Cancer Cells Produce Healthy Mice Through Clonin

Natural processes within the body can reset regulatory processes in specific types of cancer and reverse many of the components responsible for causing malignancy, according to new research.

"This settles a principal biological question,” said Dr. Rudolf Jaenisch, a professor of biology at the Massachusetts Institute of Technology (MIT, Cambridge, MA, USA). "The epigenetic elements of cancer are reversible; the genetic elements, as expected, are not.

Scientists have long known that cancer starts when specific key genes in an otherwise healthy cell mutate, and tumor growth depends on continuing, multiple alterations. Only recently, however, have researchers begun to determine the epigenetic elements of cancer--in other works, how molecules in a cell affects genes without actually changing the sequence of DNA.

The research team, from the Whitehead Institute (Cambridge, MA, USA), working with investigators from the Dana Farber Cancer Institute (Boston, MA, USA; www.dfci.harvard.edu) assessed whether any of these epigenetic influences can be reversed. First, they removed the nucleus from a melanoma cell and injected it into a denucleated egg cell (also know as nuclear transfer). After the egg cell developed into a blastocyst, the researchers harvested embryonic stem cells, which they then incorporated into healthy adult mice. This study was published in the August 2004 issue of the journal Genes and Development.

"It's important to note that the stem cells from the cloned melanoma were incorporated into most, if not all, tissues of adult mice, showing that they can develop into normal, healthy cells,” said Dr. Robert Blelloch, a researcher in the Jaenisch lab. These cells include those for immunity, skin pigmentation, and connective tissue. But in spite of this, when specific cancer-related genes in these mice were turned on, they developed malignant tumors at a much more rapid rate than the control mice.

This study opens up avenues for developing cancer animal models in which scientists could ask epigenetic questions, according to Dr. Lynda Chin of Dana-Farber's oncology department. "Although studies are ongoing, these findings have provided initial clues of the relative contributions of the epigenetic vs genetic lesions in the development of cancer. Drugs that target the cancer epigenome may prove to be a key therapeutic opportunity for diverse cancers, said Dr. Chin.




Related Links:
Whitehead Institute
Dana Farber Cancer Institute