Why the study?
Does clinical intervention of the renin-angiotensin pathway serve as an effective chemotherapeutic and/or chemopreventive modality for lung cancer?
Does clinical intervention of the renin-angiotensin pathway serve as an effective chemotherapeutic and/or chemopreventive modality for lung cancer?
Targeting the renin-angiotensin system may offer a novel chemotherapeutic or chemopreventive approach for lung cancer.
Answers are grounded in this paper and cite their sources.
RAS inhibition remains unproven for lung cancer; leaves open its role as a chemopreventive target pending trials.
Lung cancer is a leading cause of death in both men and women, with over 1,000,000 new cases diagnosed worldwide annually and a 5-year survival rate of only 14%, a figure that has improved little in the past thirty years. This poor prognosis suggests a need for novel approaches for the treatment and prevention of lung cancer. The reninangiotensin system is an established, primary regulator of blood pressure, homeostasis, and natriuresis; however, compelling evidence indicates that the angiotensin peptides also play a role in cell proliferation and inflammation. Angiotensin II is a vasoconstrictor, a mitogen, and an angiogenic factor, while angiotensin-(1-7) has vasodilator, antiproliferative, and anti-angiogenic properties. This review focuses on studies examining the renin-angiotensin system in pulmonary cancers and whether clinical intervention of this pathway may serve as an effective chemotherapeutic and/or chemopreventive modality for lung cancer.
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Gallagher et al. (2011) studied this question.
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