Patients’ Chances of Recovery Linked to Cancer Type : Health: Some cancers respond better to treatment than others. Doctors are learning that the form the disease takes has a lot to do with it.

The news recently that former Democratic presidential candidate Paul E. Tsongas survived a recurrence of his cancer less than a year after bone-marrow transplants in 1986 shows that, regardless of how he fared at the polls, he is one of the luckiest men in America.

He was lucky to have skilled doctors and nurses, a good hospital, a daring treatment, an optimistic family and a courageous attitude.

Most of all, he was lucky that his cancer was lymphoma.

Among cancers, lymphoma is one of the more treatable. And among types of lymphoma, the low-grade kind he had is the most treatable. It does not diminish the work of his healers to say that Tsongas’ disease was the single most important variable in his therapy.

Tsongas, then a U.S. senator, discovered his cancer in 1983. He underwent a pioneering course of treatment in 1985, after his condition deteriorated, that involved removing bone marrow, administering radiation and chemotherapy and then replacing the bone marrow. About seven months later, doctors discovered a cancerous lymph node, and Tsongas underwent radiation therapy. Today, his doctors said, he is cancer-free.

For cancer patients, relapse and recurrence are perhaps the most dreaded words in the language. But for some patients, they do not necessarily mean a death sentence.

Although never a good sign, the recurrence of lymphoma after treatment is inherently less a cause for alarm than the reappearance of so-called “solid” tumors, such as breast cancer or colon cancer. That is because lymphoma is by nature a diffuse disease. It is a cancer of the lymph nodes, which are scattered encampments of the immune system.

“It is normal for lymphocytes (which are formed in the lymph nodes) to traffic throughout the body,” explained Walter J. Urba, a researcher at the National Cancer Institute. “When lymphoma shows up in a new site, it does not necessarily mean the cells have to be more resistant then the original ones.”

In contrast, cancer appearing in the lungs or bones after breast cancer surgery is dire news. To survive in foreign environments, cancerous breast tissue must acquire new traits, including the ability to get into the bloodstream or lymphatic channels, take hold far away and ultimately grow. Such “metastatic” cells are extremely abnormal and as a rule much less easily killed than most lymphoma cells.

Advances in cell biology are just beginning to shed light on why some cancers are more aggressive than others, more resistant to chemotherapy or radiation treatment and more likely to return.

Cancer describes a condition in which cells demonstrate uncontrolled growth. Except for that single--and crucial--characteristic, however, there is little in common among the many dozens of diseases that are called cancer.

The avenues leading to the cancer cell’s uncontrolled growth are varied and distinctive. All cancer involves changes in the encyclopedia of genetic information--the DNA--but damage in some cases is as small as a typographical error and in others is as huge as a garbled reshuffling of whole volumes. Some cells become malignant by losing the function of “tumor suppressor genes,” while others get there by turning on cancer-causing genes, the so-called “oncogenes.” These genes, when activated by radiation or a virus, can cause a normal cell to become cancerous.

The cancer cells often are influenced by the organs in which the malignant tumors occur. Every cancer has a “cell of origin.” Lymphomas come from lymphocytes, a type of white blood cell. Gliomas come from glia, the cells that nurture and support the nerves of the brain and spinal cord; colon carcinoma comes from the cells that line the inner surface of the large intestine.

The gene mechanisms and the origin of any particular cancer presumably govern their clinical behavior and treatability, although scientists are only getting the first glimmers of how.

About 85% of the lymphomas of the sort Tsongas had begin with a break in a chromosome, one of the 46 strings of DNA that carry genetic information. The break occurs at a spot where the DNA normally undergoes rearrangement when the young lymphocyte grows into a mature cell of the immune system.

Although clearly a mistake, this event is in some sense a variation of normal cellular behavior and, by itself, does not cause lymphoma. Instead, scientists theorize that the disease begins when the DNA suffers a “second hit” that turns on an oncogene or some other stimulus to uncontrolled growth. The result is cancer, but the route taken appears to be less complicated and tortured than that of many other tumors.

In comparison, there is evidence that some of the more deadly cancers undergo as many as five or six accidents. Very fast-growing colon cancers, for example, may result from the loss of two tumor suppressor genes and the activation of several oncogenes. This piling up of mutations may make colon cancer cells much more abnormal--and much less treatable--than lymphoma cells, even though both are cancer.

“One might be concerned that with multiple genetic aberrations, these cells may be harder to kill. With lymphoma, there may be fewer genetic alterations to overcome with therapy,” said Stanley J. Korsmeyer, an oncologist and researcher at Washington University in St. Louis.

It is also likely that highly malignant tumors can withstand treatment because their cells exhibit “normal” behavior.

Many cancers of the colon, liver and kidney, for example, have an active “multiple drug resistance gene” that allows a cell to kick toxic substances it has absorbed back out into the environment without being damaged.

The purpose of this mechanism, however, is not drug resistance. Instead, it appears to be an evolutionary adaptation that allows these cells to protect themselves from damaging chemicals they meet in their routine work of digestion and excretion. Consequently, most of these tumors are resistant to chemotherapy from the outset.