Olsen R J, Tarantolo S R, Hinrichs S H
Department of Pathology and Microbiology University of Nebraska Medical Center Omaha NE 69198-6495 USA.
Sarcoma. 2002;6(1):27-42. doi: 10.1080/13577140220127530.
Soft tissue sarcomas comprise a heterogeneous group of aggressive tumors that have a relatively poor prognosis. Although conventional therapeutic regimens can effectively cytoreduce the overall tumor mass, they fail to consistently achieve a curative outcome. Alternative gene-based approaches that counteract the underlying neoplastic process by eliminating the clonal aberrations that potentiate malignant behavior have been proposed. As compared to the accumulation of gene alterations associated with epithelial carcinomas, sarcomas are frequently characterized by the unique presence of a single chromosomal translocation in each histological subtype. Similar to the Philadelphia chromosome associated with CML, these clonal abnormalities result in the fusion of two independent unrelated genes to generate a unique chimeric protein that displays aberrant activity believed to initiate cellular transformation. Secondary gene mutations may provide an additional growth advantage that further contributes to malignant progression. The recent clinical success of the tyrosine kinase inhibitor, STI571, suggests that therapeutic approaches specifically directed against essential survival factors in sarcoma cells may be effective. This review summarizes published approaches targeting a specific molecular mechanism associated with sarcomagenesis. The strategy and significance of published translational studies in six distinct areas are presented. These include: (1) the disruption of chimeric transcription factor activity; (2) inhibition of growth stimulatory post-translational modifications; (3) restoration of tumor suppressor function; (4) interference with angiogenesis; (5) induction of apoptotic pathways; and (6) introduction of toxic gene products. The potential for improving outcomes in sarcoma patients and the conceptual obstacles to be overcome are discussed.
软组织肉瘤是一组异质性的侵袭性肿瘤,预后相对较差。尽管传统治疗方案能有效减少肿瘤总体积,但它们并不能始终实现治愈。有人提出了基于基因的替代方法,通过消除增强恶性行为的克隆畸变来对抗潜在的肿瘤发生过程。与上皮癌相关的基因改变积累情况相比,肉瘤的特征通常是在每个组织学亚型中独特地存在单一染色体易位。与慢性粒细胞白血病相关的费城染色体类似,这些克隆异常导致两个独立的不相关基因融合,产生一种独特的嵌合蛋白,该蛋白表现出被认为启动细胞转化的异常活性。继发性基因突变可能提供额外的生长优势,进一步促进恶性进展。酪氨酸激酶抑制剂STI571最近在临床上的成功表明,针对肉瘤细胞中基本生存因子的治疗方法可能有效。本综述总结了针对与肉瘤发生相关的特定分子机制的已发表方法。介绍了在六个不同领域已发表的转化研究的策略和意义。这些领域包括:(1)破坏嵌合转录因子活性;(2)抑制生长刺激的翻译后修饰;(3)恢复肿瘤抑制功能;(4)干扰血管生成;(5)诱导凋亡途径;(6)引入有毒基因产物。讨论了改善肉瘤患者预后的潜力以及需要克服的概念障碍。