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c-kit受体及其配体可能参与神经纤维瘤组织中肥大细胞数量的增加。

Possible involvement of c-kit receptor and its ligand in increase of mast cells in neurofibroma tissues.

作者信息

Hirota S, Nomura S, Asada H, Ito A, Morii E, Kitamura Y

机构信息

Department of Pathology, Osaka University Medical School, Suita, Japan.

出版信息

Arch Pathol Lab Med. 1993 Oct;117(10):996-9.

PMID:7692836
Abstract

Many mast cells are present in the tumor tissues of neurofibromatosis 1. We investigated the mechanism of the mast cell increase. Since the stem cell factor (SCF) induces development of mast cells and since the receptor of SCF is encoded by the c-kit gene, we examined the expression of SCF mRNA and c-kit mRNA in neurofibroma tissues. In situ hybridization demonstrated strong expression of c-kit messenger RNA in mast cells in the neurofibroma, but the expression of SCF mRNA was not demonstrable by in situ hybridization in either neurofibroma tissues or control normal skin tissues. When RNA extracted from neurofibroma tissues or normal skin tissues was reverse transcribed and then amplified by the polymerase chain reaction, the amount of SCF cDNA was greater in neurofibroma tissues than in normal skin tissues. The results suggest that SCF and the c-kit receptor are associated with the increase of mast cells in neurofibroma tissues.

摘要

在1型神经纤维瘤病的肿瘤组织中有许多肥大细胞。我们研究了肥大细胞增多的机制。由于干细胞因子(SCF)可诱导肥大细胞的发育,且SCF的受体由c-kit基因编码,因此我们检测了神经纤维瘤组织中SCF mRNA和c-kit mRNA的表达。原位杂交显示神经纤维瘤中的肥大细胞有强烈的c-kit信使RNA表达,但在神经纤维瘤组织或对照正常皮肤组织中,原位杂交均未显示SCF mRNA的表达。当从神经纤维瘤组织或正常皮肤组织中提取的RNA进行逆转录,然后通过聚合酶链反应进行扩增时,神经纤维瘤组织中SCF cDNA的量比正常皮肤组织中的多。结果表明,SCF和c-kit受体与神经纤维瘤组织中肥大细胞的增多有关。

相似文献

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Possible involvement of c-kit receptor and its ligand in increase of mast cells in neurofibroma tissues.c-kit受体及其配体可能参与神经纤维瘤组织中肥大细胞数量的增加。
Arch Pathol Lab Med. 1993 Oct;117(10):996-9.
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Localization of stem cell factor (SCF) and c-kit mRNA in human placental tissue and biological effects of SCF on DNA synthesis in primary cultured cytotrophoblasts.干细胞因子(SCF)和c-kit mRNA在人胎盘组织中的定位以及SCF对原代培养的细胞滋养层细胞DNA合成的生物学效应。
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Identification of mutations in the coding sequence of the proto-oncogene c-kit in a human mast cell leukemia cell line causing ligand-independent activation of c-kit product.在人肥大细胞白血病细胞系中鉴定原癌基因c-kit编码序列中的突变,该突变导致c-kit产物的配体非依赖性激活。
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