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Cancer risks associated with X-rays, CT scans are only theoretical: Study

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New York: The widespread belief that radiations from X-rays and CT scans can cause cancer has flaws and is based on an unproven theoretical model, suggests a study.

To estimate cancer risk from low-dose radiation, scientists used a model known as linear no-threshold (LNT) in the study published in the American Journal of Clinical Oncology.

But risk estimates based on this model “are only theoretical and, as yet, have never been conclusively demonstrated by empirical evidence”, wrote researcher James Welsh from the Loyola University in Chicago.

The use of the LNT model drives unfounded fears and “excessive expenditures on putative but unneeded and wasteful safety measures”, Welsh noted.

In the LNT model, the well-established cancer-causing effects of high doses of radiation are extended downward in a straight line to very low doses.

The model dissuades many physicians from using appropriate imaging techniques and “discourages many in the public from getting proper and needed imaging, all in the name of avoiding any radiation exposure”, the researcher explained.

This model assumes there is no safe dose of radiation, no matter how small.

However, the human body has evolved the ability to repair damage from low-dose radiation that naturally occurs in the environment.

Studies of atomic bomb survivors and other epidemiological studies of human populations have never conclusively demonstrated that low-dose radiation exposure can cause cancer, according to the study.

Any claim that low-dose radiation from medical imaging procedures is known to cause cancer “should be vigorously challenged, because it serves to alarm and perhaps harm, rather than educate”, the scientists suggested.

The LNT model “should finally and decisively be abandoned”, the authors concluded. (IANS)(Photo: www.continentalhospitals.com)

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New Therapy for Drug-Resistant Skin Cancer Suggested by Researchers

A team of researchers has managed to exploit a vulnerability in melanoma or skin cancer that develops resistance to a targeted therapy, providing a potential new therapeutic strategy to selectively kill the drug-resistant cancer cells.

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The reason for increased bleeding is not known. It may be because rivaroxaban is more 'potent', the paper published in the Journal of Clinical Oncology said. (IANS)
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A team of researchers has managed to exploit a vulnerability in melanoma or skin cancer that develops resistance to a targeted therapy, providing a potential new therapeutic strategy to selectively kill the drug-resistant cancer cells.

The study has shown that when cancer cells develop drug resistance, they also acquire a new vulnerability, the Xinhua reported.

The researchers, led by Rene Bernards of the Netherlands Cancer Institute and Oncode Institute in Denmark, exposed this new vulnerability in melanoma that has developed resistance to treatment with a BRAF inhibitor — a targeted therapy that blocks a signalling pathway in the cancer cell through which it gets the message to keep on dividing.

Since more than half of all melanoma patients have a mutation in this BRAF gene, the BRAF-inhibitor stops tumour growth in those patients.

But within a few months, the tumour cell adapts the original signalling pathway and becomes active again, and even hyperactive.

The researchers, however, found that the hyperactive resistant melanoma cells produced large amounts of reactive oxygen species, but cancer cells still sensitive to the drug did not do so.

Combining the new compound with vitamin D allowed certain protective genes to be expressed at much higher levels than they are in diseased cells.
Representational image, pixabay

The study, published in the journal Cell, found that the abundance of free radicals caused the resistant melanoma cells to stop dividing, but they did not die.

When tested on mice along with an existing drug, vorinostat, which is known to stimulate the production of free oxygen radicals, the researchers saw tumours shrink under the influence of the drug, the report said.

This laid the foundation for a new therapeutic strategy: Treating patients with BRAF-mutated melanoma, as usual, with signal pathway inhibitors.

When the tumour becomes resistant, stop giving those inhibitors and immediately treat the patients with vorinostat to kill the resistant cancer cells.

Also Read: Leukemia Progression in Kids Can be Delayed Through Bone Density Treatment

“It is not a combination drug. It is very important that you first stop the signalling pathway inhibitors because they suppress the free radicals and thus eliminate the effects of vorinostat,” Bernards said. (IANS)

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