Researchers in Edinburgh have discovered how a molecular mechanism drives the growth of bile duct cancer, a rare form of the disease for which there are few treatment options.
The mechanism, known as the ‘Wnt’ pathway, is well-known to cancer
experts. It consists of a network of proteins that carry signals inside
cells. Experimental drugs that block it are already being tested in patients with other cancers. But the latest study, led by the University of Edinburgh, gives the
first indication that bile duct cancer may be particularly susceptible
to these drugs.
“Identifying the signals that control bile duct cancer’s growth will
allow us to design better treatments that are urgently needed,” said Dr
Luke Boulter, of the MRC Human Genetics Unit at the University of
Edinburgh, who led the research.
Plans are now in the pipeline to find out whether the drugs will be effective in patients.
“These drugs are being tested in clinical trials for other types of
cancer. The next step will be to find out if this treatment would
benefit patients with bile duct cancer. There are very few treatment
options for this disease, so research into new therapies is essential.”
Bile duct cancer, also known as cholangiocarcinoma, is a rare but
aggressive type of cancer that affects the network of tubes that carries
bile from the liver to the digestive system. It is often diagnosed at
an advanced stage, meaning it is very difficult to treat with surgery.
Around 2,100 people are diagnosed with bile duct cancer each year in the UK.
This site is for information on the various Chemo treatments and Stem Cell Therapies since 1992. This journey became bitter sweet in 2014, with the passing of my beautiful and dear wife. Sherry, had fought Non - Hodgkins Lymphoma(NHL) since 1990, in and out of remissions time and time again. From T-Cell therapies(1990's) to Dual Cord Blood Transplant(2014), she was in Clinical Trials over the years. This site is for informational purpose only and is not to promote the use of certain therapies.
Subscribe to:
Post Comments (Atom)
No comments:
Post a Comment