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Cancer research: Breakthrough achieved?
In what could be a breakthrough, researchers say that increasing our understanding of genes may make it possible for them to eventually develop ways of stopping many people at increased risk of bowel cancer from developing the disease altogether.

SCIENTISTS FROM the Institute of Cancer Research and the London Research Institute of Cancer Research, UK have identified and isolated two stretches of genetic code that, they hope, could provide a breakthrough in cancer research. The genetic mutations detected by them can play a significant role in successful treatment of bowel cancer. Organs of the large bowel form the alimentary canal of the digestive system, which is somewhat like a sewage treatment system. Lying between the cecum and rectum, they are subjected to the dirtiest and most corrosive environment. Over a period of time, a type of tumour-like growth called polyps develops on the inner walls of ascending colon, descending colon and sigmoid colon. Sometimes, they start bleeding painfully and may turn cancerous.

 

The life sciences journal Nature Genetics reports the finding of the scientists who detected two areas near specific genes that strongly influence the risk of cancerous polyps. The two genes individually do not create any trouble. When one of them is present alone, its effect is quite insignificant. However, in cases when either of them combines with two other high-risk genetic variants, the risk of developing bowel cancer increases dramatically to three times the average population.

 

According to Dr Lesley Walker, Director of Cancer Information of Cancer Research, UK, the organisation has launched a series of genome-wide studies, including searches for genes that influence cancer risk. About 8,000 cancer patients were followed up as part the study. “Increasing our understanding of genes like this may make it possible for scientists to eventually develop ways of stopping many people at increased risk of bowel cancer from developing the disease altogether,” claims joint lead researcher Professor Ian Tomlinson.

 

Critics of the huge funds channelled to genetic research out of the total available funds consider the isolation of the ‘cancer-causing genes’ a non-solution. According to Dr Lorriman, the main problem is not genes but the excessive consumption of substances for which human beings are not designed. He says, “Before we turn to genes, and the ‘non-solution’ they offer, we should concentrate on items that affect our immune system.”  Cancers are supposed to be mopped up by the immune system and they thrive when the system is compromised. Diet research scientists say that today’s foods are a major cause of such compromise. The original ‘hunter-gatherer diet’ ensured the maximum compatibility to man’s immune system. When humans took up farming as a source of food, diet moved 90 degrees away from the optimum immune resistance. Farmers’ manipulations caused even fruits in ‘agro diet’ to become laden with sugar. Today’s ‘industrial diets’ are removed 180 degrees away from the optimal. Immuno-suppressing vegetable oils like sunflower oil, forming part of modern diet have almost completely destroyed the capacity of resisting cancer.

 

Genetic scientists counter this by pointing out that to turn back to ‘original’ diet is unimaginable whatever the merits of such a diet are. So, all that is left is genetic improvement to fit our new lifestyle. Apart from genetically modifying the food sources to suit us, scientists are now concentrating on improving our genes to adapt us to pollution and disease.  Researchers specialising in molecular medicine and immunology at Mayo Clinic have reported a milestone in this direction. They used the body’s own cells and a virus to destroy cancer cells, which take a tumour from its origin to other parts of the body.

 

While primary tumours cause discomfort and some pain, the growth of secondary tumours, a process called metastasis, is very painful and is almost fatal. Metastasis is carried out through the lymphatic system, which consists of the bone marrow, spleen, thymus and lymph nodes. Like the circulatory system with its arteries and veins, the lymphatic system is spread throughout the body with lymph vessels.  The Mayo Clinic-led study, spearheaded by principal investigator Dr Richard Vile, hypothesized that the spread of cancer could be controlled through the lymphatic system by manipulating the immune system. The scientists first studied the threats faced by the immune system when it delivers cancer-destroying virus to the tumour. They concentrated on immature T-cells from bone marrow and programmed them to respond to specific threats.

 

T-cells were removed from a healthy mouse. They were loaded with the virus and injected back into the mouse. The virus was observed to detach itself from the T-cells when it returned to lymph nodes and spleen. These virus-loaded cells selectively replicated within tumour cells, extracting tumour cells from those areas. Dr Vile summarized the results from the study: “If you kill tumour cells directly in the tumour itself, you can get a weak immunity against the tumour. But, if you use this virus to kill tumour cells in the lymph nodes, you get a higher immunity against the tumour.”

 

Although studies so far have been limited to the mouse, the technology is relatively easy to translate to humans. Taking T-cells from the patient and injecting them back is already in vogue. Radioactive tracers are attached to the T-cells before re-injecting, as a diagnostic method to find the source of infection in patients.  Dr Vile says, “Taking T-cells from the patient is  something routinely done today – loading them with this virus and then putting those T-cells back (should help) patients whose cancer has spread to lymph nodes, who are at high risk of the cancer spreading to other parts of the body or who are at high risk of succumbing to the cancer.”

 

Scientists are hoping to translate the results into clinical trials. However, until those trials are done, it is difficult to be certain that the phenomenon seen in mouse models will clearly translate to humans. Dr Vile told Nature Medicine, “We’re hopeful that will be the case.”

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