Background: The incidence of cutaneous squamous cell carcinoma (cSCC) continues to increase, and it is now predicted that the number of deaths from cSCC will surpass that of melanoma within the next 5 years. Although most cSCCs are successfully treated, there exists an important subset of high-risk tumors that have the highest propensity for local recurrence (LR), nodal metastasis (NM), and disease-specific death (DSD).
Objective: We investigated the clinical outcomes of high-risk cSCCs treated with Mohs surgery (MS) alone, analyzing LR, NM, distant metastasis, and DSD.
The MYC oncogene is dysregulated in most human cancers and hence is an attractive target for cancer therapy. We and others have shown experimentally in conditional transgenic mouse models that suppression of the MYC oncogene is sufficient to induce rapid and sustained tumor regression, a phenomenon known as oncogene addiction. However, it is unclear whether a therapy that targets the MYC oncogene could similarly elicit oncogene addiction.
View Article and Find Full Text PDFNevus lipomatosus cutaneous superficialis (NLCS) is an idiopathic hamartomatous condition characterized by the presence of mature adipose tissue in the dermis. We report a case of NLCS initially misdiagnosed as condyloma acuminata in a 14-year-old boy. This case highlights classic clinical and histologic features of NLCS.
View Article and Find Full Text PDFAn increased number of melanocytic nevi and lentigines have been reported in patients with two types of autosomal recessive congenital ichthyosis (ARCI): lamellar ichthyosis and nonbullous congenital ichthyosiform erythroderma. These melanocytic lesions may have clinical and dermoscopic features of atypia, necessitating close surveillance. Here, we report two interesting cases of pediatric patients with harlequin ichthyosis (HI) who developed increased melanocytic nevi and lentigines.
View Article and Find Full Text PDFMYC is a potential target for many cancers but is not amenable to existing pharmacologic approaches. Inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase) by statins has shown potential efficacy against a number of cancers. Here, we show that inhibition of HMG-CoA reductase by atorvastatin (AT) blocks both MYC phosphorylation and activation, suppressing tumor initiation and growth in vivo in a transgenic model of MYC-induced hepatocellular carcinoma (HCC) as well as in human HCC-derived cell lines.
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