Christoforidou Anna V, Papadaki Helen A, Margioris Andrew N, Eliopoulos George D, Tsatsanis Christos
Department of Clinical Chemistry-Biochemistry, School of Medicine, University of Crete and University Hospital of Heraklion, 71110 Heraklion, Crete, Greece.
Mol Cancer. 2004 Dec 3;3(1):34. doi: 10.1186/1476-4598-3-34.
Tpl2/Cot oncogene has been identified in murine T-cell lymphomas as a target of MoMuLV insertion. Animal and tissue culture studies have shown that Tpl2/Cot is involved in interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-alpha) production by T-cells contributing to T-cell proliferation. In the present report we examined a series of 12 adult patients with various T-cell malignancies, all with predominant leukemic expression in the periphery, for the expression of Tpl2/Cot oncogene in order to determine a possible involvement of Tpl2/Cot in the pathogenesis of these neoplasms.
Our results showed that Tpl2/Cot was overexpressed in all four patients with Large Granular Lymphocyte proliferative disorders (LGL-PDs) but in none of the remaining eight patients with other T-cell neoplasias. Interestingly, three of the LGL-PD patients displayed neutropenia, one in association with sarcoidosis. Serum TNF-alpha levels were increased in all Tpl2/Cot overexpressing patients while serum IL-2 was undetectable in all subjects studied. Genomic DNA analysis revealed no DNA amplification at the Tpl2/Cot locus in any of the samples analyzed.
We conclude that Tpl2/Cot, a gene extensively studied in animal and tissue culture T-cell models may be also involved in the development of human LGL-PD and may have a role in the pathogenesis of immune manifestations associated with these diseases. This is the first report implicating Tpl2/Cot in human T-cell neoplasias and provides a novel molecular event in the development of LGL-PDs.
Tpl2/Cot癌基因在鼠T细胞淋巴瘤中被鉴定为莫洛尼鼠白血病病毒(MoMuLV)插入的靶点。动物和组织培养研究表明,Tpl2/Cot参与T细胞产生白细胞介素-2(IL-2)和肿瘤坏死因子-α(TNF-α),促进T细胞增殖。在本报告中,我们检测了12例患有各种T细胞恶性肿瘤的成年患者,所有患者外周血中均以白血病表现为主,以确定Tpl2/Cot癌基因的表达情况,从而确定Tpl2/Cot是否可能参与这些肿瘤的发病机制。
我们的结果显示,在所有4例大颗粒淋巴细胞增殖性疾病(LGL-PD)患者中Tpl2/Cot均过度表达,但在其余8例患有其他T细胞肿瘤的患者中均未检测到。有趣的是,3例LGL-PD患者出现中性粒细胞减少,其中1例与结节病有关。所有Tpl2/Cot过度表达的患者血清TNF-α水平均升高,而在所有研究对象中均未检测到血清IL-2。基因组DNA分析显示,在所分析的任何样本中,Tpl2/Cot基因座均未发生DNA扩增。
我们得出结论,Tpl2/Cot是一个在动物和组织培养T细胞模型中得到广泛研究的基因,它可能也参与了人类LGL-PD的发生发展,并且可能在与这些疾病相关的免疫表现的发病机制中发挥作用。这是首篇将Tpl2/Cot与人类T细胞肿瘤相关联的报告,并为LGL-PD的发生发展提供了一个新的分子事件。