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头颈部鳞状细胞癌中的癌基因与肿瘤抑制基因

Oncogenes and tumour-suppressor genes in squamous cell carcinoma of the head and neck.

作者信息

Field J K

机构信息

School of Dentistry, University of Liverpool.

出版信息

Eur J Cancer B Oral Oncol. 1992 Jul;28B(1):67-76. doi: 10.1016/0964-1955(92)90016-t.

Abstract

Cancer is now considered to be a multi-hit process which involves a number of aberrant genetic events culminating in malignant transformation. In squamous cell carcinoma (SCC) of the head and neck the action of both oncogenes and tumour-suppressor genes has been identified during the course of the disease. Cytogenetic analysis of these carcinomas has demonstrated chromosomal breakpoints, particularly in the regions of 1p22 and 11q13 together with frequent amplification of the proto-oncogenes in the 11q13 amplicon; int-2, hst-1 and bcl-1. Ras mutations have been infrequently identified in the Western World whereas ras over-expression has been a common finding and may be associated with the early development of head and neck cancer. C-myc over-expression appears to correlate with a poor prognosis for these patients. The tumour-suppressor gene p53 is also thought to be involved in the development of SCC in head and neck tumours and its aberrant expression is associated with a history of heavy smoking and heavy drinking. E-cadherin, a putative tumour-suppressor gene is down-regulated in poorly differentiated head and neck SCC and maybe important in nodal metastasis. A recent study has indicated that the Human Papilloma Virus (HPV 16 and 33) has a role in the aetiology of tonsillar carcinomas and HPV has been shown to produce transforming proteins which bind to and inactivate the p53 tumour suppressor gene. This evidence suggests that the possibility of a viral mechanism for the development of SCC in the head and neck should be considered. This paper proposes a series of genetic events to explain the development of SCC of the head and neck.

摘要

癌症现在被认为是一个多步骤过程,涉及许多异常的基因事件,最终导致恶性转化。在头颈部鳞状细胞癌(SCC)中,在疾病过程中已确定了癌基因和肿瘤抑制基因的作用。对这些癌的细胞遗传学分析已证明存在染色体断点,特别是在1p22和11q13区域,同时11q13扩增子中的原癌基因(int-2、hst-1和bcl-1)频繁扩增。在西方世界,Ras突变很少被发现,而Ras过表达是常见现象,可能与头颈部癌的早期发展有关。C-myc过表达似乎与这些患者的预后不良相关。肿瘤抑制基因p53也被认为参与头颈部肿瘤中SCC的发生发展,其异常表达与大量吸烟和大量饮酒史有关。E-钙黏蛋白是一种假定的肿瘤抑制基因,在低分化头颈部SCC中表达下调,可能在淋巴结转移中起重要作用。最近的一项研究表明,人乳头瘤病毒(HPV 16和33)在扁桃体癌的病因学中起作用,并且已证明HPV产生与p53肿瘤抑制基因结合并使其失活的转化蛋白。这一证据表明,应考虑头颈部SCC发生发展的病毒机制的可能性。本文提出了一系列基因事件来解释头颈部SCC的发生发展。

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