A team of US engineers have developed a prototype wearable device that can continuously collect live cancer cells directly from a patient’s blood in an advance that could help patients avoid biopsy as well as get treatment for cancer more effectively.
Most cancer cells cannot survive in the bloodstream, but those that do are more likely to start a new tumour.
Typically, it is these satellite tumours, called metastases, which are deadly, rather than the original tumour. They can release more than 1,000 cancer cells into the bloodstream in a single minute.
This means cancer cells captured from blood could provide better information for planning treatments than those from a conventional biopsy, the researchers explained.
“Nobody wants to have a biopsy. If we could get enough cancer cells from the blood, we could use them to learn about the tumour biology and direct care for the patients. That’s the excitement of why we’re doing this,” said Daniel F. Hayes, Professor at the University of Michigan.
The wearable device contains a cell-grabbing chip, which in animal tests trapped 3.5 times as many cancer cells per millilitre of blood as it did running samples collected by a blood draw, according to the paper published in the journal Nature Communications.
The chip uses nanomaterial graphene oxide to create dense forests of antibody-tipped molecular chains, enabling it to trap more than 80 per cent of the cancer cells in the blood that flows across it.
It can also be used to grow the captured cancer cells, producing larger samples for further analysis.
The team estimates the device could begin human trials in three to five years. It would be used to help optimise treatments for human cancers by enabling doctors to see if the cancer cells are making the molecules that serve as targets for many newer cancer drugs. (IANS)
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.
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.
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.
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)