And then, there's the aging process itself. "There's an old saying in biology, which is ontogeny recapitulates phylogeny, which means the development of the individual recapitulates the development of the species. So at some point during your early gestation, you had a tail and webbed hands and webbed feet, because biology is built on itself. Through evolution, however, you don't need the webbing anymore, so your genes take care of killing that growth. It's called apoptosis, programmed cell death," Slamon says while taking a tissue sample out of a large freezer, where it's stored at 70 degrees below zero.

"Well, the same thing happens during aging. There's programmed cell death. Cells are eventually lost, and when they aren't replenished it results in organ failure. That's what we call it. From nature's point of view it's probably an entirely appropriate function. You're done, it's time for you to go away and a new individual or group to come. Again, if we can interfere with or manipulate the signals, we can stop programmed cell death and stop the aging process. That's the scariest part of the story, and I don't want to be around to think about it."

Surprisingly, the high-tech bet of the moment in research labs around the country is not directed at killing cancer cells, or even at trying to fix what's broken in the cell that's causing unregulated growth. While there are labs doing this kind of work, of course, the avenue of hot pursuit is an all-out effort to find an effective weapon to interfere with the signals involved in tumor growth. In order to flourish, tumors need nourishment; they need to be fed. This is accomplished by the formation of new blood vessels, a process called angiogenesis.

The idea is simple: Cut off a tumor's food supply, and it can't grow. Equally significant, and one of the key reasons angiogenesis is such an attractive target, is the hope that any successful treatment would be generic. All tumors, whether in the lung, breast, prostate, or colon, need nourishment. Scientists also believe angiogenesis may provide a big payoff as a point of attack because the cells involved in blood-vessel growth don't mutate. Cancer cells, on the other hand, are quite volatile and do tend to mutate to form resistance to drugs, which is why strategies that specifically target tumor cells tend to fail.

The theory was first proposed by Dr. Judah Folkman of Children's Hospital in Boston in the early seventies. However, back then, whatever the merits of the idea itself, the biology and the technology to take a serious shot at this strategy didn't really exist.

But the precocious Folkman, who's become almost a cult figure, thanks to a front-page New York Times piece about his work nearly two years ago, was denied a grant for his research by the National Institutes of Health even as recently as 1992. Today, however, there are nineteen separate clinical trials under way for anti-angiogenesis drugs, including Endostatin, one of the two that have come out of Folkman's lab in conjunction with the company EntreMed (Folkman's other drug is Angiostatin, not yet in trials).

When the Times piece by Gina Kolata was published, Folkman was still working only with mice. Nevertheless, DNA discoverer and Nobel winner James Watson, a towering figure in science, was quoted saying he believed Folkman would cure cancer in two years (that would be this May, although Watson claimed his comments were not accurately represented). Though Folkman's work was no secret -- and in fact, there were already anti-angiogenesis drugs that were farther along than his -- the story caused a remarkable frenzy.

Folkman was overwhelmed by thousands of calls from seriously ill cancer sufferers pleading for help, and, of course, from the media. The episode is a stark illustration of the fine line researchers have to walk when they start making hopeful predictions about cancer treatments and potential cures. It's also an indication of just how quickly things are moving: Less than two years ago, there was outrage at what was viewed as the excessive optimism of the Times piece.

Ironically, however, since Folkman is the recognized father of the field, researchers I spoke with do not believe his drugs are among the most promising. "Angiostatin and Endostatin are, in a way, a throwback to the old days," says one scientist in the field. "By that I mean nobody, including Folkman, has any idea how they work. The mechanism of action is completely unknown."

Using Folkman's basic premise, however, there are a number of specifically targeted compounds in clinical trials now for which the expectations are much brighter. Biotech companies like Sugen and Genentech, just to name two, both have drugs in the later stages of patient testing.

While Sugen's compound (SU5416) targets a receptor in the signal-transduction process, Genentech's (anti-vascular endothelial growth factor, or anti- VEGF) is aimed, as you can tell from its name, at a growth factor. Again, going back to the basic biology of the cell and how one cell communicates with another, the effort here is to find a vulnerable point somewhere along the lines of communication and disrupt it.

As an adult, you don't need to form new blood vessels, except perhaps in rare instances, such as to help heal a major wound. Nevertheless, cells have all the information required to carry out the process. And when there is a cancer, the renegade cells that are wildly reproducing set the cycle in motion. It's known that certain conditions in the body can begin the signalling to start angiogenesis. A decrease in the flow of oxygen in a specific part of the body, for example, can cause the cells in that area to elicit VEGF.

This growth factor then instigates the production of endothelial cells, which actually begin to form the first part of the new blood vessel. As more and more of these cells are produced, they eventually coalesce into a tube. The building process is complex and requires at least three or four receptors working in concert to be successful.