- Comparative Analysis of Serum Mannose-Binding Lectin in Normal Population and Patients with Different Types of Cancer.
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Bum Joon Kim, Young Sik Kim, Eun Mee Han, Eung Seok Lee, Nam Hee Won, Geung Hwan Ahn, Dale Lee, Bom Woo Yeom
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Korean J Pathol. 2004;38(5):306-310.
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 Abstract
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- BACKGROUND
Mannose-binding lectin (MBL) is a serum protein of innate immunity. Its genetic mutations lead to deficiency of serum MBL and recurrent pyogenic infection in childhood.
However, little is known about the frequency of its gene mutations or serum levels in Korean population and patients with cancers.
METHODS
We studied the mutational genotypes of MBL exon 1 codon 52, 54, and 57 or serum MBL levels from 102 normal adults and 228 cases of breast, stomach, colon, uterine cervical, and lung cancers by allele-specific PCR and enzyme-linked immunosorbent assay.
RESULTS
MBL gene mutations were found in 32 of 102 normal adults (31.4%), and were restricted only to exon 1 codon 54 showing homozygous (n=5, 4.9%) or heterozygous mutations (n=27, 26.5%). Mean and median serum MBL in the patients with cancers were increased (2,647+/-1,742 and 2,915 ng/mL, mean+/-S.D. and median) than those of normal adults (1,906+/-1,359 and 1,758 ng/mL). Serum MBL level was significantly increased in the patients with stomach, uterine cervical, colon, and lung cancers.
CONCLUSION
Our results indicate that the frequency and pattern of MBL gene mutations and its serum level is very similar among northeastern Asian populations. In addition, MBL might be involved in an immunologic response against common cancers, although further studies are needed.
- Expression of Cancer-Related Genes in Epstein Barr Virus-Infected Burkitt's Lymphoma Cell Line Treated with Mitomycin C.
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Woo Bom Yeom, Seol Hee Park, Min Kyung Kim, Chul Hwan Kim, In Sun Kim, Dale Lee
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Korean J Pathol. 2001;35(4):271-277.
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Abstract
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- BACKGROUND
Infection of Epstein Barr virus (EBV) into B cells drives the infected cells into the cell cycle and frequently results in lymphoblastoid cells. Mitomycin C inhibits DNA synthesis of epithelial cells as well as lymphoid cells by cross-linking with DNA. Many of the cancer cells have various pathways for escaping the responsiveness to the negative growth-regulatory effects of mitomycin C and gaining the immortalized property. The auther performed a cell culture of an EBV infected Jijoye lymphoma cell line, and compared the cell cycle and cancer related genes between the mitomycin treated- and non-treated group.
METHODS
DNA and RNA were extracted from the Jijoye cells; and EBV nuclear antigen (EBNA)-1, 2 and latent membrane protein (LMP) of EBV and p53 and p21 mRNA analyse was performed.
RESULTS
Mitomycin C blocked G2/M phase, however, mitomycin did not affect the expression of EBNA-1, 2 and LMP.
Mitomycin C also increased the p21 mRNA expression without p53 mRNA increase.
CONCLUSIONS
Mitomycin C induces B cell apoptosis by blocking the G2/M phase and by increasing p21 mRNA independent to p53, which reveals the presence of an alternative pathway of p21 induction by mitomycin C in EBV positive lymphoma cells
- K-ras Gene Mutations and Expression of K-ras, p16, Cyclin D1 and p53 in Synchronous Lesions of The Colon Adenoma-Carcinoma Sequences.
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Hwa Eun Oh, Seong Jin Cho, Nam Hee Won, Dale Lee, Insun Kim, Bom Woo Yeom
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Korean J Pathol. 2001;35(4):291-298.
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Abstract
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- BACKGROUND
The colorectal adenoma-carcinoma sequence represents a well-known para-digm for the sequential development of cancer driven by the accumulation of genomic defects. Although the colorectal adenoma-carcinoma sequence has been well investigated, the studies about tumors of different dignity co-existent in the same patient are rare.
K-ras mutation is an early genetic change in colon cancer.
The genes involved in the cell cycle such as cyclin D1, p16, and p53 are important in the tumorigenesis of the colon. The aims of this study were to determine K-ras gene mutation and expression of K-ras, p16, cyclin D1 and p53 in synchronous lesions of the colon adenoma-carcinoma sequences and their possible relationship with K-ras mutation.
METHODS
The materials included 45 colonic adenocarcinomas which were accompanied by adenoma (22 low grade and 26 high grade). By using polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP), we detected K-ras mutation of codon 12. An aberrant K-ras, p16, cyclin D1 and p53 expressions were stained using an immunohistochemical method. RESULTS: K-ras mutation was 52.4% (11/21) of high grade adenomas. K-ras expression was 65.4% (17/26) of high grade adenomas. p16 and cyclin D1 expressions were 50% (11/22) and 90.9% (20/22) of low grade adenomas, respectively. p53 expression was 75.6% (34/45) of adenocarcinomas. There were statistical correlations among K-ras, p16 and cyclin D1.
CONCLUSIONS
These results indicate that the ras gene mutation is an early event and the overexpressions of p16, cyclin D1 and p53 are associated with K-ras mutation and expression in adenoma-carcinoma sequences.
- E-Cadherin Expression in Renal Cell Carcinoma according to the Mainz Classification.
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Ju Han Lee, Hyun Deuk Cho, Dale Lee, Nam Hee Won
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Korean J Pathol. 1999;33(12):1131-1138.
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Abstract
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- According to the Mainz classification, renal cell carcinoma (RCC) consists of three subtypes: each has characteristic genetic alterations within the chromosomal or mitochondrial DNA. The three subtypes are: clear cell type, chromophil type, and chromophobe type. E-cadherin is a Ca++-dependent adhesion molecule which plays a major role in the maintenance of intercellular adhesion in epithelial tissues. In a normal kidney, E-cadherin is expressed in the distal tubule and the collecting duct, but not in the proximal tubule. We reclassified 110 cases of RCC according to mainz classification.
Immunohistochemical staining for E-cadherin was done on twenty eight cases of RCC, including 18 cases of clear cell type, four cases of chromophil type, and six cases of chromophobe type. The results were as follows: 1) of the 110 cases of RCC, 96 cases (87.3%) were of clear cell type, four cases (3.6%) of chromophil type, and ten cases (9.1%) of chromophobe type, 2) there was no significant correlation between the nuclear grade and clinical stage according to each subtype, 3) E-cadherin expression showed a strong positive reaction along the cell membranes in all six cases of chromophobe type.
The differential expression of E-cadherin in RCC may suggest that the chromophobe type may have different biologic characteristics from other types of RCC.
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