ken_akiba, on May 22 2010, 03:21 PM, said:
I reckon it was done most likely on 'junk' part of DNA that current mainstream science believes serves no function to anything, on which, I disagree wholeheartedly.
I think it is the junk DNA that holds the key to the quandry that clones always end up having unexpected, mysterious genetic defects.
Maybe no more : http://www.eurekaler...ol-dd043010.php
Researchers from the University of Leeds, UK, the Charité University Medical School and the Max Delbrück Centre for Molecular Medicine (MDC) in Berlin, Germany, have discovered a new driving force behind cancer growth.
Their studies have identified how 'junk' DNA promotes the growth of cancer cells in patients with Hodgkin's lymphoma. Professor Constanze Bonifer (University of Leeds) and Dr Stephan Mathas (Charité, MDC) who co-led the study suspect that these pieces of 'junk' DNA, called 'long terminal repeats', can play a role in other forms of cancer as well. The work is published in Nature Medicine.*
The researchers uncovered the process by which this 'junk DNA' is made active, promoting cancer growth.
"We have shown this is the case in Hodgkin's lymphoma, but the exact same mechanism could be involved in the development of other forms of blood cancer," said Prof. Bonifer. "This would have implications for diagnosis, prognosis, and therapy of these diseases."
'Long terminal repeats' (LTRs) are a form of 'junk DNA' - genetic material that has accumulated in the human genome over millions of years. Although LTRs originate from viruses and are potentially harmful, they are usually made inactive when embryos are developing in the womb