1993 Fiscal Year Final Research Report Summary
Analysis of transformation mechanism from differentiated to undifferentiated thyroid cancer
| Project/Area Number |
04454316
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
General surgery
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| Research Institution | Osaka University |
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Principal Investigator |
KOBAYASHI Tetsuro Osaka University Medical School Department of Surgery II Staff, 医学部, 助手 (40162002)
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| Co-Investigator(Kenkyū-buntansha) |
TOMITA Naohiro Osaka University Medical School Department of Surgery II Staff, 医学部, 助手 (00252643)
NISHISYO Isamu Osaka University Medical School Department of Medical Genetics Assitant Professo, 医学部, 助教授 (10228182)
TAKAI Shin-ichiro Osaka University Medical School Department of Sugical Oncology Professor, 医学部, 教授 (80028513)
TAKEDA Tsutomu Osaka University Medical School Department of Surgery II Staff, 医学部, 助手 (80236471)
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| Project Period (FY) |
1992 – 1993
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| Keywords | anaplastic transformation / p53 / anaplastic thyroid cancer / human monoclonal antibody / cell line / papillary thyroid cancer |
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| Research Abstract |
1. Analysis of genetic level
Mutation of p53 gene was studied for undifferentiated (anaplastic) and differentiated (papillary) thyroid carcinoma. An abnormal basic sequence was found only in anaplastic cancer specimens. This result suggests that mutation of p53 may trigger the anaplastic transformation from the papillary thyroid cancer.
2. Analysis of protein level
Human monoclonal antibody prepared from cervical lymph nodes taken from patients with anaplastic thyroid cancer with differentiated thyroid cancer specimens. Antigen recognized by this monoclonal antibody was even expressed in differentiated thyroid cancer. This monoclonal antibody may be useful tool for studying the mechanism of anaplastic transformation of thyroid cancer.
3. Analysis of cell kinetics
Four anaplastic thyroid cancer cell lines and 3 poorly differentiated cancer cell lines were established. K-199, an anaplastic cancer cell line, secretes granulocyte-colony stimulating factor (G-CSF), which may play some role in the growth of anaplastic thyroid cancer with an autocrine or paracrine mechanism. By adding a differentiated thyroid cancer cell line provided by fellow investigators, we were able to prepare a cell panel, which covered both highly and poorly differentiated and also undifferentiated thyroid cancer, ncluding differentiated thyroid cancer cell line, presented by other investigator, we can prepare the cell panel of thyroid cancer covering from differentiated to poorly and further undifferentiated thyroid cancer. As shown in genetic study, abnormal expression of p53 relationg anaplastic transformation was also found in this cell panel.
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