VIRUS VS. CANCER
OCTOBER 18, 1996
Charlayne Hunter-Gault reports on new hope in the war against cancer.
CHARLAYNE HUNTER-GAULT: The news comes from two potentially important studies on cancer published today in the Journal "Science." One involves a link between cancer and the common cold. The other involves a new scientific link between smoking and lung cancer. To explained, we're joined by Dr. Richard Klausner, director of the National Cancer Institute. Thank you for joining us. Let's start with this intriguing link between the common cold and cancer. What is it and how significant is it?
DR. RICHARD KLAUSNER, National Center Institute: Well, what these researchers reported today in “Science” is the result of a search for a long sort goal, and that is a virus that would only kill cancer cells and not kill normal cells. These researchers started with a common respiratory virus, which can kill normal cells and cancer cells. They found that by genetically engineering that virus by altering it, it can no longer kill normal cells but can only kill a certain common type of cancer cell, and what it does, it recognizes a molecular difference between cancer cells and normal cells, representing the fulfillment of the type of dream that if we understood the molecular difference between a cancer cell and a normal cell, we can begin to move from therapy that's random or poisons everything to targeted therapy, and that's what this virus is about.
CHARLAYNE HUNTER-GAULT: And how does it work, I mean, you inject cold cells into a tumor?
DR. KLAUSNER: No, it's not like that. This is a virus that can cause colds normally, and then they modify the virus, it can't cause colds anymore. When that, the normal virus gets inside cells, it makes a lot more of itself and kills the cell. But in order to do that, it has to turn off a particular protein present in all normal cells. Now 50 percent of cancer cells develop because that protein is lost. That protein normally is a guardian of the cell against cancer. The way that protein called P-53 works is by constantly looking at the DNA, the genetic material in a cell and looking for mistakes, looking for damage to the DNA, when it finds it, it tells the cell to stop and to fix the damage. If the cell can't fix the damage, that same protein tells a cell to commit suicide. In order for this cold virus to normally affect a cell, it has to turn off that protein. These scientists destroyed the ability of the virus to turn off that protein, so now the virus can only grow and kill cells that don't have that protein. It turns out that 50 percent of all human cancer, whether it's breast cancer or prostate cancer or colon cancer, brain cancer, lung cancer, have lost the P-53 gene or lost the function of the protein that the P-53 gene instructs the cells to make. So this altered virus will kill any cancer cell that's lost the P-53 function.
CHARLAYNE HUNTER-GAULT: Now so far, most of the work on this has been done in animals, right?
DR. KLAUSNER: All the work that's been reported has been done in animals, but it has been tested in humans in what we call Phase 1 clinical trials where it's given to people in a clinical research setting to see whether there's any toxicity. So the first step in testing a new treatment is to see whether there is unacceptable toxicity.
CHARLAYNE HUNTER-GAULT: So how hopeful are we that this is really going to be a major breakthrough?
DR. KLAUSNER: Well, we're very intrigued by it, uh, but as with many encouraging laboratory findings, it's a long way to go to proving that it can be used in humans. The most difficult problem to overcome with this particular virus is the human immune system, which will limit the infection in a cancer patient. So it may be very difficult to wipe out all the cancer cells, but we are all very excited about this new approach and looking to see whether it does work.
CHARLAYNE HUNTER-GAULT: All right. The second study, linking, scientifically linking smoking to cancer, what's new about that?
DR. KLAUSNER: Well, let me just say this new study is also about the P-53 gene, and it provides a specific molecular mechanistic connection between chemicals in cigarette smoke and specific damage to the gene that tells the cells to make P-53, the same guardian of the genome. We didn't need this study to tell us that smoking causes lung cancer, but this does make an additional specific connection between what's in the cigarette smoke and how it actually causes the cancer.
CHARLAYNE HUNTER-GAULT: And this never had existed before.
DR. KLAUSNER: This we didn't have before, and it has larger implications. The P-53 gene is altered in 50 to 60 percent of lung cancers. The P-53 gene has about over 1,000 pieces of information in it, and any one of them can be changed, but when we look at lung cancers, there's three specific places in a gene that seem to be changed again and again and again in most patients. What it turns out is this one component of cigarette smoke exactly produces that exact fingerprint of molecular changes. Now what that tells us is that the reading of the molecular fingerprint will be an incredibly important tool in our attempt to be detectives and find what in the environment may cause cancer, because each chemical in the environment may leave a specific fingerprint, and by being able to read the fingerprint may be able to go back and finally uncover chemical and environmental causes of cancer that are otherwise incredibly difficult to find out.
CHARLAYNE HUNTER-GAULT: So this is--what you're saying is this goes beyond--I mean, it's important enough to definitively establish the link between smoking and, and cancer, but this goes beyond that, is what you're saying?
DR. KLAUSNER: This goes beyond that, and this tells us just like if we try to catch a thief, we don't have to watch the thief break into a house, the thief leaves fingerprints. The thief may leave something behind. Chemicals that can cause cancer leave fingerprints. That's what this tells us.
CHARLAYNE HUNTER-GAULT: Briefly, what's the next step in this?
DR. KLAUSNER: The next step in this is first of all to identify other chemicals and the types of fingerprints that they leave in particular cancer-causing genes and begin finally to understand in exquisite detail how things that we eat, things that we're exposed to actually cause particular cancers.
CHARLAYNE HUNTER-GAULT: All right. Well, Dr. Klausner, as you said, we've a long way to go, but this is very interesting and, indeed, intriguing news. Thank you for joining us.
DR. KLAUSNER: Well, thank you very much.