London, April 15 (IANS) Cancer cells force neighbouring healthy tissue into helping with the disease’s growth and spread, a new study has found, shedding light on how cancer cells and normal cells communicate with each other.
The findings showed that cancer cells use an altered gene to persuade healthy cells to release unique growth signals, which cancer cells can use to multiply but cannot secrete them.
Also, the faulty versions of the KRAS gene – often altered in cancer – can have an important effect on healthy tissues.
Normal KRAS makes occasional signals that asks a cell to divide, but when altered the gene becomes hyperactive and helps drive cancer cells’ rapid and uncontrolled growth.
“What our research underlines is that cancer cells do not drive the growth and spread of tumours alone – they can bully their healthy neighbours into helping them,” said one of the researchers Chris Tape from The Institute of Cancer Research, in London.
Further, the altered KRAS gene also plays an important role in turning healthy ‘stromal cells’ — connective tissue cells of any organ — into cancer’s allies.
In addition, the researchers discovered that healthy cells were responding with a totally new message – a message that doubled the capacity for KRAS to drive malignant behaviour in the cancer cells.
They also recognised well-known pathways that KRAS uses to communicate with neighbouring healthy cells.
“We have discovered exactly how cancer cells can persuade stromal tissue to secrete key growth signals, and in doing so opened up exciting new possibilities for treatment,” Tape added.
The study, published in the journal Cell Scientists, showed for the first time that there is a communication loop with a cancer-causing gene controlling cancer via healthy stromal cells and opens up avenues for new approaches to cancer treatment.
“We have identified a key role played by the most commonly mutated gene in cancer in communicating with healthy cells. Blocking its effects could be an effective cancer treatment,” explained lead author Claus Jorgensen researcher at the University of Manchester.
The team studied communication networks in cells from a type of pancreatic cancer called pancreatic ductal adenocarcinoma – one of the most deadly forms of cancer.
KRAS is altered in more than 90 per cent of pancreatic cancer, and in nearly 20 per cent of all cancers.
The team studied thousands of different growth factors, proteins, and receptors across different pancreatic ductal adenocarcinoma cells to see how signals were being transmitted.
Implantable device may soon shrink pancreatic tumours in humans
Washington, April 15 (IANS) In pioneering research, researchers from Massachusetts Institute of Technology (MIT) and Massachusetts General Hospital have developed a small, implantable device that delivers chemotherapy drugs directly to pancreatic tumours.
In a study of mice, they found that this method was up to 12 times more effective than giving chemotherapy drugs by intravenous injection which is how most pancreatic cancer patients are treated.
The researchers are now preparing to design a clinical trial for human patients.
“It’s clear there is huge potential for a device that can localise treatment at the disease site,” says Laura Indolfi, post-doc in MIT’s institute for medical engineering and science (IMES).
“You can implant our device to achieve a localised drug release to control tumour progression and potentially shrink [the tumour] to a size where a surgeon can remove it,” Indolfi added.
The thin, flexible film could also be adapted to treat other hard-to-reach tumours.
The team engineered a flexible polymer film that is made from a polymer called PLGA widely used for drug delivery and other medical applications.
The film can be rolled into a narrow tube and inserted through a catheter, so surgically implanting it is relatively simple.
Once the film reaches the pancreas, it unfolds and conforms to the shape of the tumour.
“Because it’s very flexible it can adapt to whatever size and shape the tumor will have,” Indolfi noted.
Drugs are embedded into the film and then released over a pre-programmed period of time.
The film is designed so that the drug is only secreted from the side in contact with the tumour, minimising side effects on nearby organs.
The researchers compared two groups of mice carrying transplanted human pancreatic tumours.
One group received the drug-delivery implant loaded with the chemotherapy drug paclitaxel and the other received systemic injections of the same drug for four weeks which mimics the treatment human patients usually receive.
In mice with the drug-delivery implant, tumour growth slowed and in some cases, tumours shrank.
The localised treatment also increased the amount of necrotic tissue (dead cancer cells that are easier to remove surgically). Additionally, by acting as a physical barrier, the film was able to reduce metastasis to nearby organs.
“This combination of local, timed and controlled release, coupled with the judicious use of critical compounds, could address the vital problems that pancreatic cancer has provided as obstacles to pharmacological therapy,” says Elazer Edelman, the Thomas D. and Virginia W. Cabot professor of health sciences and technology at MIT.
The greatest benefit of this device is the ability to implant it with minimally invasive procedures so “we can give a tool to oncologists and surgeons to reach tumours that otherwise would be difficult to reach,” Indolfi pointed out in a paper reported in the journal Biomaterials.