Already the first phase of results from the study funded partially by the CRBCM and MDHonors are completed. This is a study on lung cancer detection completed on 50 tissues provided by a tissue bank from the University of Virginia. Preliminary results coming from the University of Texas in El Paso seem to suggest that the genes involved appear consistently in all cancers no matter the stage of disease, types and race of individual bearing the disease. This fact is strong because it attest to the early occurrence of these mutations in the neoplastic transformation. It could subsequently point to cure if indeed these mutations are no longer detected since they appear undisturbed no matter the stage of disease.
The test could therefore detect non only the disease early, but cure of the disease, an unprecedented event...But don't let CRBCM jump ahead of its conclusions which have not been finalized until the publication of our first paper. Big heads will fight these finding as skepticism is stylish , remember the CRBCM is making the research happen, we do not micro-manage the outcomes! Facts are being fed to us, and they look promising! Our purpose is to explore, find the facts, and feed them to the community at large, and in the process learn! learn! and do the deed ......CRBCM, hard at work!
The second phase is to complete the same PCR based tests in matched serum (sera) of individuals who gave the tissues and spin the same tests to confirm the presence of these mutation in the serum. We intend to show that the mutations are detectable in blood. Should we demonstrate that the serum can give us the same result, early detection could be demonstrated in blood. There are caveats however and many have to do with determining that the findings are indeed found in lung cancer. Detection through PET in positive individual (who carry these mutations without evident mass) is just another hurdle we will have to face.
Corollary detection of specific mutations that makes tumors susceptible to Avastin will be conducted as part of this series. One of the curious fact performed by the researcher at UTEP is to use Actin as the reference standard. A fact that is peculiar and call for questions when we meet next to draft the preliminary draft of the 1st article. For CRBCM actin could potentially be used as a predictive Biomarker for Taxane and or Platinum effects! or is-it? We are at the entrance of bigger things we presume!
The CRBCM...advancing deliberately without big brother breathing down our neck. Science should be free of political pressures! It makes the thruth even more powerful...We are not closed to criticism, just bringing an argument!
What is important with this exercise is learning to do scientific stuff! That is what the people watching did not understand...yes the study has been done in some form, but doing stuff open new doors to a active mind, and a new institution!
Thursday, February 6, 2014
Tuesday, February 4, 2014
TRPM7 (and PLBC)
It is potentially a dangerous gene when mutated (TRPM)
Its autophosphorylation capacity makes it a potential DRIVER gene...
And it is an Ion Channel and therefore has direct implications on cellular depolarisation
Use of Calcium as a co-factor put it center to all function calcium does. It's importance in Traumatic Brain Injury cannot be undermined. It seemed to be at the center of neuronal death. It also may impact the NFAT...
1. Its implication of Alzheimer needs assessment
2. Its role in the endothelium leads to
"Defects in this gene have been associated to magnesium deficiency in human microvascular endothelial cells.[3]" wikipedia
3.It also has a significant relation with P38 or MAPK and therefore reaches ATF2, C-MYC,PAX6 and P53
And again through P38, this gene impact the epigenic event commanded by ELK1, ETS1 and MK2 by which it reach the CREB, RAR, and the NFkB/P65.
4.Through the PLBC, it reaches the Inositiol based pathway.
5. It is unclear if it participates in Micro-vascular disease seen on so many Brain MRI in elderly, raising the issue of whether this will be a biomarker for this silent disease and whether Aspirin is the best course.
6.?Disruption here is accompanied by disturbance of calcium in blood, or dysfunction of Parathyroid?
Focusing on P38!
Its autophosphorylation capacity makes it a potential DRIVER gene...
And it is an Ion Channel and therefore has direct implications on cellular depolarisation
Use of Calcium as a co-factor put it center to all function calcium does. It's importance in Traumatic Brain Injury cannot be undermined. It seemed to be at the center of neuronal death. It also may impact the NFAT...
1. Its implication of Alzheimer needs assessment
2. Its role in the endothelium leads to
"Defects in this gene have been associated to magnesium deficiency in human microvascular endothelial cells.[3]" wikipedia
3.It also has a significant relation with P38 or MAPK and therefore reaches ATF2, C-MYC,PAX6 and P53
And again through P38, this gene impact the epigenic event commanded by ELK1, ETS1 and MK2 by which it reach the CREB, RAR, and the NFkB/P65.
4.Through the PLBC, it reaches the Inositiol based pathway.
5. It is unclear if it participates in Micro-vascular disease seen on so many Brain MRI in elderly, raising the issue of whether this will be a biomarker for this silent disease and whether Aspirin is the best course.
6.?Disruption here is accompanied by disturbance of calcium in blood, or dysfunction of Parathyroid?
Focusing on P38!
Monday, February 3, 2014
Meaning of cancer recurrence
1-Meaning of recurrence
2-disease only slowed down
3-new development of new bypass pathway
4-additional escape mechanism or pathway
5-resistant disease
6-a virus act on a promoter
ie
--------------------------------------------------------------------------------------------------
YY1 and RYB are fair targets for further investigation.
note RYB gene relation with caspase 10!
2-disease only slowed down
3-new development of new bypass pathway
4-additional escape mechanism or pathway
5-resistant disease
6-a virus act on a promoter
ie
Transcriptional repression by YY1, a human GLI-Krüippel-related protein, and relief of repression by adenovirus E1A protein
Yang Shi*,et al.--------------------------------------------------------------------------------------------------
YY1 and RYB are fair targets for further investigation.
note RYB gene relation with caspase 10!
Sunday, February 2, 2014
Then it goes on to destroy the quote: another political game by excluding us! can't make up this stuff !
just a reminder and CRBCM agrees with the following quote:
"The best discoveries in science aren’t predictable,” says HHMI President Robert Tjian. “One of the things that sets HHMI apart from other organizations that support biomedical research is that we free our researchers to follow their scientific instincts—to follow things that pop up unexpectedly.”
HHMI encourages its investigators to push their research fields into new areas of inquiry. By employing scientists as HHMI investigators—rather than awarding them research grants—the Institute is guided by the principle of “people, not projects.” HHMI investigators have the freedom to explore and, if necessary, to change direction in their research. Moreover, they have support to follow their ideas through to fruition—even if that process takes many years.
“The flexibility that comes with HHMI support allows people to move into new scientific areas more easily,” said Erin K. O’Shea, vice president and chief scientific officer. “I can’t emphasize enough how difficult that kind of movement can be with traditional sources of funding.”
Candidates apply directly to HHMI. Applications must be received by June 3, 2014. Successful candidates are expected to meet the following criteria:
HHMI announced its last open competition in 2012. That competition resulted in the selection of 27 of the nation’s top biomedical scientists as HHMI investigators in 2013. Once selected, HHMI provides each investigator with his or her full salary, benefits, and a research budget over their initial five-year appointment. The Institute will also cover other expenses, including the purchase of critical equipment.
Through the HHMI Investigator Program, the Institute has joined with more than 70 distinguished U.S. universities, hospitals, institutes, and medical schools to create an environment that provides flexible, long-term support for more than 300 Hughes scientists and members of their research teams. HHMI investigators are widely recognized for their creativity and research accomplishments: 172 HHMI investigators are members of the National Academy of Sciences and there are currently 17 Nobel laureates who are HHMI investigators.'"
The Howard Hughes Medical Institute
The Howard Hughes Medical Institute plays an influential role in advancing scientific research and education in the United States. Its scientists, located across the United States, have made important discoveries that advance our fundamental understanding of biology and its relation to human disease. In a complementary program at HHMI's Janelia Farm Research Campus in Loudoun County, Virginia, leading scientists are pursuing long-term, high-risk, high-reward research in a campus designed to bring together researchers from disparate disciplines. The Institute also aims to transform science education into a creative, interdisciplinary endeavor that reflects the excitement of real research. For more information, visit www.hhmi.org.
The Institute’s endowment at the close of fiscal 2013 was about $16.9 billion. HHMI’s headquarters are located in Chevy Chase, Maryland, just outside Washington, D.C.
"The best discoveries in science aren’t predictable,” says HHMI President Robert Tjian. “One of the things that sets HHMI apart from other organizations that support biomedical research is that we free our researchers to follow their scientific instincts—to follow things that pop up unexpectedly.”
HHMI encourages its investigators to push their research fields into new areas of inquiry. By employing scientists as HHMI investigators—rather than awarding them research grants—the Institute is guided by the principle of “people, not projects.” HHMI investigators have the freedom to explore and, if necessary, to change direction in their research. Moreover, they have support to follow their ideas through to fruition—even if that process takes many years.
“The flexibility that comes with HHMI support allows people to move into new scientific areas more easily,” said Erin K. O’Shea, vice president and chief scientific officer. “I can’t emphasize enough how difficult that kind of movement can be with traditional sources of funding.”
Candidates apply directly to HHMI. Applications must be received by June 3, 2014. Successful candidates are expected to meet the following criteria:
- Hold a PhD, and/or MD or equivalent degree.
- Hold a tenured or tenure-track position as Assistant Professor or higher academic rank (or the equivalent) at an eligible U.S. institution. Federal government employees are not eligible.
- Have more than 5 but no more than 15 years of post-training, professional experience.
- Be the principal investigator on one (or more) active, national, peer-reviewed research grants with a duration of at least three years.
HHMI announced its last open competition in 2012. That competition resulted in the selection of 27 of the nation’s top biomedical scientists as HHMI investigators in 2013. Once selected, HHMI provides each investigator with his or her full salary, benefits, and a research budget over their initial five-year appointment. The Institute will also cover other expenses, including the purchase of critical equipment.
Through the HHMI Investigator Program, the Institute has joined with more than 70 distinguished U.S. universities, hospitals, institutes, and medical schools to create an environment that provides flexible, long-term support for more than 300 Hughes scientists and members of their research teams. HHMI investigators are widely recognized for their creativity and research accomplishments: 172 HHMI investigators are members of the National Academy of Sciences and there are currently 17 Nobel laureates who are HHMI investigators.'"
The Howard Hughes Medical Institute
The Howard Hughes Medical Institute plays an influential role in advancing scientific research and education in the United States. Its scientists, located across the United States, have made important discoveries that advance our fundamental understanding of biology and its relation to human disease. In a complementary program at HHMI's Janelia Farm Research Campus in Loudoun County, Virginia, leading scientists are pursuing long-term, high-risk, high-reward research in a campus designed to bring together researchers from disparate disciplines. The Institute also aims to transform science education into a creative, interdisciplinary endeavor that reflects the excitement of real research. For more information, visit www.hhmi.org.
The Institute’s endowment at the close of fiscal 2013 was about $16.9 billion. HHMI’s headquarters are located in Chevy Chase, Maryland, just outside Washington, D.C.
Related Links
For More Information
NEVER LEAVE YOUR MIND AT PEACE WHEN IT COMES TO GENES (PROGNOSIS OF SENESCENCE)
It is by now quite clear that Senescence is clearly linked to the health of your eyes (given the frequency of cataract in elderly) and intrinsic deterioration of the heart muscle and muscles in general. Elderly's muscles seem to become hypothrophic without control. Kidney deterioration seem to follow closely as if an organ shutdown is in the work. Indeed some genes seems to be at work in a very discrete way indicating to the eyes, the heart, the muscles, and peripherally the kidney that it is time to shut this thing down. The proof is that keeping exercising seems to fool this message keeping people "young".
At cellular or gene level, the genes that form the muscles must be implicated! The Myb, MyoD,Myogenein, Myf5, MEF2, GNA12 ...some of which interacts with MDFI (watch out because it is an gene inhibitor): (look at the leukemias'story when it comes to interacting with inhibitors (our eyes is square and fare in the SIX1)) six1 talks to PAX (Melanoma) (how this is liked to Breast cancer...well? did you see E2A? It's here though!)
MDFI (don't say we at CRBCM did not warned you) AND IF YOUR EYES ARE RIVETED ON THIS ONE, DON'T FORGET MDFIC AS A TARGET! OH! BY THE WAY LOOK-UP ECRG2 (esophageal cancer ) AND RBEL1 WHILE ON THIS! (Why? because it is a rebel gene! think about that!)
"UniProtKB/Swiss-Prot: MDFI_HUMAN, Q99750
At cellular or gene level, the genes that form the muscles must be implicated! The Myb, MyoD,Myogenein, Myf5, MEF2, GNA12 ...some of which interacts with MDFI (watch out because it is an gene inhibitor): (look at the leukemias'story when it comes to interacting with inhibitors (our eyes is square and fare in the SIX1)) six1 talks to PAX (Melanoma) (how this is liked to Breast cancer...well? did you see E2A? It's here though!)
MDFI (don't say we at CRBCM did not warned you) AND IF YOUR EYES ARE RIVETED ON THIS ONE, DON'T FORGET MDFIC AS A TARGET! OH! BY THE WAY LOOK-UP ECRG2 (esophageal cancer ) AND RBEL1 WHILE ON THIS! (Why? because it is a rebel gene! think about that!)
"UniProtKB/Swiss-Prot: MDFI_HUMAN, Q99750
ACTIVITIES AT CRBCM AS OF FEBRUARY 2014!
It is critical to our readers to know that CRBCM is still alive, maturing and quickly expanding its reach...
It is mind "troubling" to think where despite our struggles we have position ourselves. It point to one thing, the need for CRBCM and institution such this one is "critically" great. We are at
1. having chemotherapy patients needing us
2. patients from El Paso depending on us
3.in a week we are presenting at a local Hospital breaking news on gene studies in Breast cancers
4.Last week we were featured in "University of Texas in El Paso (UTEP) news". At least our MDHONORS/CRBCM financed work on Lung cancer work was featured.
5.We are solicited for presentation and article reviews.
6. Our work on Traumatic Brain Injury (TBI) is selected for potential publication
7.We have presented our work on TBI through the hall of the prestigious UMC (University Medical Center)
And we the reinstitution of CPRIT, we are poised to submit another research proposal (participating is key, our expectation is "zero" for CPRIT is tricky. We still don't know what this institution is trying to be...
8.We are still "medical Director" at a local Griffols/Talecris Plasma Center. And completed our work there!
9. We have taken over an over 30 year old prominent Medical Practice
10. We still have completed our mission in the snow covered Indianapolis
And yesterday when you were stretching your legs, enjoying a week-end, the CRBCM attended to more than 10 outpatient and inpatient patients who rely on this new clinic for immediate and future care!
11.On February 10, 2 Nursing students will start Rotation at CRBCM,
We will be at NIH, SBIR, and other funding institution submissions,
and most importantly we will continue our blog
now followed internationally, with more than 35,000 reviews in 1 year!
The CRBCM....the year is still young, we are going to keep moving!
It is mind "troubling" to think where despite our struggles we have position ourselves. It point to one thing, the need for CRBCM and institution such this one is "critically" great. We are at
1. having chemotherapy patients needing us
2. patients from El Paso depending on us
3.in a week we are presenting at a local Hospital breaking news on gene studies in Breast cancers
4.Last week we were featured in "University of Texas in El Paso (UTEP) news". At least our MDHONORS/CRBCM financed work on Lung cancer work was featured.
5.We are solicited for presentation and article reviews.
6. Our work on Traumatic Brain Injury (TBI) is selected for potential publication
7.We have presented our work on TBI through the hall of the prestigious UMC (University Medical Center)
And we the reinstitution of CPRIT, we are poised to submit another research proposal (participating is key, our expectation is "zero" for CPRIT is tricky. We still don't know what this institution is trying to be...
8.We are still "medical Director" at a local Griffols/Talecris Plasma Center. And completed our work there!
9. We have taken over an over 30 year old prominent Medical Practice
10. We still have completed our mission in the snow covered Indianapolis
And yesterday when you were stretching your legs, enjoying a week-end, the CRBCM attended to more than 10 outpatient and inpatient patients who rely on this new clinic for immediate and future care!
11.On February 10, 2 Nursing students will start Rotation at CRBCM,
We will be at NIH, SBIR, and other funding institution submissions,
and most importantly we will continue our blog
now followed internationally, with more than 35,000 reviews in 1 year!
The CRBCM....the year is still young, we are going to keep moving!
Friday, January 31, 2014
Many Invitations, so little time!
SENT TO CRBCM
===================================================================
===================================================================
Good morning,
The Office of Continuing Medical Education has been
in communication with the El Paso County Medical Society to submit
abstracts for consideration for publication in their journal.
Dr. Alan Tyroch, MD, the Program Director for the Rio Grande Trauma
Conference invites you to participate in the submission process. If you
would like for our office to forward the abstract you provided for the
14th Annual Rio Grande Trauma Conference
on December 5th and 6th, 2013 for consideration
for publication in the El Paso Medical Society’s next issue, please sign
the letter attached and send to
jesia.boykin@ttuhsc.edu or fax to 915-783-6220 by
Friday, February 7, 2014.
=====================================================
BUT ONE THING FOR SURE, WE WILL BE IN LAS-VEGAS FOR THE ANNUAL UPDATE IN HEMATOLOGY!
Thursday, January 30, 2014
In Lymphoproliferative disorder, particular of dangerous genes
1*Highly conserved Molecule: This means the molecule has stood the test of time and has been used under that form for years, and may have become critical in basic cellular functions. In the human cell, some genes that are now "conserved" came from or were adopted from invading Virus. For such an adoption to occur, the gene must be critical and acquired without antigenicity. It is believed that ELK-1, ETS, Myb,ERG,ETV EWS, or TEL, could be an evolutive genes that are characterized with high level of co-association and remains most of all within the epigenic zone. TEL-JAK2 has been suggested in Leukemia(Lacronique et al)
while TMPRSS-ERG has been demonstrated in Prostate cancer (clark et al).
In Breast cancer, "Elk1 also interacts with BRCA1 splice variants, namely BRCA1a and BRCA1b. This interaction enhances BRCA1-mediated growth suppression in breast cancer cells. Elk1 may be a downstream target of BRCA1 in its growth control pathway. Recent literature reveals that c-fos promoter activity is inhibited, while overexpression of BRCA1a/1b reduces MEK-induced activation of the SRE. These results show that one mechanism of growth and tumor suppression by BRCA1a/1b proteins acts through repression of the expression of Elk1 downstream target genes like Fos.[20]" wikepedia
Watson et al suggested :"
It has been over 15 years since Ets was originally identified as one of the two genes (Ets and Myb) transduced by the avian leukemia virus, E26 (Watson et al., 1990);" again suggesting these gene that control epigenetic events may be evolutive as suggested above, and keeps attractive co-association capability that may have help them escape cellular immunity ! Their location at the epigenetic location show the points to a cellular zone of weakness. But it also could point to the importance of inhibitor of de-Acetylators in human cancer and point to why we need further efforst to understand epigenetic events. The fact is that medication targeting Retinoic Acid took over by surprise the world when it comes to treatment of Promyelocytic Leukemias, re-enforces this notion...
To know more about how gene elements described above interact further with P53, histone de-acetylators, and the Telomeres, read our blog of 1 year ago on 01/31/2013.
========================================================================
I cannot pass to the next step without pointing to the fact that distant effect of Traumatic Brain injury (TBI) are not far from these region since they all depend on secondary release of Cytokines which originate from these regions!
=======================================================================================
AND SO MUCH STILL TO TALK ABOUT!
2*young selective development:
3*JAK/STAT involvement
4*The cell wants to achieve selective terminal differentiation and criss cross with gene repair and gene of variable region
5*membranous event with coexistence of Death Receptor
6*factor BSAP expression
7*Activity at TLE4, a negatve regulator of PAX5
8*relation with Ibrutinib
9*Daxx gene
10*The intervention pf the Variable region of IG
11*role of RAG1
12*emu enhancer
13*role of AML1
14*role of TATA and the Retinoblastoma genes
15*Intervention of the Telomere
16*Acetylated P53 (see blog 01/31/2013)
while TMPRSS-ERG has been demonstrated in Prostate cancer (clark et al).
In Breast cancer, "Elk1 also interacts with BRCA1 splice variants, namely BRCA1a and BRCA1b. This interaction enhances BRCA1-mediated growth suppression in breast cancer cells. Elk1 may be a downstream target of BRCA1 in its growth control pathway. Recent literature reveals that c-fos promoter activity is inhibited, while overexpression of BRCA1a/1b reduces MEK-induced activation of the SRE. These results show that one mechanism of growth and tumor suppression by BRCA1a/1b proteins acts through repression of the expression of Elk1 downstream target genes like Fos.[20]" wikepedia
Watson et al suggested :"
It has been over 15 years since Ets was originally identified as one of the two genes (Ets and Myb) transduced by the avian leukemia virus, E26 (Watson et al., 1990);" again suggesting these gene that control epigenetic events may be evolutive as suggested above, and keeps attractive co-association capability that may have help them escape cellular immunity ! Their location at the epigenetic location show the points to a cellular zone of weakness. But it also could point to the importance of inhibitor of de-Acetylators in human cancer and point to why we need further efforst to understand epigenetic events. The fact is that medication targeting Retinoic Acid took over by surprise the world when it comes to treatment of Promyelocytic Leukemias, re-enforces this notion...
To know more about how gene elements described above interact further with P53, histone de-acetylators, and the Telomeres, read our blog of 1 year ago on 01/31/2013.
========================================================================
I cannot pass to the next step without pointing to the fact that distant effect of Traumatic Brain injury (TBI) are not far from these region since they all depend on secondary release of Cytokines which originate from these regions!
=======================================================================================
AND SO MUCH STILL TO TALK ABOUT!
2*young selective development:
3*JAK/STAT involvement
4*The cell wants to achieve selective terminal differentiation and criss cross with gene repair and gene of variable region
5*membranous event with coexistence of Death Receptor
6*factor BSAP expression
7*Activity at TLE4, a negatve regulator of PAX5
8*relation with Ibrutinib
9*Daxx gene
10*The intervention pf the Variable region of IG
11*role of RAG1
12*emu enhancer
13*role of AML1
14*role of TATA and the Retinoblastoma genes
15*Intervention of the Telomere
16*Acetylated P53 (see blog 01/31/2013)
New Challenges to the human cell
In a world where new stimulants and new conditions are created, the human cell, deep in our systems, is confronted and forced to adapt and conform to new environment constantly. And doing so with the human genes that it possesses at the moment. Yes, while a chemist work hard to create new chemical product to improve our lives (I really hope this), the cell somewhere in the human body does not know it will face this new challenge once it comes to contact with it. To deal with this new product as a stimulant, the cell has to use its potentials. It has sometime to rearrange its mechanisms to deal with the new stimulant! While most of the time quick adaptation to the new product is limited in its impact on the life of the cell, certain stimulants will lead to receptor desensitization, transcription factors amplifications (particularly if gene autophosphorylation is allowed, shutdown of regulators occurs, alteration in splicing, and special miRNA are transcribed,etc.). The point is even Receptor desensitization itself may lead to shutdown of critical genes.
One of the things that makes the cell vulnerable to the effect of new stimulant, is not only its reliance to old techniques to fight new challenges (ie, activation of the NF-kB) but also proximity and interactivity of the genes particularly those in the proximity of the initial inducing events. But in a lightening fast action, distant genes are also involved. The proximity of basic cellular functions is also a player. Indeed it is common that one event could affect various cellular functions such as proliferation,growth and differentiation. In fact the ease of recruiting neighbor gene is impressive. It does not take much for a stimulant to induce de-differentiation to return cellular omnipotence to deal with the new comer, but cellular omnipotence is sitting next to shutting Apoptosis so that the new challenge does not kill the cell, But as seen in many cases, gene repair mechanisms are raised to the ready (in some cases shut down to tolerate mistakes), splicing machines are set in motion to make new RNA to create adapted novel proteins, multiplication machinery are also ready to clone resistant cells, messaging machinery is put in a "work" mode to notify surrounding cells in case they don't know already. The most sensitive function of all is the machinery to induce JAK/STAT and the variable domain of immunoglobulins. Once these are engaged, a potential neoplastic transformation is possible if attachment to the involved gene occurs!
An example of this is what happen in Hodgkin disease, if you read about PAX genes, you will find cellular de-differentiation, PAX1-engage MOX1 but surprise-surprise-BRCA1 is not far. You will argue that PAX5 is the one in 97% of some Hodgkin Lymphomas, but follow the TLE4, Daxx, AML1,TATA,and RAG1....you will find that the same story repeats itself!
The CRBCM is following the trail!
One of the things that makes the cell vulnerable to the effect of new stimulant, is not only its reliance to old techniques to fight new challenges (ie, activation of the NF-kB) but also proximity and interactivity of the genes particularly those in the proximity of the initial inducing events. But in a lightening fast action, distant genes are also involved. The proximity of basic cellular functions is also a player. Indeed it is common that one event could affect various cellular functions such as proliferation,growth and differentiation. In fact the ease of recruiting neighbor gene is impressive. It does not take much for a stimulant to induce de-differentiation to return cellular omnipotence to deal with the new comer, but cellular omnipotence is sitting next to shutting Apoptosis so that the new challenge does not kill the cell, But as seen in many cases, gene repair mechanisms are raised to the ready (in some cases shut down to tolerate mistakes), splicing machines are set in motion to make new RNA to create adapted novel proteins, multiplication machinery are also ready to clone resistant cells, messaging machinery is put in a "work" mode to notify surrounding cells in case they don't know already. The most sensitive function of all is the machinery to induce JAK/STAT and the variable domain of immunoglobulins. Once these are engaged, a potential neoplastic transformation is possible if attachment to the involved gene occurs!
An example of this is what happen in Hodgkin disease, if you read about PAX genes, you will find cellular de-differentiation, PAX1-engage MOX1 but surprise-surprise-BRCA1 is not far. You will argue that PAX5 is the one in 97% of some Hodgkin Lymphomas, but follow the TLE4, Daxx, AML1,TATA,and RAG1....you will find that the same story repeats itself!
The CRBCM is following the trail!
Wednesday, January 29, 2014
Diet is important in cancer control:(case in point, Breast cancers!)
I knew this from the Bottom of my heart but pinning the genetic reason was here before me and I just did not see it. Supply of sugar will ultimately increase Insulin which will increase the demand for Insulin receptor which in cancer is a bad actor. The increase in Insulin receptor will interact with major genes that affect cancer. First it affect the JAK /STAT pathways, which leads to Proliferation, second it affects the Gerb gene family which is a "wild" gene, meaning a gene just connected to too many others that will be influenced. But one of the aspect mostly forgotten by survivors, is the receptor connection to the PTPN11. A gene that has many links but one particular link is its relation with LAIR1, " is a protein forming a receptor found in the plasma membrane of cells involved in receptor-mediated endocytosis. In humans, the LRP1 protein is encoded by the LRP1 gene.[wikipedia
Involvement of this LAIR1 is bad for you if it leads to consumption of Thrombospondin-1(THBS1 ) which help the cell grow its feet for walking away and metastasizing (Breast cancer has done done quite a bit! Through the interaction with PGDFR, this pathway will affect even blood clots (destruction of Caveolin) possibly inducing clot to move away and cause strokes and Myocardial infarction (science here is still growing). Drop of Thrombospondin is a major event involving CD38, and certain Integrins (be very careful which! ) and release of Metallo-proteases. It is amazing that we do not monitor THBS1 today since its drop marks Metastatic disease. (and stroke and MI presumably). And all this is induced by diet. Not changing diet in cancer helps residual disease spread.
One of the thing that is important to note, most Estrogen Receptor are covered by a sugar, and Heparan sulfate is in most case the cover. Guess what, THBS1 interact with Heparan for potentially its removal. Making thrombospondin potentially a mechanism for cessation of Receptor desensitization. What would happen in people depending on the preservation of the Receptor function (Tamoxifen)? can we also infer there is a benefit for sulfur products here?
If you follow this line of thinking, you will also find that cholesterol use by the brain will be affected. Another effect of LAIR1, opening another Pandora Box!
Eat less sugar is critical to cancer spread.....The CRBCM, work is still ahead.....
Tuesday, January 28, 2014
Questions for researchers! Melanoma as an example !
When a cancer continues to rise
-it means it is more environmental?
-It means its central mechanism continue to escape us
-It means the isoforms of the genes causing it, is more frequently found in the population
-It means that many isoforms can lead to it, again here we need to know the basics? does the frequency of cancer in society firmly linked to the frequency of the gene Isoforms?
-does the frequency means we keep missing the fundamentals?
-Or does it means the tumor has greater facility to penetrate the neoplastic transformation, or reach easily the "wild genes" or genes of importance in differentiation...
or genes capable of autoregulation?
or genes capable of suppressing other genes
or genes susceptible to Vitamin depletion
The prominence of Vitamin and hormones in society seem to suggest this last point! Or is it vitamin imbalance?
In Melanoma for example it is established that the disease seems to occur more frequently in patients who burn rather than tan. And that sunburn would more likely be the trigger! What that tells you about their MCIR gene, their FAK and induction of the Wnt (association with LEF1), and Notch, Now that we are speaking MITF, and GNAQ/GNA11, or is it a deficiency of the SOCS family gene?
-Association with moles? Dysplastic moles have up to 80% risk of Melanoma development, particularly when familial tendencies are implicated? what that tells us about what gene is involved is it MITF still?or is it PPP3CA (interferes with dephosphorylation of DNM1L, HSPB1 and SSH1)(will Etoposide helps here?with Cisplatin may be? When you say this, is it POLR2C, the culprit?
or is it PAX3,MEF2, or Calsarcin-3.
well don't forget insufficiency of p16/CDKN2A when insufficiency of inhibitor of this major pathway relieve the block on cell division...
What gets BRAF so involved Or is it the involvement of Rho/ROCK. What BRAF has to do with MITF
why inability to cope with change in skin color shuts down apoptosis? Can interfering with splicing affects
What the hell Xeroderma has to do any how?RAD2, ERCC,DDB2,POLH,XPA,XPB.
Or simply BRAF is locked in Autoregulation, being truly a driver mutation, or relieved of its blocker or ubiquitinating substrate? Is the PTEN present or not (is it more involved in internal Melanoma-lung?)
what about POU3F2 and PIAS, and miRNA-211, should we block TAF15? (sparing TATA and HSP27?)
can blocking the FGF worth while?
what about the expression of c-Kit (lentigo), where are the DNA repair genes? Should we focus on abilty of this cell to deal with hypoxia? (it seems to enjoy this path?)
There is much to be done, but where are we....
AT CRBCM, we are still at work!
-it means it is more environmental?
-It means its central mechanism continue to escape us
-It means the isoforms of the genes causing it, is more frequently found in the population
-It means that many isoforms can lead to it, again here we need to know the basics? does the frequency of cancer in society firmly linked to the frequency of the gene Isoforms?
-does the frequency means we keep missing the fundamentals?
-Or does it means the tumor has greater facility to penetrate the neoplastic transformation, or reach easily the "wild genes" or genes of importance in differentiation...
or genes capable of autoregulation?
or genes capable of suppressing other genes
or genes susceptible to Vitamin depletion
The prominence of Vitamin and hormones in society seem to suggest this last point! Or is it vitamin imbalance?
In Melanoma for example it is established that the disease seems to occur more frequently in patients who burn rather than tan. And that sunburn would more likely be the trigger! What that tells you about their MCIR gene, their FAK and induction of the Wnt (association with LEF1), and Notch, Now that we are speaking MITF, and GNAQ/GNA11, or is it a deficiency of the SOCS family gene?
-Association with moles? Dysplastic moles have up to 80% risk of Melanoma development, particularly when familial tendencies are implicated? what that tells us about what gene is involved is it MITF still?or is it PPP3CA (interferes with dephosphorylation of DNM1L, HSPB1 and SSH1)(will Etoposide helps here?with Cisplatin may be? When you say this, is it POLR2C, the culprit?
or is it PAX3,MEF2, or Calsarcin-3.
well don't forget insufficiency of p16/CDKN2A when insufficiency of inhibitor of this major pathway relieve the block on cell division...
What gets BRAF so involved Or is it the involvement of Rho/ROCK. What BRAF has to do with MITF
why inability to cope with change in skin color shuts down apoptosis? Can interfering with splicing affects
What the hell Xeroderma has to do any how?RAD2, ERCC,DDB2,POLH,XPA,XPB.
Or simply BRAF is locked in Autoregulation, being truly a driver mutation, or relieved of its blocker or ubiquitinating substrate? Is the PTEN present or not (is it more involved in internal Melanoma-lung?)
what about POU3F2 and PIAS, and miRNA-211, should we block TAF15? (sparing TATA and HSP27?)
can blocking the FGF worth while?
what about the expression of c-Kit (lentigo), where are the DNA repair genes? Should we focus on abilty of this cell to deal with hypoxia? (it seems to enjoy this path?)
There is much to be done, but where are we....
AT CRBCM, we are still at work!
Sunday, January 26, 2014
Puzzling c-KIT
C-kit presence has been used in the definition of GIST and its presence has been used for the sensitivity to TKI (Gleevec). But this is proven when C-kit is a driver Mutation (driven by localized or in-situ) autoregulation), in other disease C-kit could be present as a secondary event (mitigated response in response to upstream gene overexpression-this conditioned by normal suppressive downregulation), in those cases, TKI will have a minimal effect....
Can Monteluskast or Zafirlukast improve outcome
or does blocking IL3 receptor change outcome
or should we introduce a JAK-STAT inhibitor to affect outcome since the SOCS genes seems to be involved? SOCS1 is described as a negative inhibitor of JAK/STAT pathway! Activators of SOCS1 are being looked at in Hepatoma, How frequently is c-Kit positivity in this disease? What is the meaning of c-Kit in Adenoid Carcinoma (driver Vs secondary)? Interesting questions indeed!
Can Monteluskast or Zafirlukast improve outcome
or does blocking IL3 receptor change outcome
or should we introduce a JAK-STAT inhibitor to affect outcome since the SOCS genes seems to be involved? SOCS1 is described as a negative inhibitor of JAK/STAT pathway! Activators of SOCS1 are being looked at in Hepatoma, How frequently is c-Kit positivity in this disease? What is the meaning of c-Kit in Adenoid Carcinoma (driver Vs secondary)? Interesting questions indeed!
In Melanoma, Tribulations of the MITF gene!
The gene is a "wild" gene and can auto-regulate, 2 charateristics that make MITF a dangerous gene! Moreover, it is implicated in cellular differentiation, it regulates the BCL-2, and shows up when resistance to BRAF inhibitor come to be demonstrated. It causes a deformation and intervene in cellular ability to resist Hypoxia. Therefore VEGF amplification is a secondary event meaning it is not a driver Mutation, and Anti-VEGF will have a minimal effect in Melanoma.(This is debatable in Uveal melanoma However - Here it is the GNAQ/GNA11 thing! And PKC and MEK inhibitors may be actors). Mutations in MITF lead to Tietz syndrome[5] and Waardenburg syndrome type IIa.[6]wikipedia
Blocking Wnt 3a, and the Cyclic AMP could be meaningful and alpha MSH could be a bio-marker for BRAF resistance. Look at PAX3 role and POU3F2! Interaction with LEF-1 is under scrutiny. Briefly, we have our eyes on Melanoma and its activity. The Melanocortin Receptor is also under review...Briefly we know that the cell has predicted that MITF is an agent of differentiation and adaptation (splicing and miRNA 211), it also has planned that if the cell cannot differentiate and adapt, it should quickly die through apoptosis...let melanoma cell choose this natural pass for the cure!
?Does failure to Braf points to susceptibility to Cisplatin or Melphalan? good question to explore, again is alpha MSH a meaningful Bio-marker under these circumstances? a good question to further explore!
Blocking Wnt 3a, and the Cyclic AMP could be meaningful and alpha MSH could be a bio-marker for BRAF resistance. Look at PAX3 role and POU3F2! Interaction with LEF-1 is under scrutiny. Briefly, we have our eyes on Melanoma and its activity. The Melanocortin Receptor is also under review...Briefly we know that the cell has predicted that MITF is an agent of differentiation and adaptation (splicing and miRNA 211), it also has planned that if the cell cannot differentiate and adapt, it should quickly die through apoptosis...let melanoma cell choose this natural pass for the cure!
?Does failure to Braf points to susceptibility to Cisplatin or Melphalan? good question to explore, again is alpha MSH a meaningful Bio-marker under these circumstances? a good question to further explore!
CRBCM staying in the news!
Improving the Odds Against Lung Cancer
- Last Updated on Thursday, 23 January 2014 15:39
UTEP News Service
For many, lung cancer is diagnosed too late.
“About 85 percent of people diagnosed with lung cancer will die of that condition,” said Mutombo Kankonde, M.D., referring to the most fatal cancer in the United States.
Mutombo
Kankonde, M.D. (left), a local El Paso oncologist, and Jianying Zhang,
Ph.D., a cancer biologist at UTEP, are working together to develop a
test for the early detection of lung cancer. Photo courtesy of Dr.
Kankonde.Those striking statistics — more people die of lung cancer each year than of colon, breast and prostate cancer combined — are what compelled Kankonde to study the disease and recently assemble a team of local scientists to develop a test to detect lung cancer much earlier.
“I haven’t done much work on lung cancer myself, but I have been able to identify biomarkers of liver cancer,” said Jianying Zhang, Ph.D., a biologist at The University of Texas at El Paso who forms part of the research team. “Dr. Kankonde knows this and wants to apply the same approach that I used in my lab to detect lung cancer earlier.”
Lung cancer is currently diagnosed after a CT scan, MRI or chest X-ray — when the tumor has already become visible as a mass in the lung and is at an advanced stage.
“If we use that sort of technology for diagnosis, it’s usually too late for the patient,” Zhang said. “That’s why we want to find a way to identify the cancer before there’s a tumor.”
In an effort to develop a breakthrough kit that detects lung cancer with either blood or saliva samples, Zhang, the oncologist, and Brad Bryan, Ph.D., a biomedical scientist at Texas Tech University Health Sciences Center, are studying 50 lung cancer tissue samples and the genes that compose them for phase one of the project.
The specialists are searching for three particular cancer-related genes in the tissue that have been associated with lung cancer at an early stage.
“We want to know, ‘What is the frequency of these gene abnormalities in these known lung cancer samples?’” said Kankonde, who is interested in the genetics of cancer.
If the genes are overexpressed in the tissue samples, as the team suspects they will be, they can be used as biomarkers, or early indicators of the disease.
The next phase of the project would be to develop a test kit that can detect the specific cancer-related genes in a patient’s blood or saliva, and test the diagnostic method on frequent smokers — who are at the highest risk for lung cancer. If a smoker tests positive for the genes, he or she would undergo a PET scan to see if a tumor is present.
“This has the potential to achieve cancer intervention at an early stage,” Zhang said. “In this way, the patient can still survive and have surgery done before it’s too late.”
If the team’s research is successful, they’ll eventually be able to put their test kit on the market for doctors to use on patients who are at risk for lung cancer.
Kankonde added that another team objective is to determine which lung cancers are sensitive to Avastin, a standard drug used to reduce the size of lung tumors.
Not all patients respond to the drug, and Kankonde believes this also may be linked to a patient’s particular genetics.
“We want to identify genetically why some patients are sensitive to Avastin and why some are not,” he said.
If they can determine and validate the gene that causes a reaction, doctors could potentially determine whether Avastin will be a worthwhile treatment for a patient with lung cancer on a case-by-case basis.
Kankonde, who operates his own oncology clinic in El Paso, says he has positive expectations for the outcome of the study.
If he’s right, he may well be applying the tests in his own clinic one day.
One of the reason we have kept silence these few days is our return to Indianapolis to complete the various tasks that keeps CRBCM a float! Many contracts remain to be fulfilled, and CRBCM intends to accomplish one and every single contract to the fullest...so we are sometime on the move. Indiana was covered with snow so the mission was perilous (looking at your plane de-icing makes one critically uncomfortable, particularly when the de-icing fluid freezes on your plane window), but we are seeing the light as we progress deliberately! We still keep staying in the news though! Our research was posted in the UTEP NEWS!
Friday, January 24, 2014
DO NOT UNDERESTIMATE THE POWER OF ONE (RECEPTOR)
"IRAK1b, a Novel Alternative Splice Variant of Interleukin-1 Receptor-associated Kinase (IRAK), Mediates Interleukin-1 Signaling and Has Prolonged Stability*"
Liselotte E. Jensen‡"Please just go to article, but it is clear that TGF Beta is clearly important particularly in Breast Cancer. Anything that can autophosphorylate should make any-researcher nervous because it can set its self up and initiate something up (driver mutation). When it is a molecule that can help cancer cell elude autoimmune destruction, when it help the auto-growth, and avoid apoptosis through death receptor or otherwise, when it interfere with cellular differentiation, when its level is require at strong presence, and when it is a conserved mechanism, it is an important part of the neoplastic transformation. Through the Tollip, it can be reached by targeting the Tankyrase! CRBCM is on it!
IRAK-1 is a critical component to cancer production!
Involvement of the NFKB suggests it (through TRAF 6, PKC, and TAB)
Through the RACs and RICs, IRAK reaches Metastasis (Rho/ROCK) and the BARC1 (breast cancers). (by touching Myd...of course).
Its activity through tampering with a gene regulator (IKK) should make you double nervous and doubling with autophosphorylation means it can be a driver on its own and achieve autocrine role for the new Cancer!
Through the CHUK it acts as a multiple site hitting of the NFkB but also reaches the Wnt through CTNNB1. Hitting NCOA means the engagement of all other Hormone receptors including the "wild" gene, Andogene receptors! Once again The Tankyrases better be your Target to stop all this upstream...
And you know through the Dead Box, P53 will be spared and through mechanisms shared above, your Retinoblastoma gene will soon come into play. And I guess I should not mention the Ubiquitin C or the NOTCH!...they all are involved!
The lesson here is that it is not the gene to look at when you are trying to find a therapeutic intervention, it is its common Receptor or substrate. Don't look at IL-1, look at their receptors ...such as IRAK-1!
Thursday, January 23, 2014
BAD THINGS LOOK ALIKE, BUT TRY TO WALK WITH ME THROUGH THE MAZE OF GENES! LIGHT IS BORN!
AMBRY-GENETICS"
"Pancreatitis Panel includes concurrent full gene analysis for PRSS1, SPINK1 and CFTR. Pancreatitis Panel can detect 99% of PRSS1 and SPINK of known mutations and 97-98% of of CFTR mutations. Testing does not include CTRC gene analysis."
BUT DO YOU REMEMBER SPINK5
IN THE NETHERTON SYNDROME
WHERE THEY SPEAK OF ICHTHYOSIS AND LEKTI
AND STRATUM BASALE
AND PSORIASIS AND STRATUM BASALE, WHERE BASAL LIKE CELL COME FROM AND SEEN IN TRIPLE NEGATIVE BREAST CANCER,
REALLY LOOK IT UP, IN PSORIASIS THEY SPEAK OF CCHCRA1
WELL DOWNSTREAM THIS WE FIND POLR2C WHICH TALK TO TAF15 THEN SAFB WHICH ACTIVATES ESTROGEN RECEPTOR AND HNRPD WHICH INTERACTS WITH HSP27 AND LATER SPEAKS WITH TGFB AND PTPN12 AND BAMMMMM! IT REACHES BCAR1. AND BRCA1 BECOMES FOUND IN TRIPLE NEGATIVE BREAST CANCER WHICH IS NOT FAR FROM PANCREATIC PROCESSES. BUT IN ALL THE MAZE OF GENES OUR FOCUS REMAINS ON SP1, EP300,SIN3A,GATA1.
THE FACT REMAINS THAT TATA SPEAKS ALSO TO POLR2C, THE SAME POLR2C THAT SPEAKS TO TAF15. HMMMM....AND TATA binding protein SPEAKS TO TAF15.
PTPN12 INTERACTS WITH SHC1 BUT WATCH IT ATTACKING SHC1 (REGULATOR OF APOPTOSIS) BECAUSE IT HAS THE FAMOUS SH2 DOMAIN LIKE A GAZILLION OF OTHER MOLECULE INCLUDING THE STATS AND THE JAKs. YOU JUST DON'T KNOW WHAT YOU WILL TOUCH.
ON THE OTHER HAND UBIQUITICN C KEEPS ATTRACTING RESEARCHER FOR WHAT IT CAN DELIVER! ONE NEEDS TO STRATEGIZE THIS APPROACH!
"Pancreatitis Panel includes concurrent full gene analysis for PRSS1, SPINK1 and CFTR. Pancreatitis Panel can detect 99% of PRSS1 and SPINK of known mutations and 97-98% of of CFTR mutations. Testing does not include CTRC gene analysis."
BUT DO YOU REMEMBER SPINK5
IN THE NETHERTON SYNDROME
WHERE THEY SPEAK OF ICHTHYOSIS AND LEKTI
AND STRATUM BASALE
AND PSORIASIS AND STRATUM BASALE, WHERE BASAL LIKE CELL COME FROM AND SEEN IN TRIPLE NEGATIVE BREAST CANCER,
REALLY LOOK IT UP, IN PSORIASIS THEY SPEAK OF CCHCRA1
WELL DOWNSTREAM THIS WE FIND POLR2C WHICH TALK TO TAF15 THEN SAFB WHICH ACTIVATES ESTROGEN RECEPTOR AND HNRPD WHICH INTERACTS WITH HSP27 AND LATER SPEAKS WITH TGFB AND PTPN12 AND BAMMMMM! IT REACHES BCAR1. AND BRCA1 BECOMES FOUND IN TRIPLE NEGATIVE BREAST CANCER WHICH IS NOT FAR FROM PANCREATIC PROCESSES. BUT IN ALL THE MAZE OF GENES OUR FOCUS REMAINS ON SP1, EP300,SIN3A,GATA1.
THE FACT REMAINS THAT TATA SPEAKS ALSO TO POLR2C, THE SAME POLR2C THAT SPEAKS TO TAF15. HMMMM....AND TATA binding protein SPEAKS TO TAF15.
PTPN12 INTERACTS WITH SHC1 BUT WATCH IT ATTACKING SHC1 (REGULATOR OF APOPTOSIS) BECAUSE IT HAS THE FAMOUS SH2 DOMAIN LIKE A GAZILLION OF OTHER MOLECULE INCLUDING THE STATS AND THE JAKs. YOU JUST DON'T KNOW WHAT YOU WILL TOUCH.
ON THE OTHER HAND UBIQUITICN C KEEPS ATTRACTING RESEARCHER FOR WHAT IT CAN DELIVER! ONE NEEDS TO STRATEGIZE THIS APPROACH!
Wednesday, January 22, 2014
For fun, we also do!
Hello Clement Albert,(or DR Kankonde)
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We think you'll agree that Radio Airplay is a better promotional tool than ever. More than 50,000 artists rely on Airplay to get their music out there, and here's why:
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Cancer research questions, so many it is mind troubling!
1.Can disruption of the Nuclear CAP be used as therapeutic intervention in dividing cell?
lewis et al:
"The defects in splicing and U1 snRNP binding caused by CBC depletion can be specifically reversed by recombinant CBC. In summary, efficient recognition of the cap-proximal 5' splice site by U1 snRNP is facilitated by CBC in what may be one of the earliest steps in pre-mRNA recognition. Data in Colot et al. (this issue) indicate that this function of CBC is conserved in humans and yeast."
It is a conserved process for a reason! CAN INTERFERING WITH SPLICING BE USED IN CANCER THERAPY?
2. Could blocking Transportins (1,2) or A1 be a novel therapeutic approach in Breast cancers since levels of Molecule transfer seems of importance in this disease.
Can these molecules (transporters in general) be biomarkers of cellular activities in breast cancers. What is the role of targeting the poly tail (A) of RNA, should that limit the movement of these RNA
3. Should BH3 domains, presence of BNIP3 activation, BCL2, NOTCH activation, be surrogates for anti-apoptosis in cancer biology? what about SHC1
4. Should presence of activity at CD47 be consider a biomarker of BCL-2 activity? Anti-apoptosis?
CD47 (IAP).
wikipedia:"By blocking TSP1 from binding to its cell surface receptor (CD47) normal tissue becomes nearly immune to cancer radiation therapy and assists in tumor death."
5.GIPC 1 could turn out to be an important Target in Ovarian cancers! because of DAB2 and LRP interactions.
So many things to test, it is mind "troubling" or is it "mind buggling",they say!
lewis et al:
"The defects in splicing and U1 snRNP binding caused by CBC depletion can be specifically reversed by recombinant CBC. In summary, efficient recognition of the cap-proximal 5' splice site by U1 snRNP is facilitated by CBC in what may be one of the earliest steps in pre-mRNA recognition. Data in Colot et al. (this issue) indicate that this function of CBC is conserved in humans and yeast."
It is a conserved process for a reason! CAN INTERFERING WITH SPLICING BE USED IN CANCER THERAPY?
2. Could blocking Transportins (1,2) or A1 be a novel therapeutic approach in Breast cancers since levels of Molecule transfer seems of importance in this disease.
Can these molecules (transporters in general) be biomarkers of cellular activities in breast cancers. What is the role of targeting the poly tail (A) of RNA, should that limit the movement of these RNA
3. Should BH3 domains, presence of BNIP3 activation, BCL2, NOTCH activation, be surrogates for anti-apoptosis in cancer biology? what about SHC1
4. Should presence of activity at CD47 be consider a biomarker of BCL-2 activity? Anti-apoptosis?
CD47 (IAP).
wikipedia:"By blocking TSP1 from binding to its cell surface receptor (CD47) normal tissue becomes nearly immune to cancer radiation therapy and assists in tumor death."
5.GIPC 1 could turn out to be an important Target in Ovarian cancers! because of DAB2 and LRP interactions.
So many things to test, it is mind "troubling" or is it "mind buggling",they say!
Monday, January 20, 2014
Importance of cancer Metastasis
One thing for sure Metastasis is just not another characteristic of Cancer. It is one of the characteristics of tumoral cells that make them cancerous. Cancer will not kill anybody unless it spreads (with the exception of Brain cancer, but even in this disease, it is the tentacular infiltrations of these cells that ultimately kill. Cancer on the move kills. So it is important to focus on genes that lead to cancer spread. Prostate cancer or colon cancers will not kill if invasion and metastasis will not occur. And survivors will not be at risk if the disease stopped popping up somewhere else (in most cases, since local recurrence could be dealt with vehemently with an aggressive local treatment!). Spread has become sophisticated, from Putative genes such as MTS1, to motion evidence with non muscle Myosin (II, and sometime V)/Actin, to SNAIL and SLUG (E-Cadherin). It goes on to hiding behind P53 of which activation can increase phosphorylation of MK5 and you know what effect this will have on RAS. In Breast cancers in particular, you know about RSK dependent TGF accumulation of MK2. Increase of RSK4, decrease CXCL family member which in turn activates the Claudins...Other pathways of importance VEGF,LIMK1,P38. Putative role of RhoA/Rock. MLCK, BNIP and even LAR genes. We have so many chances to act but sit on our hands...talking to governors who have nothing to do with these markers...The Ultimate blocker to cancer research is still Human...wearing Tuxedo, unaware or innocent to science! Work with CRBCM to stop cancer, not find reasons...and you know the rest....CRBCM progressing slowly but surely ... we will continue to fight until we find a cure...and enemies become irrelevant to the fight! (So many markers, so many chances to stop cancer, but nothing substantial done to capture the moment! and politics keep going...they lost their soul! )
Sunday, January 19, 2014
?new Breast cancer Biomarker
There must be a marker in Breast cancer displaying a mutation in the fanconi like gene.
We know that disturbance in Fanconi disease affect mobilization of molecule such as Cystine.
And Fanconi gen alteration is cited a lot in Breast cancer, Is there a Beta albumin secretion when SLC gene is abnormal in Breast Cancer. take serum and Breast cancer specimen, if mutation in SLC gene is found, does the serum gives us a Beta-albumin like molecule in the serum? easy to find a biomarker...ok let's go to work.
Is SLC gene marker a surrogate of Crizotinib activity? secondary reason for investigation?
PALB2 is associated with BRCA-2, is there a secretion of protein linked to it?
We know that disturbance in Fanconi disease affect mobilization of molecule such as Cystine.
And Fanconi gen alteration is cited a lot in Breast cancer, Is there a Beta albumin secretion when SLC gene is abnormal in Breast Cancer. take serum and Breast cancer specimen, if mutation in SLC gene is found, does the serum gives us a Beta-albumin like molecule in the serum? easy to find a biomarker...ok let's go to work.
Is SLC gene marker a surrogate of Crizotinib activity? secondary reason for investigation?
PALB2 is associated with BRCA-2, is there a secretion of protein linked to it?
Saturday, January 18, 2014
CAMPTEN ! IN NEURO-ENDOCRINE TUMORS!
Somethings make you scratch your head,
and now you wonder what made them think of it...
In life revisiting stuff is not bad after all...
WHO HAD THOUGHT OF THAT
AND THEN IT MAKES YOU RUN BACK TO THE DRAWING BOARD
COMBINATION OF XELODA AND TEMODAR IN NEURO-ENDOCRINE TUMOR?
THE RESULT IS UNEXPECTEDLY GOOD!
WHAT IS THE GENETIC BASIS OF THIS, CRBCM WONDERS! LET'S GO BACK HERE....THE SEARCH SHOULD NOT BE LONG, I GUESS......to be this effective the mode of action go to be additive which in gene may mean a more total blockade of a specific gene or pathway, or blockade of 2 competing gene/pathways or may be blockade of 1 pathway and its rescue process. We have got to go deeper. And why Neuroendocrine ? Is that mean where Etoposide may work such as in the epigenetic area where Histone Deacetylase are king, or is it in the mitochondria where the CREB genes , BCL-2 are in effect. Xeloda aims a Thymidilate synthase impairing S-phase but what that have to do with silencing th MGMT gene that unleashes Temodar alkylating effect...does blocking synthase and the need in S phase give a better out look...well we need dig in further...and why neuro endocrine, why the hormone? here focus on epigenetic phenomena is warranted...
and now you wonder what made them think of it...
In life revisiting stuff is not bad after all...
WHO HAD THOUGHT OF THAT
AND THEN IT MAKES YOU RUN BACK TO THE DRAWING BOARD
COMBINATION OF XELODA AND TEMODAR IN NEURO-ENDOCRINE TUMOR?
THE RESULT IS UNEXPECTEDLY GOOD!
WHAT IS THE GENETIC BASIS OF THIS, CRBCM WONDERS! LET'S GO BACK HERE....THE SEARCH SHOULD NOT BE LONG, I GUESS......to be this effective the mode of action go to be additive which in gene may mean a more total blockade of a specific gene or pathway, or blockade of 2 competing gene/pathways or may be blockade of 1 pathway and its rescue process. We have got to go deeper. And why Neuroendocrine ? Is that mean where Etoposide may work such as in the epigenetic area where Histone Deacetylase are king, or is it in the mitochondria where the CREB genes , BCL-2 are in effect. Xeloda aims a Thymidilate synthase impairing S-phase but what that have to do with silencing th MGMT gene that unleashes Temodar alkylating effect...does blocking synthase and the need in S phase give a better out look...well we need dig in further...and why neuro endocrine, why the hormone? here focus on epigenetic phenomena is warranted...
Friday, January 17, 2014
c-MYC, a trouble maker in Breast Cancer
The expression of c-MYC suggests downregulation of BCL-2 and may open the road to use of anti-Topoisomerases.
The danger of c-MYC is through its relation with ZBTB17(Zinc Finger) which affects the Host Cell Factor 1 which in turn hits SP1 and the POU2F1. The latest activates:
"POU2F1 has been shown to interact with SNAPC4,[3][4] Ku80,[5][6] Glucocorticoid receptor,[7][8][9] Sp1 transcription factor,[10][11] NPAT,[12] POU2AF1,[4][13][14] Host cell factor C1,[15][16] TATA binding protein,[17] RELA,[18] Nuclear receptor co-repressor 2,[19] EPRS,[20] Glyceraldehyde 3-phosphate dehydrogenase,[12] MNAT1[21] and Retinoid X receptor alpha.[7][22]"wikipedia
Touching the RELA in an uncontrolled fashon is generally a mistake. It is a "wilder" gene affecting all functions and marks the Wnt/NFkB involvement, and Brings in the Casein Kinases.
The involvement of PPP1R13L further brings in the SP-1, amplifying downstream events.
Amplification of the c-MYC could always be associated with repression of Myb which impacts the mi-RNA 155, and may be associated with explosive expression of the c-FOS that needs Tamper! Of course presence of c-FOS will lead to more AP-1, should c-JUN be present! Increase of c-FOS could raise the importance of Histone de-acetylators in this disease!
So the presence of c-FOS and c-MYC could potentially raise the importance of Etoposide and Histone deacetylators! An interesting trial to suggest....
The danger of c-MYC is through its relation with ZBTB17(Zinc Finger) which affects the Host Cell Factor 1 which in turn hits SP1 and the POU2F1. The latest activates:
"POU2F1 has been shown to interact with SNAPC4,[3][4] Ku80,[5][6] Glucocorticoid receptor,[7][8][9] Sp1 transcription factor,[10][11] NPAT,[12] POU2AF1,[4][13][14] Host cell factor C1,[15][16] TATA binding protein,[17] RELA,[18] Nuclear receptor co-repressor 2,[19] EPRS,[20] Glyceraldehyde 3-phosphate dehydrogenase,[12] MNAT1[21] and Retinoid X receptor alpha.[7][22]"wikipedia
Touching the RELA in an uncontrolled fashon is generally a mistake. It is a "wilder" gene affecting all functions and marks the Wnt/NFkB involvement, and Brings in the Casein Kinases.
The involvement of PPP1R13L further brings in the SP-1, amplifying downstream events.
Amplification of the c-MYC could always be associated with repression of Myb which impacts the mi-RNA 155, and may be associated with explosive expression of the c-FOS that needs Tamper! Of course presence of c-FOS will lead to more AP-1, should c-JUN be present! Increase of c-FOS could raise the importance of Histone de-acetylators in this disease!
So the presence of c-FOS and c-MYC could potentially raise the importance of Etoposide and Histone deacetylators! An interesting trial to suggest....
Thursday, January 16, 2014
Today CRBCM at work
===========if you don't see a country, we just have fewer reviews!
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In triple negative breast cancer, so many things can go wrong!
One of the thing that goes wrong in triple negative breast cancer is that up to 40% of these cancer are BRCA mutation positive. Decrease in BRCA activity because of Mutation is followed by amplification of ELK1 which in turn engages the Serum Response Element (SRE), a devilish gene that engage among other gene the TEAD1 which affects MAX and the C-MYC, and the MSH2 and all breaks loose. Just by amplifying activity or the SER, the RELA gets excited and breast cancer of the aggressive kind develops quickly. It is not just Apoptosis that is reduced but the level of dedifferentiation in cellular development open doors to therapeutic options of new kinds that have been insufficiently explored, making the job at CRBCM even more undertaking, we have yet to sleep! looking at P38,JNK,ERK,ELK1, Sap1, HSP27, CRE and SRF as potential targets!
And what with Mutations at the ATF1 and CREBBP...and the cogitations go on!
Increase in ELK1 activates MEK and ....target ? well let's keep going...
And who would have guest that C-fos would be an important Biomarker? got me totally fooled!
And what with Mutations at the ATF1 and CREBBP...and the cogitations go on!
Increase in ELK1 activates MEK and ....target ? well let's keep going...
And who would have guest that C-fos would be an important Biomarker? got me totally fooled!
Wednesday, January 15, 2014
To the survivors, Peace could come through the CENP-F, importin, EGF repeats! But we don't know what we know!
Yes it is true that when survivors of a cancer meet their Doctors, they look to him to tell them if the disease is back or if they should rest some more at peace. The truth is that science has not work enough to provide good indicators of cancer recurrence particularly when it comes to those cancers missing standard markers. For example if you follow a colon or ovarian cancer, the CEA and CA-125 will be respectively good markers to follow . Most clinicians will do these tests serially, and patient find comfort in following these related number of markers as their disease progresses. The Marker's number help with decision to move forward with various therapeutic options before both the physician and the patient. ie. if the PSA is increasing following a series of treatments, Prostate cancer will be supposed to progress or resist the said treatments, and often decision to change treatment will ensue. On the other hand, Response to a treatment for metastatic prostate cancer will be judged based on how much it drops or decrease the PSA, a valid response criteria in Prostate Cancer. So clearly, Bio-markers are here for us to be used in clinical practice.
However both the patient and their doctors remain silence when it comes to very dangerous cancers. Sarcoma, Melanoma or even Brain cancers have no standardized Markers to follow. It is sad to wait for the mass to grow in a convincing way to tell the patient that the tumor is on the move. Often as we have our eyes on this tumor, somewhere else something happens to tell us the tumor is indeed on the move. But one thing for sure, a tumor to grow need to multiply, use more proteins, its nucleus will tell us "I am at work more here" and we have ways to tell. Mitosis and cell division is always in play when cancer Multiply and CENP-F will tell us, Notch is in play and EGF repeats will tell the message (amplification of c-MYC will tell us), level of CSL genes will tell us NOTCH is hot or not! level of Importin or BRAP- all these genes are at our disposal to tell something is up! And even level of Myosin and use of NLSs (Nuclear localization signals) can tell a story, but despite our big talk, we have not done enough to tell our patients the truth because those with means have not let us investigate these potentials to their fullest. Researchers, the coalition want answers, in breast cancer, Wnt (CTNNB gene) and Notch (EGF repeats) are at work, when we sleep at the wheel.! wake-up! The Nuclear localisation signals are winking at us, we don't wink back!
However both the patient and their doctors remain silence when it comes to very dangerous cancers. Sarcoma, Melanoma or even Brain cancers have no standardized Markers to follow. It is sad to wait for the mass to grow in a convincing way to tell the patient that the tumor is on the move. Often as we have our eyes on this tumor, somewhere else something happens to tell us the tumor is indeed on the move. But one thing for sure, a tumor to grow need to multiply, use more proteins, its nucleus will tell us "I am at work more here" and we have ways to tell. Mitosis and cell division is always in play when cancer Multiply and CENP-F will tell us, Notch is in play and EGF repeats will tell the message (amplification of c-MYC will tell us), level of CSL genes will tell us NOTCH is hot or not! level of Importin or BRAP- all these genes are at our disposal to tell something is up! And even level of Myosin and use of NLSs (Nuclear localization signals) can tell a story, but despite our big talk, we have not done enough to tell our patients the truth because those with means have not let us investigate these potentials to their fullest. Researchers, the coalition want answers, in breast cancer, Wnt (CTNNB gene) and Notch (EGF repeats) are at work, when we sleep at the wheel.! wake-up! The Nuclear localisation signals are winking at us, we don't wink back!
Monday, January 13, 2014
Use of genetic in the future (full of controversial speculations to see if you are following!) careful with genes!
1.Today we can assume that alzheimer reflects disturbance in CREB and related genes
tomorrow, alcoholic will be judge by their level of CREB. It will be nice to tell someone that because of your isoform of CREB, don't even try Alcohol at all! you will become an alcoholic!
And just tell a man that your memory capacity is doubtful given your CREB activity, your strength is else where (comprehension or other capacity). Patient with post traumatic syndrome could be evaluated by the status of their CREB! have they become too forgetful....disturbance of CREB could point to old age?
Other genes for this purpose, ELK1 of course which is close by in the viscinity!But also CREBBP!
tomorrow, alcoholic will be judge by their level of CREB. It will be nice to tell someone that because of your isoform of CREB, don't even try Alcohol at all! you will become an alcoholic!
And just tell a man that your memory capacity is doubtful given your CREB activity, your strength is else where (comprehension or other capacity). Patient with post traumatic syndrome could be evaluated by the status of their CREB! have they become too forgetful....disturbance of CREB could point to old age?
Other genes for this purpose, ELK1 of course which is close by in the viscinity!But also CREBBP!
Sunday, January 12, 2014
CANCER RESEARCH FUNDING, A RIGGED GAME
Time and again, MAN comes up with the reason why progress is not achieved to the fullest. And the allocation of scarce funding does not escape the malignancy of human politics. The reflex to profit only those we know is entrenched in the core of humans, it bubbles inside of us, somewhat repressed by conscience and known rules of the game, but ultimately suppressed when it comes to reel deeds. Whether mischievious or unintended, these deeds corrupt the ultimate outcome, unintended or not.
In Texas the early years of CPRIT have been just that. Although the CPRIT concept was sane and well intended, putting in development was given to fund raisers of Universities. And what they put in place was a corrupt system which funneled funding to a few Universities and not the community of researchers as a whole. It took a few years to blow up in their face. You don't send to the moon or anywhere men in a political ship. Only a ship that is guided by solid unbiased science will make it through the peripetia of a natural world governed by true physics, mathematical and natural laws.
Although it is said that the review process is independent, you got to be an innocent kind to believe that reviewers are not hand picked, and trained to recognize the source of the submission. Indeed the CRBCM critics continue to write: "the project is ambitious, however the PI (principal investigator) is unknown". The merit went to prior knowledge of the man, but not the idea he submitted. The CRBCM will continue to submit ideas to these organizations because may be, just may there be a chance that one unique good soul is left in that institution, because even crooked minds can have a moment of lucidity and clairvoyance. So we will keep challenging them...and maybe our efforts help framing our argument as we use their free criticism, biased or not.
A friend of mine was working at NIH and told me, we usually receive a call to submit or write up a proposal on this or that at the last minute, and often we get the grant! and when I told him, I am writing a grant proposal, the answer was: "you are crazy wasting your time!"...It is who you know in the end!
Our fight is right, we believe strongly, because it is funded on facts, women continue to die of Breast cancer, and somehow we are managing to grow as if something, somewhere keeps us alive...January 1st, we acquired a new medical office (a retiring physician allowed us to take over his business). This has increased our foot print tremendously. These things happen for a reason, our true, just and innocent purpose of our coalition. Self funding is our true objective and desired position. Because anything less corrupts. CRBCM, still advancing purposefully!
In Texas the early years of CPRIT have been just that. Although the CPRIT concept was sane and well intended, putting in development was given to fund raisers of Universities. And what they put in place was a corrupt system which funneled funding to a few Universities and not the community of researchers as a whole. It took a few years to blow up in their face. You don't send to the moon or anywhere men in a political ship. Only a ship that is guided by solid unbiased science will make it through the peripetia of a natural world governed by true physics, mathematical and natural laws.
Although it is said that the review process is independent, you got to be an innocent kind to believe that reviewers are not hand picked, and trained to recognize the source of the submission. Indeed the CRBCM critics continue to write: "the project is ambitious, however the PI (principal investigator) is unknown". The merit went to prior knowledge of the man, but not the idea he submitted. The CRBCM will continue to submit ideas to these organizations because may be, just may there be a chance that one unique good soul is left in that institution, because even crooked minds can have a moment of lucidity and clairvoyance. So we will keep challenging them...and maybe our efforts help framing our argument as we use their free criticism, biased or not.
A friend of mine was working at NIH and told me, we usually receive a call to submit or write up a proposal on this or that at the last minute, and often we get the grant! and when I told him, I am writing a grant proposal, the answer was: "you are crazy wasting your time!"...It is who you know in the end!
Our fight is right, we believe strongly, because it is funded on facts, women continue to die of Breast cancer, and somehow we are managing to grow as if something, somewhere keeps us alive...January 1st, we acquired a new medical office (a retiring physician allowed us to take over his business). This has increased our foot print tremendously. These things happen for a reason, our true, just and innocent purpose of our coalition. Self funding is our true objective and desired position. Because anything less corrupts. CRBCM, still advancing purposefully!
Proposed Genetic Biomarker of fibrosis: SOCS3
1.The fact that administration of GCSF may increase frequency lung induced toxicity in patients on Bleomycin,
2.The fact that IL-6 is now the target for therapy in multiple sclerosis
"
Interleukin-6: a new therapeutic target in systemic sclerosis?
Steven O'Reilly"
3. and some believe IL-10 recruits fibroblasts
==========================================
All these facts point to one and only one gene to watch, SOCS3 and therefore the involvement of the JAK-STAT pathways. Indeed all Myelofibrosis end up in fibrosis and therefore a focus on SOCS3 is more than warranted. SOCS3 is first know as an inhibitor of the JAK/STAT pathways.
wikipedia: "The expression of this gene is induced by various cytokines, including IL6, IL10, and interferon (IFN)-gamma. The protein encoded by this gene can bind to JAK2 kinase, and inhibit the activity of JAK2 kinase."
SOCS3 is not only an enhancer of KRAS pathways in colon cancer by removing the pathway break (RasGAP), (it should be SOCS3 we should be watching!), but SOCKS3 through its activity with PTPN11, brings you the CEACAM-1 connection (which we follow as CEA in colon cancer) and beyond the CEACAM, SOCS3 brings Annexin-1 the road to fibrosis. Remember how Mucinous Gastric cancers end up producing so much fibrosis in the peritoneum that patient die of intestinal obstruction, it is we as Doctors do not monitor IL-6, IL-10, Interferon levels, SOCS3 activity, CEA, and Annexin-1 for that matter. We think PEG tube instead of blocking Annexin activities!
If you happen not to believe, you should read Wikipidia:
" Patients with a subset of Noonan syndrome PTPN11 mutations also have a higher prevalence of juvenile myelomonocytic leukemias (JMML). Activating Shp2 mutations have also been detected in neuroblastoma, melanoma, acute myeloid leukemia, breast cancer, lung cancer, colorectal cancer.[7] These data suggests that Shp2 may be a proto-oncogene. However, it has been reported that PTPN11/Shp2 can act as either tumor promoter or suppressor.[8] In aged mouse model, hepatocyte-specific deletion of PTPN11/Shp2 promotes inflammatory signaling through the STAT3 pathway and hepatic inflammation/necrosis, resulting in regenerative hyperplasia and spontaneous development of tumors. Decreased PTPN11/Shp2 expression was detected in a subfraction of human hepatocellular carcinoma (HCC) specimens.[8] The bacterium Helicobacter pylori has been associated with gastric cancer, and this is thought to be mediated in part by the interaction of its virulence factor CagA with SHP2.[9] wikipedia
=================================================================
why do you believe CEA is elevated in Gastric,colon or even Breast cancers! This pathway is indeed in effect!
Even GUO et al spoke about this in their observation focused on Caveolin in Fibrosis, but stumbled on SOCS3 (Their Caveolin was not far from SOCS3):
" Real-time PCR revealed that the expression of the mandarin fish Mx, IRF-1, SOCS1, and SOCS3 genes involved in the poly(I:C)-induced Jak-Stat signaling pathway was impaired by the mCav-1 scaffolding domain peptide (mSDP)."
"
SOCS3 is a powerful gene
and at CRBCM we still believe that a gene that can induce Malformation, is powerful.
SOCS3/PTPN11 is a powerful association:
Missense mutations in the PTPN11 locus are associated with both Noonan syndrome and Leopard syndrome.
It has also been associated with Metachondromatosis.[4]wikipidia
"
To muscle up both Leonard and Noonan syndromes ("il faut le faire" the french will tell you!) et le faire fort!(DO IT STRONGLY)
AND THEY MANAGE TO DO THIS THROUGH MITF!
2.The fact that IL-6 is now the target for therapy in multiple sclerosis
"
Interleukin-6: a new therapeutic target in systemic sclerosis?
Open
Steven O'Reilly"3. and some believe IL-10 recruits fibroblasts
"New concepts of IL-10-induced lung fibrosis: fibrocyte recruitment and M2 activation in a CCL2/CCR2 axis.
Sun L, Louie MC"==========================================
All these facts point to one and only one gene to watch, SOCS3 and therefore the involvement of the JAK-STAT pathways. Indeed all Myelofibrosis end up in fibrosis and therefore a focus on SOCS3 is more than warranted. SOCS3 is first know as an inhibitor of the JAK/STAT pathways.
wikipedia: "The expression of this gene is induced by various cytokines, including IL6, IL10, and interferon (IFN)-gamma. The protein encoded by this gene can bind to JAK2 kinase, and inhibit the activity of JAK2 kinase."
SOCS3 is not only an enhancer of KRAS pathways in colon cancer by removing the pathway break (RasGAP), (it should be SOCS3 we should be watching!), but SOCKS3 through its activity with PTPN11, brings you the CEACAM-1 connection (which we follow as CEA in colon cancer) and beyond the CEACAM, SOCS3 brings Annexin-1 the road to fibrosis. Remember how Mucinous Gastric cancers end up producing so much fibrosis in the peritoneum that patient die of intestinal obstruction, it is we as Doctors do not monitor IL-6, IL-10, Interferon levels, SOCS3 activity, CEA, and Annexin-1 for that matter. We think PEG tube instead of blocking Annexin activities!
If you happen not to believe, you should read Wikipidia:
" Patients with a subset of Noonan syndrome PTPN11 mutations also have a higher prevalence of juvenile myelomonocytic leukemias (JMML). Activating Shp2 mutations have also been detected in neuroblastoma, melanoma, acute myeloid leukemia, breast cancer, lung cancer, colorectal cancer.[7] These data suggests that Shp2 may be a proto-oncogene. However, it has been reported that PTPN11/Shp2 can act as either tumor promoter or suppressor.[8] In aged mouse model, hepatocyte-specific deletion of PTPN11/Shp2 promotes inflammatory signaling through the STAT3 pathway and hepatic inflammation/necrosis, resulting in regenerative hyperplasia and spontaneous development of tumors. Decreased PTPN11/Shp2 expression was detected in a subfraction of human hepatocellular carcinoma (HCC) specimens.[8] The bacterium Helicobacter pylori has been associated with gastric cancer, and this is thought to be mediated in part by the interaction of its virulence factor CagA with SHP2.[9] wikipedia
=================================================================
why do you believe CEA is elevated in Gastric,colon or even Breast cancers! This pathway is indeed in effect!
Even GUO et al spoke about this in their observation focused on Caveolin in Fibrosis, but stumbled on SOCS3 (Their Caveolin was not far from SOCS3):
" Real-time PCR revealed that the expression of the mandarin fish Mx, IRF-1, SOCS1, and SOCS3 genes involved in the poly(I:C)-induced Jak-Stat signaling pathway was impaired by the mCav-1 scaffolding domain peptide (mSDP)."
"
SOCS3 is a powerful gene
and at CRBCM we still believe that a gene that can induce Malformation, is powerful.
SOCS3/PTPN11 is a powerful association:
Missense mutations in the PTPN11 locus are associated with both Noonan syndrome and Leopard syndrome.
It has also been associated with Metachondromatosis.[4]wikipidia
"
To muscle up both Leonard and Noonan syndromes ("il faut le faire" the french will tell you!) et le faire fort!(DO IT STRONGLY)
AND THEY MANAGE TO DO THIS THROUGH MITF!
more speculative notes on triple negative breast cancers
Through the TIAF gene, inhibition of JAK3 could have a role in triple negative Breast cancer.
The RELA,UBE2I and MITF genes could have a prominent role in the development of triple negative breast cancer,
Blocking FGF could shield FGFR in the pathogenesis of triple negative Breast Cancers
POLR2A is our link to Psoriasis and the Basal like morphology! And you really are talking to BRCA genes
If you reach the RELA, you are in the Sp-1 and SF-1 territory and with POU2F1, you are deep in the belly of the beast!
and with SF-1, you are really exploring the MYC gene through the PUF-FUS (MyC gene/Xeroderma pigmentosus)
Basal cell like triple negative breast cancer has deep connections with autoimmune disease and therefore race (and probably gender)distribution through these mazes of genes. At CRBCM, we are tracking it down!
The RELA,UBE2I and MITF genes could have a prominent role in the development of triple negative breast cancer,
Blocking FGF could shield FGFR in the pathogenesis of triple negative Breast Cancers
POLR2A is our link to Psoriasis and the Basal like morphology! And you really are talking to BRCA genes
If you reach the RELA, you are in the Sp-1 and SF-1 territory and with POU2F1, you are deep in the belly of the beast!
and with SF-1, you are really exploring the MYC gene through the PUF-FUS (MyC gene/Xeroderma pigmentosus)
Basal cell like triple negative breast cancer has deep connections with autoimmune disease and therefore race (and probably gender)distribution through these mazes of genes. At CRBCM, we are tracking it down!
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