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A surprise
“Spark” for Pre-Cancerous Colon Polyps
Newswise — Researchers at the Huntsman
Cancer Institute (HCI) at the University of
Utah studied the events leading to colon
cancer and found that an unexpected protein
serves as the “spark” that triggers
formation of colon polyps, the precursors to
cancerous tumors.
“Our findings will certainly raise some
eyebrows,” says oncological sciences
graduate student Reid Phelps, first author
of the study, which was published
Friday, May 15 in the journal Cell.
“We expect the conventional wisdom regarding
colon tumor development to be reconsidered,
together with some resistance to our
alternative explanation.”
The study in zebrafish and human cells
discovered that a protein, known as
C-terminal binding protein 1, or CTBP1, was
the spark that initiated colon polyp
formation, not the protein beta-catenin, as
previously thought.
With this new information, future treatments
that prevent tumor progression can be
developed.
The research centered on the mutation of a
tumor-suppressor gene called APC – a
mutation previously found to be present in
85 percent of all colon cancers.
Since then, research labs around the world
have developed theories about how the gene
works in colon cancer development.
“Our work reveals new information about how
the APC protein functions to prevent colon
tumor formation. This new information opens
new possibilities treating and preventing
colon cancer. ” says David Jones, Ph.D., a
professor of oncological sciences at the
University of Utah and senior director of
early translational research at HCI.
“We want to know what happens immediately
following mutation of the APC gene mutation
as a way of understanding how we might
intervene.
"If
you’re trying to match therapies with a
specific genetic mutation, it helps to
understand the earliest steps in tumor
formation, as well as the downstream
consequences.”
APC stands for adenomatous polyposis coli.
It is classified as a tumor suppressor gene.
Before the new study, scientists believed
that following APC mutation, faulty cell
communication caused by a particular protein
known as beta-catenin resulted in colon
polyp formation. Colon polyp formation
precedes the development of colon cancer.
While considerable evidence implicates
dysregulated Wnt/beta-catenin signaling as
the initiating event underlying colon
adenoma formation following loss of APC,
several studies examining human FAP adenomas
raised the possibility that APC loss alone
is insufficient to promote aberrant Wnt/beta-catenin
signaling.
These findings suggest that beta-catenin
dependent intestinal cell proliferation may
contribute to adenoma progression, rather
than initiation following loss of APC.
According to the National Cancer Institute,
there are about 108,070 new cases of colon
cancer and 40,740 new cases of rectal cancer
each year in the United States. Colon and
rectal cancers together claim 49,960 lives
in the country annually.
Huntsman Cancer Institute (HCI) at the
University of Utah marks its 10th
anniversary in 2009.
HCI was founded by Jon M. Huntsman to
fulfill his dream of finding a cure for
cancer through genetic research.
In the last 10 years, HCI has grown to
become one of America’s major cancer
research centers. HCI is part of the
University of Utah healthcare system and is
ranked consistently by U.S. News & World
Report as one of the top cancer hospitals in
the country.
For more information about HCI, please visit
www.huntsmancancer.org
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