1.CDH 17
The change in expression of this gene in advance pancreatic cancer does not come as a surprise
because by now we have become familiar with the fact that advance cancer is on the move and should metastasize, CDH belong to the Cadherin family, the family of adhesion molecule, cells need to detach and go. Takamura M et al. have shown that the Liver-intestine Cadherins reduction correlated with Colon cancer metastatic to lymph nodes.
CDH17 appears to be a gene of differentiation and could help determine the origin of of tissue in those ambivalent cases where we are dealing with an cancer of unknown primary. It is a proton pump dependent cellular membrane structure. What is fascinating is the fact that how quickly these structures are internalized or their stimulation effect is transmitted to the Nucleus at splicing center to be expressed as differentiation agents.
Zhu at al. have suggested that the hepatic Nuclear factor 1 and CDX2 participate in the regulation of CDH17 expression. (larger speculation Where is the p molecule counterpart? since this cadherin is on 8q)
2. PSCA: PROSTATE stem cell Antigen
When the prostate lends a hand to the pancreas you know this is bad news. This antigen does not exist in the normal pancreas. But when it appears in the Pancreas you know the disease is advanced. Even in the Prostate the amplification of this antigen marks very high Gleason at presentation or bone Metastatasis. It is not PSA we should be looking for, but PCR overexpression of PSCA. By its name it says it all "Stem cell" meaning the cancer is now OMNIPOTENT and Incredibly resistant. The presence of this antigen is not only predictive but also prognosis. The makers of SIPULEUCEL-T should be incubating patient dendritic cells with with this antigen rather than PAP to be active in pancreatic cancers.
One interesting observation was made by Moore et al. while they were knocking down rats to further study this gene, they noted an over-expression of the AURORA kinases, these genes that regulate mitosis by controlling events at the Centrosomes. It is interesting because it raises the possibility of using the PSCA as an indicator for use of Aurora inhibitors (Hesperadin, ZM447439,Tozasertib,VX680). Also recent evidence of activity of Abraxane in Pancreatic cancer would open up the opportunity to use Abraxane in combination with Aurora kinase inhibitor in this disease. Clearly if P53 is dysregulated, we can safely assume the Aurora kinase may have a role since they are more likely over-expressed.
SO: new target Therapy in Pancreatic cancer ABRAXANE with an Aurora MutiKinase Inhibitor would be the next step if we want to introduce target therapy in Pancreatic cancers.
A recent TV documentary showed that a chemical compound that the EPA is investigating because it has contaminated the drinking waters in the USA caused cells to have Multiple Centrosomes in exposed cells, clearly is it affecting the AURORA and most likely AURORA A. It raised the possibility that Metallic based chemical compound toxicity may have a larger weight on this pathways. I wonder what Arsenic Trioxyde would add to this! remember the anti-Aurora have a secondary anti-Histone (3) activity contributing to their effect in CML.
3. MYC:
*a GLOBAL AMPLIFIER OF ALL GENES INCLUDING PROLIFERATIVE GENES.
*RECRUITER OF HISTONES DEACETYLASE PROTEIN
*OVERACTION OF CBF LIKE MOLECULES
*IT HAS IRES THE INTERNAL RIBOSOME ENTRY SITES WHICH IS THE KEY TO THE DOOR TO RIBOSOME FOR PROTEIN FORMATION (REGULATOR FOR MATION) AND HAS A THE ZIPPER TO ATTACH AND OPEN WIDE DNA FOR TRANSLATION. OVER-EXPRESSION OF MYC DRIVES PROLIFERATION AT HIGH PACE!
WIKIPEDIA SAYS IT ALL
Myc protein is a transcription factor that activates expression of many genes through binding on consensus sequences (Enhancer Box sequences (E-boxes)) and recruiting histone acetyltransferases (HATs). It can also act as a transcriptional repressor. By binding Miz-1 transcription factor and displacing the p300 co-activator, it inhibits expression of Miz-1 target genes. In addition, myc has a direct role in the control of DNA replication.[4]
Myc is activated upon various mitogenic signals such as Wnt, Shh and EGF (via the MAPK/ERK pathway).
By modifying the expression of its target genes, Myc activation results
in numerous biological effects. The first to be discovered was its
capability to drive cell proliferation (upregulates cyclins, downregulates p21), but it also plays a very important role in regulating cell growth (upregulates ribosomal RNA and proteins), apoptosis (downregulates Bcl-2), differentiation and stem cell self-renewal. Myc is a very strong proto-oncogene and it is very often found to be upregulated in many types of cancers. Myc overexpression stimulates gene amplification,[5] presumably through DNA over-replication."
"
Showing posts with label colon cancer. Show all posts
Showing posts with label colon cancer. Show all posts
Saturday, March 16, 2013
Thursday, March 7, 2013
NEWS from ASCO
*Avastin-Folfoxiri better than Avastin-Folfiri, no news there. It is just a repeat of things we knew would happen.
*In Colon cancer patients with Wild type KRAS Panitumumab (Vectibix) associated to 5-FU based combination gave an outcome comparable to results obtained in a different study with Avastin and 5-FU based combination. 2 phase II trials but 2 similar outcomes. And this in first line and 2nd line. Can't wait to see a phase III.
*40% Glioblastoma express EGFR
20% have EGFRvIII
with Lapatinip being looked at for treatment, will wait to see.
*In Colon cancer patients with Wild type KRAS Panitumumab (Vectibix) associated to 5-FU based combination gave an outcome comparable to results obtained in a different study with Avastin and 5-FU based combination. 2 phase II trials but 2 similar outcomes. And this in first line and 2nd line. Can't wait to see a phase III.
*40% Glioblastoma express EGFR
20% have EGFRvIII
with Lapatinip being looked at for treatment, will wait to see.
Tuesday, February 26, 2013
REGORAFENIB, A DEFINITIVE ADVANCEMENT IN CANCER MEDICINE!
Those of us who had treated metastatic colon cancer know that patients only dies when you have exhausted possible options. It is sobering moment to see a human being deteriorating before your eyes while you have nothing to offer!
So, when something new comes along that appears effective, we embrace it in this disease. We know our patients will be offered it at one given point. Colon cancer seems to wait until you have finished all you can do! This behavior is particular as opposed to lung cancer which appears to kill despite your doing!
The power of Regorafenib seems to reside in the number of kinases affected by this drug:VEGFR3, TIE2, PDGFR, FGFR, KIT and RET.
Through KIT, it has found its Approval for GIST.
A slew of Genes are affected by this drug (on top of those mentioned, DDR2, TrK2A, Eph2A, RAF-1,BRAF, BRAF v600E, SAPK2,PTK5, and Abl) have been included in its repertoire.
The CORRECT trial introduced us to this drug in Metastatic colon cancer. Thumbs up!
Dose approved: 160 mg orally daily!
DDR2 has been commented on plenty here in various notes!
TrK2A seems to relate to transmembranes channel allowing survival in low K+ conditions
Eph2A is downstream the MAPK and is the feedback regulator. once activated it comes back on its membrane receptor and sens inhibitory influx to shut down the MAPK. Cancer quickly desactivates this to keep the signal transduction pathway on. It kinds of remind me of the Sons of the Sevenless (my favorite).
(to be continued)
Regorafenib, the power of a good Multikinase, the next generation Multikinase!
-------------------------------------------------------------------------------
RAF-1 OR c-RAF
Remember RAS-RAF-MAPK, while c-RAF is RAF-1, people are more talking about b-RAF or BRAF.
RAF-1
"-The phosphorylated form of RAF1 (on residues Ser-338 and Ser-339, by PAK1) phosphorylates BAD/Bcl2-antagonist of cell death at 'Ser-75'.
- Phosphorylates adenylyl cyclases: ADCY2, ADCY5 and ADCY6, resulting in their activation. Phosphorylates PPP1R12A resulting in inhibition of the phosphatase activity.
- Phosphorylates TNNT2/cardiac muscle troponin T. Can promote NF-kB activation and inhibit signal transducers involved in motility (ROCK2), apoptosis (MAP3K5/ASK1 and STK3/MST2), proliferation and angiogenesis (RB1).
-Can protect cells from apoptosis also by translocating to the mitochondria where it binds BCL2 and displaces BAD/Bcl2-antagonist of cell death.
-Regulates Rho signaling and migration, and is required for normal wound healing. Plays a role in the oncogenic transformation of epithelial cells via repression of the TJ protein, occludin (OCLN) by inducing the up-regulation of a transcriptional repressor SNAI2/SLUG, which induces down-regulation of OCLN. Restricts caspase activation in response to selected stimuli, notably Fas stimulation, pathogen-mediated macrophage apoptosis, and erythroid differentiation." (Reviewed, UniProtKB/Swiss-Prot)
Abnormality at RAF-1 causes the NOONAN and the LEOPARD syndromes, "short stature" from genetic stand point, gives you the largest gift in genetic finding. Again do not discriminate and round up short stature people!
SAPK-1
It is the stress induced MAPK-8 or c-JUN, block ubiquitination of P53 and therefore up-regulates it.
By involving SAPK-1, Regorafenib is indeed one of the rare drug that can impact growth factors, cyclins, TNF in a more significant way in diseases where this pathway is very amplified (from cancer to inflammatory disease and infections!)
So, when something new comes along that appears effective, we embrace it in this disease. We know our patients will be offered it at one given point. Colon cancer seems to wait until you have finished all you can do! This behavior is particular as opposed to lung cancer which appears to kill despite your doing!
The power of Regorafenib seems to reside in the number of kinases affected by this drug:VEGFR3, TIE2, PDGFR, FGFR, KIT and RET.
Through KIT, it has found its Approval for GIST.
A slew of Genes are affected by this drug (on top of those mentioned, DDR2, TrK2A, Eph2A, RAF-1,BRAF, BRAF v600E, SAPK2,PTK5, and Abl) have been included in its repertoire.
The CORRECT trial introduced us to this drug in Metastatic colon cancer. Thumbs up!
Dose approved: 160 mg orally daily!
DDR2 has been commented on plenty here in various notes!
TrK2A seems to relate to transmembranes channel allowing survival in low K+ conditions
Eph2A is downstream the MAPK and is the feedback regulator. once activated it comes back on its membrane receptor and sens inhibitory influx to shut down the MAPK. Cancer quickly desactivates this to keep the signal transduction pathway on. It kinds of remind me of the Sons of the Sevenless (my favorite).
(to be continued)
Regorafenib, the power of a good Multikinase, the next generation Multikinase!
-------------------------------------------------------------------------------
RAF-1 OR c-RAF
Remember RAS-RAF-MAPK, while c-RAF is RAF-1, people are more talking about b-RAF or BRAF.
RAF-1
"-The phosphorylated form of RAF1 (on residues Ser-338 and Ser-339, by PAK1) phosphorylates BAD/Bcl2-antagonist of cell death at 'Ser-75'.
- Phosphorylates adenylyl cyclases: ADCY2, ADCY5 and ADCY6, resulting in their activation. Phosphorylates PPP1R12A resulting in inhibition of the phosphatase activity.
- Phosphorylates TNNT2/cardiac muscle troponin T. Can promote NF-kB activation and inhibit signal transducers involved in motility (ROCK2), apoptosis (MAP3K5/ASK1 and STK3/MST2), proliferation and angiogenesis (RB1).
-Can protect cells from apoptosis also by translocating to the mitochondria where it binds BCL2 and displaces BAD/Bcl2-antagonist of cell death.
-Regulates Rho signaling and migration, and is required for normal wound healing. Plays a role in the oncogenic transformation of epithelial cells via repression of the TJ protein, occludin (OCLN) by inducing the up-regulation of a transcriptional repressor SNAI2/SLUG, which induces down-regulation of OCLN. Restricts caspase activation in response to selected stimuli, notably Fas stimulation, pathogen-mediated macrophage apoptosis, and erythroid differentiation." (Reviewed, UniProtKB/Swiss-Prot)
Abnormality at RAF-1 causes the NOONAN and the LEOPARD syndromes, "short stature" from genetic stand point, gives you the largest gift in genetic finding. Again do not discriminate and round up short stature people!
SAPK-1
It is the stress induced MAPK-8 or c-JUN, block ubiquitination of P53 and therefore up-regulates it.
By involving SAPK-1, Regorafenib is indeed one of the rare drug that can impact growth factors, cyclins, TNF in a more significant way in diseases where this pathway is very amplified (from cancer to inflammatory disease and infections!)
Monday, February 4, 2013
CELLULAR LANGUAGE (II)
In Cellular Language I published recently that we tried to emphasize that big functions of the cell start up with an on-and-off switch. The Tic and The Tan like in MORSE language, the 1and 0 of the computer. While this is true, there are many other simple things at the molecular level that are just as simple, but full of physiologic and scientific implications.
1.ON and OFF switch:
--------------------------
Events that lead to cancer are sometimes an exaggeration of a signal. The K-RAS (there exist many RAS (es) as we discussed in differentiation) has a switch called the Sons of the Sevenless which can stay on, sending signals down the cell continuously. Activated RAS will light on 3 signal pathways:
-MAP kinase (through RAF)--->FOS, JUN (stress), MYC (the dangerous leading to Burkitt)-TF
-RAL/CDC42 (important in the movement of the membrane, Metastasis)
-PI3K (leading to affect on AKT/MTOR) FOXO downstream hiding the PUMA-remember)
Mutations at the RAS itself can also cause it to stay on, as opposed to knocking it out.
Remember, Mutations of RAS occur in 80% of Pancreatic cancers and 50% of colon cancer.
Therefore, a simple switch can kill you with one of the most devastating diseases.
2. Change of shape:
---------------------
To confuse and look smart, your scientist calls this post-translational conformation to emphasize that this change has occurred later because of the nteraction with another molecule (in general).
At the surface of the membrane, there are here and there some Molecules called INTEGRINS; these are of various types and increasing molecular diversity and are best known as Receptors. They are large complexes of molecules gathered in chunks called 'subunits'. They basically cross the thickness of the cellular membrane and, outside the cell, they sense what is going on. Integrins serve many great purposes including cell division, proliferation, migration, adhesion to each either, differentiation, sensing etc. You name it, they do it! Only division of DNA, this, they don't do. But the membrane has to be divided also to make 2 cells in cell divison. Even anti-coagulation happens here. The versatility of the integrins is linked to the variety of subunits it is composed with. Some are nature of cell specific and some are contact specific. By contact specific, I mean what molecule outside the cell it will attach to (ie fibronectin Vs GPIIb).
Suffice is to say that kinking of the Integrins causes exposure of some parts of the Integrin molecule not naturally exposed. If one looks at the skin of the joint at the back of the finger, one will see folded skin. if you forcefully bend your finger, the fold you were looking at will unfold and the bottom of the fold will come out. This is what happen to the integrin when it meets outside the cell another molecule such as TALIN.
That bending triggers the attachment of other molecules or ions (phosphorylation) to the now exposed skin, lighting up the Integrins for the cascade of events which will unfold, including the activation of SRC in Sarcoma.
The shape imposed by the bending is also Molecule specific. Despite the resemblance of SRC with the c-ABL (leukemia), their bending does not offer the same shape, and therefore, different parts of the molecule are exposed and 2 different diseases result.
CELL ADHESION- "join at the hip"
----------------------------------------
At many points the cells are joined to each other at the hips of the Talins. Say, at the hip of the Talin which linked to one Integrin, there is a PLUS SIGN at Cell A, and at the next TALIN attached to the Integrin of cell B, there is a NEGATIVE sign. These 2 integrins will be attached, and cell adhesion is achieved. Simple as that!
Wheels of cellular migration,
-----------------------------,
Cells can roll over other cells by progressively attaching Talin to Talins and breaking the talin-talins (integrin-integrin) behind, engulfing the integrins and using them again in the forthcoming attachment like a wheel touching the ground. The cell is that smart at the membrane.
More simple things to come...
Hiding the PUMA behind the FOXO to have a death TRAP (Apoptsosis) in case the FOXO is compromised!
Just simple, but effective tricks ...
1.ON and OFF switch:
--------------------------
Events that lead to cancer are sometimes an exaggeration of a signal. The K-RAS (there exist many RAS (es) as we discussed in differentiation) has a switch called the Sons of the Sevenless which can stay on, sending signals down the cell continuously. Activated RAS will light on 3 signal pathways:
-MAP kinase (through RAF)--->FOS, JUN (stress), MYC (the dangerous leading to Burkitt)-TF
-RAL/CDC42 (important in the movement of the membrane, Metastasis)
-PI3K (leading to affect on AKT/MTOR) FOXO downstream hiding the PUMA-remember)
Mutations at the RAS itself can also cause it to stay on, as opposed to knocking it out.
Remember, Mutations of RAS occur in 80% of Pancreatic cancers and 50% of colon cancer.
Therefore, a simple switch can kill you with one of the most devastating diseases.
2. Change of shape:
---------------------
To confuse and look smart, your scientist calls this post-translational conformation to emphasize that this change has occurred later because of the nteraction with another molecule (in general).
At the surface of the membrane, there are here and there some Molecules called INTEGRINS; these are of various types and increasing molecular diversity and are best known as Receptors. They are large complexes of molecules gathered in chunks called 'subunits'. They basically cross the thickness of the cellular membrane and, outside the cell, they sense what is going on. Integrins serve many great purposes including cell division, proliferation, migration, adhesion to each either, differentiation, sensing etc. You name it, they do it! Only division of DNA, this, they don't do. But the membrane has to be divided also to make 2 cells in cell divison. Even anti-coagulation happens here. The versatility of the integrins is linked to the variety of subunits it is composed with. Some are nature of cell specific and some are contact specific. By contact specific, I mean what molecule outside the cell it will attach to (ie fibronectin Vs GPIIb).
Suffice is to say that kinking of the Integrins causes exposure of some parts of the Integrin molecule not naturally exposed. If one looks at the skin of the joint at the back of the finger, one will see folded skin. if you forcefully bend your finger, the fold you were looking at will unfold and the bottom of the fold will come out. This is what happen to the integrin when it meets outside the cell another molecule such as TALIN.
That bending triggers the attachment of other molecules or ions (phosphorylation) to the now exposed skin, lighting up the Integrins for the cascade of events which will unfold, including the activation of SRC in Sarcoma.
The shape imposed by the bending is also Molecule specific. Despite the resemblance of SRC with the c-ABL (leukemia), their bending does not offer the same shape, and therefore, different parts of the molecule are exposed and 2 different diseases result.
CELL ADHESION- "join at the hip"
----------------------------------------
At many points the cells are joined to each other at the hips of the Talins. Say, at the hip of the Talin which linked to one Integrin, there is a PLUS SIGN at Cell A, and at the next TALIN attached to the Integrin of cell B, there is a NEGATIVE sign. These 2 integrins will be attached, and cell adhesion is achieved. Simple as that!
Wheels of cellular migration,
-----------------------------,
Cells can roll over other cells by progressively attaching Talin to Talins and breaking the talin-talins (integrin-integrin) behind, engulfing the integrins and using them again in the forthcoming attachment like a wheel touching the ground. The cell is that smart at the membrane.
More simple things to come...
Hiding the PUMA behind the FOXO to have a death TRAP (Apoptsosis) in case the FOXO is compromised!
Just simple, but effective tricks ...
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!
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!
Friday, December 21, 2012
STUDY OF GENETIC PREDISPOSITION TO CANCER.
Human genome has been uncovered, and laboratories can now give us our genomes quickly. What took years to develop is now readily available. Pretty soon we are all going to have a credit card/ID with our genome on it. Already, scientists are working at studying the patterns of DNA as they relate to disease development. It will soon become obligatory to write the patient's genome sequence to support the diagnosis doctors give to their patients before insurance will pay for the drug.
For Colon cancer, people will be swallowing disposable cameras to detect early masses. Colonoscopies will be things of the past (it will be indicated just for biopsies of masses seen on cameras). Hemocult test as we know it, will be replaced by gene detection on the stool sample.
Presence of Mismatch repair gene, APC gene, loss of 5q,18q,17q,8q (these numbers are not random, this is how cancer evolves from a normal cell to a cancer cell in Colon cancer). If a stool sample gives you a 8q, you know pretty much this man or woman has more likely the cancer, based on the current model of colon cancer genetic evolution.
In families with many cancers, comparing sequences of genes of family members is now being further improved. Who actually develops the cancer and who stays safe, is being mapped to see the differences that triggered cancer development (phylogenetics). As we are uncovering DRIVER ONCOGENES, our treatment will be computer generated. No one will be able to remember all the genes and their heterogeneous presentations.
We got to face this, our future is to have a Gene Card for ID. There is no Doctor who will know all the gene abnormalities, so the first thing you do when you enter the medical office is to hand over your gene card. We put it in a READER and we have your disease, real, or tendencies and all potential treatments you may benefit from. Drs will be there to hold your hand and give you some additional comforting advice.
Our infectious disease specialist will be giving a prescription with the genes of the infectious agent spelled out, with the likely Antibiotic to give. Science is moving forward, let's embrace it!
Human genome has been uncovered, and laboratories can now give us our genomes quickly. What took years to develop is now readily available. Pretty soon we are all going to have a credit card/ID with our genome on it. Already, scientists are working at studying the patterns of DNA as they relate to disease development. It will soon become obligatory to write the patient's genome sequence to support the diagnosis doctors give to their patients before insurance will pay for the drug.
For Colon cancer, people will be swallowing disposable cameras to detect early masses. Colonoscopies will be things of the past (it will be indicated just for biopsies of masses seen on cameras). Hemocult test as we know it, will be replaced by gene detection on the stool sample.
Presence of Mismatch repair gene, APC gene, loss of 5q,18q,17q,8q (these numbers are not random, this is how cancer evolves from a normal cell to a cancer cell in Colon cancer). If a stool sample gives you a 8q, you know pretty much this man or woman has more likely the cancer, based on the current model of colon cancer genetic evolution.
In families with many cancers, comparing sequences of genes of family members is now being further improved. Who actually develops the cancer and who stays safe, is being mapped to see the differences that triggered cancer development (phylogenetics). As we are uncovering DRIVER ONCOGENES, our treatment will be computer generated. No one will be able to remember all the genes and their heterogeneous presentations.
We got to face this, our future is to have a Gene Card for ID. There is no Doctor who will know all the gene abnormalities, so the first thing you do when you enter the medical office is to hand over your gene card. We put it in a READER and we have your disease, real, or tendencies and all potential treatments you may benefit from. Drs will be there to hold your hand and give you some additional comforting advice.
Our infectious disease specialist will be giving a prescription with the genes of the infectious agent spelled out, with the likely Antibiotic to give. Science is moving forward, let's embrace it!
Sunday, November 11, 2012
Hypothesis for Cancer Research: Mucinous Cancer
One of the bad types of gastroenterologic cancers such as Gastric and Colon cancers is the one known as Mucinous Cancer. Basically, this cancer produces a Mucin assumed to be a viscous liquid surrounding the cell. This tumor spreads early and deeply. At the time it is found, most of the time, the cancer is in advanced stage. Researchers have explained this phenomenon by stating that this Mucin contains many ingredients suppressive to immunity (including Cytokines), and soluble Molecules (such as Prostaglandin E2) that may down regulate local immunity against the cancer. It may also have those metalloproteases that we discussed in our earlier post for research suggestions on Oct, 14, 2012
Prostaglandins in general respond to anti inflammatory agents.
CAN WE MEASURE THE LEVEL OF TISSUE PROSTAGLANDINS IN MUCINOUS CANCERS AS A PREDICTOR OF ANTI-INFLAMMATORY (ASPIRIN) MAINTENANCE THERAPY POST PRIMARY TREATMENT TO DECREASE RATE OF METASTASIS IN COLON AND GASTRIC CANCERS?
CAN ANTI-MUCIN (AFTER WE KNOW THE REAL CONTENT FOR SPECIFIC CANCER TISSUE) PROVIDE AN INCREASE OF ANTIBODY BINDING TO CANCER CELLS?
TREG CELLS are cells involved in tolerance of our own cells. They work to stop us from killing our own cells. ARE THEY INCREASED IN CANCERS TO DECREASE CELLULAR IMMUNITY AGAINST CANCERS?
CANCER CELLS SEEMS TO HAVE A SELF GROWTH HORMONE WHICH IS SECRETED IN ITS IMMEDIATE SURROUNDING. THIS HORMONE ACTS THROUGH RECEPTORS ON THE EXTERNAL MEMBRANE OF THE CELL. THE PROFILE OF RECEPTORS ON CANCER MEMBRANES IS DEFINITELY DIFFERENT FROM THE NORMAL CELL. WHY CAN'T WE PRACTICE "PROFILING" BY INVENTORYING ALL THE RECEPTORS (OR CRITICAL RECEPTORS)?
RECEPTORS ARE MADE BY GENES MOSTLY, WE CAN CONTROL THESE THROUGH OUR KNOWLEDGE OF GENETICS. IF WE KNOW RECEPTORS EXCLUSIVE TO CANCER CELLS,
CAN WE DEVELOP ANTIBODY TO THESE RECEPTORS?
Prostaglandins in general respond to anti inflammatory agents.
CAN WE MEASURE THE LEVEL OF TISSUE PROSTAGLANDINS IN MUCINOUS CANCERS AS A PREDICTOR OF ANTI-INFLAMMATORY (ASPIRIN) MAINTENANCE THERAPY POST PRIMARY TREATMENT TO DECREASE RATE OF METASTASIS IN COLON AND GASTRIC CANCERS?
CAN ANTI-MUCIN (AFTER WE KNOW THE REAL CONTENT FOR SPECIFIC CANCER TISSUE) PROVIDE AN INCREASE OF ANTIBODY BINDING TO CANCER CELLS?
TREG CELLS are cells involved in tolerance of our own cells. They work to stop us from killing our own cells. ARE THEY INCREASED IN CANCERS TO DECREASE CELLULAR IMMUNITY AGAINST CANCERS?
CANCER CELLS SEEMS TO HAVE A SELF GROWTH HORMONE WHICH IS SECRETED IN ITS IMMEDIATE SURROUNDING. THIS HORMONE ACTS THROUGH RECEPTORS ON THE EXTERNAL MEMBRANE OF THE CELL. THE PROFILE OF RECEPTORS ON CANCER MEMBRANES IS DEFINITELY DIFFERENT FROM THE NORMAL CELL. WHY CAN'T WE PRACTICE "PROFILING" BY INVENTORYING ALL THE RECEPTORS (OR CRITICAL RECEPTORS)?
RECEPTORS ARE MADE BY GENES MOSTLY, WE CAN CONTROL THESE THROUGH OUR KNOWLEDGE OF GENETICS. IF WE KNOW RECEPTORS EXCLUSIVE TO CANCER CELLS,
CAN WE DEVELOP ANTIBODY TO THESE RECEPTORS?
Subscribe to:
Posts (Atom)