Minority Predoctoral Fellowship Program

少数族裔博士前奖学金计划

• 批准号: 6985460
• 负责人: SERINA D ORTIZ
• 金额: $ 2.56万
• 依托单位: BECKMAN RESEARCH INSTITUTE/CITY OF HOPE
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-08-01 至 2010-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6985460
• 关键词: SDS polyacrylamide gel electrophoresis; T cell receptor; biological signal transduction; carcinogenesis; cell death; cell growth regulation; cell line; cell proliferation; clone cells; enzyme activity; flow cytometry; gene expression; green fluorescent proteins; human T cell leukemia; immunoprecipitation; leukocyte activation /transformation; liquid chromatography mass spectrometry; matrix assisted laser desorption ionization; molecular oncology; neoplastic cell; predoctoral investigator; protein tyrosine kinase; proteomics

DESCRIPTION (provided by applicant): T-cell leukemia, including T-lineage acute lymphoblastic leukemia, is among the most common and aggressive form of hematologic malignancy in both children and adults. This malignancy represents a heterogeneous group of lymphoid cancers with varied morphologic and immunologic features of transformed T-cells originated from normal T-cell precursors. Syk, a non-receptor tyrosine kinase, plays critical roles in cell signaling events mediated by hematopoietic receptors such as T-cell receptor. Interestingly, expression of Syk inhibits human breast cancer cell growth and metastasis, perhaps by suppressing malignant growth of the breast cancer cells. Like in breast cancer cells, Syk expression is reduced in T-lineage leukemia cells. Our previous studies have demonstrated that expression of Syk in leukemic T-cells inhibits the proliferation and activation-induced-cell-death of these cells. The working hypothesis of the candidate's dissertation project is that expression of an activated Syk can control the growth and tumorigenicity of T-lineage leukemia cells. My study will test this hypothesis using both in vitro analyses and in vivo animal studies to determine the molecular and cellular mechanisms of how Syk expression may regulate the growth of leukemic T-cells.

描述（由申请人提供）：T细胞白血病，包括T-Linege急性淋巴细胞白血病，是儿童和成人中最常见和最具侵略性的血液学恶性肿瘤形式之一。这种恶性肿瘤代表了一组异质的淋巴癌，具有转化的T细胞的形态和免疫学特征，源自正常的T细胞前体。 SYK是一种非受体酪氨酸激酶，在由造血受体（如T细胞受体）介导的细胞信号事件中起关键作用。有趣的是，SYK的表达抑制了人类乳腺癌细胞的生长和转移，也许是通过抑制乳腺癌细胞的恶性生长。像在乳腺癌细胞中一样，T-Linege白血病细胞中SYK表达降低。我们以前的研究表明，Syk在白血病T细胞中的表达抑制了这些细胞的增殖和激活诱导的细胞死亡。候选人论文项目的工作假设是激活的SYK的表达可以控制T-Linege白血病细胞的生长和肿瘤性。我的研究将使用体外分析和体内动物研究来检验这一假设，以确定SYK表达如何调节白血病T细胞生长的分子和细胞机制。