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Медицинская библиотека · Oncology reports · 2005

Two different global gene expression profiles in cancer cell lines established from etiologically different oral carcinomas.

Ruutu Merja, Johansson Bo, Grenman Reidar, Syrjänen Stina

Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

cDNA arrays were used to characterize the gene expression profiles in 6 oral carcinoma cell lines (UT-SCC-10, UT-SCC-14, UT-SCC-37, UT-SCC-54A and UT-SCC-54B, UT-SCC-74) established from 5 patients with different etiological backgrounds, including young patients, classical risk factors and lichen-derived lesions. In addition, 2 human papillomavirus (HPV)-positive cell lines (hypophraryngeal cancer and HPV16 E6/E7-transformed oral keratinocytes) were similarly tested. Two distinct global gene expression profiles with down-regulated and up-regulated patterns were identified, which closely related to the etiologic backgrounds of the primary tumors. Typically in cluster analysis, interferon or interferon-related genes and T- and B-lymphocyte-related genes were up-regulated in lichen-derived carcinoma cell lines. Common to all carcinoma cell lines were 6 genes, which were up- or down-regulated (IgC mu heavy chain constant region, semaphorin, T-cell growth factor, cAMP-dependent protein kinase beta-catalytic subunit, desmocollin 1A/1B precursor and recA-like protein HsRad51). In HPV-positive cell lines, 13 genes were identified with similar down-regulation as shown in our previous studies on HPV-positive genital cell lines. Importantly, all of these genes were also down-regulated in 3 of the 6 oral cancer cell lines. These data suggest that oral carcinomas with different etiological backgrounds can be distinguished by their different global gene expression patterns.

Для цитирования: Ruutu Merja, Johansson Bo, Grenman Reidar, Syrjänen Stina. Two different global gene expression profiles in cancer cell lines established from etiologically different oral carcinomas.. Oncology reports. 2005.

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