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Charles Shuler

Publications and source records attributed to Charles Shuler.

3 recordsLinked to original sources
PubMed2006

Expression of complement restriction factors (CD46, CD55 & CD59) in head and neck squamous cell carcinomas.

BACKGROUND: Tumor cells can escape complement-dependent cytotoxicity (CDC) by expressing complement restriction factors (CRFs), CD46, CD55 and CD59. CRF-expression in non-neoplastic mucosa of the head and neck was compared with biopsies of the head and neck squamous cell carcinoma (HNSCC) and cell lines derived from oral squamous cell carcinomas (OSCC). METHODS: Normal mucosa and HNSCC tumor tissue (poor, moderate, or well differentiated) specimens were immunostained with anti-CRF monoclonal antibodies. Immunostaining of the OSCC cell lines (SCC12 and SCC71) was examined under laser scan fluorescence microscopy. RESULTS: CD46, CD55 and CD59 were highly expressed in HNSCC cells including T1/T2N0M0 stages. The CRF expression was much lower or absent in non-neoplastic squamous epithelia or in the submucosa of both normal and tumor tissues. CONCLUSIONS: Enhanced staining of tumor tissues at stages T1/T2 indicates that the CRFs are overexpressed by primary tumors before metastasis to either lymph nodes or organs (N0M0 stage) suggesting that CRFs are formed early during tumorigenesis.

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PubMed2003

Microphthalmia resulting from MSX2-induced apoptosis in the optic vesicle.

PURPOSE: Microphthalmia is a relatively common ocular malformation. Molecular mechanisms that lead to this dire condition are largely unknown. Msx genes have been shown to be expressed in the developing eye. In the Msx1;Msx2, double mutant mouse, eye development arrests early in embryogenesis. To investigate possible functions of Msx2 in early ocular development, we created transgenic animals that overexpress Msx2. METHODS: Msx2 transgenic embryos and nontransgenic littermates were examined histopathologically. The effect of Msx2 overexpression on retinal cell proliferation was assayed by bromodeoxyuridine (BrdU) incorporation and immunohistochemical staining. Apoptosis was determined by TUNEL labeling. Expression of retina and retinal pigmented epithelium (RPE)-specific genes was investigated by performing in situ hybridization or immunohistochemical staining. RESULTS: Forced expression of the Msx2 gene resulted in optic nerve aplasia and microphthalmia in all transgenic animals. In developing retinas of Msx2 transgenic animals, proliferation was significantly reduced and increased numbers of retinal cells underwent apoptosis. Marker analysis showed suppression of Bmp4 and induction of Bmp7 gene expression in the optic vesicle. Ectopic concurrent expression of the RPE cell markers Cx43 and Trp-2 in the neural retinal layer suggests cell fate respecification. CONCLUSION: These results indicate that forced expression of Msx2 perturbs BMP signaling in the developing eye and is accompanied by an increase in retinal cell death and a reduction in cell proliferation. Thus, deregulated Msx2 gene expression may be a plausible genetic mechanism by which the autosomal dominant form of congenital microphthalmia may arise.

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