Abstract: Poster Presentations |


Peter J. Mazzone, MD*; Carol Farver, MD
Author and Funding Information

The Cleveland Clinic, Cleveland, OH


Chest. 2008;134(4_MeetingAbstracts):p156002. doi:10.1378/chest.134.4_MeetingAbstracts.p156002
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PURPOSE: AMP-activated protein kinase (AMPK) is a key cellular energy sensor. When cells are faced with energy stresses, such as in environments with low oxygen and/or glucose concentrations, AMPK functions to restore energy balance by inhibiting synthetic pathways and stimulating catabolic pathways. Activation of AMPK leads to phosphorlyation of acetyl-coA carboxylase. AMPK is the only upstream kinase for acetyl-coA carboxylase. Thus, detection of phosphorylated acetyl-coA carboxylase implies activation of AMPK. Tumor microenvironments are often hypoxic and deprived of glucose, conditions that lead to activation of AMPK. Controversy exists about the role of AMPK in cancer development. Some feel that activation inhibits tumor growth while others feel that activation of AMPK is necessary to protect cancer cells while they are finding means to receive their energy supply. We aimed to assess the prevalence of activated AMPK in lung adenocarcinomas that had undergone curative intent resection and to assess for differences in survival amongst those with and without activated AMPK.

METHODS: Immunohistochemistry staining of paraffin embedded tissue for phosphorylated acetyly-coA carboxylase was performed on resected lung adenocarcinoma specimens. Levels of activation were graded. Survival was compared for different levels of activation.

RESULTS: 69 resected stage I adenocarcinoma specimens were evaluated. 46% did not stain positive for activated AMPK, 22% had rare positivity, 25% were positive in <5% on the specimen, 4% in 5–50% of the specimen, and 3% in >50% of the specimen. Of those with any visible staining for activated AMPK 54% have survived at least 5 years from resection compared to 41% in those with no visible staining (p=0.2). Preliminary observation suggests increased staining in more well-differentiated areas of the tumor specimen (e.g. BAC, AAH).

CONCLUSION: Activated AMPK is found in at least 32% of early stage lung adenocarcinoma. The presence of AMPK activation did not affect survival. Increased AMPK activation may be seen in more well differentiated areas of the tumor.

CLINICAL IMPLICATIONS: Additional study to clarify the role of AMPK activation in tumor progression is warranted.

DISCLOSURE: Peter Mazzone, No Financial Disclosure Information; No Product/Research Disclosure Information

Wednesday, October 29, 2008

1:00 PM - 2:15 PM




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