of our collaboration attempts with the University Medical Center in El Paso, and the UTEP (University of Texas in El Paso).  With this award, the CRBCM will continue to march toward the cure day by day, and with confidence and focused vision.   And with this steady progression, victory is certain.  MDHonors revived our hope in the belief that we still have a chance to succeed if we try hard enough!
The cure is within reach, we got to keep on believing that it is reachable, and not get discouraged by politicians and malicious institutions which are distracting our progress toward the cure! 
We can not thank MDHonors enough ; for now let's go to work as we face international scrutiny and the true challenge of a cure for cancers!

And God Bless CRBCM
La lucha continua !

Dr Kankonde.

Thursday, March 28, 2013

S100A4, AN IMPORTANT TARGET FOR SURE! LOCATED AT 1q21

The importance of a molecule in the body is determined  by its chemical properties, the pathogenesis of the disease in which it is  participating or how critical a function it is performing in the cascade of a pathway. The importance of a gene is determined by its product's shape and function which is sometimes defined by atoms hanging at its periphery, ready for business of attracting other electrons or ions.  It is also determined by genes in a linkage relationship at the chromosome level. This last point is important to be clarified by researchers who have the tools to explore the coexistence of genes on an arm of a specific chromosome.  And a lot of research forgets to look at that aspect of the problem gene. (don't forget "q" most of the time portends for worse prognosis than "p" , that is it may induce a malignant phenotype.  In fact, co-expression of homologue "p" will mitigate the phenotype. And the homologue gene is on a p arm and on a different numbered chromosome)

By now you also know that cell life is directed in one direction at a time frequently.  Cells are under function performance, differentiation, proliferation or neoplastic transformation.  Neoplastic cells are in concert with surrounding cells from which it avoids to be in conflict with to escape detection.  Neoplastic Cells will be soon stressed because of their increased needs and through the c-JUN -FOS will increase a Tumor Growth factor liberated from the cellular membrane with concomittent release of Metalloproteases in the extracellular membrane through flippase-floppase activity.  The Metalloprotease goes out, the Growth factor goes in.
IT WOULD BE GOOD TO KNOW WHICH METALLOPROTEASE IS SPECIFICALLY LINKED TO WHICH PROTEIN IN ORDER TO KNOW WHAT IS GOING ON INSIDE THE CELL JUNK BY DETERMINING WHICH OF THE METALLOPROTEASE   FAMILY MEMBER IS IN THE EXTRACELLULAR SPACE OR BLOOD!   NICE LITTLE PROJECT RIGHT THERE.  "WHICH TYPE OF METALLOPROTEASE FOR WHICH CANCER"  I BET, BRAIN TUMOR WILL RELEASE A DIFFERENT METALLOPROTEASE THAN OVARIAN CANCER.  BECAUSE THE GROWTH HORMONE RELEASED IN THE CELL WILL BE DIFFERENT.

By now you also know that in certain proliferative processes, there is an increased aspect of only 1 or 2 functions.  In Leukemias, for example, it is amplification of a certain Core binding complex which attaches certain molecules with specific functions.  And the cell follows the cascade of functions to go in a certain cell life trend.  Some of these proteins are gene regulators.  In fact, Leukemia would be better controlled if we just determined the proteins on CBF and the regulators that are promoted in the cell.  ANOTHER EASY PROJECT : THE PATTERNS OF GENE REGULATORS IN A SPECIFIC LEUKEMIA (BY WETERN OR SOUTHERN BLOT).

One of those regulators is the S100A4, a potent regulator which not only is at the differentiation, meaning when mutated or amplified it will create phenotypic havoc for sure.  It is handling Calcium, therefore will affect some Microtubules (good or bad for Taxanes?):  Time to find out more! Read these articles!

NOTE HBXIP S100A4:  AN IMPORTANT TARGET FOR CERTAIN!

Wednesday, March 27, 2013

LOX Lysyl-Oxidase

This gene found in gastric and bladder cancer is prognostic.  Its amplification allows the cell to deal with austere conditions in Metastatic conditions.  It seems to be amplifying under the impetus of HIF (Hypoxia induced factor). Its amplification appears more reactive than driving the resulting dowstream reaction.It can affect the structure of laminin and collagen through its formation of Aldehyde.
It can push proliferation by acting as a co-factor at nuclear level.
It can affect AKT (Protein Kinase B).
Recently, a study in Sarcoma using a Doxorubicin isoform was set in motion. Expression of LOX should be included in the analysis since Hypoxia was a component of the treatment.
LOX would not be a principal target in a treatment strategy since it addresses mostly metastasis, it either an adjunct treatment, or will have a role in Maintenance therapy.

Sunday, March 24, 2013

INTERESTING FACTS

Most Oncologists get more practice changing information from the JCO and the New England Journal of Medicine than from BLOOD which has turned "Molecular" on them!  Blood has become more of a research tool than of impact on day to day Oncology/Hematology practice.  A balance is needed guys over there!  Even the Lancet is now better perceived by "practitioners"!
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*Researchers keeps ahead of Oncology practice, and that is good.
While we are still coming or waking to the reality of the existence of Crizotinib.

Crizotinib

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Crizotinib
Systematic (IUPAC) name
3-[(1R)-1-(2,6-dichloro-3-fluorophenyl)ethoxy]-5-(1-piperidin-4-ylpyrazol-4-yl)pyridin-2-amine
Clinical data
Trade names Xalkori
MedlinePlus a612018
Licence data US FDA:link
Pregnancy cat. D (US)
Legal status -only (US)
Routes Oral
Pharmacokinetic data
Half-life 46 hours
Identifiers
CAS number 877399-52-5 
ATC code L01XE16
PubChem CID 11626560
DrugBank DB08700
ChemSpider 9801307 Yes
UNII 53AH36668S Yes
KEGG D09731 Yes
ChEMBL CHEMBL601719 Yes
Synonyms PF-02341066
1066
Chemical data
Formula C21H22Cl2FN5O 
Mol. mass 450.337 g/mol
  (what is this?)  (verify)
Crizotinib (trade name Xalkori,[1] Pfizer), is an anti-cancer drug acting as an ALK (anaplastic lymphoma kinase) and ROS1 (c-ros oncogene 1) inhibitor, approved for treatment of some non-small cell lung carcinoma (NSCLC) in the US and some other countries, and undergoing clinical trials testing its safety and efficacy in anaplastic large cell lymphoma, neuroblastoma, and other advanced solid tumors in both adults and children.[2]
 -------------------------------

RESEARCHERS ARE MOVING FORWARD
LOOKING NOW IN COMBINATION OF
1.  FIG-ROS1
2.  SLC34a2-ROS1
3.  COEXISTENCE  OF EGFR AND ROS1

THIS IS A GOOD SIGN.
IT IS ONCE AGAIN A SIGN OF HOW A CELLULAR PROCESS GETS COMPLICATED QUICKLY JUST AS YOU START UNDERSTANDING.

LESS THAN 0.5% OF ONCOLOGIST HAVE USED CRIZOTINIB TO DATE!

Friday, March 22, 2013

Meat consumption and mortality - results from the European Prospective Investigation into Cancer and Nutrition



Results
As of June 2009, 26,344 deaths were observed. After multivariate adjustment, a high consumption of red meat was related to higher all-cause mortality (hazard ratio (HR) = 1.14, 95% confidence interval (CI) 1.01 to 1.28, 160+ versus 10 to 19.9 g/day), and the association was stronger for processed meat (HR = 1.44, 95% CI 1.24 to 1.66, 160+ versus 10 to 19.9 g/day). After correction for measurement error, higher all-cause mortality remained significant only for processed meat (HR = 1.18, 95% CI 1.11 to 1.25, per 50 g/d). We estimated that 3.3% (95% CI 1.5% to 5.0%) of deaths could be prevented if all participants had a processed meat consumption of less than 20 g/day. Significant associations with processed meat intake were observed for cardiovascular diseases, cancer, and 'other causes of death'. The consumption of poultry was not related to all-cause mortality.
Conclusions
The results of our analysis support a moderate positive association between processed meat consumption and mortality, in particular due to cardiovascular diseases, but also to cancer.
Keywords:

Socioeconomic patient characteristics predict delay in cancer diagnosis: a Danish cohort study


http://www.biomedcentral.com/1472-6963/8/49

JAMA Network | JAMA | DELAY IN DIAGNOSIS AND TREATMENT OF CANCER

This is an article from 1950 that already pointed out what matters to improve patient's survival outcomes:

JAMA Network | JAMA | DELAY IN DIAGNOSIS AND TREATMENT OF CANCER

Friday, March 8, 2013

CHANGES ARE COMING TO YOU, LIKE IT OR NOT!

SOME PEOPLE REALLY BELIEVE THEY ARE THEY TOO BIG FOR CRITICISM, THEY FEEL OFFENDED WHEN YOU CONFRONT THEM WITH A TRUTH THEY CAN'T BELIEVE.
Everyday Big professors are reminded how important they are by our praises and regular consultations.  Professors grow on us because they have knowledge we believe to be the truth, and because often they are right rather than wrong.  But every time they are solicited, they practice a certain logic they have perfected to come to a logical conclusion.  They pass on this logical process to their students and friends and, as a result, a university culture is created and passed on!  Such a system, however, needs to be challenged once in a while to be made better.  It is made better when it accepts change, because accepting new plausible changes prepares us to wider sorts of challenges, it is the strength of diversity, it prepares us against challenges to come, challenges we will have to reckon with at one point or another. It is the strength of these United States. It is why this country is better prepared than other countries which is somewhat monolithic, culture wise!

When monolithic systems are confronted, when our professors are confronted and when they refuse to face the truthful difference, they reject it with anger and become defensive and somewhat violent (not necessarily physical violence) in their tone.
I was in a recent meeting where I suggested to an eminent oncologist that we look into potential new targeting therapy for a rare type of sarcoma.  An eminent man who I admire became irate or vexed at an unexpected level which surprised me.  It is the truth that everyone nowadays should be looking to target therapy for answers in cancer.  But his reaction was off the wall!   I can understand that evidence based medicine forces us to argue only what has been proven,  but in a university setting, the non-proven should challenge us to look for more, it should be where we start if the goal is to push the envelope further.  I don't know what was in the man's drink to be so offended by the truth we all face, the puzzle that is cancer. I don't know under what "University environment" political pressure he finds himself, so I give him a break, give him slack !  He was just defending his turf !

But one thing for sure, let's be more receptive to change, because it will come, and impose on us whether we like it or not!  You can resist it for a while, but one of these days even your own son or a dear friend will wake you up to it!

Monday, February 25, 2013

STILL LOOKING FOR NEW TARGETS FOR THE CURE OF CANCER?

WELL I GIVE YOU THESE TARGETS DEEP IN THE NUCLEUS

1. Esap 1
2. Esw-1
3. Esc-2 and 8
and the mighty NPT-1 gene

Here you are at the heart of cell survival
as you touch on Histone Deacetylase, gene silencing (Including Ribosomal genes or RNA) and Telomeres.
and I gave you a clue, Antibiotic from fungi can help!
The cure is at the door, open it!


Friday, February 22, 2013

ANTI-MEK ARE BETTER ANTI-VEGF

Based on what we know now, it is easy to see that in those diseases where Avastin has failed FDA approval, Anti-MEK will do better.  MEK is down stream and MEK is involved in much more, including VEGF expression.  MEK is part of the MEK/MAPK pathways, it is the door to Mesenchymal transformation (that is it the door to epithelial-mesenchymal transition), and therefore to angiogenesis, and to metastatic spread.
Anti-MEK also removes the negative inhibitory effect of the PTEN driven forces of the PI3K/MTOR pathways.

PTEN inhibits insulin-stimulated MEK/MAPK activation andcell growth by blocking IRS-1 phosphorylation and IRS-1/Grb-2/Sos complex formation in a breast cancer model

Watch it now as Cabozantinib, Selumtinib, and Trametinib will rise in anything Avastin has touched.
Metastatic Colon Cancer is the Primary target!

Only the MTOR inhibitors add to these drugs

Inability of Doxorubicin to add to DTIC in Melanoma is due to amplification of these 2 pathways.

Anti-MEK and MTOR combination will do far better in Melanoma and Pancreatic cancers, mark my words.  We just need to brace ourselves to a new set of side effects.

Monday, January 28, 2013

DIET FAILURES

With any kind of diet, by the time you reach the 6-12 week mark,  the selected strategy has given you its maximum benefit.  Hopefully, by then you will have achieved the 10% reduction of your total weight which is the realistic goal to pursue.  If you did it right, 1-2 pound per week of weight loss, you would have lost at least 10 pound by now.  After this, maintenance is the challenge and your body's response is even more of a challenge.
The body wants to get back to the size it knows you can achieve.  Make no mistake, size is the major killer.  Just look at the tumor, when it gets too big, areas of necrosis soon happen because some areas will suffer ischemia.

Your body will start asking for food, will try to tell you that just this small thing will not be harmful, and it will tell this throughout the day.   TIMING, WHEN YOU CAN AFFORD TO EAT SOMETHING IS AN IMPORTANT STRATEGY TO PUT IN PLACE.  KEEP CONTROL OVER THIS.  REMEMBER ONE THING IS FOR SURE: BY THIS TIME, GROWTH HAS STOPPED AND THAT THIS IS ALREADY A GREAT GOAL ACHIEVED. KEEP IT THERE.

To go further down, avoid staying home near the refrigerator.  Go out, walk at the mall without money, just your ID! Or best go to the gym or call your support buddy.  When the diet effect is maximized, that is when you need to exercise the most, and that's when you need Calorie control the most, and your vitamins.  Whatever you do, do not increase your Carbohydrate intake, or any excess calories. Remember, you will not increase your weight doing this.  The body will fight back, trying to use what you have given it to its maximum advantage, using everything to its advantage, constipation will set in to prolong intestinal absorption and reduce stool size, but work on staying "regular".  Constipation is a proven risk of Colon cancer.  Take it out. At this stage, it also is hard to exercise. Your body will tell your brain not to exercise.  Any excuses will come to mind.  Double down and keep exercising.  A walk will be good any time.  Remember, staying home with the refrigerator in the house is one of the brain challenges.  If you do reach for the refrigerator, have safe options.  Very cold water, sweet non sugary options or a fruit.  Dried vegetable chips or low calorie nuts.  Here, frequency to the refrigerator needs to be controlled by a schedule.

So, schedule or time your eating, when you reach to eating, find options that are safe, and keep on moving or exercising; this should be your strategy.  And remember, if you do not increase your weight, that's an objective success already.  We will keep trying to find more and let you know!

Saturday, January 26, 2013

PRELIMINARY DISCUSSION ON THE 4TH LAW. THE 4TH LAW IS BEST UNDERSTOOD AS THE SET OF FORCES THAT DRIVE THE CELL FUNCTIONS IN A PARTICULAR ELECTED DIRECTION.

THE 4TH LAW IS BEST UNDERSTOOD AS THE SET OF FORCES THAT DRIVE THE CELL FUNCTIONS IN A PARTICULAR ELECTED DIRECTION.
At molecular level, this is enforced by GENE AMPLIFICATION.  That is if the cell is going toward differentiation, the cell will make cellular processes to direct all the cellular function to that aim.  for specific cancer this equivalent to the notion of DRIVER Mutation.   Cellular functions are not totally random and living things do not stay still!  life is always on the go, and on the go for survival.  And once it has chosen a direction, it direct its functions toward an overall goal which at cellular level is to ensure survival.  The drive, the stamina, the direction is battery powered and purposeful!
In the cell that drive is powered and to ensure that it has direction,  AMPLIFICATION GENES go to work.

One good example of this is what happens with some Viruses.  A number of viruses when the enter the host cell, will incorporate their viral genome into the genome of the host to manage to use the host survival machinery to their advantage.  Insertion in the genome of the host sometimes is not enough to trigger the use of the Viral genome in the host machinery, the Virus has to recruit a "growth factor" most of the time called FACTOR-1 to ensure amplification of its genetic material.  (this is known for HIV infection)

In cancer cells, there are amplification genes toward the completion and survival of the cancerous process.
In lung and thyroid cancers, TTF-1 represent such a gene.  found amplified in about 10 % of tumors.  Scientist have had trouble defining its role.  But they know its AMPLIFICATION is bad news for the host.  It is a driver gene for the cancerous process.   In the cell, there are several levels of GENE AMPLIFICATIONS.

The first level is mission driven.  If the mission is to differentiate, this 4th law push to achieve the mission.
if the mission is to grow a cancer, the cell uses all its resources to make a "perfect cancer."  This means, tolerate error in the DNA multiplication, down-regulate the repair mechanism, down-regulate or mutate the  regulator of P53, MDM2. Amplify VGEF so that the tumor has plenty of good blood vessels.

The second level of amplification is actually originating from the stimulus, the cause of the transformation.  the cause could be a change in Oxygen level, a break of shorten Telomerase tail, Tumor growth factor (FGF-1), Cyclins, or an oncogenic mutation or break of DNA strands.  This will ultimately stimulate receptors with subsequent signal transduction pathways flow that could be amplified by way of  intensity of the signals, but also enzymatic up-regulation and nuclear transcription amplification.   Amplification can be then cancerous based, but also stimuli caused.

the 3rd amplification is what occurs at the DRIVER Mutation due to growth factors or increased catalytic rate from related enzymes.

It is hard to measure cancer driven gene Amplification.  Most of the study keeps taking Metothrexate and its mechanism of Resistance because amplification of Dehydrofolate Reductase is the mechanism of resistance.  every body focus on this enzyme to measure resistance.   But when you look at amplification at this various levels, it is not  hard to see that these measurements are missing the point or are just misleading.

We will discuss the relevant Genes under the section or Rubric "NOMENCLATURE".  Frankly speaking, we have not finished yet the genes for the 3rd law.

We are working hard at CRBCM!

Saturday, December 29, 2012

AS WE SEARCH FOR THE CURE, IT IS IMPORTANT TO REMEMBER THAT:
Molecular Biology offers tremendous opportunities to fight cancer.  In fact, it is surprising that we seem so early (or late, depending on how you understand this) in the game.  The cell can be affected in so many ways that we are late reacting. Using integrated methods and our computer abilities, we should by now be involved in developing patterns of attacks by cancer cell type.
We should define clearly the major drivers by type of cancer, and pick the counter attacks specifically per type of cancer.  We should be at the stage where each patient who presents to us has his genotype defined, changes in his membrane receptors described, driver mutations enunciated,  status of P53,  level of major Cyclins and various cell protections (P-gp, Bcl-2), status and quantitative expression of transcription factors, expression of Metastatic potential (E-Cadherin, Metallo-protease, TGF), histone conformation, level of Endonuclases, status of mitotic speed, types of protein Anchor at cell membranes, and Kinesins (Kif2a,b,c) and so on so forth, all spelled out on his file!

IT IS ONLY WITH THIS LEVEL OF DEFINITION, THAT WE CAN PICK AND CHOOSE AN APPROPRIATE TREATMENT, OR UNDERSTAND THE SHORTCOMINGS OF OUR CURRENT STANDARD TREATMENTS.  Computers should also be used to tell us if combination treatments should be used sequentially or concurrently, and at which sequences, order and time our therapeutics should be given.

Molecular Biology, so many "distractions" and stuff that some scientists are spending days on, and may lead to something some day, but as we work in a race against death situation, and people are dying every day, it is time to pause and regroup, look at how to create this panel per patient, and develop computer supported patterns of therapy.  And every 2-5 years make a stop, update our computer and reload for the Cure!

Tuesday, December 25, 2012

"I say to you today, my friends that in spite of the difficulties and frustrations of the moment, I still have a dream"

Christmas Reflections at CRBCM!

"I say to you today, my friends that in spite of the difficulties and frustrations of the moment, I still have a dream" and with this dream we will rise again to fight another day because we have understood that as long as we live another day, a door may be opened again, another chance may come along, we got to stay prepared and keep looking forward for an opportunity.  There are in life many pits, but all have a bottom here on earth, and even in the darkness of those pits, as long as we live, our imagination will help us rise again.  It is our call, the cause is too important to quit.
Those who came before us have left these words because they lived the horrors of life, went through them and came out the other side still whole.  They left these words so that we do not give up, but instead keep strategizing even when faced by a wall of negative forces.  We need to keep on advancing because only positive steps can generate new consequences.  Not doing a thing is to lose control of the outcome.  So at CRBCM we believe in new steps until life is irreversibly taken from us.  So in these Christmas days, let celebrate persistence and resolve.  What we fight against will not go away until we stand up to it!  Merry Christmas to all.

Sunday, December 23, 2012

IT IS A CIVIL RIGHT ISSUE, CURE OF CANCER FOR VULNERABLE POPULATION.

We have found an El Paso Chapter of the NAACP.  We at CRBCM have understood that the field is not leveled given the limited funds available.  Larger organizations will crush us and lead us to oblivion.  But we will fight until the enemies relent!  They have built futile barriers and discriminatory processes to shield us away from participation, they have put propaganda to cast doubt in the community while they are ripping the goods!  What they are afraid of is the competition in this race for the cure!  What they don't know  is that they cannot deny the facts that some people are more vulnerable to cancers, and that huge institutions gobbling up all the resources do not necessarily you in mind as a priority.  Do not believe that someone else will think of you as a priority.  The proof is in the pudding!  EL PASO HAS BEEN FORGOTTEN.  CPRIT SENT LESS THEN 1 PERCENT OF CLOSE TO A BILLION DOLLARS TO EL PASO WHICH IS THE 6TH LARGEST CITY IN TEXAS! AND IT IS NOT BECAUSE EL PASO DID NOT ASK FOR THE MONEY.   GRANT APPLICATIONS ARE BEING SYSTEMATICALLY REJECTED AT THE HEST OF SO-CALLED REVIEWERS WHO ARE UNIVERSITY BIASED REPRESENTATIVES!  OTHER APPLICATIONS ARE "ADMINISTRATIVELY WITHDRAWN" WITHOUT ANY REVIEW!  They call a party, but El Paso is not allowed to dance and show how good it is really.  Not even a chance to be reviewed!

They claim we have been removed from the competition because the Coalition did not have a product to be produced!  What is services to our community?  Under the survivorship program well detailed in our plan, most of the services are reimbursed by the federal government. This will assure survival and revenues for El Paso.  No, in their mind, services are not a product. They prefer gambling away money in research that will yield less 10-20% possible return in 10-15 years.  At the pace of progress,  most of these research RESULTS will be old by then.  Changes need to be implemented today to yield results in the near future.  Lifestyle need modifications today for a better Texas tomorrow.   If we agree that close to 3000 African women are dying yearly  from a breast cancer that could be prevented, when do you prefer having a solution? Now or in 10 years?  At CRBCM we believe that denying people participation in a race for the cure, is a civil right issue.  We call to the senses of our leaders to take positive steps to reduce politics!

Greed has entered the fray. Universities are shaping and packaging their products to fit funding requirements.
Since the old CPRIT was avidly gobbling up companies located outside Texas, old patents/research products developed in Texas, are quickly being sold to outside Companies so that CPRIT money is relocating these old patents to Texas!  and believe this, this has been funded reportedly! And funded 5 times the millions it was originally sold by the TEXAS university!  Do not tease me because I have the facts!  CPRIT now has been renovated, the new CPRIT will not let itself untangled in politics, at least we believe and hope!

We will continue our planned talk with the local chapter of the NAACP, because it is a CIVIL RIGHTS' issue to protect women from a disease they could be saved from today!


Wednesday, December 19, 2012

THIORIDAZINE, A PHENOTHIAZINE WHICH IS AN INHIBITOR OF CALMODULIN WILL HAVE ANTITUMOR EFFECT AS DEMONSTRATED BY CANADIAN RESEARCHERS WHEN THEY DESCRIBED A 50 PERCENT DECREASE OF STEM CELLS.  WE AT CRBCM BELIEVE THIS EFFECT IS OF COURSE LINKED TO THE RELEASE OF CALCIUM IN THE CYTOSOL LEADING TO ENDONUCLEASE STIMULATION WITH THE RESULTING ATTACK ON DNA.
THE FACT IS THIS EFFECT WILL BE MORE ON MEMBRANE WHERE CALMODULIN IS MOSTLY LOCATED.  THEREFORE LIBERATION OF CALCIUM AFFECTS ELECTRICAL POLARITY AT THE MEMBRANE. TORSADE DE POINTE CAN RESULT AND HAD LED TO THE BANNING OF THIORIDAZINE IN CANADA.
THIORIDAZINE ACTS ALSO AS AN ANTIGROWTH FACTOR IN GENERAL. THIS FACT COULD CONTRIBUTE TO ITS ANTI-CANCER ACTIVITY.  IN OUR PREVIOUS NOTES, WE
HAD SUGGESTED ADDING THE ANTI-CALMODULIN TO AVASTIN AS A STRATEGY TO TREAT RECURRENT BRAIN TUMOR.

Tuesday, December 18, 2012

Leukemia inhibitory factor

From Wikipedia, the free encyclopedia

Leukemia inhibitory factor

PDB rendering based on 1LKI.
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols LIF; CDF; DIA; HILDA; MLPLI
External IDs OMIM159540 MGI96787 HomoloGene1734 GeneCards: LIF Gene
RNA expression pattern
PBB GE LIF 205266 at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 3976 16878
Ensembl ENSG00000128342 ENSMUSG00000034394
UniProt P15018 P09056
RefSeq (mRNA) NM_001257135.1 NM_001039537.1
RefSeq (protein) NP_001244064.1 NP_001034626.1
Location (UCSC) Chr 22:
30.64 – 30.64 Mb
Chr 11:
4.26 – 4.27 Mb

PubMed search [1] [2]

Leukemia inhibitory factor, or LIF, is an interleukin 6 class cytokine that affects cell growth by inhibiting differentiation. When LIF levels drop, the cells differentiate.

Function LIF derives its name from its ability to induce the terminal differentiation of myeloid leukemic cells, thus preventing their continued growth. Other properties attributed to the cytokine include: the growth promotion and cell differentiation of different types of target cells, influence on bone metabolism, cachexia, neural development, embryogenesis and inflammation. p53 regulated LIF has been shown to facilitate implantation in the mouse model and possibly in humans.[1] It has been suggested that recombinant human LIF might help to improve the implantation rate in women with unexplained infertility.[2]

Binding/activation

LIF binds to the specific LIF receptor (LIFR-α) which forms a heterodimer with a specific subunit common to all members of that family of receptors, the GP130 signal transducing subunit. This leads to activation of the JAK/STAT (Janus kinase/signal transducer and activator of transcription) and MAPK (mitogen activated protein kinase) cascades.[citation needed]

Expression

LIF is normally expressed in the trophectoderm of the developing embryo, with its receptor LIFR expressed throughout the inner cell mass. As embryonic stem cells are derived from the inner cell mass at the blastocyst stage, removing them from the inner cell mass also removes their source of LIF.

Use in stem cell culture

Removal of LIF pushes stem cells toward differentiation, but they retain their proliferative potential or pluripotency. Therefore LIF is used in mouse embryonic stem cell culture. It is necessary to maintain the stem cells in an undifferentiated state, however genetic manipulation of embryonic stem cells allows for LIF independent growth, notably overexpression of the gene Nanog.
LIF is not required for culture of human embryonic stem cells.[3][4]
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These comments from Wikepedia introduce our discussion today,
first of all, patient with leukemia have their cells stopped at various stage of differentiation
meaning some are stopped at baby stage, some at teenager stage, some at adult stage. And at each stage, the leukemia takes a different Name, agressiveness and prognosis. In General, the younger the stage the bad/worse the prognosis. So there is a benefit to HELP ALONG THE CELL TO GROWTH, IT ACTUALLY IS HELPFUL FOR THE CELL TO MATURE SO THAT THE TUMOR GETS A GOOD OR BETTER PROGNOSIS.
AS A MATTER OF FACT, THE MORE MATURE THE CELL BECOMES, THE LESS LIKELY IT WILL DIVIDE REDUCING THE LOAD OF THE TUMOR.  THE MORE MATURE IT GETS, THE MORE LIKELY IT WILL GET OLD AND DIE OF A NATURAL DEATH. 
ON THE OTHER END HOWEVER, THE MORE LIKELY IT MATURES, THE MORE LIKELY IT MAY COMPLETE OR PERFORM ITS NATURAL FUNCTION. SO IF ITS FUNCTION WAS TO BE ABLE TO SPREAD, THE MATURE CELL CAN SPREAD FASTER.  THAT'S WHY SCIENTISTS ARE REPORTING THAT AN INHIBITOR TO THIS LIF  MAY STOP THE SPREAD OF CANCER.  THE MD ANDERSON HAS BEEN WORKING ON THIS AND HAVE REPORTED SOME SUCCESS! THE FIGHT IS ON!