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Ever since the FDA's April approval of Viagra, the little blue pill giving insurance companies a headache, the media have been infatuated with male impotence and its potential cure. U.S. pharmacists dispensed more than 215,000 Viagra prescriptions within the first four weeks of availability, sending manufacturer Pfizer Inc.'s stocks soaring and journalists buzzing. Everyone from porn magazine editors to former presidential hopefuls have expounded upon the supposed sociocultural impact of a wonderdrug clinically proven to, shall we say, make man's best friend stand up and salute the flag. use of cialis

other medicines that treat high blood pressure discount cialis about cialis and cialis typesSetting The Record Straight: Erectile DysfunctionThe RAS/RAF/mitogen-activated protein kinase and extracellular signal–regulated kinase (ERK) kinase (MEK)/ERK signaling pathway couples signals from cell surface receptors to transcription factors and regulates cell fate downstream of receptor tyrosine kinases, cytokines, and heterotrimetric G-protein–coupled receptors.1 Melanoma is a major public health problem, particularly in the Western world,2 with 76?000 estimated new cases in the United States in 2012.3 The biological mechanism underlying melanoma development is complex, with the RAS/RAF/MEK/ERK pathway playing a key role in melanoma cell proliferation and survival.1 Hyperactivation of ERK has been found in most human melanomas, commonly regulated through BRAF (OMIM *164757) or NRAS (OMIM *164790) somatic mutations.1,4 Approximately 50% of melanoma tumors have BRAF mutations (mostly V600E mutation), leading to elevated kinase activity.5,6 Drugs inhibiting this pathway, particularly targeting BRAF, have shown therapeutic efficacy.6,7 The cyclic guanosine monophosphate (cGMP)–specific phosphodiesterase (PDE) 5A was recently demonstrated as a downstream target of BRAF.8,9 Through the MEK/ERK cascade, activated BRAF down-regulates PDE5A, which lowers cGMP degradation and leads to an increase in intracellular calcium ion Ca2+, triggering invasion and metastasis of melanoma cells.8- 11 In contrast, rescuing expression of PDE5A in melanoma cells decreased their invasiveness.8 Down-regulation of PDE5A was also seen in NRAS-mutant cell lines, indicating that activation of mitogen-activated protein kinase signaling leads to PDE5A down-regulation in melanoma cell lines, irrespective of genetic background.8 Phosphodiesterase 5A is the target of sildenafil citrate, commercially known as Viagra, which has been widely prescribed for erectile dysfunction (ED).12,13 Treatment with sildenafil and other PDE5A inhibitors can promote melanoma cell invasion, particularly in the BRAF-mutated melanoma cell lines.8 This indicates that PDE5A suppression by sildenafil use mimics an effect of BRAF/NRAS activation and thus may potentially function as one of the “hits” for melanomagenesis. Most recently, 2 PDE5 inhibitors were shown to promote melanin synthesis,14 which may exacerbate melanoma development.15 These pieces of evidence prompted our hypothesis regarding the potential link between sildenafil use and melanoma.16 Hearing loss

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