Do We Know What Causes Bile Duct Cancer?
We don’t know the exact cause of most bile duct cancers, but researchers have found several risk factors that make a person more likely to develop bile duct cancer (see the section “ What are the risk factors for bile duct cancer?”). There seems to be a link between this cancer and things that irritate and inflame the bile ducts, whether it’s bile duct stones, infestation with a parasite, or something else.
Scientists are starting to understand how inflammation might lead to certain changes in the DNA of cells, making them grow abnormally and form cancers. DNA is the chemical in each of our cells that makes up our genes – the instructions for how our cells function. We usually look like our parents because they are the source of our DNA. But DNA affects more than how we look.
Some genes control when cells grow, divide into new cells, and die. Genes that help cells grow, divide, and stay alive are called oncogenes. Genes that slow down cell division or cause cells to die at the right time are called tumor suppressor genes. Cancers can be caused by DNA changes (mutations) that turn on oncogenes or turn off tumor suppressor genes. Changes in several different genes are usually needed for a cell to become cancerous.
Some people inherit DNA mutations from their parents that greatly increase their risk for certain cancers. But inherited gene mutations are not thought to cause very many bile duct cancers.
Gene mutations related to bile duct cancers are usually acquired during life rather than being inherited. For example, acquired changes in the TP53 tumor suppressor gene are found in most bile duct cancers. Other genes that may play a role in bile duct cancers include KRAS, HER2, and MET. Some of the gene changes that lead to bile duct cancer might be caused by inflammation. But sometimes what causes these changes is not known. Many gene changes might just be random events that sometimes happen inside a cell, without having an outside cause.
Last Medical Review: November 1, 2014 Last Revised: January 20, 2016