A new piece of medical technology unveiled by NPL will help improve the success rates of radiotherapy cancer treatments.
The new clinical electron linear accelerator (linac), a £1.5 million government-funded investment, will help ensure patients are treated with accurate doses of radiation.
Radiotherapy is used to treat cancer by using ionising radiation such as high-energy X-rays or electron beams to destroy cancer cells.
Every hospital needs to ensure that its radiotherapy equipment is stable and accurate because delivering correct radiation doses is critical.
If the dose is too low, the cancer may continue to grow. If they are too high, the patient may be endangered by healthy tissue being damaged.
NPL's new clinical linac’s ability to provide highly stable beams and accurate doses will enable calibrations with smaller uncertainties.
The new technology allows it to calibrate the full range of beam qualities currently in therapeutic use in the UK in a very short period of time. This will allow hospitals to deliver more accurate and effective radiation doses to cancer patients.
The new facility helps the UK respond to a recent report from the National Radiotherapy Advisory Group which states that the UK has a huge gap between the number of people treated with radiotherapy and optimal treatment levels.
For further information, please contact James Manning
Find out more about NPL's research in Ionising Radiation
Showing posts with label cancer hope. Show all posts
Showing posts with label cancer hope. Show all posts
Friday, July 29, 2011
Monday, June 6, 2011
Targeted cancer therapy kills prostate tumor cells
A new targeted therapy for prostate cancer halts tumor growth in animals with advanced prostate cancer that is resistant to hormone therapy, a new study finds.
The results will be presented Saturday at The Endocrine Society’s 93rd Annual Meeting in Boston.
“This targeted therapy may provide a treatment breakthrough that will extend the lives of men with advanced, hormone-refractory prostate cancer,” said lead investigator Shuk-mei Ho, PhD, chairwoman of the Department of Environmental Health at the University of Cincinnati.
Men with prostate cancer that has recurred or has spread outside the prostate routinely receive androgen deprivation therapy, which blocks the action of the male hormones.
This castration occurs through surgical removal of both testes or more often with medications. Although effective, this hormone-blocking treatment eventually stops working in some patients, Ho said.
“These patients are left with very few treatment options and usually succumb quickly to the disease,” she said.
Ho’s team previously found they can inhibit the growth of prostate cancer cell lines in culture by targeting and activating a protein called G protein-coupled receptor 30 (GPR30) using the experimental drug G-1, a GPR30 agonist, or stimulator.
In their new study, funded by the Veterans Affairs and the National Institutes of Health, Ho and her co-workers tested G-1 in an animal model of castration-resistant prostate cancer.
They implanted human prostate cancer cells beneath the skin of male mice. The established tumor regressed upon castration and after the cancer relapsed, they injected the mice with a low dose of G-1.
They also gave G-1 to noncastrated, or “intact,” male mice that had prostate tumors. In these intact mice that still had male hormones, G-1 did not stop growth of the prostate tumors or cause substantial death of tumor cells (necrosis), they found.
“Surprisingly, G-1 was highly effective in halting the growth of the tumors that re-emerged after castration,” Ho said.
The castration-resistant tumors showed a 65 percent necrosis. These mice had increased expression of GPR30 after castration, which Ho believes sensitised prostate tumors to the cell growth-inhibiting effects of G-1.
“These results mean G-1 won’t work without androgen deprivation therapy,” she said.
Therefore, Ho reported, the window of time when this targeted therapy might be effective for treating hormone-resistant prostate cancer is after androgen deprivation therapy.
She said she believes G-1 can make androgen blockade more effective. G-1 caused no harm to the prostate or other vital organs in mice, she added.
Although GPR30 may have a role in cell growth in female tissues, Ho said it appears to have the opposite effect in men with hormone-resistant prostate cancer.
“The beauty of this GPR30 is that it does not have any estrogen, and so it will not cause any estrogen related side effects.” she said.
The results will be presented Saturday at The Endocrine Society’s 93rd Annual Meeting in Boston.
“This targeted therapy may provide a treatment breakthrough that will extend the lives of men with advanced, hormone-refractory prostate cancer,” said lead investigator Shuk-mei Ho, PhD, chairwoman of the Department of Environmental Health at the University of Cincinnati.
Men with prostate cancer that has recurred or has spread outside the prostate routinely receive androgen deprivation therapy, which blocks the action of the male hormones.
This castration occurs through surgical removal of both testes or more often with medications. Although effective, this hormone-blocking treatment eventually stops working in some patients, Ho said.
“These patients are left with very few treatment options and usually succumb quickly to the disease,” she said.
Ho’s team previously found they can inhibit the growth of prostate cancer cell lines in culture by targeting and activating a protein called G protein-coupled receptor 30 (GPR30) using the experimental drug G-1, a GPR30 agonist, or stimulator.
In their new study, funded by the Veterans Affairs and the National Institutes of Health, Ho and her co-workers tested G-1 in an animal model of castration-resistant prostate cancer.
They implanted human prostate cancer cells beneath the skin of male mice. The established tumor regressed upon castration and after the cancer relapsed, they injected the mice with a low dose of G-1.
They also gave G-1 to noncastrated, or “intact,” male mice that had prostate tumors. In these intact mice that still had male hormones, G-1 did not stop growth of the prostate tumors or cause substantial death of tumor cells (necrosis), they found.
“Surprisingly, G-1 was highly effective in halting the growth of the tumors that re-emerged after castration,” Ho said.
The castration-resistant tumors showed a 65 percent necrosis. These mice had increased expression of GPR30 after castration, which Ho believes sensitised prostate tumors to the cell growth-inhibiting effects of G-1.
“These results mean G-1 won’t work without androgen deprivation therapy,” she said.
Therefore, Ho reported, the window of time when this targeted therapy might be effective for treating hormone-resistant prostate cancer is after androgen deprivation therapy.
She said she believes G-1 can make androgen blockade more effective. G-1 caused no harm to the prostate or other vital organs in mice, she added.
Although GPR30 may have a role in cell growth in female tissues, Ho said it appears to have the opposite effect in men with hormone-resistant prostate cancer.
“The beauty of this GPR30 is that it does not have any estrogen, and so it will not cause any estrogen related side effects.” she said.
Labels:
cancer hope,
drug therapy,
prostrate,
study,
treatment
Saturday, June 20, 2009
Drug-trial cancer patients recover: Magic Bullet found! Ipilimumab

Two men with advanced and inoperable prostate cancer have staged dramatic recoveries after being treated with an experimental antibody drug.
Both are now cancer-free and have returned to normal life after they took part in a trial of a drug called ipilimumab that boosts the immune system.
Before treatment at the Mayo Clinic in Rochester, Minnesota, US, each of them had aggressive tumours that had grown well beyond the prostate gland into abdominal areas.
Trial leader Dr Eugene Kwon said: "The goal of the study was to see if we could modestly improve upon current treatments for advanced prostate cancer.
"The candidates for this study were people who didn't have a lot of other options. However, we were startled to see responses that far exceeded any of our expectations."
First, the patients received traditional hormone therapy to remove testosterone, which fuels prostate cancer. Researchers then introduced a single dose of ipilimumab. The drug is an antibody which builds on the hormone therapy and boosts the immune system's response to the cancer.
Both patients saw their prostate specific antigen (PSA) levels drop to the point where they became eligible for surgery. PSA is a protein in the blood that allows doctors to monitor prostate cancer.
When the surgeons made their incisions, they had a surprise. Mayo clinic urologist Dr Michael Blute said: "The tumours had shrunk dramatically. I had never seen anything like this before. I had a hard time finding the cancer. At one point the pathologist asked if we were sending him samples from the same patient."
Further research is now planned to understand more about the mechanisms of the antibody and how best to use it on patients, but Dr Kwon added: "This is one of the holy grails of prostate cancer research. We've been looking for this for years."
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