Postmenopausal women keeping abreast of tipsy genes!

First it was diet coke, now it seems that alcohol could possibly increase the chances of breast cancer in women. This was determined by Dr Peter Shields, professor of medicine and oncology based at Georgetown University's Lombardi Comprehensive Cancer Center in Washington DC, and Dr Jo Freudenheim, chair of social and preventive medicine at the State University of New York in Buffalo. It was found that two genes that code for enzymes that breakdown alcohol, ADH1B and ADH1C, are possibly linked to increased risk of breast cancer in postmenopausal women who favour a drink or two. Lead author of the study, Dr Catalin Marian stated the obvious, saying: "The higher their alcohol consumption, the higher their risk."(Medical news today, 2008).
The study showed that the variations in the DNA sequences of the two genes caused significant increases in the susceptibility towards breast cancer. In the case of the ADH1B gene, women possessing the gene variant who consumed alcohol were twice as susceptible to breast cancer compared to the women who abstained from drinking alcohol. Alternatively, the ADH1C gene actually provides some protection against breast cancer; but as alcohol consumption increases, the effectiveness of this protection decreases, thus causing a contrasting, but nevertheless significant increase in the risk of breast cancer.
“The results showed that increased breast cancer risk in postmenopausal women was linked to variations in DNA sequences in two genes: ADH1B (sequence rs1042026) and ADH1C (sequence rs1614972).Among postmenopausal women with the ADH1B (sequence rs1042026) gene variant, the risk of breast cancer for the alcohol drinkers was nearly double that of the abstainers.Among women with the ADH1C (sequence rs1614972) gene variant, there was a protective effect against breast cancer risk that varied inversely with the amount of alcohol: the more alcohol a woman with this gene variant consumed, the less protection offered, and the higher the risk of breast cancer. (Conversely, this could be viewed as the protection conferred by the gene appeared to get stronger as alcohol consumption dropped).” (Medical news today, 2008).
In light of this obviously depressing news, there maybe some cause for celebration, in that the aforementioned Dr Catalin Marian implied that more research was needed to validate the findings and show that the genes are more than just ‘linked’ to the risk of breast cancer, and have yet to be proven to be a potential cause of breast cancer. "We have to keep in mind that the gene sequence variations we observed are not located directly in coding regions, but they may be associated and inherited together with other variations that have this effect on the enzyme function." Says Marian

Nathan Crouch (41453627)
References:
http://www.medicalnewstoday.com/articles/103911.php
http://www.cbsnews.com/stories/2008/04/14/health/webmd/main4014147.shtml
http://imagecache2.allposters.com/images/pic/153/817586~Blood-Alcohol-Posters.jpg

Healing faster

Have you ever wished a cut or burn would heal faster and leave no scars? Research from the University of Bristol suggests that this can happen in the future by simply applying a gel. When a cut or burn occurs, blood vessels constrict to decrease the amount of blood loss. After a blood clot is formed by the platelets, in response to the completion of the clot the blood vessel enlarges to allow white blood cells to fight off the foreign invaders In addition the white blood cells bring collagen to help heal the skin, which also produces the scar. One of the genes responsible for scars is the osteopontin (OPN). Therefore by creating a gel that suppresses this gene, it could accelerate healing and leave no scar.

Reference:
University of Bristol (2008, January 24). Skin Care: Scar-free Healing Shown With Gene Suppression. ScienceDaily. Retrieved April 16, 2008, from
http://www.sciencedaily.com¬ /releases/2008/01/080121080355.htm

http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Skin_cuts_and_abrasions?Open

Hung Le
41724288

Errors in Mitochondrial DNA the source of cancer spreading

The way in which a cancer spreads is through the process of metastasis, wherein primary cancer cells breaks away from the main tumour, travels through the lymph system or in the bloodstream, settles in a new area and begins to form a new tumour. It is this process which differentiates the less dangerous benign tumours from the deadly malignant kind and preventing it would result in a tumour being easily excisable once identified. A recent study has shown that mutations in Mitochondrial DNA may be responsible for metastasis, and that curing cancer may be as easy as treating a patient with antioxidants.

Mitochondria are organelles within eukaryotic cells that produce energy molecules to fuel cellular processes. They also have their own DNA, referred to as mtDNA, found within the mitochondria itself, rather than the nucleus where most of the cell’s genetic material is stored. This allows the mitochondrion to replicate themselves (with some assistance from the nucleus) depending on the energy needs of the cell, though replication is still controlled by genes within the nucleus. Unfortunately, the protein packaging and self-repair abilities of mtDNA are not as effective as that of nuclear genetic material and so are more susceptible to mutations. It is these mutations that have been suspected of being closely related to metastasis in cancer cells. An earlier study on cancer cells showed that the mitochondria of these cells possessed many more mutations than that of healthy cells, though whether this was a result of the cancer or the cancer was a result of the mutations was unknown.

Researchers at the University of Tsukuba in Japan have recently performed a study on whether mtDNA mutations were responsible for metastasis. The experiment involved swapping the mtDNA of a tumour cell that tends to metastasize with one that does not and injecting the cells into mice. What their results showed was that when these cells were injected into mice the rarely metastasising tumour cells, now containing mtDNA from metastasising tumours, did in fact metastasise, while the originally metastasising tumour cells containing mtDNA from non-metastasising cells did little. This would imply that the basis for tumours metastasising is mtDNA.

Further study showed that the mutations in the mtDNA caused the Mitochondria to produce an excess of reactive oxygen species molecules, which are damaging to DNA. Since mtDNA appears to be the root of metastasis in tumour cells it can be inferred that it is these oxygen species molecules that damage the nuclear genetic material of healthy cells, creating cancer cells. Perhaps most interesting is that these oxygen species molecules can be neutralised with antioxidants and that when mice that had been injected with metastatic tumour cells were treated with these antioxidants, they showed little to no new tumour growth. As a result, antioxidant treatment of malignant cancer has warranted further study.

Original article:

http://sciencenow.sciencemag.org/cgi/content/full/2008/403/1

Image source:

http://www.a3243g.com/image_mitochondria.asp

Kiel Headrick, 4176059

Weather NOT too hot to handle for "superplants"

A new study by the University of Toronto is planning to find how plants "breathe" so that can help us breed plants that would better survive the hot summers.
This study shows the first example of a gene that controls how leaves close their surface pores. "It's very exciting," says university's botany professor and senior author Malcolm Campbell. "This is a gene that helps regulate carbon dioxide uptake. If plants are the Earth's lungs, we've just discovered a key piece of information about how the Earth breathes."
The pores on the surface of plant leaves, called stomata, function like little mouths that open and close in response to cues such as light, temperature, and water availability. Using mouse-ear cress, a relative of mustard, cabbage and radish plants, Campbell and co-authors from the university,together with the University of Lancaster, then compared the cooling rates of plants with normal, high and low levels of gene activity. From their data, they were able to link the gene to plant exhalation.
This discovery is another step in understanding how plants might respond to their environment. In hot temperatures, plants keep their mouths "shut" longer than usual, to avoid losing gases and water through evaporation. However, they must open their stomata at some point, both to pick up carbon dioxide needed for photosynthesis and to release oxygen back into the atmosphere. This information will be important to plant breeders looking to improve crop resistance to drought, as well as to those seeking to understand plants' evolutionary responses to climate.
"These genes are of high importance. They allow plants to adapt to changes in light, carbon and water availability. Ultimately, they shape the flux of carbon and water throughout entire ecosystems and affect the carbon cycle on a global-scale." says Campbell.
The study was supported by the University of Toronto, the Natural Sciences and Engineering Research Council of Canada and the Biotechnology and Biological Sciences Research Council of the U.K.

links : http://www.sciencedaily.com/releases/2005/07/050718214711.htm

by,
Zulaikha Razali ( 41600720 )

Gene Splicing: The key human success?

It has now been proven that chimpanzees are the closest living relatives to humans on this planet with genomes that are almost 99% identical to our own. But if we really are that closely related on paper, what are the causes of the vastly different structural, behavioural, and mental variations that occur between the two species? With the help of innovative new research from the University of Toronto's Centre for Cellular and Biomolecular Research, potential new explanations to this conundrum have finally been uncovered. In performing several comparisons between the heart and brain tissue extracted from humans and chimpanzees, University of Toronto Professor Benjamin Blencowe and his team, including graduate student researcher John Calarco, have discovered considerable differences in the way mRNA is spliced during protein production (ScienceDaily, 2007).

"It's clear that humans are very different from chimpanzees on several levels, but we wanted to find out if it could be the splicing process that accounts for some of these fundamental differences," says Blencowe, a professor with the Banting and Best Department of Medical Research and Department of Molecular Genetics (ScienceDaily, 2007).

"The surprising thing we found was that six to eight per cent of the alternative splicing events we looked at were showing differences, which is quite significant. And those genes that showed differences in splicing are associated with a range of important processes, including susceptibility to certain diseases" (ScienceDaily, 2007).

mRNA splicing is the process of protein production that occurs following the transcription phase of protein production in which the primary RNA transcript is modified before leaving the nucleus to be translated by a ribosome. This process of modification involves the attachment of a splicesome, formed from several ribozymes and protein molecules, to the pre-mRNA molecule which then removes the non-coding portions of RNA called introns and splices together the two adjacent exons. The variation that comes about from this process is determined by a function called alternative RNA splicing, in which different sections of the genetic code are treated as exons during RNA splicing, thus allowing many different proteins to be created from the same gene. The new findings have confirmed that this rocess of exon recognition differs significantly between humans and chimpanzees, thus creating some of the major differences between the two species.

The study, which has now made its appearance in the Journal of Genes and Development, is likely to have positive implications for the future study of disease in chimpanzees and humans. This study is one of the essential steps in identifying and understanding why different diseases will have large effects one species and not the other.

To learn more about this interesting topic please consult the following websites:

http://www.sciencedaily.com/releases/2007/11/071114151513.htm

http://www.mukto-mona.com/Articles/jaffor/evolution080306.htm

http://www.genesdev.org/cgi/content/full/21/22/2963?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=Blencowe&searchid=1&FIRSTINDEX=0&volume=21&issue=22&resourcetype=HWCIT

Reference:

University of Toronto (2007, November 15). Humans And Chimps Differ At Level Of Gene Splicing. ScienceDaily. Retrieved April 15, 2008, from http://www.sciencedaily.com­ /releases/2007/11/071114151513.htm

By: Thomas Bennett, 41761902

Gene Splicing: The key human success?

It has now been proven that chimpanzees are the closest living relatives to humans on this planet with genomes that are almost 99% identical to our own. But if we really are that closely related on paper, what are the causes of the vastly different structural, behavioural, and mental variations that occur between the two species? With the help of innovative new research from the University of Toronto's Centre for Cellular and Biomolecular Research, potential new explanations to this conundrum have finally been uncovered. In performing several comparisons between the heart and brain tissue extracted from humans and chimpanzees, University of Toronto Professor Benjamin Blencowe and his team, including graduate student researcher John Calarco, have discovered considerable differences in the way mRNA is spliced during protein production (ScienceDaily, 2007).

"It's clear that humans are very different from chimpanzees on several levels, but we wanted to find out if it could be the splicing process that accounts for some of these fundamental differences," says Blencowe, a professor with the Banting and Best Department of Medical Research and Department of Molecular Genetics (ScienceDaily, 2007).

"The surprising thing we found was that six to eight per cent of the alternative splicing events we looked at were showing differences, which is quite significant. And those genes that showed differences in splicing are associated with a range of important processes, including susceptibility to certain diseases" (ScienceDaily, 2007).

mRNA splicing is the process of protein production that occurs following the transcription phase of protein production in which the primary RNA transcript is modified before leaving the nucleus to be translated by a ribosome. This process of modification involves the attachment of a splicesome, formed from several ribozymes and protein molecules, to the pre-mRNA molecule which then removes the non-coding portions of RNA called introns and splices together the two adjacent exons. The variation that comes about from this process is determined by a function called alternative RNA splicing, in which different sections of the genetic code are treated as exons during RNA splicing, thus allowing many different proteins to be created from the same gene. The new findings have confirmed that this rocess of exon recognition differs significantly between humans and chimpanzees, thus creating some of the major differences between the two species.

The study, which has now made its appearance in the Journal of Genes and Development, is likely to have positive implications for the future study of disease in chimpanzees and humans. This study is one of the essential steps in identifying and understanding why different diseases will have large effects one species and not the other.

To learn more about this interesting topic please consult the following websites:

http://www.sciencedaily.com/releases/2007/11/071114151513.htm

http://www.mukto-mona.com/Articles/jaffor/evolution080306.htm

http://www.genesdev.org/cgi/content/full/21/22/2963?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=Blencowe&searchid=1&FIRSTINDEX=0&volume=21&issue=22&resourcetype=HWCIT

Reference:

University of Toronto (2007, November 15). Humans And Chimps Differ At Level Of Gene Splicing. ScienceDaily. Retrieved April 15, 2008, from http://www.sciencedaily.com­ /releases/2007/11/071114151513.htm

By: Thomas Bennett, 41761902

INJECTION OF HOPE - Alzheimer’s Vaccine

A revolutionary drug that stops Alzheimer’s disease could be available within a few years.

It could prevent people from reaching the devastating final stages of the illness in which sufferers lose the ability to work, talk or even swallow, and end up totally dependent on others.

Alzheimer's, the most common cause of dementia, affects about 200,000 Australians. Possibly thousands of others are undiagnosed or in the very early stages of the disease.

Existing drugs can delay the progress of the symptoms, but their effect wears off relatively quickly, allowing the disease to take its devastating course. In contrast, the new vaccine may be able to hold the disease at bay indefinitely, known as CAD106, showed it is highly effective at breaking up the sticky protein that clogs the brain in Alzheimer’s destroying vital connections between brain cells.

The vaccine uses a tiny section of the amyloid protein attached to an empty virus shell to trick the immune system into attaching and breaking up deposits of protein clogging the brain.

The development of tests capable of detecting the disease in its earliest stages would allow the jab to be given as early as possible and also used to keep the disease at bay in those with a strong family history of the illness.

But while the jab may stop the disease in its tracks, it is not expected to repair dear tissue, so will not be a cure.

HOW IT WORKS:

Step 1) Amyloid plaque builds up on the brain. Connections between brain cells are destroyed, causing memory loss.
Step 2) A series of vaccine injections are give to patient. Vaccine produces antibodies which trigger break-up of the plaque.
Step 3) Levels of antibodies are kept high by booster injections and the disease is halted.

Original post: Courier Mail 23/06/07 Saturday.

By Chiung-Yin Tu #4138534