TKTL1 is overexpressed in a large portion of non-small cell lung cancer specimens.

TKTL1 is overexpressed in a large portion of non-small cell lung cancer specimens.
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DOI:
10.1186/1746-1596-3-35
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发表时间:
2008-08-12
影响因子:
2.6
通讯作者:
Goldmann T
Goldmann T
中科院分区:
医学4区
文献类型:
--
作者:
Schultz H;Kähler D;Branscheid D;Vollmer E;Zabel P;Goldmann T

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在几种肿瘤中,转酮醇酶活性与增殖相关,所述转酮醇酶活性阿利亚由戊糖磷酸途径的酶控制,所述戊糖磷酸途径是糖酵解的替代能量产生反应级联。硫胺素依赖性转酮酶反应的增加尤其是通过上调转酮酶样酶1(TKTL 1)活性诱导的;这表明TKTL 1是肿瘤增强的厌氧葡萄糖降解的致病酶。我们研究了TKTL 1的表达在88人,福尔马林固定的非小细胞肺癌组织和24个乳腺癌的免疫组化染色应用0至3染色评分系统(3 =最强的表达)。对于验证方法,我们使用HOPE技术对40例NSCLC固定和石蜡包埋标本进行了额外染色;结果与福尔马林固定石蜡包埋标本相当(未显示)。研究了与年龄、性别、TNM分类参数和肿瘤分级以及肿瘤转录因子1(TTF 1)和表面活性蛋白A(SPA)表达的潜在相关性。40.9%的分析肺肿瘤弱表达TKTL 1(评分1),38.6%中度表达(评分2),17.1%强表达(评分3)。3例肿瘤被诊断为TKTL 1阴性(3.4%;评分0)。所有乳腺癌标本染色均为阳性,评分为1:32%;评分为2:36%;评分为3:32%。肺泡巨噬细胞和肺泡上皮细胞II型也被发现是TKTL 1阳性。未发现列出的临床参数显示与TKTL 1信号外观显著相关。虽然我们描述了TKTL 1在肺癌中的表达,但我们需要声明,到目前为止,还没有基于这些发现的任何治疗方案的科学指征。
In several tumors the transketolase activity, controlled inter alia by enzymes of the pentose phosphate pathway which is an alternative, energy generating reaction-cascade to glycolysis, has been correlated with proliferation. The increase of thiamine-dependant transketolase enzyme reactions is induced especially through upregulated transketolase-like enzyme 1 (TKTL1)-activity; that shows TKTL1 to be a causative enzyme for tumors enhanced, anaerobic glucose degradation. We investigated TKTL1-expression in 88 human, formalin-fixed non-small cell lung cancer tissues and 24 carcinomas of the breast by immunohistochemical stainings applying a 0 to 3 staining-score system (3 = strongest expression). For means of validation we additionally stained 40 NSCLC fixed and paraffin-embedded utilizing the HOPE-technique; showing comparable results to the formalin-fixed, paraffin-embedded specimens (not shown). Potential correlations with age, sex, TNM-classification parameters and tumor grading as well as tumor transcription factor 1 (TTF1) and surfactant protein A (SPA) expression were investigated. 40.9% of the analyzed lung tumors expressed TKTL1 weakly (Score 1), 38.6% moderately (score 2) and 17.1% strongly (score 3). 3 tumors were diagnosed TKTL1-negative (3.4%; score 0). All Breast cancer specimen stainings were positive and scored 1: 32%; scored 2: 36%; scored 3: 32%. Alveolar macrophages and Alveolar Epithelial Cells Type II were also found to be TKTL1-positive. None of the listed clinical parameters could be found to show a significant correlation to TKTL1 signal appearance. Although we describe the expression of TKTL1 in lung cancers, we need to state that up till now there is no scientific indication for any treatment regimens based upon these findings.
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影响因子: 3.6
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