BackgroundChlamydia is a common bacterial pathogen responsible for many diseases. Methods for transforming this important organism using a β-lactamase as a selection marker have been developed very recently. However, the National Institutes of Health Guidelines for Research Involving Recombinant DNA Molecules do not permit transformation experiments with β-lactamase gene-containing vectors for certain human chlamydial pathogens. Therefore, a different selection marker is urgently needed for transformation of those chlamydiae.ResultsAfter transformation of plasmid-free Chlamydia trachomatis with pGFP:SW2, which carries a β-lactamase and a chloramphenicol acetyltransferase gene fused to a green fluorescence protein gene, transformants were obtained by selection with either ampicillin or chloramphenicol. Stable chloramphenicol-resistant, but ampicillin-sensitive, transformants were obtained using a pGFP:SW2 derivative without the β-lactamase. All transformants expressed green fluorescence protein and had glycogen synthesis activity restored.ConclusionsChloramphenicol resistance may be used as a selection marker for genetic experiments in Chlamydia. This eliminates the requirement for the use of β-lactamase, of which dissemination to some C. trachomatis serovars may jeopardize clinical treatment of chlamydial infections in pregnant women. Chloramphenicol acetyltransferase may also serve as a useful secondary selection marker for genetic analyses in β-lactamase-transformed chlamydial strains.

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In the past several decades obesity has become an increasingly problematic public health concern in developed countries. The strong correlation between high birth weights, obesity in adolescence and cancer is now evident. However, the molecular mechanism connecting obesity and cancer has yet to be elucidated. Here we review current literature investigating this relationship at both hormonal and biochemical levels. We also explore recent publications for novel cancer therapies that target pathways in which cancer manipulates host metabolism. The hormone leptin, which is upregulated in obese individuals, signals satiety and has been shown to play a role in signaling pathways promoting metastasis in a number of different cancers. Furthermore, leptin receptors are increased in some cancers and as a result these cells begin to utilize aerobic glycolysis for energy production as opposed to oxidative phosphorylation. Tumorigenic cells use alternative splicing to select for specific metabolic enzymes, which then serve as metabolic tools to promote tumor proliferation. A hypoxic environment can lead to the activation of AMP-activated protein kinase (AMPK), which in turn activates glycolytic machinery. It also upregulates transcription factors that promote tumor angiogenesis and allow sustained tumor growth. A more detailed understanding of metabolic aberrations due to obesity and their contribution to the onset of cancer is critical for the development of new therapies in the fight against both diseases.