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抗细胞生长因子药物在肿瘤治疗中的研究进展 总被引:1,自引:0,他引:1
肿瘤细胞的生长,一方面需要无限制的自分泌生长因子,刺激肿瘤细胞生长;另一方面旁分泌各种血管生成因子,刺激周围血管内皮细胞生长、新生血管形成,为肿瘤细胞的生长提供必要的养分. 相似文献
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成纤维细胞生长因子受体5(fibroblast growth factor receptor 5, FGFR5)是FGFR5家族中的一个新型受体,是由胞外区、穿膜区及胞内区构成的穿膜受体。然而,与其他经典FGFRs不同,其胞内区缺乏信号转导所必须的酪氨酸激酶,这一特征决定了其生物学功能有别于其他FGFRs。FGFR5激活时可抑制细胞增殖,促进细胞黏附和融合,提示该蛋白是一个潜在的抑癌因子,其分子机制有待进一步研究阐明。研究表明,FGFR5在肿瘤及非肿瘤疾病的发生发展中扮演了独特的角色。 相似文献
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碱性成纤维细胞生长因子与肿瘤 总被引:13,自引:0,他引:13
碱性成纤维细胞生长因子(bFGF)作为一种细胞丝裂原和促血管生成因子,在许多肿瘤的生长中起着重要的作用,许多实验研究提示肿瘤组织或患者体液中的bFGF水平能作为诊断或判断预后的指标,目前,阻止bFGF产生及抑其生物学活性的发挥,作为一种有效的抗肿瘤策略已得到广泛的发展,具有良好的应用前景。 相似文献
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表皮生长因子受体与酪氨酸激酶抑制剂在肿瘤防治中的应用进展 总被引:9,自引:0,他引:9
表皮生长因子受体(epidermal growth factor receptor,EGFR)信号传递系统可调控细胞周期,调节细胞生长与分化,促进损伤修复。EGFR在包括非小细胞肺癌(non-small-cell lung cancer,NSCLC)在内的多种上皮源性肿瘤中过表达预示存活率低、预后差、转移可能性大,可作为肿瘤基因治疗的靶位。酪氨酸激酶抑制剂(tyrosine kinase inhibitors,TKIs)可选择性抑制EGFR酪氨酸激酶活性,抑制肿瘤生长,增加放化疗敏感性。 相似文献
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靶向表皮生长因子受体的肿瘤生物治疗方法研究进展 总被引:5,自引:0,他引:5
肿瘤生物治疗(cancer biotherapy)已经成为继手术、放疗和化疗三大经典肿瘤治疗模式后的第四模式。在肿瘤生物治疗中,表皮生长因子受体(epidermal growth factor receptor,EGFR)靶点扮演着重要角色。EGFR为一种相对分子质量为170 000的酪氨酸蛋白激酶型受体,在多种恶性肿瘤存在过表达,在肿瘤发生、发展中起着重要作用。靶向EGFR的肿瘤生物治疗方法主要包括:基因沉默治疗、显性负性治疗、单克隆抗体(monoclonal antibody,McAb)治疗、生物“导弹”治疗、EGFR酪氨酸激酶抑制剂(EGFR tyrosine kinase inhibitor,EGFR TKI)治疗、双特异性抗体(bispecific antibody,BsAb)治疗方法等。目前靶向EGFR的肿瘤生物治疗研究已经取得较大进展,随着研究的进一步深入,肿瘤的治疗必将跨入一个全新的时代。 相似文献
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肺癌是全球第六大死因,也是恶性肿瘤的主要死因之一,非小细胞肺癌(non-small cell lung cancer,NSCLC)是其最常见的类型.表皮生长因子受体(epidermal growth factor receptor,EGFR)基因突变是NSCLC的常见突变之一.针对EGFR基因突变的晚期NSCLC患者,... 相似文献
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表皮生长因子受体在多种肿瘤中存在过度表达.在三苯氧胺耐药(TAM-R)的乳腺癌细胞中表皮生长因子受体(EGFR)的过度表达预示着肿瘤预后不良.研究乳腺癌TAM-R的机制及寻找克服耐药的方案十分重要.已有大量临床前研究显示EGFR信号通路的激活导致乳腺癌细胞产生TAM-R,临床上已有应用EGFR抑制剂于TAM-R乳腺癌的报道,但并非所有患者都能从中获益.EGFR抑制剂的原发或继发耐药是临床上遇到的新难题. 相似文献
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Activation of insulin-like growth factor I receptor signaling pathway is critical for mouse plasma cell tumor growth 总被引:7,自引:0,他引:7
Plasma cell neoplasia in humans generally occurs as multiple myeloma, an incurable form of cancer. Tumors with marked similarity can be induced in mice by a variety of agents, including chemicals, silicone, and oncogene-containing retroviruses, suggesting the use of murine tumors as an informative model to study plasma cell disease. Herein, we have focused on the role of insulin-like growth factor I receptor (IGF-IR) signaling in the development of plasma cell disease. The insulin receptor substrate 2/phosphatidylinositol 3'-kinase/p70S6K pathway was found to be either constitutively or IGF-I-dependently activated in all plasma cell tumors. Biological relevance was demonstrated in that plasma cell lines with up-regulated IGF-IR expression levels exhibited mitogenic responses to IGF-I. More importantly, expression of a dominant-negative mutant of IGF-IR in these lines strongly suppressed tumorigenesis in vivo. Taken together, these results demonstrate that up-regulation and activation of IGF-IR and the downstream signaling pathway involving insulin receptor substrate 2, phosphatidylinositol 3'-kinase, and p70S6K may play an important role in the development of a broad spectrum of plasma cell tumors. 相似文献
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人类表皮生长因子受体2(HER-2)是目前研究最为透彻的人类原癌基因之一.研究表明在人类乳腺癌、胃癌、卵巢癌及其它肿瘤中均存在HER-2过表达的现象,这种过表达使其成为药物研发中的理想靶点.与传统的化疗药物相比,靶向药物和抑制剂类药物,能更好地改善患者的预后,提高患者的生存率,安全性和有效性也更加明显.本文综述了HER-2阳性肿瘤靶向药物的研究现状及治疗进展,为HER-2相关药物开发和临床治疗提供有价值的参考. 相似文献
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Somatic mutations of epidermal growth factor receptor signaling pathway in lung cancers 总被引:14,自引:0,他引:14
Shigematsu H Gazdar AF 《International journal of cancer. Journal international du cancer》2006,118(2):257-262
Somatic mutations in the tyrosine kinase (TK) domain of the epidermal growth factor receptor (EGFR) gene in lung cancers have generated enormous interest, because they predict for sensitivity to TK inhibitors (TKIs). While mutational status is of great importance in determining response to TKIs, it is not the sole factor, and evidence is accumulating that EGFR gene amplification, other members of the EGFR family (HER2, HER3) and genes downstream of EGFR signaling (KRAS, BRAF), may be involved in cancer pathogenesis and the response of TKIs. EGFR mutations occur in highly selected subpopulations of lung cancer patients: adenocarcinoma histology, never-smoker status, East Asian ethnicity and female gender. The recent finding of "a resistance associated" mutation for TKIs also provides new insights into this complicated mechanism. Thus, molecular-based studies to analyze the biological functions and to assess TKI sensitivity depending on the type of mutations are required. Epidemiological studies to identify possible carcinogenic factor(s) affecting different subpopulations are also of interest. In addition, for optimal therapeutic approach a comprehensive understanding of the genes related to EGFR signaling pathway, including RAS/RAF/MAPK and PI3K-AKT pathways, are required. 相似文献
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