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MOLECULAR EPIDEMIOLOGY OF AIDS-ASSOCIATED LYMPHOMA

MOLECULAR EPIDEMIOLOGY OF AIDS-ASSOCIATED LYMPHOMA
艾滋病相关淋巴瘤的分子流行病学
批准号:
2428981
负责人:
OTONIEL MARTINEZ-MAZA
金额:
$26.42万
依托单位国家:
美国
项目类别:
财政年份:
1997
资助国家:
美国
项目状态:
已结题
起止时间:
1997-09-30 至 2001-08-31

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中文摘要
翻译
描述(改编自摘要):非霍奇金B细胞淋巴瘤是 在获得性免疫缺陷综合征中, (艾滋病)和感染人类免疫缺陷病毒(HIV)。在 本申请,主要研究者提出研究,以阐明 艾滋病淋巴瘤的分子流行病学。在初步工作中, 主要研究者发现,血清sCD 23水平升高,以及 其他免疫系统分子(IgE,sCD 27)水平升高,先于 艾滋病淋巴瘤的外观。此外,sCD 23水平升高, 在艾滋病淋巴瘤之前,可能是由于肿瘤产生这种分子 细胞在拟定的研究中,研究者和同事将检测 假设sCD 23(和其他分子)的过度表达, 艾滋病之前的淋巴瘤反映:(1)免疫功能障碍导致B细胞 过度激活和增强的IG同种型转换,可能有助于 这种癌症中常见的c-myc:IG基因染色体易位,或 或者,(2)这些物质(sCD 23和其他)的产生 分子)的淋巴瘤细胞本身,或(3)EBV的再活化 感染此外,他们还将检查表达式的预测值 艾滋病淋巴瘤的这些分子,以及这些分子的表达 与艾滋病毒感染无关的淋巴瘤,包括非洲流行病 伯基特淋巴瘤。其具体目标是:(1)确定 sCD 23在AIDS淋巴瘤出现前的表达;(2) 确定/确认哪些免疫系统分子,除了sCD 23, (3)在发展艾滋病淋巴瘤的人中升高;(3)确定 测量血清中除sCD 23以外的分子水平, 预测艾滋病淋巴瘤出现的额外信息;以及 (4)确定sCD 23或其他免疫系统分子是否升高, 与HIV感染无关的非霍奇金B细胞淋巴瘤,或 血友病患者的艾滋病淋巴瘤这些具体目标的实现 将为我们对分子生物学的理解提供有价值的新信息, 艾滋病-淋巴瘤的流行病学,以及免疫功能障碍在 这种癌症的产生和发展。
英文摘要
DESCRIPTION (adapted from the Abstract): Non-Hodgkin's B-cell lymphoma is seen in greatly-elevated frequency in the acquired immunodeficiency syndrome (AIDS) and in infection with the human immunodeficiency virus (HIV). In this application, the Principal Investigator proposes studies to elucidate the molecular epidemiology of AIDS-lymphoma. In preliminary work, the Principal Investigator found that elevated serum levels of sCD23, as well as elevated levels of other immune system molecules (IgE, sCD27), precede the appearance of AIDS-lymphoma. Also, the elevated levels of sCD23 seen to precede AIDS-lymphoma may be due to the production of this molecule by tumor cells. In the proposed studies, the Investigator and associates will test the hypotheses that the over-expression of sCD23 (and other molecules) that precedes AIDS-lymphoma reflects: (1) immune dysfunction leading to B-cell hyper-activation and enhanced Ig isotype switching, perhaps contributing to the c-myc:Ig gene chromosomal translocation commonly seen in this cancer, or alternatively, (2) the production of these substances (sCD23 and other molecules) by the lymphoma cells themselves, or (3) reactivation of EBV infection. Also, they will examine the predictive value of the expression of these molecules for AIDS-lymphoma, and the expression of these molecules in lymphoma not associated with HIV infection, including African endemic Burkitt's lymphoma. Their specific aims are to: (1) define the pattern of expression of sCD23 prior to the emergence of AIDS-lymphoma; (2) determine/confirm which immune system molecules, other than sCD23, are elevated in those who develop AIDS-lymphoma; (3) determine if the measurement of serum levels of molecules other than sCD23 provides additional information for predicting the appearance of AIDS-lymphoma; and (4) determine if sCD23 or other immune system molecules are elevated in non-Hodgkin's B-cell lymphoma not associated with HIV infection, or in AIDS-lymphoma in hemophiliacs. The accomplishment of these specific aims will add valuable new information to our understanding of the molecular epidemiology of AIDS-lymphoma, as well as the role of immune dysfunction in the generation and growth of this cancer.
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