OPCML Is a Broad Tumor Suppressor for Multiple Carcinomas and Lymphomas with Frequently Epigenetic Inactivation

Background: Identification of tumor suppressor genes (TSGs) silenced by CpG methylation uncovers the molecular mechanism of tumorigenesis and potential tumor biomarkers. Loss of heterozygosity at 11q25 is common multiple tumors including nasopharyngeal carcinoma (NPC). OPCML, located at 11q25, is one of the downregulated genes we identified through digital expression subtraction. Methodology/Principal Findings: Semi-quantitative RT-PCR showed frequent OPCML silencing in NPC and other common tumors, with no homozygous deletion detected by multiplex differential DNA-PCR. Instead, promoter methylation of OPCML was frequently detected in multiple carcinoma cell lines (nasopharyngeal, esophageal, lung, gastric, colon, liver, breast, cervix, prostate), lymphoma cell lines (non-Hodgkin and Hodgkin lymphoma, nasal NK/T-cell lymphoma) and primary tumors, but not in any non-tumor cell line and seldom weakly methylated in normal epithelial tissues. Pharmacological and genetic demethylation restored OPCML expression, indicating a direct epigenetic silencing. We further found that OPCML is stress-responsive, but this response is epigenetically impaired when its promoter becomes methylated. Ecotopic expression of OPCML led to significant inhibition of both anchorage-dependent and -indendent growth of carcinoma cells with endogenous silencing. Conlusions/Significance: Thus, through functional epigenetics, we identified OPCML as a broad tumor suppressor, which is frequently inactivated by methylation in multiple malignancies. © 2008 Cui et al.published_or_final_versio

Clinical, genomic, and metagenomic characterization of oral tongue squamous cell carcinoma in patients who do not smoke: Clinical and genomic study of nonsmokers with oral tongue cancer

Evidence suggests the incidence of oral tongue squamous cell carcinoma is increasing in young patients, many who have no history of tobacco use

Innervation options for gracilis free muscle transfer in facial reanimation

Gracilis free muscle transfer (GFMT) is considered the gold standard in dynamic smile reanimation in patients with long-standing facial paralysis. There are multiple motor nerves in the head and neck that can be used to provide innervation to the GFMT, either alone or in combination. In this article, we review the literature about these donor nerve options and discuss their advantages and disadvantages in terms of smile excursion, spontaneity, reliability, and timing. Furthermore, we discuss the use of multiple donor nerve sources in dually-innervated GFMT and areas for future investigation

Contemporary techniques for nerve transfer in facial reanimation

Nerve transfer procedures have the potential to restore innervation and function to the native facial musculature. This review summarizes the existing literature on facial nerve injury, regeneration, and reinnervation techniques with a focus on nerve transfer and its various options. Utilizing nerve transfer as early as possible, and ideally during the first 12 months of paralysis, is recommended. Prolonged paralysis is frequently not amenable to nerve transfer. The masseteric nerve provides excellent smile restoration after coapation to midfacial nerve branches with minimal morbidity. Several modifications to the hypoglossal nerve transfer have been described to limit its morbidity in speech and swallowing. The cross facial nerve, while appealing and able to achieve a true spontaneous smile, has limitations in terms of axonal load, time to reinnervation, unpredictable outcomes, and utility in older patients, who have less regenerative potential. Finally, there are exciting new developments in the field, combining reanimation techniques to harness advantages of various donor nerves, and research in peripheral nerve regeneration

MAGEB2 is Activated by Promoter Demethylation in Head and Neck Squamous Cell Carcinoma

Purpose: Although promoter hypermethylation has been an accepted means of tumor suppressor gene inactivation, activation of otherwise normally repressed proto-oncogenes by promoter demethylation has been infrequently documented