CYTOGENETICS AND BIOCHEMISTRY OF PROSTATE CANCER
CYTOGENETICS AND BIOCHEMISTRY OF PROSTATE CANCER
批准号:
6475794
负责人:
THOMAS G PRETLOW
金额:
$37.88万
依托单位国家:
美国
项目类别:
财政年份:
1992
资助国家:
美国
项目状态:
已结题
起止时间:
1992-07-23 至 2003-11-30
关键词:
JAK kinase athymic mouse biological signal transduction cell growth regulation cell line cellular oncology cellular pathology cytogenetics cytokine receptors human tissue mass tissue /cell culture matrigel molecular oncology neoplasm /cancer genetics neoplasm /cancer transplantation neoplastic cell neoplastic growth prostate neoplasms prostate specific antigen protein tyrosine kinase xenotransplantation
中文摘要
这是对CA57179的竞争性续订申请,这项授权是
作为RFA的结果,在过去4年零3个月内获得资金
与前列腺癌(PCA)有关。目前,这笔赠款支持一个
对细胞遗传学、分子生物学感兴趣的教职员工之间的合作努力
生物学、病理学和泌尿学。续订申请代表
继续追求选定的先前目标。这项研究的重点是
是否使用来自手术的前列腺癌组织(A)试图确定
控制PCAs生长的因素并可能导致显著的
在不同患者中观察到的攻击性差异和(B)至
使用从这些研究和其他研究中获得的信息
实验室创造条件,使我们能够从
大部分PCa患者的组织被切除。直到最近,大多数PCA都在发挥作用
研究实验室依赖于三种细胞系:PC-3,DU 145,
和LNCaP。其中两条线路,PC-3和DU 145,缺乏证据表明
功能正常的雄激素受体,未能使前列腺特异性
抗原--前列腺量最丰富的蛋白质产物
上皮细胞。虽然已经开发了一些其他的主成分分析模型,
它们(A)不是普遍可用的,(B)仍然非常有限
反映了在PCA中看到的广泛的疾病范围。小才是
了解PCA中的增长控制。通常很长的时间
(5-20年)前列腺癌患者的生存使其成为一种疾病
个别患者的肿瘤生长能力可能会有不寻常的
长期的翻译意义。如果我们能够实现我们的
目标,这种方法可能使发展知识成为可能
特定患者的肿瘤将促进更具特异性的
基因治疗的靶向方法,针对特定基因的治疗
酪氨酸激酶、抗肿瘤化疗和免疫治疗。这个
这些患者的长期存活可能使人们能够提炼出这些
在患者经历旷日持久之前的特定肿瘤处理方法
和严重的骨痛,折磨着大多数死亡的患者
都是由前列腺癌引起的。
英文摘要
This is a competitive renewal application for CA57179, a grant that was
funded for the past 4 years and three months as the result of an RFA
related to prostate cancer (PCA). Currently, this grant supports a
collaborative effort among faculty interested in cytogenetics, molecular
biology, pathology, and urology. The renewal application represents a
continued pursuit of selected previous goals. The focus of this study
is the use of PCA tissues derived from surgery (a) to attempt to define
the factors that control the growth of PCAs and may cause the marked
differences in aggressiveness observed in different patients and (b) to
use the information derived from these studies and from other
laboratories to devise conditions that will permit us to grow PCAs from
tissues resected from most PCA patients. Until recently, most PCA work
in research laboratories has relied on three cell lines: PC-3, DU 145,
and LNCaP. Two of these lines, PC-3 and DU 145, lack evidence of
functioning androgen receptors and fail to make prostate specific
antigen, quantitatively the most abundant protein product of prostatic
epithelial cells. While a few other models of PCA have been developed,
they are (a) not generally available and (b) still very limited in their
reflection of the broad spectrum of disease seen in PCA. Little is
understood about the control of growth in PCA. The usually lengthy
(5-20 years) survival of patients with PCA makes PCA a disease in which
the ability to grow the tumors of individual patients might have unusual
long-term translational significance. If we are able to achieve our
goals, this approach might make it possible to develop knowledge of
specific patients tumors that would facilitate a more specifically
targeted approach to gene therapy, therapy directed against specific
tyrosine kinases, antineoplastic chemotherapy, and immunotherapy. The
long survival of these patients might allow one to refine these
approaches to specific tumors before patients experience the protracted
and severe bone pain that afflicts the majority of patients whose deaths
are caused by prostate cancer.
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海外基金