• Title/Summary/Keyword: Salivary protein polymorphism

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Genetic Polymorphism of Parotid Middle Band protein(Pm) in a Korean Population (이하선 타액내 Parotid Middle-Band Protein(Pm)의 유전적 다형현상에 관한 연구)

  • Ha-Jin Kim;Chong-Youl Kim
    • Journal of Oral Medicine and Pain
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    • v.18 no.1
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    • pp.45-53
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    • 1993
  • It is known that human saliva includes various kinds of salivaru proteins that show genetic polymorphism. Withrespect to salivary protein polymorphism, this study was conducted on 160 healthy Koreans between the ages of 20 and 29 chosen randomly : their parotid slaiva was collected, freeze-dried, and horizontally electrophoresed over acid-urea starch gel. Aluminum lactate-lactic acid was also used as buffer solution. The gel was stained with amidoblack 10B/1% acetic acid solution, and then destained with 0.5M H2SO4 solution. Accordingly, the parotid middle-band protein(Pm) identified, and its phenotypes and gene frequency were obtained. The obtined results were as follows : 1. The phenotypes of parotid middle band protein(Pm) observed in parotid saliva of the 160 Koreans were Pm(+) in 91 people (56.9%) and Pm(-) in 69 people (43.1%) 2. The gene frequency of Pm+ was 0.343, and that of Pm-waw 0.657. 3. The gene frequency of parotid middle band protein (Pm) obtained from Korean's parotid saliva was midway between that of Japanese and Chinese.

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A study on the Polymorphisms in Salivary Parotid Middle-band Protein of the Patients with Diabetes Mellitus (당뇨병 환자의 이하선 타액내 Pm의 다형현상에 대한 연구)

  • Jae-Duk Kim
    • Journal of Oral Medicine and Pain
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    • v.20 no.1
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    • pp.247-255
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    • 1995
  • The purpose of this study was to evaluate the polymorphism in parotid middle-band protein(Pm) of the patients with diabetes mellitus. Saliva from the parotid glands was collected from 60 healthy Korean who were live in Kwan-ju and from 33 diabetes mellitus patients who had more than 140mg/dl of fasting blood sugar for on week. In the saliva collected from parotid glands, Pm was analyzed to evaluate the distribution of phenotype using acid-urea starch gel elecrophores is The following results were obtained : 1. The phenotypes of parotid middle band protein(Pm) observed in parotid saliva of the control group(60 people) were Pm(+) in 38 people (63.3%) and Pm(-) in 22 people (36.7%). The gene frequency of Pm+ was0.394, and that of Pm- was 0.606. 2. The phenotypes of parotid middle band protein(Pm) observed in parotid saliva of the diabetes mellitus patient group(33 patients) were Pm(+) n 21 patients(63.6%) and Pm(-) in 12 patients (36.4%). The gene frequency of Pm+ was 0.397, and that of Pm- was 0.693 3. Pm dose not have significant differences between phenotypes on both the control group and the diabetes mellitus patient group.

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Molecular Biologic Analysis of c-kit Gene in Salivary Gland Carcinoma (타액선암에서 c-kit 유전자에 대한 분자생물학적 연구)

  • Seo Kyu-Hwan;Jung Kwang-Yoon;Woo Jung-Soo;Baek Seung-Kuk;Choi Sung-Bae;Kim Sang-Hee;Kim In-Sun;Kwon Soon-Young
    • Korean Journal of Head & Neck Oncology
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    • v.19 no.2
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    • pp.121-126
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    • 2003
  • Objectives: The c-kit gene encodes a transmembrane receptor-type tyrosine kinase, which is known to have a significant role in the normal migration and development of germ cells and melanocytes. In the previous studies of c-kit gene, c-kit expressions showed only in adenoid cystic carcinomas, lymphoepithelioma-like carcinomas and myoepithelial carcinomas, but not in others and mutation was not found in any types of salivary carcinoma. We investigate the c-kit expression which may be useful to differentiating adenoid cystic carcinomas from others, and mutation of the gene which may not be exist nor the mechanism of c-kit activation in salivary carcinomas. Material and Methods: The archival tissue samples from 42 salivary carcinomas of major and minor salivary glands were studied for c-kit expression by immunohistochemistry and gene mutation by polymerase chain reaction amplification and single strand conformational polymorphism. Results: The c-kit expressions were noted in 22/24 adenoid cystic carcinomas, 7/9 mucoepidermoid carcinomas, 2/3 acinic cell carcinomas, 3/4 malignant mixed tumors, and one undifferentiated carcinoma. The mutation of c-kit gene was found in 3/24 adenoid cystic carcinomas, 3/8 mucoepidermoid carcinomas, one acinic cell carcinoma, and 2/4 malignant mixed tumors. Conclusion: c-kit protein overexpression is seen in a variety of salivary gland carcinomas, and the mutation of the gene may be the mechanism of c-kit activation in these neoplasms.