ABSTRACT
Amyloidosis results from the deposition of insoluble, fibrous amyloid proteins, nearly always in the extracellular spaces of organs and tissues. There are several varieties of amyloidosis, each of which is identified by the immunochemical nature of amyloid protein fibrils. Amyloid goiter is a very rare clinical entity and can be confused with a neoplasm. We have experienced a case of amyloid goiter with hypothyroidism secondary to tuberculosis. A 20 years old women with 5 months history of pulmonary tuberculosis was admitted with complaints of diarrhea, abdominal pain, weight loss at one year ago. She had a non-tender, diffuse and firm goiter. Also she had normal thyroid function at the first admission but was found to be hypothyroid at the second admission, 10 months later. Histologic examination revealed amyloid deposition in thyroid gland, stomach, colon and rectum.
Subject(s)
Female , Humans , Young Adult , Abdominal Pain , Amyloid , Amyloidogenic Proteins , Amyloidosis , Colon , Diarrhea , Extracellular Space , Goiter , Hypothyroidism , Plaque, Amyloid , Rectum , Stomach , Thyroid Gland , Tuberculosis , Tuberculosis, Pulmonary , Weight LossABSTRACT
PURPOSE: Alteration of p53 and telomerase activity may be responsible for gastric carcino- genesis. In this study, we tried to observe modulation of telomerase activity by wild type p53 in gastric cancer cell lines. MATERIALS AND METHODS: We used five gastric cancer cell lines (KATO-III, AGS, SNU-1, SNU-5, SNU-16). In order to find p53 mutation, we used western blot and PCR-SSCP. The TRAP-eze kit which supplied by Oncor (Gaithersburg, MD) was used to detect telomerase activity of the five gastric carcinoma cell lines. The wild type p53 gene was transfected by electroporation method. RESULTS: The expression of p53 protein was increased in four gastric carcinoma cell lines and one cell line (KATO-III) did not express. We found p53 point mutation in exon 5 and 8, and the p53 gene was deleted in KATO-III. The telomerase activity were observed in all five gastric carcinoma cell lines and there were no difference in telomere repeat length among five cell lines. After transfection with wild type p53, we could not find the change of telomerase activity in KATO-III. CONCLUSION: Although activation of telomerase activity and mutation of p53 gene may be needed in gastric carcinogenesis, the telomerase activity was not affected by restoration of p53 function in gastric carcinoma cell lines.