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Researchers from the University of Pittsburgh School of Medicine in Pennsylvania say they have discovered a mechanism which causes cancer activity to increase in head and neck cancer. The discovery may lead to new treatments for the disease.
Senior author of the study, Dr. Jennifer Grandis, says the team found that heightened activity of an oncogene (a gene that potentially causes cancer) called signal transducer and activator of transcription 3 (STAT3) may be a result of dysfunctional proteins that are meant to control the oncogene.
Their findings are published in the Proceedings of the National Academy of Sciences.
According to Dr. Grandis, previous research has found that increased signaling and activation of STAT3 is linked to poor cancer prognosis. She says that STAT3 prompts the production of other proteins that trigger cancer cell growth and survival.
But she notes that the cause of increased STAT3 signaling and activation has been unknown.
In order to determine what triggers increased STAT3 activity, the research team searched for mutations in a variety of proteins linked to the oncogene.
The investigators note that STAT3 must be phosphorylated in order to be activated. This is done by adding a phosphate group to the protein.
Some cancer drugs suppress enzymes called kinases that boost the phosphorylation process. But for this study, the researchers analyzed the opposite process, in which enzymes called phosphatases remove phosphates, therefore stopping the phosphorylation process and deactivating the proteins.
From this, the investigators were surprised to find that head and neck tumors that possessed increased STAT3 activity were linked to mutations in phosphatases that are a part of the PTPR (protein tyrosine phosphatase receptor) family.
The research team duplicated these mutations in both laboratory and computation models, and found that they caused phosphatases to become defected.
Explaining the findings, Dr. Grandis says:
"Because the phosphatases don't work properly, phosphate groups don't get removed from STAT3 appropriately, and it stays activated. These mutations essentially get rid of the brakes that might otherwise slow or even stop cancer development."
Dr. Grandis adds that it may be possible in the future to screen tumors for PTPR mutations, which could then be treated with drugs that hinder STAT3 activity.
In other news related to head and neck cancer, a study reported by Medical News Today in September 2013 suggested that dental cavities are linked to lower risk of the disease, while another study suggested that swallowing exercises help aid recovery from the cancer.
Written by Honor Whiteman
Copyright: Medical News Today
Not to be reproduced without the permission of Medical News Today.
Frequent mutation of receptor protein tyrosine phosphatases provides a mechanism for STAT3 hyperactivation in head and neck cancer, doi: 10.1073/pnas.1319551111, Vivian Wai Yan Lui, Noah D. Peyser, Patrick Kwok-Shing, Jozef Hritz, Yan Zeng, Yiling Lu, Hua Li, Lin Wan, Breean R. Gilbert, Ignacio J. General, Ivet Bahar, Zhenlin Ju, Zhenghe Wang, Kelsey P. Pendleton, Xiao Xiao, Yu Du, John K. Vries, Peter S. Hammerman, Levi A. Garraway, Gordon B. Mills, Daniel E. Johnson, and Jennifer R. Grandis, published in the Proceedings of the National Academy of Sciences, January 2014. Abstract
No ‘Brakes’ — Pitt Study Finds Mechanism for Increased Activity of Oncogene in Head and Neck Cancers, news release from the University of Pittsburgh School of Medicine, accessed 7 January 2014.
Visit our Cancer / Oncology category page for the latest news on this subject.
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