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Mobile phones can actually cause cancer: Study

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A man talks on his mobile phone in the village of Devmali in the desert state of Rajasthan, India June 14, 2016. REUTERS/Himanshu Sharma
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London, July 25,2015:  Your fears are not completely unfounded. Mobile phones can actually cause cancer, says a study.

A metabolic imbalance caused by radiation from your wireless devices could be the link to a number of health risks, such as various neuro-degenerative diseases and cancer, the study suggested.

This imbalance, also known as oxidative stress, is defined as “an imbalance between the production of Reactive Oxygen Species (ROS) and antioxidant defense” by the authors.

The hazardous effects of radiation from wireless devices could be realized through the “classical mechanisms” of oxidative impairments in living cells, the researchers said.

The study, published in the journal Electromagnetic Biology & Medicine, explored experimental data on the metabolic effects of low-intensity Radio Frequency Radiation (RFR) in living cells.

Study co-author Igor Yakymenko from the National University for Food Technologies said the oxidative stress due to RFR exposure could explain not only cancer, but also other minor disorders such as headache, fatigue, and skin irritation, which could develop after long-term exposure.

“These data are a clear sign of the real risks this kind of radiation poses for human health,” Yakymenko said.

“ROS are often produced in cells due to aggressive environments, and can also be provoked by ordinary wireless radiation,” he added.

In 2011, the International Agency for Research on Cancer classified RFR as a possible carcinogen for humans. But clear molecular mechanisms of such effects of RFR were a bottleneck in acceptance of a reality of risk.

Yakymenko and his colleagues call for a precautionary approach in using wireless technologies, such as cell phones and wireless internet. (IANS)

 

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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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