Partridge M, Kiguwa S, Langdon J D
Dept Oral and Maxillofacial Surgery, King's College School of Medicine and Dentistry, Denmark Hill, London, U.K.
Eur J Cancer B Oral Oncol. 1994 Jul;30B(4):248-51. doi: 10.1016/0964-1955(94)90006-x.
Evidence suggests that the accumulation of genetic lesions in dominant oncogenes and tumour suppressor genes is involved in the development of human cancers. We have used restriction fragment length polymorphism analysis to identify chromosomal deletions which may indicate the location of potential tumour suppressor genes. Deletion of chromosome 3p was found in 17/21 (81%) of informative primary oral squamous cell carcinoma (SCC) using a polymorphic probe recognising the D3F15S2 locus (3p21). Loss of heterozygosity (LOH) was not confined to patients exposed to recognised risk factors such as heavy smoking or alcohol consumption and was present at an early stage in the disease suggesting that this genetic alteration may be a fundamental event for oral cancer.
有证据表明,显性癌基因和肿瘤抑制基因中遗传损伤的积累与人类癌症的发生有关。我们利用限制性片段长度多态性分析来识别可能指示潜在肿瘤抑制基因位置的染色体缺失。使用识别D3F15S2位点(3p21)的多态性探针,在21例信息充分的原发性口腔鳞状细胞癌(SCC)中有17例(81%)发现3号染色体短臂缺失。杂合性缺失(LOH)并不局限于接触过大量吸烟或大量饮酒等公认风险因素的患者,且在疾病早期就已出现,这表明这种基因改变可能是口腔癌的一个基本事件。