Re: cellular mutation and cancer

Re: cellular mutation and cancer - or lack thereof.

Zack,

I think the problem is a little bit more complex than what is presented. The nuclei were transferred from cells that had already differentiated from the original fertilized egg into brain cells back into an undifferentiated, denucleated cell.

To me, it appears that certain factors (proteins, RNA, etc.) in the new cells (1) did not respond to the genetic mutation in the transplanted nuclei, or (2) factors in the new cell, that were not present in the differentiated brain cells modified (repaired?) or responded to other areas in the DNA. It would be interesting to see if the brain cells became cancerous as they underwent further differentiation, or if another promoter is needed to cause cancer. Also, I would like to know what the mean that cells were reprogrammed. Do they mean no expression of cancer? Was the DNA reprogrammed (repaired)?

I think this will have nothing to do with the LNT, unless you are talking about transferring mutated nuclei in irradiated people into undifferentiated cells.

Zack Clayton <zclayton@YAHOO.COM> wrote:

I just wonder what this news means for radiological cancer induction
and the LNT? Cellular mutations apparently DON'T cause cancer by
themselves.

http://www.sciencedaily.com/releases/2003/06/030604084515.htm

Source:
St. Jude Children's Research Hospital

Date:
2003-06-04

Cloning Embryos From Cancer Cells

MEMPHIS, TENN. (June 3, 2003) -- Nuclei removed from mouse brain tumor
cells and transplanted into mouse eggs whose own nuclei have been
removed, give rise to cloned embryos with normal tissues, even though
the mutations causing the cancer are still present. This research, from
scientists at St. Jude Children's Research Hospital, appears in the
June 1 issue of Cancer Research.

The finding demonstrates that the cancerous state can be reversed by
reprogramming the genetic material underlying the cancer, according toJames Morgan, Ph.D., a member of the St. Jude Department of
Developmental Neurobiology, and lead author of the study. The findings
also indicate that genetic mutations alone are not always sufficient to
cause a cell to become cancerous.

“Specifically, it shows that so-called epigenetic factors are key
elements in the development and maintenance of tumors,” Morgan said.

Epigenetic factors are those that influence the cell’s behavior.
Examples include environmental effects and chemical modification.

“The concept of epigenetic factors having a role in cancer is already
largely accepted,” Morgan said. “In fact, it’s already known that
epigenetic alterations of chromosomes can cause certain rare forms of
cancer. And some anti-cancer agents actually target epigenetic changes.
But this is the first formal proof of the theory in a living animal.”

Unlike mutations, epigenetic modifications of DNA are potentially
reversible mo! lecular events that cause changes in gene expression. Some
genes that help prevent the development of cancer (e.g., tumor
suppressor genes) can be targets of epigenetic factors. The
inactivation of such a gene might make the DNA more vulnerable to
developing a cancer-causing mutation.

The St. Jude researchers used nuclei from mouse medulloblastoma cells
to create the clones. Medulloblastomas are brain tumors that tend to
spread to the spinal cord. They account for about 20 percent of
childhood brain tumors and most often occur in children under ten years
of age.

The team, led by Morgan and department chair Tom Curran, Ph.D., placed
nuclei from medulloblastoma cells into mouse eggs whose own DNA had
been removed.

“Since the embryos did not develop tumors, we conclude that the
cancerous properties were removed by reprogramming,” Morgan said.

“The use of mouse eggs to reprogram cancer cell DNA represents a new
strate! gy for investigating the molecular basis of cancer,” Curran said.
“By studying this model we hope to identify which epigenetic factors
may contribute to this form of brain tumor. In addition, it also gives
us a valuable tool for testing new therapies.”
. . .

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