Sunday May 20, 2018

Indian-origin scientist Ravi Majeti, turns cancer cells into harmless cells

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By Anurag Paul

An Indian-origin researcher at the Stanford University in the US has found a method that can cause dangerous leukemia cells to mature into harmless immune cells known as macrophages.

Assistant professor of medicine Ravi Majeti made the key observation after collecting leukemia cells from a patient and trying to keep the cells alive in a culture plate.

During the study, Majeti and post-doctoral scholar Scott McClellan found that some of the cancer cells in culture were changing shape and size into what looked like macrophages.

The team confirmed that the methods shown to have altered the destiny of the mouse progenitor cells years ago could be used to transform these human cancer cells into macrophages which can engulf and digest cancer cells and pathogens.

“We were giving everything at them to help them hold out,” said Majeti in a report that appeared in the journal Proceedings of the National Academy of Sciences. B-cell leukemia cells are in many ways progenitor cells that are forced to stay in an immature state.

B-cell acute lymphoblastic leukemia with a variation called the Philadelphia chromosome is a especially aggressive cancer with poor results.

“So finding potential treatments is especially exciting,” Majeti added.

Majeti and his colleagues have some reason to hope that when the cancer cells become macrophages, they will not only be neutralized but may actually assist in fighting the cancer.

“Because the macrophage cells came from the cancer cells, they will already carry with them the chemical signals that will distinguish the cancer cells, causing an immune attack against the cancer more likely,” Majeti explained.

The researchers’ next steps would be to find out if they can discover a drug that will incite the same reaction and that could function as the groundwork for a therapy for the leukemia.

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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.
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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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