FAU physicians pinpoint genetic causes of tumours in ulcerative colitis
Researchers from Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) have discovered a protein which produces interleukin–6 (IL–6), a cytokine that promotes tumour growth. This insight could pave the way for a new therapy to prevent bowel tumours. The study has recently been published in the journal ‘Cancer Research’.
Ulcerative colitis is a chronic disease of the colon which usually occurs in recurrent attacks. The number of patients affected in Germany is estimated at approximately 168,000. Typical complaints are frequent diarrhoea with blood or mucus, pain in the left lower abdomen, permanent urge to defecate, fever and general physical weakness. As the inflammation of the colon proceeds, the symptoms become more pronounced and the risk of bowel cancer rises. So far, it has been impossible to identify the precise cause of the disease and the high probability of subsequent cancer despite worldwide research on the topic.
A group of researchers under the supervision of Dr. Benno Weigmann at the Medical Department 1 of the Universitätsklinikum Erlangen (University Hospital) has been carrying out research on the molecular factors causing ulcerative colitis for years. “We hope to gain a better understanding of the progression of the disease. Of particular interest is the question of why colon tumours frequently occur in the later stages of the disease,” says Benno Weigmann. “If we succeed, the chances for an effective therapy are very good.”
The group are focusing on NFAT transcription factors (a special family of proteins), especially NFATc2 which is important in the activation of T-cells and has been linked to ulcerative colitis before. FAU physicians have now succeeded in showing that NFATc2 also plays a role in the later development of colon tumours. “First, we were able to demonstrate an increased level of NFATc2 in patients’ colon tumours,” Benno Weigmann explains. “In subsequent experiments, we were able to prove that NFATc2 promotes tumours.”
NFATc2 controls apoptosis (programmed cell death) and cell proliferation. If there is insufficient NFATc2, many more cells die and degenerated cells are removed from the body much more quickly, preventing tumours from forming. NFATc2 controls the production of interleukin–6, which plays an important role in the development of cancer and facilitates metastases. With rising IL–6 levels in the patient’s serum, the risk of a tumour rises as well, which was also demonstrated by the research.
Identifying NFATc2 as key regulator of the tumour-promoting cytokine IL–6 was an important step in understanding the carcinogenesis of chronic inflammation processes. Dr. Weigmann and his colleagues hope that their findings will lead to a new form of therapy helping to prevent the development of tumours in patients with chronic bowel disease.
Further information for the press:
Dr. Benno Weigmann
uni | media service | research No. 30/2012 on 1.8.2012