Honjo Noriyasu, Gunduz Mehmet, Fukushima Kunihiro, Cengiz Beyhan, Beder Levent B, Gunduz Esra, Nagatsuka Hitoshi, Xiao Jing, Shimizu Kenji, Nishizaki Kazunori
Department of Otolaryngology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.
Otolaryngol Head Neck Surg. 2007 Jul;137(1):119-25. doi: 10.1016/j.otohns.2007.01.017.
We sought to assess loss of heterozygosity (LOH) profiles of 3p, 6q, 8q, 10q, 12q, 13q, and 17p and to identify the tumor suppressor genes involved in salivary gland neoplasms.
LOH analysis was performed using 26 microsatellite markers by polymerase chain reaction-polyacrylamide gel electrophoresis method in 20 benign and 6 malignant salivary gland tumors.
Overall, LOH was detected in at least one informative locus in 18 of 20 (90%) of benign tumors and in all of 6 cases of malignant tumors. High LOH frequencies were revealed at the loci D3S1307 (22%, 3p26), D3S966 (41%, 3p21), D6S255 (27%, 6q25), D8S166 (25%, 8q12), D8S199 (21%, 8q24), and D10S1765 (28%, 10q23) in benign tumors, defining the hotspot regions for putative tumor suppressor genes.
The hotspot regions defined by the present study suggest that new tumor suppressor genes related to the development of salivary gland tumors may reside at several chromosomal loci, including loci at 3p, 6q, 8q and 10q.
我们试图评估3p、6q、8q、10q、12q、13q和17p的杂合性缺失（LOH）图谱，并确定参与涎腺肿瘤的肿瘤抑制基因。
采用聚合酶链反应-聚丙烯酰胺凝胶电泳法，使用26个微卫星标记对20例良性和6例恶性涎腺肿瘤进行LOH分析。
总体而言，20例良性肿瘤中有18例（90%）在至少一个信息位点检测到LOH，6例恶性肿瘤均检测到LOH。在良性肿瘤的D3S1307（22%，3p26）、D3S966（41%，3p21）、D6S255（27%，6q25）、D8S166（25%，8q12）、D8S199（21%，8q24）和D10S1765（28%，10q23）位点发现高LOH频率，确定了假定肿瘤抑制基因的热点区域。
本研究确定的热点区域表明，与涎腺肿瘤发生相关的新肿瘤抑制基因可能存在于几个染色体位点，包括3p、6q、8q和10q位点。
