Cancer-the most dreaded word in the English language. Americans have watched cancer statistics steadily rise to frightening proportions. We all know someone who has fought cancer and lost the battle. Healthy people, young people, athletes. No one is exempt from the rising cancer rate.
What is the common denominator linking those destined to develop malignant cells? Scientific speculation includes diet, exercise, environment, pollution, stress, genetics, and combinations of all these factors. Are the excesses of a modern society relative to the growing cancer rate? What is causing the national cancer rate to accelerate from one-in five, to one-in-four, to one-in-three, despite millions of dollars of research? Cancer treatment protocols are becoming more effective, but what about identifying specific causal relationships?
If scientists cannot identify specific causes, how can we hope to effect preventive measures? If the cancer rate continues to rise unchecked, are we, as a race, destined to develop cells which mutate in response to our changing society and environment? It is an issue that must be dealt with on a medical, psychological, and financial level.
Smoking has been positively linked to lung cancer, but what explains case histories of eighty year old men with a thirty-year history of smoking two packs a day of unfiltered cigarettes and no incidence of lung disease? Is it possible that we inherit the ability to ward off cancer? Do our genes protect us from malignancies that would develop in someone who did not possess the protective genes?
Pat Steeg, Chief of the Woman's Cancer Section at the National Institutes of Health is determined to answer these questions. She has been working literally night and day to prove that the gene she discovered eight years ago determines whether small malignant tumors will spread. She has had cancer herself, and knows the horrifying experience of living with a disease that territorially and diligently claims human tissue in its progressive path.
Dr. Steeg and her colleagues were studying skin cancers in mice when the gene was discovered. They were trying to determine the difference between tumors that spread and tumors that remained intact. They found a total of 24 genetic abnormalities related to metastasis of the original tumor. Of the 24 abnormalities identified, the 23rd revealed the most pro-found gene defect, the one they believed to be responsible for the spread of cancer cells. They named the gene NM-23.
Steeg discovered that in every mouse skin cancer that did not spread, the NM-23 gene was normal. In cancers that metastasized, the NM-23 gene was defective. It was obvious that the NM-23 gene was involved in preventing the metastatic process, but exactly how it worked was a mystery. Their hypothesis is that the gene is able to control the spread of cancer cells by acting like a sort of biological glue. When the activity of the NM-23 gene is turned off, tumor cells spread very quickly. When the gene is functional, the cancer cells stay glued together.
After pinpointing the exact gene responsible for halting the spread of cancer cells, Steeg set out to prove that actual transfection of the gene would turn metastasizing cells into ones that stuck to each other, thus preventing them from spreading through the body. A stationary cancer is much easier to treat than one constantly moving and growing. In some cases, the body's own immune system effectively eliminates small and stationary cancer cells.
Steeg's experiment involved transplanting working copies of the NM-23 gene into live metastasizing breast cancer cells. She implanted 40 mice with cancer cells that contained copies of the NM-23 gene. Another 40 mice received only the live cancer cells. Tumors developed in all 80 mice at the site the cancer cells were implanted. Steeg and her staff then waited an interminable four months to see if the tumors would spread equally in both groups of mice.
To determine the effectiveness of the "corrected gene", tissue-sample slides were prepared from each mouse. The cancer had spread in the mice who did not receive the NM-23 gene, while the mice who received cancer cells with the corrective gene showed only 10-50% as much metastatic disease. This starling data rep-resents a significant genetic breakthrough. Looking for the exact gene responsible for a minuscule genetic mistake is like trying to find one specific grain of sand on a ten-mile beach.
Our DNA is made up of literally billions of "letters". Clues that signal genetic mistakes hide within this megamass of letters. Gene Hunters are scientists trained to track down these well hidden clues. They look for markers in the chromosomes which indicate inherited disease. Detecting the altered genetic sequence would allow for early removal of malignant cells, cells that are so small they can be removed by simple needle biopsy. In breast cancer, for instance, it would mean saving the entire breas t by avoiding surgery, radiation, and chemotherapy as well as attendant physical and emotional scars.
If we can control inherited mutated genes, can we stop all forms of cancer from growing? No, because 90% of cancers are caused by gene mutation related to our environment.1 The leading causes may include smoking, herbicides and pesticides sprayed on the food supply, chemicals in the air and water, and radiation. The other 10% of cancers are genetically inherited. Dr. Steeg and other gene researchers have proven that the off/on switch for cancer cells is within us at all times and is found in the genes that program our cells.
Until methodologies are perfected which control the growth of cancer cells from gene defects or environmental causes, the best treatment is prevention. Given the vast amount of scientific data linking free radicals and cancer, it would be wise to adopt a sound preventive program that includes
Does Dr. Steeg's research mean that we have a cure for cancer? Unfortunately not. But the clinical application translates to a reduction in metastatic burden in breast cancer by 90%. Since the majority of cancer deaths are due to metastasis of the main tumor, slowing down the spread of cancer cells allows for an appreciable increase in long term survival time. Buying time also means that surgical removal of the main tumor could end the disease.
Pat Steeg's research has recently been published in the journal Oncogene,3 and has been presented at multiple conferences of the world's top cancer researchers. Hopefully, this accumulation of ground-breaking data will result in accelerated gene research and therapies that will be available to cancer patients. "I look for the day when we can custom design a treatment to the molecular characteristics of the tumor that each individual has" states Dr. Steeg.
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