Universal cure for the spread of cancer

Scientists closer to understanding how cancer spreads

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

How can Identical Twins Be Genetically Different?

Scientists at the University of Michigan Medical School has conducted studies on 11 pairs of monozygotic twins which are genetically identical but one of them suffers from rheumatoid arthritis.

The researchers compared gene expression patterns of each twin and found that three genes where significantly over-expressed in the rheumatoid arthritis suffers when compared to their healthy twin. The three genes were not known to be associated with the disease before.

Because monozygotic twins start out with nearly identical genetic information, scientists stated that the differences in the expression of the genes were caused by environmental factors that modify DNA. They also stated that using identical twins represented the best experimental system to address how two patients can have the same genes but different disease outcomes.

The first over-expressed gene codes for a protein called laeverin. Scientists hypothesize that this would promote tissue damage of the joint in the rheumatoid arthritis sufferer. The second gene over-expressed codes for a protein that helps deactivates the hormone cortisol which is involved in anti-inflammatory effects. The third gene codes for Cyr61, which is used in a process that recruits new blood vessels which is needed in the early stages of rheumatoid arthritis.

Associate professor at the University of Michigan Medical School , Joseph Holoshitz stated that, “The newly discovered genes provide important insights into the nature of the disease and facilitate the design of novel treatment strategies for rheumatoid arthritis”.

Sources:
http://www.sciencedaily.com/releases/2006/07/060726091919.htm
http://en.wikipedia.org/wiki/Twin

Ibrahim Sedic 41294101

Identical Twins Genetically Different

A study carried out by Swedish, Dutch and American scientists has found that identical twins are not actually completely genetically identical. The scientists studied ten pairs of identical (or monozygotic) twins, in which one twin from nine of the pairs had an hereditary disease (e.g. Parkinson’s or Dementia) and the other did not. In the past it was known that differences between twins were caused by environmental factors and epigenetic factors (which influence the expressions of a gene). This study has now shown that there are minuscule differences in the actual genetic make up of identical twins, contrary to past assumptions. This may explain the subtle differences in the phenotypes (outward appearance) of twins who come from the same embryo.

"When we started this study, people were expecting that only epigenetics would differ greatly between twins,” said Jan Dumanski, a professor of genetics at the University of Alabama at Birmingham and an author of the study. “But what we found are changes on the genetic level, the DNA sequence itself.”

It is not known yet whether this change occurs at the embryonic level of production and/or as the individual ages. This study, published in the American Journal of Human Genetics may help scientists understand and treat genetically induced diseases more fully by being able to easily identify the different gene between the two twins, consequently finding the gene/s which cause the disease. In the meantime, the common assertion that “no two people are genetically the same, except identical twins” will have to be modified, and numerous biology textbooks reprinted!

Laura Fenlon

41732126

http://www.ajhg.org/AJHG/fulltext/S0002-9297(08)00102-X

http://www.nytimes.com/2008/03/11/health/11real.html?bl&ex=1205726400&en=5a8aba53a3148fae&ei=5087

http://www.lswn.it/en/press_releases/2008/identical_twins_not_as_identical_as_originally_thought