My site in google
Hello everyone, finally my site has started coming in the first page of google when I typed my full name. This has given me a new identity. Check out the screen shot.
Wednesday, 28 March 2007
Thursday, 22 March 2007
Obesity and cancer
Source: Science Daily
Researchers have found out that people who are obese and diagnosed with prostrate cancer have a greater chance to die because of it than a normal person having the same level of cancer.
Shocking? Same here!!!
I would like to type some more here but I think it will be best if you read what the scientist who pursued this research says:
"If a man is obese at the time of diagnosis, he faces a 2.6-fold greater risk of dying as compared to a normal-weight man with the same diagnostic profile, regardless of whether he has a radical prostatectomy or radiation therapy, whether or not he gets androgen-deprivation therapy, whether he has low- or high-grade disease and whether he has localized, regional or distant disease."
Prostatectomy is a surgical procedure where tissues of the prostate gland is removed. This is usually done to remove the tumour from the prostate gland.
And thats not all... In obese men, there is a 3.6 fold increased risk of metastasis ie... spreading of cancer to distant regions of the body, than in normal weight persons.
The reason or mechanism that relates obesity and cancer development that the researchers point out is the amount of growth factors and serum estrogens which could promote cancer growth.
Researchers have found out that people who are obese and diagnosed with prostrate cancer have a greater chance to die because of it than a normal person having the same level of cancer.
Shocking? Same here!!!
I would like to type some more here but I think it will be best if you read what the scientist who pursued this research says:
"If a man is obese at the time of diagnosis, he faces a 2.6-fold greater risk of dying as compared to a normal-weight man with the same diagnostic profile, regardless of whether he has a radical prostatectomy or radiation therapy, whether or not he gets androgen-deprivation therapy, whether he has low- or high-grade disease and whether he has localized, regional or distant disease."
Prostatectomy is a surgical procedure where tissues of the prostate gland is removed. This is usually done to remove the tumour from the prostate gland.
And thats not all... In obese men, there is a 3.6 fold increased risk of metastasis ie... spreading of cancer to distant regions of the body, than in normal weight persons.
The reason or mechanism that relates obesity and cancer development that the researchers point out is the amount of growth factors and serum estrogens which could promote cancer growth.
Vitamin C and cancer
Source: Science Daily, Wikipedia, http://www.envtox.ucdavis.edu/CEHS/TOXINS/chromium6.htm
I'm sure you must be eagerly waiting to see what is the connection between Vitamin C and cancer. I won't make wait anymore. I'll jump into it straight away.
Researchers have found out that interaction between chromium 6 and Vitamin C inside the cells could trigger mutations and DNA damage thereby leading to cancer.
I think I'll type in something about chromium 6 and Vitamin C before proceeding to the news. Chromium is found in water, rocks and soils. It is also found in small traces in our food. It is usually found in two forms namely chromium 3 and chromium 6.
Chromium 3 is found more and it has some health benefits like metabolising sugars and participating in many enzyme reactions. Chromium 6 is the carcinogen.
Vitamin C is very important for our body because it acts as an anti-oxidant, preventing cells from undergoing free radical damage. Outside the cells, it is Vitamin C that converts chromium 6 to chromium 3 thereby preventing it from entering into the cells.
But what happens when there is an interaction between Vitamin C and Chromium 6 inside the cells?
Researchers worked on this and they found startling results. The activity of Vitamin C on Chromium 6 brought about heavy damage to the chromosome and DNA.
And the thing is that even if chromium 6 is in trace amounts inside the body, it could give rise to such a tremendous reaction in the presence of Vitamin C.
The Chromium 6 issue came to light in the 1990s thanks to the movie "Erin Brockovich".
I'm sure you must be eagerly waiting to see what is the connection between Vitamin C and cancer. I won't make wait anymore. I'll jump into it straight away.
Researchers have found out that interaction between chromium 6 and Vitamin C inside the cells could trigger mutations and DNA damage thereby leading to cancer.
I think I'll type in something about chromium 6 and Vitamin C before proceeding to the news. Chromium is found in water, rocks and soils. It is also found in small traces in our food. It is usually found in two forms namely chromium 3 and chromium 6.
Chromium 3 is found more and it has some health benefits like metabolising sugars and participating in many enzyme reactions. Chromium 6 is the carcinogen.
Vitamin C is very important for our body because it acts as an anti-oxidant, preventing cells from undergoing free radical damage. Outside the cells, it is Vitamin C that converts chromium 6 to chromium 3 thereby preventing it from entering into the cells.
But what happens when there is an interaction between Vitamin C and Chromium 6 inside the cells?
Researchers worked on this and they found startling results. The activity of Vitamin C on Chromium 6 brought about heavy damage to the chromosome and DNA.
And the thing is that even if chromium 6 is in trace amounts inside the body, it could give rise to such a tremendous reaction in the presence of Vitamin C.
The Chromium 6 issue came to light in the 1990s thanks to the movie "Erin Brockovich".
Monday, 19 March 2007
New antibodies towards cancer treatment
Source: huliq.com
Wikipedia
My second post of the day... This is also very interesting.
Researchers are working on making antibodies to stimulate the immune system to attack cancer cells better. The antibodies they are using are monoclonal antibodies and their aim is to target these antibodies towards boosting boosting the immune system so that it will evoke a stronger response against cancer.
So...what are these monoclonal antibodies?
Monoclonal antibodies are antibodies that are identical because they are produced by the same cell for a particular antigen. How is it done? Answer is invitro ie... in a lab. I'll elaborate on the significance of monoclonal antibodies.
Basically, in the body, antibodies are produced by the B cells for binding to the various epitopes of an antigen. Such an antibody mixture is called polyclonal antibody. Monoclonal antibodies are synthesised by removing the B cells from mouse for example which has already been exposed to the particular antigen so that it can produce the antibody. Invitro, these B cells cannot continuously produce antibodies since they cannot survive under invitro conditions. So inorder to make them produce indefinitely, they fuse the B cells with myeloma cells (cancerous B cells) so that they can produce the antibodies indefinitely. The fused cell is called a hybridoma cell.
Apart from boosting the immune system, researchers are also trying to tag radioactive isotopes so that the spread of cancer can be detected in the body.
One such antibody anti-CTLA-4 was used to treat melanoma in patients in 1999 and they found significant results (Reduction in tumour). Apart from this, some more monoclonal antibodies are being tested. Its results are not yet out but the researchers expect to get something positive from it.
Wikipedia
My second post of the day... This is also very interesting.
Researchers are working on making antibodies to stimulate the immune system to attack cancer cells better. The antibodies they are using are monoclonal antibodies and their aim is to target these antibodies towards boosting boosting the immune system so that it will evoke a stronger response against cancer.
So...what are these monoclonal antibodies?
Monoclonal antibodies are antibodies that are identical because they are produced by the same cell for a particular antigen. How is it done? Answer is invitro ie... in a lab. I'll elaborate on the significance of monoclonal antibodies.
Basically, in the body, antibodies are produced by the B cells for binding to the various epitopes of an antigen. Such an antibody mixture is called polyclonal antibody. Monoclonal antibodies are synthesised by removing the B cells from mouse for example which has already been exposed to the particular antigen so that it can produce the antibody. Invitro, these B cells cannot continuously produce antibodies since they cannot survive under invitro conditions. So inorder to make them produce indefinitely, they fuse the B cells with myeloma cells (cancerous B cells) so that they can produce the antibodies indefinitely. The fused cell is called a hybridoma cell.
Apart from boosting the immune system, researchers are also trying to tag radioactive isotopes so that the spread of cancer can be detected in the body.
One such antibody anti-CTLA-4 was used to treat melanoma in patients in 1999 and they found significant results (Reduction in tumour). Apart from this, some more monoclonal antibodies are being tested. Its results are not yet out but the researchers expect to get something positive from it.
Around 50 genes discovered which slows down cancer
Source: Science Daily
This article that was posted in science daily has a lot in common with what I'm working on...What I mean is that I deal with analysing all the possible aspects of cancer and its behaviour and this article deals with a part of it. So the following lines will have some points from my work as well. I may have missed explaining a few points here and there. So if you have any doubts, feel free to email me. If it is in my limits, I'll definitely help you out. This post according to me is very important if you want to about cancer mechanism.
It is a well known fact that cancer cells are not "normal cells". The normal molecular mechanisms are disrupted or modified in a cancer cell. In a normal cell, signals are generated which provokes it to undergo proliferation and also to halt the same. But in a cancerous cell, the signals for inhibiting cell proliferation is disrupted. Hence, they keep on multiplying. You can say this as the basic concept behind a cancerous cell.
It is also an obvious fact that it is the gene that controls all the activities of a cell. Hence, researchers wanted to find out the genes that bring about the cell division inhibition so that in the future, the defects could be rectified and normalcy could be restored by gene therapy.
So the research started...
The signals which stimulate cell proliferation are the growth factors like Epidermal GF, Vascular Endothelial GF, etc... Non cancer readers... forgive me... just take these names as it is. Just consider them as some proteins helping in cell proliferation. (Actually they are!!!)
These GFs stimulate a host of other molecules in a cascade like fashion bringing about cell proliferation. Also, some genes are stimulated by certain other factors which bring about inhibiton of the same. To find out the genes, researchers collaborated with a lot of mathematicians, biologists, physicists, computer scientists, etc... to sieve through the enormous data that they had in their hands.
What they found out was that the phenomenon of cell division and its regulation takes place at different times. Initially, genes are activated that bring about cell division, then after a few hours, certain other genes are activated which bring about its inhibition thereby we have a controlled growth.
The researchers found out that about 50 genes played a role in bringing about cell division inhibition. They found out that these genes produce proteins which hinder the cell proliferation.
I'll give you an example from my project analysis : We have a protein called cyclin D which forms a complex with another protein CDK and brings about cell proliferation. Another protein called P27 is also synthesised which binds to this CDK thereby preventing the complex formation. Hence cyclin D alone cannot do the job and thus cell proliferation is prevented.
The main aim of the research is to give tailor made therapies to the patients according to their genetic makeup so that the effect of the treatment will be good and also the side effects and associated problems can be prevented.
This article that was posted in science daily has a lot in common with what I'm working on...What I mean is that I deal with analysing all the possible aspects of cancer and its behaviour and this article deals with a part of it. So the following lines will have some points from my work as well. I may have missed explaining a few points here and there. So if you have any doubts, feel free to email me. If it is in my limits, I'll definitely help you out. This post according to me is very important if you want to about cancer mechanism.
It is a well known fact that cancer cells are not "normal cells". The normal molecular mechanisms are disrupted or modified in a cancer cell. In a normal cell, signals are generated which provokes it to undergo proliferation and also to halt the same. But in a cancerous cell, the signals for inhibiting cell proliferation is disrupted. Hence, they keep on multiplying. You can say this as the basic concept behind a cancerous cell.
It is also an obvious fact that it is the gene that controls all the activities of a cell. Hence, researchers wanted to find out the genes that bring about the cell division inhibition so that in the future, the defects could be rectified and normalcy could be restored by gene therapy.
So the research started...
The signals which stimulate cell proliferation are the growth factors like Epidermal GF, Vascular Endothelial GF, etc... Non cancer readers... forgive me... just take these names as it is. Just consider them as some proteins helping in cell proliferation. (Actually they are!!!)
These GFs stimulate a host of other molecules in a cascade like fashion bringing about cell proliferation. Also, some genes are stimulated by certain other factors which bring about inhibiton of the same. To find out the genes, researchers collaborated with a lot of mathematicians, biologists, physicists, computer scientists, etc... to sieve through the enormous data that they had in their hands.
What they found out was that the phenomenon of cell division and its regulation takes place at different times. Initially, genes are activated that bring about cell division, then after a few hours, certain other genes are activated which bring about its inhibition thereby we have a controlled growth.
The researchers found out that about 50 genes played a role in bringing about cell division inhibition. They found out that these genes produce proteins which hinder the cell proliferation.
I'll give you an example from my project analysis : We have a protein called cyclin D which forms a complex with another protein CDK and brings about cell proliferation. Another protein called P27 is also synthesised which binds to this CDK thereby preventing the complex formation. Hence cyclin D alone cannot do the job and thus cell proliferation is prevented.
The main aim of the research is to give tailor made therapies to the patients according to their genetic makeup so that the effect of the treatment will be good and also the side effects and associated problems can be prevented.
Thursday, 15 March 2007
Cancer genes, Beware!!! A new enemy is on the Block!!!
Source: Science Daily
Wikipedia
So...I'm pretty regular in posting new articles now!!!! Ok...let me proceed with the latest news that I've just got.
Researchers have found out a new drug which inhibits the cancer genes. This drug is a variant of vitamin A. The name of the drug is All-Trans-Retinoic Acid(ATRA). This drug stimulates and increases the amount of certain microRNA in the promyelotic leukemia cells and these miRNAs bring about inhibition of the cancer genes. Confused?
Lets get some concepts right here...
What is Promyelotic leukemia?
It is a type of cancer where abnormal white blood cells (WBCs) are produced and they outnumber the normal WBCs.
What is this microRNA?
MicroRNA are small single stranded RNA whose main function is to regulate genes. Basically, it is the mRNA which is translated into proteins. But these miRNAs are non coding RNAs ie... they don't code for any protein. Like mRNAs, they are also processed from primary transcripts and mature to form miRNAs. These have some complementary sequences to mRNAs and they go and bind to them and thus repress the genes.
Hope its clear for you now... Lets come back to the news...
The drug ATRA raises the level of 3 particular miRNAs called miRNA 15b, 16-1 and let-7. The first two bring about inhibition of the antiapoptotic gene BCL-2 so that cancer growth can be arrested. What is this antiapop... whatever?
Let me clear it...
Apoptosis is the name given to "programmed cell death" or "cell suicide". Basically, when a cell undergoes some damage, it doesn't like to stay and trouble us. So it commits suicide. This suicide is brought about by some set of factors and inhibited by another set of factors.
Now, it should be clear...
The last miRNA let-7 brings about inhibition of the RAS oncogene. RAS brings about cell proliferation and inhibition of this halts cancer growth.
How does this drug exert its function?
Researchers added the drug to leukemia cells in culture and they found out a decrease in BCL-2 gene activity and an increase in the amount of miRNAs. They confirmed the function of miRNA by adding it artificially to the cells without adding the drug. The results were the same!!!
This research has been carried out in Ohio State University.
Wikipedia
So...I'm pretty regular in posting new articles now!!!! Ok...let me proceed with the latest news that I've just got.
Researchers have found out a new drug which inhibits the cancer genes. This drug is a variant of vitamin A. The name of the drug is All-Trans-Retinoic Acid(ATRA). This drug stimulates and increases the amount of certain microRNA in the promyelotic leukemia cells and these miRNAs bring about inhibition of the cancer genes. Confused?
Lets get some concepts right here...
What is Promyelotic leukemia?
It is a type of cancer where abnormal white blood cells (WBCs) are produced and they outnumber the normal WBCs.
What is this microRNA?
MicroRNA are small single stranded RNA whose main function is to regulate genes. Basically, it is the mRNA which is translated into proteins. But these miRNAs are non coding RNAs ie... they don't code for any protein. Like mRNAs, they are also processed from primary transcripts and mature to form miRNAs. These have some complementary sequences to mRNAs and they go and bind to them and thus repress the genes.
Hope its clear for you now... Lets come back to the news...
The drug ATRA raises the level of 3 particular miRNAs called miRNA 15b, 16-1 and let-7. The first two bring about inhibition of the antiapoptotic gene BCL-2 so that cancer growth can be arrested. What is this antiapop... whatever?
Let me clear it...
Apoptosis is the name given to "programmed cell death" or "cell suicide". Basically, when a cell undergoes some damage, it doesn't like to stay and trouble us. So it commits suicide. This suicide is brought about by some set of factors and inhibited by another set of factors.
Now, it should be clear...
The last miRNA let-7 brings about inhibition of the RAS oncogene. RAS brings about cell proliferation and inhibition of this halts cancer growth.
How does this drug exert its function?
Researchers added the drug to leukemia cells in culture and they found out a decrease in BCL-2 gene activity and an increase in the amount of miRNAs. They confirmed the function of miRNA by adding it artificially to the cells without adding the drug. The results were the same!!!
This research has been carried out in Ohio State University.
Wednesday, 14 March 2007
New Antibody to track down Cancer
Source: Science Daily
Ok...I'm back with another interesting news. Here you go...
Researchers have found out a new antibody that tracks down a specific antigen found in high amounts in prostrate cancer and in tumour blood vessels. The antibody christened J591 was able to target Prostrate Specific Membrane Antigen(PSMA) and they say that this could provide a new way to treat cancer.
How? By the concept of "tagging". Researchers say that if they could tag the anti cancer drug to the antibody, then the cancer cells alone would be affected and that the normal cells would be spared. This concept is really good because it reduces the unnecessary side effects caused due to the damage caused by anti cancer treatments to normal cells.
Now how did PSMA become popular in this research?
Answer: Its presence in the Prostrate tumour and in the tumour blood vessels.
Now, the aim of the researchers is to tag the antibody with drugs that would target the blood supply of the tumours and "choke" them so that their growth and spreading could be controlled.
Ok...I'm back with another interesting news. Here you go...
Researchers have found out a new antibody that tracks down a specific antigen found in high amounts in prostrate cancer and in tumour blood vessels. The antibody christened J591 was able to target Prostrate Specific Membrane Antigen(PSMA) and they say that this could provide a new way to treat cancer.
How? By the concept of "tagging". Researchers say that if they could tag the anti cancer drug to the antibody, then the cancer cells alone would be affected and that the normal cells would be spared. This concept is really good because it reduces the unnecessary side effects caused due to the damage caused by anti cancer treatments to normal cells.
Now how did PSMA become popular in this research?
Answer: Its presence in the Prostrate tumour and in the tumour blood vessels.
Now, the aim of the researchers is to tag the antibody with drugs that would target the blood supply of the tumours and "choke" them so that their growth and spreading could be controlled.
Tuesday, 13 March 2007
New drug for Metastatic Kidney Tumour
Source: Science Daily
Its been a long time since I posted something here. So...I'm back with some more hot news. Here you go...
Researchers have found out a new drug to treat metstatic kidney cancer. The drug name is Sunitinib which is marketed under the name "Sutent".
Previously this cancer was treated using interferon(Immunotherapy). Researchers tested Sunitinib and Interferon in many patients and they found out that the former produced better results.
Now how does this drug exert its functions?
Very simple...I have already posted an article describing about "Angiogenesis". You can have a look at it here.The same principle is used by this drug.
Sunitinib halts the development of cancer by preventing the formation of new blood vessels. To be more specific about the mechanism, our body cells respond to a particular molecule or to give a better term, "ligand" with the help of receptors present on their surface. The signal generated brings about a particular function. The ligand VEGF(Vascular Endothelial Growth Factor) binds to VEGF receptor and brings about angiogenesis. This drug inhibits the receptor so that the signal is not transmitted and therefore the blood vessel formation is stopped.
Hope the concept is clear. See you soon with another interesting news.
Its been a long time since I posted something here. So...I'm back with some more hot news. Here you go...
Researchers have found out a new drug to treat metstatic kidney cancer. The drug name is Sunitinib which is marketed under the name "Sutent".
Previously this cancer was treated using interferon(Immunotherapy). Researchers tested Sunitinib and Interferon in many patients and they found out that the former produced better results.
Now how does this drug exert its functions?
Very simple...I have already posted an article describing about "Angiogenesis". You can have a look at it here.The same principle is used by this drug.
Sunitinib halts the development of cancer by preventing the formation of new blood vessels. To be more specific about the mechanism, our body cells respond to a particular molecule or to give a better term, "ligand" with the help of receptors present on their surface. The signal generated brings about a particular function. The ligand VEGF(Vascular Endothelial Growth Factor) binds to VEGF receptor and brings about angiogenesis. This drug inhibits the receptor so that the signal is not transmitted and therefore the blood vessel formation is stopped.
Hope the concept is clear. See you soon with another interesting news.
Friday, 9 March 2007
A cancer drug for Glioma
Source: Science Daily
Wikipedia
I just got this news from Science Daily. It is really interesting. The researchers at Duke University Medical Centre have found out that Avastin, an anti-angiogenic drug is able to prolong the survival of brain tumour patients.
The research was done by treating the patients this drug along with a chemotherapic agent called Irinotecan . It was found that the life span of the patients increased by three more months compared to the ordinary chemotherapic treatments. This result, they say, is very significant because the prognosis of the glioma is very grim. In such cases, an additional three months is certainly a boost for the patients.
Some facts about Glioma
A Glioma is a tumour formed in the Central Nervous System which includes the Brain and the Spinal Cord.
It usually arises from the glial cells from which the name has come.Glial cells are cells which support and protect the neurons. Usually the tumour arises behind the blood-brain barrier making it difficult to access it. Hence doctors find it hard to target the tumour using drugs since the blood-brain barrier prevents the passage of many substances including the drugs.
It is this reason that gliomas are hard to cure and the survival percentage is very low.
Some facts about Angiogenesis
Angiogenesis is basically formation of new blood vessels from existing ones.
It is very signifcant in cancer because cancer cells usually grow and proliferate faster than normal cells. Hence the food supply by the normal blood vessels is not adequate. So the cancer cells form 'extra' blood vessels inorder to have a continuous supply of food materials.
Now back to the news...
As I had stated before, Avastin is an anti-angiogenic drug. So how does it work? It acts on the new blood vessels formed by the tumours and prevents blood flow to them. In other words, it 'chokes' the cancer cells slowing down its growth and spreading and thus prolonging the survival of the patients.
Wikipedia
I just got this news from Science Daily. It is really interesting. The researchers at Duke University Medical Centre have found out that Avastin, an anti-angiogenic drug is able to prolong the survival of brain tumour patients.
The research was done by treating the patients this drug along with a chemotherapic agent called Irinotecan . It was found that the life span of the patients increased by three more months compared to the ordinary chemotherapic treatments. This result, they say, is very significant because the prognosis of the glioma is very grim. In such cases, an additional three months is certainly a boost for the patients.
Some facts about Glioma
A Glioma is a tumour formed in the Central Nervous System which includes the Brain and the Spinal Cord.
It usually arises from the glial cells from which the name has come.Glial cells are cells which support and protect the neurons. Usually the tumour arises behind the blood-brain barrier making it difficult to access it. Hence doctors find it hard to target the tumour using drugs since the blood-brain barrier prevents the passage of many substances including the drugs.
It is this reason that gliomas are hard to cure and the survival percentage is very low.
Some facts about Angiogenesis
Angiogenesis is basically formation of new blood vessels from existing ones.
It is very signifcant in cancer because cancer cells usually grow and proliferate faster than normal cells. Hence the food supply by the normal blood vessels is not adequate. So the cancer cells form 'extra' blood vessels inorder to have a continuous supply of food materials.
Now back to the news...
As I had stated before, Avastin is an anti-angiogenic drug. So how does it work? It acts on the new blood vessels formed by the tumours and prevents blood flow to them. In other words, it 'chokes' the cancer cells slowing down its growth and spreading and thus prolonging the survival of the patients.
Thursday, 8 March 2007
An RNA Splicing factor as a target for cancer therapy
Source: EurekAlert!
http://bcs.whfreeman.com/thelifewire/content/chp14/1402001.html( About RNA Splicing)
One more research news from Cold Spring Harbour Laboratory…
CSHL Researchers have found out a new RNA Splicing factor that causes cells to become cancerous. You might be wondering what an RNA Splicing factor is. Here you go…
RNA Splicing is a process by which a pre-mRNA is converted into a fully functional mRNA. Confused? Let me clear it further. Basically, the mRNA is transcribed or in simpler terms ‘formed’ from DNA. DNA has regions which code for some proteins called ‘exons’ and some regions which do not code for any protein called ‘introns’. The pre-mRNA that is initially formed from it also has the same regions. Logically, we do not need introns. We only need exons. Some factors are present which help in removing these introns from the Pre-mRNA and joining the exons thereby making it a fully functional mRNA. This process is called RNA Splicing and the factors which bring about it are called Splicing factors. This fully functional mRNA is translated into proteins.
Let’s come back to the news…
The RNA splicing factor found was called SF2/ASF. A proper RNA splicing is required for the formation of the correct protein. When something wrong happens here, it results in the formation of altered proteins which in turn could lead to disastrous effects. One of the disastrous effect could be formation of cancer.
The researchers found an abnormally high amount of this splicing factor SF2/ASF in a number of cancers like that of the colon, lung and the breast. They also found that over-expression of this factor could cause cancer in normal cells and that reducing its amount prevented cancer formation.
An example they cited was that of a protein kinase which was responsible for regulating the cell cycle and that altered RNA Splicing caused the production of a variant of this kinase which caused cancer.
http://bcs.whfreeman.com/thelifewire/content/chp14/1402001.html( About RNA Splicing)
One more research news from Cold Spring Harbour Laboratory…
CSHL Researchers have found out a new RNA Splicing factor that causes cells to become cancerous. You might be wondering what an RNA Splicing factor is. Here you go…
RNA Splicing is a process by which a pre-mRNA is converted into a fully functional mRNA. Confused? Let me clear it further. Basically, the mRNA is transcribed or in simpler terms ‘formed’ from DNA. DNA has regions which code for some proteins called ‘exons’ and some regions which do not code for any protein called ‘introns’. The pre-mRNA that is initially formed from it also has the same regions. Logically, we do not need introns. We only need exons. Some factors are present which help in removing these introns from the Pre-mRNA and joining the exons thereby making it a fully functional mRNA. This process is called RNA Splicing and the factors which bring about it are called Splicing factors. This fully functional mRNA is translated into proteins.
Let’s come back to the news…
The RNA splicing factor found was called SF2/ASF. A proper RNA splicing is required for the formation of the correct protein. When something wrong happens here, it results in the formation of altered proteins which in turn could lead to disastrous effects. One of the disastrous effect could be formation of cancer.
The researchers found an abnormally high amount of this splicing factor SF2/ASF in a number of cancers like that of the colon, lung and the breast. They also found that over-expression of this factor could cause cancer in normal cells and that reducing its amount prevented cancer formation.
An example they cited was that of a protein kinase which was responsible for regulating the cell cycle and that altered RNA Splicing caused the production of a variant of this kinase which caused cancer.
Wednesday, 7 March 2007
New Potent Anti-Cancer drug found
Source: Science Daily
This is a really good article I just read in Science Daily. Here you go...
Researchers have found out a new anti cancer drug which they say acts in a way different from the other drugs. And they also state that the drug is so potent that "a few parts" of it is enough for inducing its activities. They have also cited a very good example for "A few Parts". Its like adding a packet of sugar to a coffee cup the size of 400 Olympic swimming pools.
This new drug called Meayamycin has structural similarities with another naturally occurring anti tumour agent FR901464. FR901464 has been found to induce the G1 and G2/M phase arrest and thereby acting as a transcriptional repressor. It exerts its anti-tumour activity by some unknown means.
Researchers hope that the newly found drug would also exert similar kind of effect on the cancer cells. This research has been done by Kazunori Koide and his colleagues.
References: Masato Horigome, Hajime Motoyoshi, Hidenori Watanabe and Takeshi Kitahara, Tetrahedron Letters, Volume 42, Number 26, 12 November 2001, pp. 8207-8210(4)
This is a really good article I just read in Science Daily. Here you go...
Researchers have found out a new anti cancer drug which they say acts in a way different from the other drugs. And they also state that the drug is so potent that "a few parts" of it is enough for inducing its activities. They have also cited a very good example for "A few Parts". Its like adding a packet of sugar to a coffee cup the size of 400 Olympic swimming pools.
This new drug called Meayamycin has structural similarities with another naturally occurring anti tumour agent FR901464. FR901464 has been found to induce the G1 and G2/M phase arrest and thereby acting as a transcriptional repressor. It exerts its anti-tumour activity by some unknown means.
Researchers hope that the newly found drug would also exert similar kind of effect on the cancer cells. This research has been done by Kazunori Koide and his colleagues.
References: Masato Horigome, Hajime Motoyoshi, Hidenori Watanabe and Takeshi Kitahara, Tetrahedron Letters, Volume 42, Number 26, 12 November 2001, pp. 8207-8210(4)
Tuesday, 6 March 2007
Links found between harmless viruses and Cancer
Source: physorg.com
We already know viruses like Human Papillomavirus, Epstein-Barr virus which cause cancer. Such viruses are called Oncogenic viruses. Now the bad news is that these viruses have company. Researchers have found out links between a group of viruses which are supposedly harmless to chromosomal instability and cancer.
Ok…now let us get some concepts clear here. What is chromosomal instability? It is a phenomenon where there is a continuous occurrence of novel chromosomal mutations at a rate higher than in normal cells. These mutations disrupt the stability of the cell and the cell tends to become malignant ie…become a cancer cell.
Lets come back to the news. The researchers have found out that these ‘harmless’ viruses tend to fuse groups of cells. This abrupt fusion creates massive chromosomal instability and over time, some of these cells become malignant as already stated before.
Researchers say that if they can identify and inactivate these viruses, cancer could be prevented. They are threading the “Prevention is better than cure” path which has been pretty successful lately with methods for immunization against Human Papillomavirus and Hepatitis B bringing out good results.
This research has been done at Cold Spring Harbor Laboratory.
We already know viruses like Human Papillomavirus, Epstein-Barr virus which cause cancer. Such viruses are called Oncogenic viruses. Now the bad news is that these viruses have company. Researchers have found out links between a group of viruses which are supposedly harmless to chromosomal instability and cancer.
Ok…now let us get some concepts clear here. What is chromosomal instability? It is a phenomenon where there is a continuous occurrence of novel chromosomal mutations at a rate higher than in normal cells. These mutations disrupt the stability of the cell and the cell tends to become malignant ie…become a cancer cell.
Lets come back to the news. The researchers have found out that these ‘harmless’ viruses tend to fuse groups of cells. This abrupt fusion creates massive chromosomal instability and over time, some of these cells become malignant as already stated before.
Researchers say that if they can identify and inactivate these viruses, cancer could be prevented. They are threading the “Prevention is better than cure” path which has been pretty successful lately with methods for immunization against Human Papillomavirus and Hepatitis B bringing out good results.
This research has been done at Cold Spring Harbor Laboratory.
Friday, 2 March 2007
Threat to the Devil
Sources: The Hindu dated 01-03-2007
Wikipedia
Science News
Examiner.com
Photo Courtesy: Taken by Wayne McLean, licensed under the Creative Commons Attribution ShareAlike 2.5
You are probably wondering what this devil is. Well…it is not a horrendous monster as you imagine but a small, weasel-like animal native to Australia. Its actual name is the Tasmanian Devil and it currently is in danger of being wiped out of this world. This creature which once inhabited throughout Australia is now confined to the state of Tasmania and its population is dwindling because of a facial cancer that is affecting them. I searched about this facial cancer in the Tasmanian Devil and I found the following piece of information from Wikipedia. Here you go…
The facial tumour is called Devil Facial Tumour Disease ( DFTD)
and it is a transmittable parasitic cancer. A parasitic cancer is something that spreads from animal to animal because of the cancer cells. Basically the cancer cells behave like a bacteria or a virus. It is just an example. The transmission was found to be via aggressive mating or biting during a fight. This phenomenon actually confused the researchers and they actually concluded that the cancer could actually be caused by a virus like HPV. Researchers have found out that it is a neuroendocrinal tumour which means it is a tumour occurring at the junction of the neuro endocrine system. What happens in the devil is that the cancer first develops as a lesion and then slowly grows as a lump and prevents the animal from feeding. It therefore dies of starvation.
The research on the tumour was done by Pearse of Tasmania's Department of Primary Industries and it has shown that the tumour cell chromosomal anomalies were identical in the animals they tested and this proved that it could not have been a virus and that it could have been a single affected cell that had spread among the devils.
The only way to prevent the wiping out of the devils is to isolate those which are affected from the healthy ones.
Thursday, 1 March 2007
A Gene that could prevent multiple cancer
Source: Science Daily
This is a very interesting article that I read in Science Daily. I would like to share it with you.
Reasearchers at Cold Spring Harbor Laboratory have discovered a gene in chromosome 1 location 1p36 that could prevent cancer. The name of the gene is CHD5. They found out that when the gene is switched off, the cells lose the ability to control the growth of cancer. Basically, the gene behaves as a tumour suppressor. When the gene is switched on, the cells are able to control cancer development.
The research was actually done on mice and they wanted to see if the same was possible in humans also. For this, they collaborated with researchers from Stanford University and they found out that Glioma ( Tumour formed in the Central Nervous System) cells had deletion of CHD5 gene.
From this research, people can find out drugs that will switch ‘on’ this gene in cancer cells so as to bring about its death.
(Courtesy: Wikipedia for definition of glioma)
This is a very interesting article that I read in Science Daily. I would like to share it with you.
Reasearchers at Cold Spring Harbor Laboratory have discovered a gene in chromosome 1 location 1p36 that could prevent cancer. The name of the gene is CHD5. They found out that when the gene is switched off, the cells lose the ability to control the growth of cancer. Basically, the gene behaves as a tumour suppressor. When the gene is switched on, the cells are able to control cancer development.
The research was actually done on mice and they wanted to see if the same was possible in humans also. For this, they collaborated with researchers from Stanford University and they found out that Glioma ( Tumour formed in the Central Nervous System) cells had deletion of CHD5 gene.
From this research, people can find out drugs that will switch ‘on’ this gene in cancer cells so as to bring about its death.
(Courtesy: Wikipedia for definition of glioma)
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