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Eric or pericentromeric regions of the chromosomes, often resulting in isochromosome


Eric or pericentromeric regions of the chromosomes, often resulting Rosiglitazone in isochromosome formation or derivative whole-arm translocations involving the acrocentric chromosomes [Personal communication with Dr. Joyce L. Murata-Collins, Division of Anatomic Pathology, City of Hope, Duarte, CA]. Most notably, the partial deletion of chromosome 3 and the near-triploid karyotype of the clonal population are consistent with the HNSCCderived nature of this cell line [9]. Viral oncogene investigation detected no infection with either HPV or EBV. In this regard, 80-90 of nasopharyngeal carcinomas have been shown to be infected with EBV but very few (<1 ) of HNSCC are positive. An extensive literature report revealed only two cases of EBV + HNSCC and both cases were co-infected with HPV [21,22]. The EBV-negative characteristic of USC-HN1 further supports the origin of the tumor as a squamous and not a nasopharyngeal carcinoma. By contrast, 30 of HNSCC are infected with a subtype of HPV [12]. USC-HN1 represents a unique HPV-negative HNSCC cell PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/15501003 line inLiebertz et al. Head Neck Oncology 2010, 2:5 http://www.headandneckoncology.org/content/2/1/Page 13 ofthat it was derived from a patient who did not smoke tobacco or drink alcohol and does not have a family history of head and neck malignancies. Further characterization of the USC-HN1 cell line revealed a similar pattern of cytokine and chemokine expression compared to the pharyngeal carcinoma FaDu, a widely used HNSCC cell line. As previously reported HNSCC are highly immunomodulatory and alter their tumor microenvironment by the production of various cytokines [3]. The production of VEGFc has been correlated with increased metastatic potential in HNSCC [23], and USC-HN1 has shown a statistically increased production of VEGFc compared with FaDu. Importantly, with the exception of c-myc, the USC-HN1 cell line reveals statistically equivalent expression of proto-oncogenes and tumor-suppressor genes as FaDu and a cytokine expression profile different from FaDu, which will offer researchers yet another biomodel to study the microenvironment of HNSCC. Finally, the increased levels of activated, cleaved Notch1 found in USC-HN1 are indicative of its malignant potential, and although published reports imply various levels of Notch1 activity among HNSCC cell lines [24], it may serve as a future avenue for a new therapeutic approach since multiple trials of Notch1 inhibitors are in progress in patients with other tumor types [14]. Microarray analysis of USC-HN1 revealed a pattern of gene expression similar to HNSCC tumor samples previously reported [6]. In addition, specific up-regulated genes including CD24, E-cadherin, FABP5, keratins, heat shock protein (27 kDa), and others identified by microarray analysis were also identified by flow cytometry and immunostaining. These results support the origin of the cell line and further confirm the pathology as HNSCC.with the IHC studies, Dr. Clive Taylor for his assistance with microphotography, Dr. Dixon Gray for his help with the flow cytometry studies, and Mr. James Pang for performing the animal investigations. This work was supported in part by a grant from the American Type Tissue Collection and from funds provided by Cancer Therapeutics Laboratories, Los Angeles, CA. Author details 1 Department of Pathology, Keck School of Medicine of the University of Southern California, Los Angeles, CA 90033, USA. 2Department of Otolaryngology, Keck School of Medicine of the.

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