An interesting pair of papers on tumour suppressor genes in colorectal cancer was just published in PLoS Biology. According to the researchers,
What does that mean in reality?
Well, essentially they may have found a master switch and activating a specific gene (Atoh1), which is common to fruit flies, mice and humans, may allow cancer to be "switched off".
Why colorectal cancer, you may ask?
The research demonstrated that colorectal cancer and Merkel cell carcinoma patients show genetic and epigenetic ATOH1 loss-of-function mutations, meaning that switching off the ATOH1 gene function lead to cell differentiation and growth of those tumours. In addition, mice lacking ATOH1 developed bowel cancer, and the gene was also frequently inactivated in human patients with the disease.
Time will tell, but undoubtedly new compounds will be developed targeting the oncogene to re-activate it and slow down tumour progression to determine whether the basic research offers
proof of concept in human cancer. In a few years time, we may even see some therapeutic developments in Pharmaceutical pipelines targeting ATOH1 as a viable and valid target in human colorectal cancer.
Wouter Bossuyt, Avedis Kazanjian, Natalie De Geest, Sofie Van Kelst, Gert De Hertogh, Karel Geboes, Greg P. Boivin, Judith Luciani, Francois Fuks, Marinee Chuah, Thierry VandenDriessche, Peter Marynen, Jan Cools, Noah F. Shroyer, Bassem A. Hassan (2009). Atonal homolog 1 Is a Tumor Suppressor Gene PLoS Biology, 7 (2) DOI: 10.1371/journal.pbio.1000039
Wouter Bossuyt, Natalie De Geest, Stein Aerts, Iris Leenaerts, Peter Marynen, Bassem A. Hassan (2009). The Atonal Proneural Transcription Factor Links Differentiation and Tumor Formation in Drosophila PLoS Biology, 7 (2) DOI: 10.1371/journal.pbio.1000040