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作 者:高春涛 赵天锁 陈靖 郝继辉 Gao Chuntao;Zhao Tiansuo;Chen Jing;Hao Jihui(Department of Pancreatic Cancer,Tianjin Medical University Cancer Institute and Hospital,Key Laboratory of Cancer Prevention and Therapy,National Clinical Research Center for Cancer,Tianjin 300060,China)
机构地区:[1]天津医科大学肿瘤医院胰腺肿瘤科,国家肿瘤临床医学研究中心,天津市“肿瘤防治”重点实验室,天津市恶性肿瘤临床医学研究中心300060
出 处:《国际生物医学工程杂志》2020年第4期324-329,共6页International Journal of Biomedical Engineering
摘 要:免疫治疗在肿瘤生物学研究中至关重要,并在肿瘤靶向治疗中取得了重大进展。B7-H3(CD276)是B7家族的一个免疫关卡抑制剂,与CTLA4、PD-1和CD28等许多免疫相关因子相互作用。尽管B7-H3的受体是什么尚不明确,但确定其在多种肿瘤中过度表达。起初,有研究结果认为B7-H3可协同刺激免疫反应,但最新的研究结果表明,其在T细胞上有协同抑制作用,从而导致肿瘤细胞的免疫逃避。因此,B7-H3的过度表达与肿瘤患者的预后不良有关,且在体外实验中已证实与肿瘤的侵袭和转移有关。此外,有结果表明,除了免疫调节作用外,B7-H3还能直接影响上皮恶性肿瘤进展。旨在描述不同恶性肿瘤中B7-H3的作用、与其他免疫因子的关系以及在恶性肿瘤进展中的非免疫学功能。在肿瘤治疗中靶向B7-H3可减少肿瘤细胞增殖、抑制肿瘤进展和转移,因此这可能会改善治疗方案和取得更好的临床治疗效果。Immunotherapy plays an important role in tumor biology research,and there has been significant progress in target therapy for cancer.B7-H3(CD276)is an immune checkpoint from the B7 family of molecules,many of whom interact with known checkpoint markers including CTLA4,PD-1,and CD28.This molecule is over-expressed in many kinds of tumors,although the receptor of B7-H3 has not been characterized.Initially,B7-H3 was thought to co-stimulate the immune response,but recent studies have shown that it has a co-inhibitory role on T-cells,contributing to cancer cell immune evasion.Therefore,its over-expression has been linked to poor prognosis in human patients and to invasive and metastatic potential of tumors in in vitro models.Moreover,recent evidence has shown that B7-H3 influences cancer progression beyond the immune regulatory roles.In this review,we aim to characterize the roles of B7-H3 in different cancers,its relationship with other immune checkpoints,and its non-immunological function in cancer progression.Targeting B7-H3 in cancer treatment can reduce cell proliferation,progression,and metastasis,which may lead to improved therapeutic options and better clinical outcomes.
关 键 词:B7-H3(CD276) 免疫关卡抑制剂 上皮恶性肿瘤 侵袭 迁移
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