Saturday January 25, 2020

New Robotic Tool to Detect, Kill Cancer Cells

In the later-stage cells, the stiffening response is not as strong as they are in the early stage, though both are seemingly similar, the researchers said

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Cancer
Cancer Ribbon. Pixabay

Canadian scientists have developed a kind of magnetic tweezer that can precisely insert a minuscule bead robot into a live human cancer cell, pointing to a new option for diagnosing and killing cancer.

The study, published in the journal Science Robotics, described the design in which a magnetic iron bead about 100 times smaller than the thickness of a human hair can be coaxed into any desired position within the cell, the Xinhua reported.

The bead, about 700 nanometres in diameter, is placed on the microscope coverslip surrounded by six magnetic coils in different planes, and the cancer cell can swallow the bead into its membrane.

Then, the researchers from University of Toronto controlled the bead’s position under a microscope, using a computer-controlled algorithm to vary the electrical current through coils and shaping the magnetic field in three dimensions.

The researchers used their robotic system to study early-stage and later-stage bladder cancer cells. Previously, they had to extract the cell nuclei to examine it.

The team measured cell nuclei in intact cells instead of breaking apart the cell membrane, showing that the nucleus is not equally stiff in all directions.

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)
Representational image. Pixabay

“It’s a bit like a football in shape. Mechanically, it’s stiffer along one axis than the other,” said Professor Sun Yu.

“We wouldn’t have known that without this new technique.”

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They were able to measure how much stiffer the nucleus got when prodded repeatedly, and thus find out which cell protein or proteins might play a role in controlling this response, which could work as a new method of detecting cancer in early stage.

In the later-stage cells, the stiffening response is not as strong as they are in the early stage, though both are seemingly similar, the researchers said.

Also, the team visualised using the tiny robots to either starve a tumour by blocking its blood vessels, or destroy it directly through mechanical ablation, although those applications are still a long way from clinical uses. (IANS)

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Drugs That Treat Arthritis in Dogs Can Kill Cancer Cells: Study

Drug for arthritis in dogs can fight cancer in people

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Cancer Cells
Drugs for diabetes, inflammation, alcoholism and even for treating arthritis in dogs can also kill cancer cells. Pixabay

Drugs for diabetes, inflammation, alcoholism — and even for treating arthritis in dogs — can also kill cancer cells in the lab, according to a new health news and study.

The researchers systematically analysed thousands of already developed drug compounds and found nearly 50 that have previously unrecognised anti-cancer activity.

The findings, which also revealed novel drug mechanisms and targets, suggest a possible way to accelerate the development of new cancer drugs or repurpose existing drugs to treat cancer.

“We thought we’d be lucky if we found even a single compound with anti-cancer properties, but we were surprised to find so many,” said study researcher Todd Golub from Harvard University in the US.

Cancer Cells
Most of the non-oncology drugs that killed cancer cells in the study did so by interacting with a previously unrecognized molecular target. (Representational Image). Pixabay

The study, published in the journal Nature Cancer, yet to employ the Broad’s Drug Repurposing Hub, a collection that currently comprises more than 6,000 existing drugs and compounds that are either FDA-approved or have been proven safe in clinical trials (at the time of the study, the Hub contained 4,518 drugs).

Historically, scientists have stumbled upon new uses for a few existing medicines, such as the discovery of aspirin’s cardiovascular benefits.

“We created the repurposing hub to enable researchers to make these kinds of serendipitous discoveries in a more deliberate way,” said study first author Steven Corsello, from Dana-Farber Cancer Institute and founder of the Drug Repurposing Hub.

The researchers tested all the compounds in the Drug Repurposing Hub on 578 human cancer cell lines from the Broad’s Cancer Cell Line Encyclopedia (CCLE).

Using a molecular barcoding method known as PRISM, which was developed in the Golub lab, the researchers tagged each cell line with a DNA barcode, allowing them to pool several cell lines together in each dish and more quickly conduct a larger experiment.

The team then exposed each pool of barcoded cells to a single compound from the repurposing library, and measured the survival rate of the cancer cells.

They found nearly 50 non-cancer drugs — including those initially developed to lower cholesterol or reduce inflammation — that killed some cancer cells while leaving others alone.

Some of the compounds killed cancer cells in unexpected ways.

“Most existing cancer drugs work by blocking proteins, but we’re finding that compounds can act through other mechanisms,” said Corsello.

Cancer Cells
The researchers tested all the compounds in the Drug Repurposing Hub on 578 human cancer cells lines from the Broad’s Cancer Cell Line Encyclopedia. (Representational Image). Pixabay

Some of the four-dozen drugs researchers identified appear to act not by inhibiting a protein but by activating a protein or stabilising a protein-protein interaction.

For example, the team found that nearly a dozen non-oncology drugs killed cancer cells that express a protein called PDE3A by stabilising the interaction between PDE3A and another protein called SLFN12 — a previously unknown mechanism for some of these drugs.

These unexpected drug mechanisms were easier to find using the study’s cell-based approach, which measures cell survival, than through traditional non-cell-based high-throughput screening methods, Corsello said.

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Most of the non-oncology drugs that killed cancer cells in the study did so by interacting with a previously unrecognized molecular target.

For example, the anti-inflammatory drug tepoxalin, originally developed for use in people but approved for treating osteoarthritis in dogs, killed cancer cells by hitting an unknown target in cells that overexpress the protein MDR1, which commonly drives resistance to chemotherapy drugs. (IANS)