One word has the ability to change your life in an instant: cancer. Although those diagnosed with the disease can seek treatment and hope for remission, a cure remains elusive. However, a new study conducted by researchers from the Faculty of Medicine and Dentistry at the University of Alberta may have found a way to slow down cancer's rapid growth.

According to the Centers for Disease Control (CDC), cancer is a condition in which abnormal cells continuously divide and may potentially spread throughout the body. In the study, researchers discovered what they call an “off-switch” for cancer; a protein called TMX1 when in normal or high levels can slow down cancer’s fast spreading pace.

“Tumor tissue that is poor in TMX1 is expected to lead to more aggressive types of tumours,” said Thomas Simmen, the paper’s senior author and an associate professor in the department of cell biology at the University of Alberta, in a press release. TMX1 can be activated in normal cells via oxidative stress, and the level of the protein can help doctors determine the severity of an individual’s cancer.

“TMX1 is a biomarker for cancer progression: when it is high, more treatment options are available and the tumour is less aggressive. This allows chemotherapeutic drugs to activate the TMX1 switch and reduce tumour growth via oxidative stress. We will now investigate whether antioxidants could actually inactivate the TMX1 switch in cancer where this protein is still present, and would hence cause problems,” Simmen said in a press release.

Following this discovery, the Simmen laboratory began investigating why TMX1 levels change in tumour tissue and which stages this occurs. Simmen says for patients who are absent of their TMX1, new methods must be created to revive it to slow down the spread of cancer in a patient.

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Raturi A, Gutiérrez T, Ortiz-Sandoval C, Ruangkittisakul A, Herrera-Cruz M, Rockley J, Gesson K, Ourdev D, Lou P, Lucchinetti E, Tahbaz N, Zaugg M, Baksh S, Ballanyi K, Simmen T. TMX1 determines cancer cell metabolism as a thiol-based modulator of ER-mitochondria Ca2+ flux. Journal of Cell Biology. 2016