Medical researchers from John Hopkins University have uncovered a clue to the way the DNA molecule reproduces itself and that may reveal why cancer cells divide so rapidly and now the growth may be controlled.

The John Hopkins team discovered that the double helix making up the DNA molecule reproduces a cell by attaching itself to the cell nucleus in a continous series of loops that produce exact copies of these loops as they pass through the nucleus. The looping process explains how the lengthy strands of DNA never get entangled even though they are half a million times larger than the cell they are reproducing.

"If the cell nucleus were the size of a basketball, the strands of DNA would stretch from New York to Washington," said Dr. Bert Vogelstein of Johns Hopkins School of Medicine. "What we've done is show how the DNA can reproduce the basketball without losing itself in knots."

In better understanding how cells divide, said Dr. Donald S. Coffey, the Johns Hopkins team hopes to gain greater insight on how cancer cells multiply so rapidly.

"To understand what's wrong with a car's motor," Coffey said yesterday, "we have to know what a motor is like when it's running normally."

A cancer cell divides itself in a way that is out of control and out of step, reproducing a cell whose nucleus is abnormal in shape. This abnormality is the hallmark of the cancerous cell that spreads and invades adjacent tissue and produces an abnormal mass of tissue called a tumor.

In experiments with animal tissue, Coffey, Vogelstein and Drew M. Pardoll proved that the DNA molecule does not form an exact copy of itself by simply moving along the double helix and copying both strands at once.

The johns hopkins experiments suggest that the DNA molecule repeats itself at as many as 10,000 sites along the nucleus of the cell and that both strands of DNA are reeled through these fixed sites, forming double loops that preserve the cell after it divides.

"This system helps to understand how the DNA retains a coherent system of copying itself," Vogelstein said. "DNA is so much longer than the width of a cell's nucleus that it may be more than just an efficient way to package DNA in the nucleus; it may be involved in the way DNA is replicated (repeats itself)."

Coffey said the next step in the John Hopkins research is to find out what makes the DNA loop through 10,000 specified sites in the nuleus.

"We want to compare these mechanisms in normal cells with cancer cells," Coffey said. "If we do that, we'll begin to understand what's wrong with the car's motor."

Coffey said the nucleus of the cancer cell shows up "out of shape, disorganized and wrinkled" compared with a normal cell. He said one reason for this could be that the DNA duplication mechanism is turned on and then off in the splitting of a normal cell.

"In the cancer cell," Coffey said. "the duplication mechanism gets turned on and stays turned on. It can't be turned off."