Monday, 2 April 2012

Possible Increase in Cancer Protection, Metabolism and Longevity


One of the main focuses of genetic research is the investigation into cures and preventions of cancer. Cancer is one of the leading causes of death in the world today and it is estimated that, in Australia alone, around half of males and a third of females over the age of 85 will have been diagnosed with cancer at some point in their lives (AIHW 2010).

Cancers are caused when the cell cycle becomes unregulated and the cell rapidly and uncontrollably divides forming a tumour. The human body has certain mechanisms in place to help prevent tumours from growing. Genes called "tumour suppressors" encode certain proteins which stop the cell from dividing too quickly. A mutation or absence of these genes can prevent them from functioning properly and allow cancers to form. One particular type of tumour suppressor is a gene called PTEN, which encodes a protein called phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase (NCBI 2012). This protein is involved in a series of chemical reactions (a chemical pathway) which either signals rapidly dividing cells to stop dividing or kill the cells. This in turn prevents tumours from growing and spreading. An absence or mutation of the PTEN gene accounts for a wide range of cancer development. One study showed, "Somatic mutations or homozygous deletion of PTEN have been found in various kinds of malignant tumors, such as glioblastoma (20-75%), prostatic cancer (10-49%), small lung cancer (40%), endometrial cancer (34-50%), breast cancer and anaplastic meningiomas."(Akira, 1999)

Needless to say that research into these genes are fundamental in the development of cancer prevention methods. A recent article posted on sciencedaily.com talks about tests which were conducted using the PTEN gene in mice (Cell Press, 2012).  In the experiment an extra copy of the PTEN gene were added to the mice (Serrano, 2012).  These mice were not only protected from cancer but retained a leaner figure even after consuming more food than the control mice. In addition to this, the mice also experienced an increase in longevity that was completely separate from the fact that they were protected from cancer. This leads researchers to believe that, not only does the PTEN gene function as a tumour suppressor, it also has positive effects on the metabolic processes of certain cells.  The extra PTEN gene correlated to an increase in the formation and activity of brown adipose tissue which burns fat rather than storing it. The same effects were also exhibited when "a small compound inhibitor that mimics the effects of PTEN"(Cell Press, 2012) was applied                                                               to the mice in place of the extra PTEN gene.

The results of the experiment could have very positive implications for cancer prevention.  If the effects shown in the mice experiment were able to be replicated in humans then it is possible that we could not only experience an increase in cancer protection but also a positive increase in metabolism and longevity. Although in its early days, it is hopeful that continued research into this phenomenon may lead to significant medical breakthroughs in the field of genetic research.  

 
References
1. Cell Press (2012, March 6). "With extra gene, mice are footloose and cancer free." ScienceDaily, research article, accessed on March 16 from:
<http://www.sciencedaily.com­/releases/2012/03/120306131252.htm>

2. Manuel Serrano, et al. (March 2012) "Pten Positively Regulates Brown Adipose Function, Energy Expenditure, and Longevity," research article, accessed on March 16th from: <http://www.sciencedirect.com/science/article/pii/S1550413112000484>
3. Campbell, Neil A., et al., (2009) "Biology" (Eighth Edition, Australian Version), Pearson Australia Group Pty Ltd.

4. Akira Suzuki, José Luis de la Pompa, et al. (October 5th 1999), "High cancer susceptibility and embryonic lethality associated with mutation of the PTEN tumor suppressor gene in mice", research paper, accessed on March 16th from: <http://119.93.223.179/ScienceDirect/Current%20Biology/08-21/sdarticle_016.pdf>

5. Bonneau D, Longy M, (2000), "Mutations of the human PTEN gene." Department of Medical Genetics, University of Poitiers, Poitiers, France, Research paper. Accessed on March 16th 2011 from: <http://www.ncbi.nlm.nih.gov/pubmed/10923032>

6. Australian Institute of Health and Welfare (AIHW),  (December 16th 2010), "Cancer in Australia 2010: An Overview.", Statistics report, accessed on March 16th from: <http://www.aihw.gov.au/publication-detail/?id=6442472459>

7. Eric C. Chu, Andrzej S. Tamawski, (October 1st, 2004), "PTEN regulatory functions in tumor suppression and cell biology", Department of Medicine, Division of Gastroenterology, VA Long Beach Healtcare System and University of California, review article, accessed on March 16th from:

8. National Centre for Biotechnology Information (NCBI), Updated on March 2012, "PTEN phosphatase and tensin homolog." NCIB, research report, accessed on March 16th from: <http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=5728>

9. Cannon B, Nedergaard J, (January, 2004), "Brown adipose tissue: function and physiological significance.", research article, The Wenner-Gren Institute, The Arrhenius Laboratories F3, Stockholm University, Stockholm, Sweden. Accessed on March 16th from:  <http://www.ncbi.nlm.nih.gov/pubmed/14715917>

10. Author unknown, "Mouse experiment", image, accessed on 18th March from: <http://29.media.tumblr.com/0pr5GveTto1qxrzz1bi5hskFo1_400.jpg>

11. Author unknown, "Space-filling model of the PTEN protein (blue) complexed with tartaric acid (brown)", image, accessed on 18th March from: <http://upload.wikimedia.org/wikipedia/en/d/dc/PTEN.png>

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