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cells that cause NF1</A>   |   <A HREF="id300.htm" TARGET="_top" TITLE="Clues to Nf1">Clues to Nf1</A></div> <div> Dallas, Texas</div> <div> <B>Dallas Scientists Find Clues to Rare Disorder Marked by Tumors on Nerves </B></div> <div> <I>Knight Ridder/Tribune </I></div> <div> KRT NEWSFEATURES </div> <div> May 06, 2002 </div> <bR> <div> The Dallas Morning News </div> <div> (KRT) </div> <div> <B>DALLAS</B><FONT SIZE="3" COLOR="#000000" FACE="Arial" > </FONT>- <FONT SIZE="3" COLOR="#000000" FACE="Arial" >Dallas scientists have discovered which cells are guilty of launching tumors in a rare hereditary disease that affects the body's nerves. </FONT></div> <div> The findings could lead to new treatments for the disorder, called Neurofibromatosis type 1, which kills 15 percent of afflicted patients. </div> <div> The researchers have also proposed that the reason tumors form in Neurofibromatosis may extend to many common cancers, a theory that could change how doctors try to prevent the disease. </div> <div> "It's a wild speculation, but if it's right, it's a whole new concept," said Luis Parada, a molecular biologist at the University of Texas Southwestern Medical Center at Dallas. </div> <div> Parada, along with colleagues from UT Southwestern and France, reported the findings in Friday's issue of the journal Science. </div> <div> Neurofibromatosis type 1 affects about one in 3,500 people and can cause light brown spots, most noticeable on light-skinned patients. The disease can also cause benign tumors of nerves, some of which turn malignant. </div> <div> All people, in every one of their cells, have two "good" copies of the gene at the root of Neurofibromatosis. Normally, the gene, known as NF1, works unnoticed, quietly helping to control the natural division of cells. </div> <div> But in people with the disease, each of the body's cells carries one "good" and one "bad," or mutant, copy of the NF1 gene. According to the theory, if something causes a cell's good copy to go bad, that cell can initiate a tumor. </div> <div> The tumors that sprout in patients with Neurofibromatosis are jumbles of several types of cells. Presumably, one of those types was responsible for starting the tumor, Parada said. </div> <div> In the new research, Parada and his colleagues studied mice that were genetically engineered to develop the disease. They found that so-called Schwann cells, cells that insulate nerve fibers, are the ones that start a tumor when their good copy of the NF1 gene goes bad. </div> <div> Until now, "that was suspected to be true, but it was not nailed down," said Tyler Jacks, a cancer biologist at the Massachusetts Institute of Technology in Cambridge. </div> <div> More experiments hinted that the Schwann cells had some partners in crime, immune system cells known as mast cells. The mast cells were making their way to nerve fibers even before the tumors appeared, the scientists found. It was as if, with no good copies of the NF1 gene left, the Schwann cells attracted the mast cells, and then the mast cells helped the tumor form, Parada said. </div> <div> That means the mast cells may be the Achilles' heel doctors have been looking for. He and his colleagues are starting to give the mice drugs that prevent mast cells from migrating. </div> <div> "If our speculation is right, in five years we'll be able to greatly change the quality of life of patients with Neurofibromatosis," he said. </div> <div> A final experiment on the mice was the most interesting, Parada said. The researchers found that the genetic makeup of the mast cells was the deciding factor in whether a tumor would form. If the mast cells had two "good" copies of the NF1 gene, no tumor formed. But tumors did form when mast cells had one "bad" copy - the same situation found in human patients. </div> <div> Proof that the genetic makeup of the noncancerous cells matters is unprecedented, said Jacks, who is also a researcher with the Howard Hughes Medical Institute. </div> <div> Most cancer researchers focus on the genetic errors that occur in the tumor cells, Jacks said. And cancer drugs are usually aimed at those cells. But focusing on how the genetic makeup of other cells in the body contributes to tumors could be a new and important tactic in the war on cancer. </div> <div> And it could explain, for instance, why some people known to inherit cancer-causing mutations escape the disease, or why some smokers develop lung cancers but most don't. </div> <div> "Maybe all of us have within our genetic dowry a bunch of debilitating mutations … so we all are more or less susceptible to cancers," he said. </div> <div> Parada's colleagues were UT Southwestern's Yuan Zhu, Pritam Ghosh and Dennis Burns. </div> <div> --- </div> <div> (c) 2002, The Dallas Morning News. </div> <DIV ALIGN="LEFT"></DIV> <div> <A HREF="id23.htm" TARGET="_top" TITLE="Latest Research"><IMG SRC="054851f0.jpg" border=0 width="133" height="31" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></A></div> <div> <A HREF="index.htm" TARGET="_top" TITLE="NF TEAM"><IMG SRC="05257250.jpg" border=0 width="87" height="37" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></A></div> </td> </tr></table></body>