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乳头瘤病毒感染与肿瘤启动子的相似性。

Similarities of papillomavirus infections with tumor promoters.

作者信息

zur Hausen H

出版信息

Princess Takamatsu Symp. 1983;14:147-52.

PMID:6097579
Abstract

Papillomaviruses represent a group of small DNA-containing agents which differ in genetic organization and biological properties profoundly from other groups of viruses. Infection of cells of the basal cell layer by these viruses results in enhanced proliferation (papillomas) by retaining in part the differentiation pattern of normal cells. Virus production occurs in differentiated non-dividing cells of the stratum spinosum, granulosum, and corneum. Up to now the viruses cannot be propagated in tissue cultures. Cells induced to proliferation by papillomaviruses maintain the viral DNA frequently as free episomes in high copy number. The heterogeneity of the papillomavirus group has been revealed during the past few years. Presently 25 distinct types of human papillomaviruses have been characterized. Several animal and human systems have been reported in which papillomaviruses appear to contribute to malignant conversion. In most of these instances, besides infection by a specific type of papillomavirus, additional interaction with chemical or physical carcinogens (initiators) appears to be required. Papillomaviruses thus seem to reveal properties ascribed to tumor promoters. Moreover, clinical observations demonstrated an inhibition of papillomavirus infections by stage II inhibitors of tumor promotion, specifically by retionic acid. We investigated the role of papillomavirus infections in specific types of human cancer. Five types of papillomavirus infections (HPV 6, 10, 11, 16, and 18) were characterized in the human genital tract. HPV types 6, 10, and 11 were preferentially found in benign lesions (condylomate acuminata, cervical dysplasias), whereas HPV 16 prevails in malignant and in pre-malignant proliferations (cervical, vulval, and penile cancer, Bowenoid papulosis, Bowen's disease, carcinomata in situ).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

乳头瘤病毒是一类含小DNA的病原体,其基因结构和生物学特性与其他病毒组有很大差异。这些病毒感染基底细胞层的细胞后,部分保留正常细胞的分化模式,导致细胞增殖增强(形成乳头瘤)。病毒在棘层、颗粒层和角质层分化的非分裂细胞中产生。到目前为止,这些病毒无法在组织培养中繁殖。乳头瘤病毒诱导增殖的细胞常将病毒DNA作为游离附加体以高拷贝数形式保留。在过去几年中已揭示出乳头瘤病毒组的异质性。目前已鉴定出25种不同类型的人乳头瘤病毒。已有报道称在一些动物和人类系统中,乳头瘤病毒似乎与恶性转化有关。在大多数这些情况下,除了感染特定类型的乳头瘤病毒外,似乎还需要与化学或物理致癌物(启动剂)进行额外的相互作用。因此,乳头瘤病毒似乎具有肿瘤促进剂的特性。此外,临床观察表明,肿瘤促进II期抑制剂,特别是维甲酸,可抑制乳头瘤病毒感染。我们研究了乳头瘤病毒感染在特定类型人类癌症中的作用。在人类生殖道中鉴定出五种乳头瘤病毒感染类型(HPV 6、10、11、16和18)。HPV 6、10和11型主要见于良性病变(尖锐湿 疣、宫颈发育异常),而HPV 16型在恶性和癌前增殖病变(宫颈癌、外阴癌、阴茎癌、鲍温样丘疹病、鲍温病、原位癌)中占主导。(摘要截短于250字)

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