Journal of Pathology and Translational Medicine

Original Articles

Study of Microsatellite Alterations of 3p and 11q Chromosomes in Uterine Cervical Adenocarcinoma.: Eung Seok Lee, Hye Jin Jeong, Hee Jeoung Kim, Insun Kim; Korean J Pathol. 2001;35(2):137-143.

Abstract PDF: BACKGROUND
Uterine cervical cancer is the most prevalent cancer in Korean women, and the incidence of adenocarcinoma has been increasing. Loss of heterozygosity (LOH) analysis is used to identify regions which harbor a putative tumor suppressor gene.
METHODS
DNA was extracted from the microdissected normal and malignant lesions of 34 uterine cervical adenocarcinomas, 2 adenosquamous cell carcinomas, 13 squamous cell carcinomas, and 10 endometrial adenocarcinomas. LOH and microsatellite instability (MSI) analysis were performed using microsatellite markers, D3S4103 (3p14.2), D3S1284 (3p12), D3S1289 (3p21.2-21.1), D3S1307 (3p25-ter), THRB (3p22-24.1), and D11S35 (11q22). The expression of Fhit protein was compared with the genetic abnormalities.
RESULTS
Microsatellite alterations at 3p were detected in 37% of cervical adenocarcinomas, 16% of squamous cell carcinomas, and 43% of endometrial adenocarcinomas. The alterations of 11q were found in 17% of cervical adenocarcinomas. Microsatellite alterations of D3S1307 and D11S35 were detected in uterine cervical adenocarcinomas with high frequency. The frequency of FHIT protein loss is higher in the cervical squamous cell carcinoma than in cervical and endometrial adenocarcinomas.
CONCLUSION
Tumor suppressor gene of uterine cervical adenocarcinoma may be located in 3p25-ter and 11q22.

Loss of Heterozygosity on Chromosome 9p21, 17p13 and 3p in Human Astrocytic Tumor.: Youn Soo Lee, Chang Suk Kang, Seung Myung Dong, Jung Yong Lee, Sang In Shim, Byung Kee Kim; Korean J Pathol. 2001;35(4):330-337.

Abstract PDF: BACKGROUND
The purpose of this study was to determine the genetic abnormalities of chromosomes 9p21, 17p13.1, 3p25 and 3p14.2 in the development and progression of astrocytic tumors.
METHODS
We performed loss of heterozygosity (LOH) analysis in 41 astrocytic tumors, including 20 astrocytomas, 11 anaplastic astrocytomas and 10 glioblastomas, and correlated the results of LOH at different histopathologic grades. LOH was determined by multiplex polymerase chain reaction analysis of the DNA, which was extracted by microdissection.
RESULTS
LOH of 9p21 was found in 55.6% of astrocytomas, 54.6% of anaplastic astrocytomas and 100.0% of glioblastomas. LOH of 17p13.1 was found in 21.4% of astrocytomas, 28.6% of anaplastic astrocytomas, and 66.7% of glioblastomas. LOH of 3p25 was found in 37.5% of astrocytomas, 16.7% of anaplastic astrocytomas, and 14.3% of glioblastomas. LOH of 3p14.2 was found in 16.7% of astrocytomas, 40.0% of anaplastic astrocytomas, and 42.9% of glioblastomas. LOH on chromosome 9p21 and 17p13.1 was closely related with the histopathologic grades.
CONCLUSIONS
These results may suggest that LOH of 9p21, 17p13.1, 3p25 and 3p14.2 involves an early event of astrocytoma development and accumulates during progression. LOH of 3p25 may be involved in the tumorigenesis of astrocytoma. Identification of these LOH may illuminate the stepwise pathogenesis of astrocytic tumors and predict the possibility of malignant transformation.

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