Poorly differentiated adenocarcinoma arising from a cervical bronchial cyst.

Bronchogenic cysts with malignant change are rarely reported. We describe a case of poorly differentiated adenocarcinoma arising from a cervical bronchial cyst in a patient presenting with a thyroid mass, cervical lymphadenopathy, and initial biopsy suggestive of papillary thyroid carcinoma. The clinical presentation, intraoperative findings, radiographic images, and pathology slides are presented. To our knowledge, this is the first report of a poorly differentiated adenocarcinoma arising from a bronchial cyst in the cervical region.

Curcumin enhances the effect of cisplatin in suppression of head and neck squamous cell carcinoma via inhibition of IKKß protein of the NFκB pathway.

Previous experiments have shown that curcumin or cisplatin treatment suppresses growth of head and neck squamous cell carcinoma (HNSCC). To study the potential cooperative effect of both agents, two HNSCC cell lines were treated with curcumin or cisplatin alone or in combination. In vivo studies consisted of intravenous tail vein injection of liposomal curcumin, with intraperitoneal cisplatin, into nude mice growing xenograft HNSCC tumors. Introduction of curcumin and suboptimal concentrations of cisplatin showed a significant suppressive effect compared with treatment with either agent alone. Reduced expression of cyclin D1, IκBα, phospho-IκBα, and IKKß occurred in cisplatin- and curcumin-treated cell lines. Confocal microscopy showed expression of IKKß in the nucleus of the cell lines. Chromatin immunoprecipitation assay on DNA isolated from IKKß immunoprecipitated samples showed PCR amplification of interleukin-8 promoter sequences, a binding site of NFκB, indicating an interaction between IKKß and NFκB. Curcumin inhibited IKKß in the cytoplasm and nucleus, leading to reduced NFκB activity, with no effect on phospho-AKT. In vivo studies showed significant growth inhibition of xenograft tumors treated with a combination of liposomal curcumin and cisplatin. The suppressive effect of curcumin was mediated through inhibition of cytoplasmic and nuclear IKKß, resulting in inhibition of NFκB activity. Cisplatin treatment led to cellular senescence, indicating an effect mediated by p53 activation. The mechanisms of the two agents through different growth signaling pathways suggest potential for the clinical use of subtherapeutic doses of cisplatin in combination with curcumin, which will allow effective suppression of tumor growth while minimizing the toxic side effects of cisplatin.

Hemifacial microsomia.

Hemifacial microsomia is the second most common congenital facial anomaly, second only to cleft lip and palate. While its precise etiology is not yet known, it is likely caused by a disruption in the development of the first two branchial arches early in embryologic development. The resulting phenotype is one of varying degrees of unilateral hypoplasia of the mandible, ear deformity, and macrostomia. Early diagnosis of hemifacial microsomia is important not only to plan for surgical reconstruction of affected features, but also to lead the physician in further evaluation for associated abnormalities or disabilities. This article will introduce the reader to the most common variants seen in hemifacial microsomia, discuss the possible etiologies of the anomalies, and will highlight the importance of evaluating these patients early in life for such potentially disabling but correctable problems such as hearing loss, feeding disabilities, and neurological deformities.