The following discovery can probably stir an air of excitement among scientists making attempts to tackle cancer. A latest study led by the University of Dundee has discovered the gene behind a rare skin cancer which grows rapidly for a few weeks before healing spontaneously. It was mentioned that patients suffering from multiple self-healing squamous epithelioma (MSSE) possibly have faults in a gene called TGFBR1.
During the investigation, DNA of more than 60 MSSE patients and 110 of their unaffected relatives was thoroughly evaluated. It then appeared that MSSE patients have faults in the TGFBR1 gene that makes a receptor protein through which healthy cells receive messages from their neighbors. These messages may instruct them to carry out tasks for growth and development. However, cells from a range of cancer types reportedly interpret the ‘instructions’ transmitted by TGFBR1 in two completely different ways, depending on the maturity of the tumor.
“The unusual behaviour of this tumour has baffled scientists for about 40 years so we’re excited to have discovered the genetic faults that cause the disease. The gene we’ve identified controls part of a cell signalling pathway which is faulty in many cancers. We hope that by shedding light on how one rare cancer manages to heal itself we’ll understand more about what goes wrong in other types of tumours. There’s also a lot of interest in drugs that target these signals. Understanding how tumours that lack TGFBR1 behave will help us to predict the clinical effects of these drugs,” enlightened Dr David Goudie, Cancer Research UK scientist in the College of Medicine, Dentistry and Nursing at the University of Dundee.
In the initial stages, TGFBR1 supposedly acts as a ‘brake’ preventing the growth of early tumors in various types. Once the cancers become more advanced and aggressive, their cells presumably go through a ‘signaling switch’. The same messages from TGFBR1 are purportedly interpreted by cancer cells in a different way. In more advanced cancers, TGFBR1 apparently promotes tumor growth and spread. This reverse allegedly occurs in the self-healing tumors that have an inherited fault in the TGFBR1 gene. Those with faulty TGFBR1 are believed to develop many small tumors, but at some point there is a ‘switch’ in behavior and the tumors lacking TGFBR1 heal themselves.
The study is published in Nature Genetics.