Photoletter to the editor: Giant cutaneous horn associated with squamous cell carcinoma.

A 90-year-old patient presented with a large cutaneous horn (cornu cutaneum) of nine-year duration arising at her right cheek. The lesion was removed by surgery. Histology was reported as cornu cutaneum with a well-differentiated squamous cell carcinoma at its base.

Soluble guanylyl cyclase activation improves progressive cardiac remodeling and failure after myocardial infarction. Cardioprotection over ACE inhibition.

Impaired nitric oxide (NO)-soluble guanylate cyclase (sGC)-cGMP signaling is involved in the pathogenesis of ischemic heart diseases, yet the impact of long-term sGC activation on progressive cardiac remodeling and heart failure after myocardial infarction (MI) has not been explored. Moreover, it is unknown whether stimulating the NO/heme-independent sGC provides additional benefits to ACE inhibition in chronic ischemic heart failure. Starting 10 days after MI, rats were treated with placebo, the sGC activator ataciguat (10 mg/kg/twice daily), ramipril (1 mg/kg/day), or a combination of both for 9 weeks.

p53 regulation by TRP2 is not pervasive in melanoma.

p53 is a central tumor suppressor protein and its inhibition is believed to be a prerequisite for cancer development. In approximately 50% of all malignancies this is achieved by inactivating mutations in the p53 gene. However, in several cancer entities, including melanoma, p53 mutations are rare.

Vemurafenib induces senescence features in melanoma cells.

A large proportion of human melanomas harbor a mutation leading to permanent activation of the serine/threonine kinase BRAF, and as a consequence, they have developed dependence on BRAF/mitogen-activated protein kinase signaling. Accordingly, BRAF inhibitors such as Vemurafenib show a good anti-tumorigenic effect on metastases with the BRAF(V600E) mutation. Although an initial period of sustained tumor regression is usually observed after Vemurafenib treatment, tumors often relapse at the same site, and apoptosis induction of melanoma cells in vitro is incomplete.