Activation of the Par-4 Extrinsic Pathway of rSuppression of Lung Cancer

Grants and Contracts Details

Description

Lung cancer deaths in women in the U.S. currently exceed those from breast cancer. Administration of estrogen during hormone replacement therapy (HRT) greatly increases the risk of lung cancer especially in women who smoke cigarettes. Despite a decrease in the overall cigarette use over the past decades, the incidence of lung cancer in women continues to increase at a steady pace. This risk may be due, in part, to the extent to which women can convert estrogen to carcinogenic metabolites. Systemic alterations associated with lung cancer risk following estrogen replacement therapy are not fully understood. We noted that levels of the tumor suppressor protein Par-4 are down-modulated by estrogen or smoking. As Par-4 is secreted by both normal and cancer cells but induces cell death selectively in cancer cells by binding to its cell surface receptor, we hypothesize that restoration of Par-4 levels in circulation will reduce the risk of lung cancer progression and metastasis. The objective of this study is to utilize diverse approaches to up-regulate and maintain adequate levels of Par-4 in circulation in animal models and test the effect on lung cancer progression associated with estrogen and cigarette smoke. We anticipate that the findings will have therapeutic significance and can be translated for treatment of lung cancer.
StatusFinished
Effective start/end date12/1/1011/30/13

Funding

  • KY Lung Cancer Research Fund: $150,000.00

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