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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Adenocarcinoma, Animals, Biological Assay, Blotting, Western, Cricetinae, Cyclic AMP, Cyclic AMP Response Element-Binding Protein, Extracellular Signal-Regulated MAP Kinases, Lung Neoplasms, Male, Mesocricetus, Models, Animal, Nitrosamines, Phosphorylation, Random Allocation, Retinoids, Signal Transduction, Time Factors, beta Carotene.
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Does beta-Carotene promote the development of NNK-induced small airway-derived lung adenocarcinoma? Context: beta-Carotene has shown cancer-preventive effects in preclinical studies while increasing lung cancer mortality in clinical trials. We have shown that beta-carotene stimulates cAMP signalling in vitro. Here, we have tested the hypothesis that beta-carotene promotes the development of pulmonary adenocarcinoma (PAC) in vivo via cAMP signalling. PAC was induced in hamsters with the carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), followed by beta-carotene for 1.5 years. Incidence, multiplicity and size of lung tumours were recorded, and phosphorylated CREB and ERK1/2 in tumour cells were determined by Western blots. Cyclic AMP in blood cells was analysed by immunoassays, retinoids in serum and lungs by HPLC. beta-Carotene increased lung tumour multiplicity, lung tumour size, blood cell cAMP, serum and lung levels of retinoids and induced p-CREB and p-ERK1/2 in lung tumours.
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Our data suggest that beta-carotene promotes the development of PAC via increased cAMP signalling. Final Decision: yes