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Preclinical study identifies 'master' proto-oncogene that regulates ovarian cancer metastasis

g ovarian cancer tumor growth in response to stress hormones revealed the signaling pathway involved in NA-mediated Src activation. Specifically, they showed:

  • PKA (also known as cAMP-dependent protein kinase) is the switch that "turns on" NA-induced Src activation;
  • The signaling pathway occurs at a particular site on the cell known as S17; and
  • This specific mechanism is key to mediating ADRB/cAMP/PKA-induced Src activation.

Building on the Stress-Cancer Connection

For the past 13 years, Sood's research efforts have focused on the effects of chronic stress on cancer metastasis. The latest study helps form a more comprehensive picture on the impact of and biological mechanics of chronic stress on ovarian cancer, as well as the role of beta blockers in slowing disease progression. Previous studies have shown:

  • Chronic stress triggers a chain of molecular events that protects breakaway ovarian cells from destruction, as heightened levels of the fight-or-flight hormones epinephrine and norepinephrine permit more malignant cells to safely leave the primary tumor a necessary step in metastasis and cancer progression.

  • When mice with ovarian cancer are stressed, their tumors grow and spread more quickly, but the effect can be blocked using propranolol, a beta blocker commonly prescribed for heart disease.

Future research will focus on other biological mechanisms that may be affected by stress. Eventually, Sood hopes his studies will help identify the cancer patients most likely to benefit from beta blockers and other stress interventions. He is also looking at the impact of stress on other diseases, such as gastrointestinal disorders.

"This is a major step forward in understanding the biology and impact of stress on cancer progression and it opens the door to study drugs that could inhibit this unique signaling pathway," Sood said.

Contact: Scott Merville
University of Texas M. D. Anderson Cancer Center

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