Chakrabarti Susmita, Sengupta Shiladitya, Sengupta Arunava, Basak Saminendra Nath, Roy Anup, Panda Chinmay, Roychoudhury Susanta
Human Genetics and Genomics Division, Indian Institute of Chemical Biology, Kolkata, India.
Mol Carcinog. 2006 Apr;45(4):270-7. doi: 10.1002/mc.20178.
Intrinsic genomic instability of an incipient tumor cell drives the development of cancer. In colorectal cancer, an inverse relationship between microsatellite instability (MIN) and chromosomal instability (CIN) has been reported. The relationship between MIN and CIN in head and neck squamous cell carcinoma (HNSCC) is uncertain. In the present study, we examined these two types of instabilities in HNSCC using microsatellite markers and arbitrary primed PCR (APPCR) technique. HNSCC tumors showed high frequency of MIN and loss of heterozygosity (LOH). We observed that, in contrast to colorectal tumors, the frequency of LOH increased with the increase in MIN. There was no significant difference between MIN- and MIN+ groups of HNSCC tumors in the extent of overall genomic alterations; rather higher MIN+ tumors exhibited higher incidence of deletion. Thus, in sporadic HNSCC, both MIN and CIN pathways operate simultaneously to drive tumor formation.
初期肿瘤细胞的内在基因组不稳定性推动了癌症的发展。在结直肠癌中,已报道微卫星不稳定性(MIN)与染色体不稳定性(CIN)之间呈负相关。头颈部鳞状细胞癌(HNSCC)中MIN与CIN之间的关系尚不确定。在本研究中,我们使用微卫星标记和任意引物PCR(APPCR)技术检测了HNSCC中的这两种不稳定性。HNSCC肿瘤显示出高频率的MIN和杂合性缺失(LOH)。我们观察到,与结直肠肿瘤不同,LOH的频率随着MIN的增加而增加。HNSCC肿瘤的MIN-组和MIN+组在总体基因组改变程度上没有显著差异;相反,较高的MIN+肿瘤表现出更高的缺失发生率。因此,在散发性HNSCC中,MIN和CIN途径同时发挥作用以驱动肿瘤形成。