Toschi Elena, Sgadari Cecilia, Monini Paolo, Barillari Giovanni, Bacigalupo Ilaria, Palladino Clelia, Baccarini Sara, Carlei Davide, Grosso Gabriella, Sirianni Maria C, Ensoli Barbara
Laboratory of Virology, Istituto Superiore di Sanità, 00161 Rome, Italy.
Anticancer Drugs. 2002 Nov;13(10):977-87. doi: 10.1097/00001813-200211000-00001.
Kaposi's sarcoma (KS) is an angioproliferative disease of multifactorial origin arising in different clinic-epidemiologic forms, which show the same histopathological features. It generally starts as a hyperplastic reactive-inflammatory and angiogenic process, which may evolve into monomorphic nodules of KS cells that can be clonal (late-stage lesions) and resemble a true sarcoma. Infection with the human herpesvirus 8, cytokine- and angiogenic factor-induced growth together with an immuno-dysregulated state represent fundamental conditions for the development of this tumor. Several local therapies are used to eradicate early and confined skin lesions, whereas widely disseminated, progressive or symptomatic disease requires a more aggressive treatment. Although different chemotherapeutic agents have been used to treat aggressive KS, the growing understanding of the pathogenetic factors participating in KS development has provided a strong rationale for using less- or non-cytotoxic agents that block the mechanisms involved in KS pathogenesis. The angiogenic nature of KS makes it particularly suitable for using therapies based on anti-angiogenic agents. Of note on this goal, recent studies indicate that the highly active anti-retroviral therapy, including at least one human immunodeficiency virus (HIV) protease inhibitor (PI), is associated with a dramatic decrease in the incidence of AIDS-KS and with a regression of KS in treated individuals. Consistent with this, results from preclinical studies indicate that PIs have potent and direct anti-angiogenic and anti-KS activities, suggesting that they should be further investigated, alone or combined with other therapies, as a novel treatment for KS in both HIV seropositive or seronegative individuals.
卡波西肉瘤(KS)是一种多因素起源的血管增生性疾病,以不同的临床 - 流行病学形式出现,但具有相同的组织病理学特征。它通常始于增生性反应性炎症和血管生成过程,可能演变为KS细胞的单形性结节,这些结节可以是克隆性的(晚期病变),类似于真正的肉瘤。人疱疹病毒8感染、细胞因子和血管生成因子诱导的生长以及免疫失调状态是该肿瘤发生发展的基本条件。几种局部治疗方法用于根除早期局限性皮肤病变,而广泛播散、进展性或有症状的疾病则需要更积极的治疗。尽管不同的化疗药物已被用于治疗侵袭性KS,但对参与KS发生发展的致病因素的深入了解为使用较少或无细胞毒性的药物提供了有力依据,这些药物可阻断KS发病机制。KS的血管生成特性使其特别适合使用基于抗血管生成药物的治疗方法。关于这一目标值得注意的是,最近的研究表明,包括至少一种人类免疫缺陷病毒(HIV)蛋白酶抑制剂(PI)的高效抗逆转录病毒疗法与艾滋病相关KS的发病率显著降低以及治疗个体中KS的消退有关。与此一致的是,临床前研究结果表明PI具有强大而直接的抗血管生成和抗KS活性,这表明它们应作为HIV血清阳性或血清阴性个体中KS的一种新治疗方法单独或与其他疗法联合进行进一步研究。