Journal of Pathology and Translational Medicine

Original Articles

TNF-α and TNF-β Polymorphisms are Associated with Susceptibility to Osteoarthritis in a Korean Population: Lin Han, Joo Hyoun Song, Jung Hwan Yoon, Yong Gyu Park, Suk Woo Lee, Yoo Jin Choi, Suk Woo Nam, Jung Young Lee, Won Sang Park; Korean J Pathol. 2012;46(1):30-37. Published online February 23, 2012; DOI: https://doi.org/10.4132/KoreanJPathol.2012.46.1.30

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Background

The tumor necrosis factor (TNF) is believed to play an important role in the pathophysiology of osteoarthritis (OA). Evidence shows that genetic polymorphisms make substantial contributions to the etiology of OA.

Methods

We investigated the genotypes TNF-α and TNF-β in 301 OA patients and 291 healthy subjects as controls. We employed a polymerase chain reaction-restriction fragment length polymorphism and a polymerase chain reaction-single strand conformation polymorphism assay to identify the genotypes TNFA -G308A and TNFB +G252A, respectively.

Results

For TNFA -G308A, the percentages of genotypes GG, AG, and AA were 26.3% (79/301), 62.5% (188/301), and 11.3% (34/301) in OA patients and 88.7% (258/291), 11.3% (33/291), and 0% (0/291) in controls. For TNFB +G252A, the percentages of genotypes GG, AG, and AA were 15.3% (46/301), 41.9% (126/301), and 42.9% (129/301) in OA patients and 12% (35/291), 52.6% (153/291), and 35.4% (103/291) in controls. There were significant differences in genotypes and alleles of TNFA -308 between OA patients and controls (p<0.0001) and in alleles of TNFB +252 (p=0.0325). The risk of OA was significantly higher for carriers of the TNFA -308A allele and the TNFB +252 AA homozygote (p=0.0224).

Conclusions

The results suggest close relationships between TNFA -G308A and TNFB +G252A polymorphisms and individual susceptibility to OA in the Korean population.

Citations

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Copy Number Alterations of BCAS1 in Squamous Cell Carcinomas.: Yu Im Kim, Ahwon Lee, Jennifer Kim, Bum Hee Lee, Sung Hak Lee, Suk Woo Nam, Sug Hyung Lee, Won Sang Park, Nam Jin Yoo, Jung Young Lee, Sang Ho Kim, Su Young Kim; Korean J Pathol. 2011;45(3):271-275.; DOI: https://doi.org/10.4132/KoreanJPathol.2011.45.3.271

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Abstract PDF

BACKGROUND
Breast carcinoma amplified sequence 1 (BCAS1), located in 20q13, is amplified and overexpressed in breast cancers. Even though BCAS1 is expected to be an oncogene candidate, its contribution to tumorigenesis and copy number status in other malignancies is not reported. To elucidate the role of BCAS1 in squamous cell carcinomas, we investigated the copy number status and expression level of BCAS1 in several squamous cell carcinoma cell lines, normal keratinocytes and primary tumors.
METHODS
We quantitated BCAS1 gene by real-time polymerase chain reaction (PCR). Expression level of BCAS1 was measured by real-time reverse transcription-PCR and immunoblot.
RESULTS
Seven (88%) of 8 squamous cell carcinoma cell lines showed copy number gain of BCAS1 with various degrees. BCAS1 gene in primary tumors (73%) also showed copy number gain. However, expression level did not show a linear correlation with copy number changes.
CONCLUSIONS
We identified copy number gain of BCAS1 in squamous cell carcinomas. Due to lack of linear correlation between copy numbers of BCAS1 and its expression level, we could not confirm that the overexpression of BCAS1 is a common finding in squamous cell carcinoma cell lines. However, this study shows that the copy number gain of BCAS1 is a common finding in squamous cell carcinomas.

Citations

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Electrochemical Approaches for Preparation of Tailor-Made Amino Acids
Nana Wang, Jingcheng Xu, Haibo Mei, Hiroki Moriwaki, Kunisuke Izawa, Vadim A. Soloshonok, Jianlin Han
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Growth Differentiation Factor 5 (GDF5) Core Promoter Polymorphism Is Not Associated with Susceptibility to Osteoarthritis of the Knee in the Korean Population.: Zhang Cao, Hwa Sung Lee, Jae Hwi Song, Jeong Whan Yoon, Yong Kyu Park, Suk Woo Nam, Jung Young Lee, Won Sang Park; Korean J Pathol. 2010;44(4):404-409.; DOI: https://doi.org/10.4132/KoreanJPathol.2010.44.4.404

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Abstract PDF

BACKGROUND
Osteoarthritis (OA) is a common disease characterized by degenerating joint cartilage in the knee, hip, and hand. A functional single nucleotide polymorphism (SNP) +104T/C; rs143383 in the 5' untranslated region of the growth differentiation factor 5 (GDF5) gene was recently associated with susceptibility to OA in the Japanese and Chinese populations.
METHODS
To investigate whether this association is present in the Korean population, the frequency of the polymorphism was investigated in 276 patients with knee OA and 298 healthy subjects as controls. Polymorphism analysis was performed by amplifying the core promoter region of the GDF5 gene and digesting it with the BsiEI restriction enzyme.
RESULTS
The frequency of the TT, CT, and CC genotypes was 54.3% (150/276), 41.7% (115/276), and 4.0% (11/276), respectively, in patients with OA, and 53.4% (159/298), 37.9% (113/298), and 8.7% (26/298), respectively, in healthy controls. No significant differences in genotypic or allelic frequencies of the +104T/C SNP of the GDF5 gene were observed between patients with OA and controls. Also, no significant differences in allelic and genotypic frequencies were found when the individuals were stratified by age and gender.
CONCLUSIONS
The results suggest that the +104T/C; rs143383 GDF5 core promoter polymorphism is not a risk factor for OA in the Korean population.

Citations

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The association of growth differentiation factor 5 rs143383 gene polymorphism with osteoarthritis: a systematic review and meta-analysis
Yue-peng Wang, Wen-jia Di, Su Yang, Shi-lei Qin, Yun-feng Xu, Peng-fei Han, Ke-dong Hou
Journal of Orthopaedic Surgery and Research.2023;[Epub] CrossRef
Correlation between growth differentiation factor 5 (rs143383) gene polymorphism and knee osteoarthritis: an updated systematic review and meta-analysis
Bin Jia, Yaping Jiang, Yingxing Xu, Yingzhen Wang, Tao Li
Journal of Orthopaedic Surgery and Research.2021;[Epub] CrossRef
Association between GDF5 rs143383 genetic polymorphism and musculoskeletal degenerative diseases susceptibility: a meta-analysis
Xin Huang, Weiyue Zhang, Zengwu Shao
BMC Medical Genetics.2018;[Epub] CrossRef
Association of BMP-14 rs143383 ploymorphism with its susceptibility to osteoarthritis
Yi Yin, Yan Wang
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Association between GDF5 +104T/C polymorphism and knee osteoarthritis in Caucasian and Asian populations: a meta-analysis based on case-control studies
Dong Jiang, Zengtao Hao, Dongsheng Fan, Wen Guo, Pengcheng Xu, Chao Yin, Shuzheng Wen, Jihong Wang
Journal of Orthopaedic Surgery and Research.2016;[Epub] CrossRef
A comprehensive meta-analysis of association between genetic variants of GDF5 and osteoarthritis of the knee, hip and hand
Rui Zhang, Jianfeng Yao, Peng Xu, Baohu Ji, James V. Luck, Brian Chin, Shemin Lu, John R. Kelsoe, Jie Ma
Inflammation Research.2015; 64(6): 405. CrossRef
Association between GDF5 rs143383 polymorphism and knee osteoarthritis: an updated meta-analysis based on 23,995 subjects
Feng Pan, Jing Tian, Tania Winzenberg, Changhai Ding, Graeme Jones
BMC Musculoskeletal Disorders.2014;[Epub] CrossRef
Association between the +104T/C polymorphism in the 5′UTR of GDF5 and susceptibility to knee osteoarthritis: A meta-analysis
SHAO-WEN HAO, QUN-HUA JIN
Molecular Medicine Reports.2013; 7(2): 485. CrossRef
A genetic association study between growth differentiation factor 5 (GDF 5) polymorphism and knee osteoarthritis in Thai population
Tulyapruek Tawonsawatruk, Theeraroj Changthong, Sarinee Pingsuthiwong, Objoon Trachoo, Thanyachai Sura, Wiwat Wajanavisit
Journal of Orthopaedic Surgery and Research.2011; 6(1): 47. CrossRef

HgCl2 Toxicity on Cultured Renal Tubular Cells of Rabbit.: Jung Young Lee, Seong Beom Lee, Suk Hyung Lee, Won Sang Park, Nam Jin Yoo, Sang Ho Kim, Choo Soung Kim; Korean J Pathol. 1995;29(5):615-623.

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Abstract: To understand the mechanism of cell injury when exposed to HgCl2, monitoring of cytosolic ionized free Ca2+([Ca2+]i), viability test, measurement of the amount of ATP, and Ca-ATPase activity were evaluated in cultured rabbit renal tubular cells(RTC) exposed to HgCl2. The results were as follows: 1) HgCl2 was cytotoxic to rabbit RTC at all doses except 10 uM and the rate of killing displayed a dose- and time-dependent relationship. 2) The absence of extracellular Ca provided partial protection from irreversible injury induced by HgCl2. 3) The increasing pattem of [Ca2+]i varied according to the concentrations of HgCl2. At the low concentrations of HgCl2 (2.5-10 microM), the level of [Ca2+]i increased slowly over the flat 2-3 min and then achieved plateau-state. In contrast, at the high concentrations of HgCl2 (25-100 microM) the level of [Ca2+]i achieved peak within 1 min and then decreased to a plateau state under normal concentrations. 4) The level of ATP was decreased to 27.5% of that of normal control cells within 3 min by using a treatment of 100 microM HgCl2. 5) HgCl2 did not affect the Ca2+ ATPase activity by enzyme histochemical observation. These findings suggest that the elevation of [Ca2+]i in response to the HgCl2-induced injury is an important event in accelerating injury that ultimately leads to cell death. But other possibilities such as HgCl2 might have direct deleterious effects on the also should be considered.

Case Report

Primary Ovarian Leiomyosarcoma: A case report.: Won Sang Park, Seong Beom Lee, Jung Yong Lee, Sang Ho Kim, Choo Soung Kim; Korean J Pathol. 1996;30(6):548-550.

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Abstract PDF: Primary leiomyosarcoma is a rare tumor of the ovary. We experienced a case of primary ovarian leiomyosarcoma in a 68 year old woman. Microscopically, the tumor was characterized by interlacing bundles of plump spindle cells that showed immunoreactivity for alpha-smooth muscle actin, pleomorphic multinucleated giant cells and an increased mitotic rate. Ultrastructural features included abundant smooth muscle type filaments and irregular bodies. Consequently, this case has led us to propose ultrastructural and immunohistochemical criteria for primary ovarian leiomyosarcoma.

Original Articles

Loss of Heterozygosity Affecting the APC and p53 Tumor Suppressor Gene Loci in Colorectal Cancers and Its Prognostic Significance.: Eun Deok Chang, Won Sang Park, Byung Kee Kim, Sun Moo Kim, Sang In Shim; Korean J Pathol. 1997;31(3):191-200.

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Abstract PDF: Development of the human colorectal cancer is associated with several distinct genetic abnormalities involving both dominant-acting oncogenes (K-ras, c-src) and tumor suppressor genes (APC, DCC, p53) which undergo inactivation or loss. In colorectal tumors, the common molecular alteration is localized in the 17p13 and 5q21 loci encoding the p53 and the APC gene, respectively. The identification of these genes may help the understanding of the pathogenesis of colorectal neoplasia. In order to determine whether the frequency of the genetic alterations varies with sex, age, tumor size, or site, including pathologic parameters, such as degree of differentiation, tumor stage, mucin component, lymphoid reaction, tumor invasion pattern, vein and nerve invasion, lymph node metastasis, and other parameters, such as disease-free survival, distant metastasis and patient outcome, the authors analyzed the loss of heterozygosity (LOH) of the APC and the p53 genes in paraffin-embedded specimens of 48 colorectal cancers by use of the polymerase chain reaction and restriction fragment length polymorphism. The results were as follows: the LOH affecting the APC was found in 15 out of 31 (48.4%) heterozygous patients, while the LOH of the p53 locus was observed in 11 out of 26 (42.3%) patients. Among 48 patients, the LOH at both the APC and the p53 loci was observed in five (10.4%) patient. No statistically significant associations were found between the LOH of the APC gene and the proposed parameters. The relationship between the LOH of the p53 and the histologic differentiation, lymphoid reaction was significant (P<0.05), but survival was not correlated. Statistically significant associations were found between overall survival of the colorectal cancer patients and distant metastasis, Astler-Coller stage, lymphoid reaction, invasion pattern, nerve invasion, vein invasion, lymph node metastasis, and disease free survival. The above results suggest that the LOH of the p53 genes could be involved in the progression of colorectal cancers. However, neither the LOH of the APC nor that of the p53 have significant association with survival of the colorectal cancer patients.

The Role of gadd and p53 Genes in Apoptosis and Cell Cycle Delay by Genotoxic Agents.: Jung Young Lee, Jung Duk Lee, Seung Myung Dong, Eun Young Na, Min Sun Shin, Su Young Kim, Sug Hyung Lee, Won Sang Park, Nam Jin Yoo; Korean J Pathol. 1998;32(4):239-247.

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Abstract PDF: The aim of this study was to investigate the relationships between the gadd genes expression and an apoptosis induction in two different growing cell types after treatments with cisplatin and methylmethan sulfonate (MMS). We have examined the kinetics and specificity of gadd45 and gadd153 expression following cisplatin and MMS treatments to HL-60 cells and primary cultured human kidney (HKN) cells. We have also determined an induction time of apoptosis by DNA fragmentation analysis and the presence of the cell cycle arrest by a flow cytometric measurement. The results were as follows. In non-adherent HL-60 cells, a typical ladder pattern was observed within 4 hours after treatments of 20 micrometer of cisplatin and 100 microgram/ml of MMS. At the same time while adherent HKN cells failed to exhibit a ladder pattern at even higher doses of genotoxic agents. Since HL-60 cells do not have p53 gene, these findings suggest the presence of a p53-independent apoptotic pathway. The increasing patterns of the mRNA levels of gadd45 and gadd153 varied with the type of genotoxic agents. In the case of MMS treatment, the induction was rapid and transient, regardless of the cell types. The mRNA level peaked at 4 hours after MMS treatment and markedly decreased after 12 hours. On the other hand, cisplatin-induced transcriptions of gadd45 and gadd153 continued to increase for at least 24 hours and reached a peak level at 48 hours after cisplatin treatment, regardless of the cell types. HL-60 cells revealed G2 arrest following 24 hours after cisplatin and MMS treatments. These findings suggest that the regulation mechanism of apoptosis between adherent and non-adherent cells, might be different and that gadd45 and gadd153 might have an important role in DNA repair rather than apoptosis. Also, the findings suggest that an expression pattern of gadd45 and gadd153 might be different according to the type of genotoxic agents.

Identification of Differentially Expressed Genes Using RNA Fingerprinting in Cell after DNA Damage.: Jung Young Lee, Min Sun Shin, Seung Myung Dong, Eun Young Na, Su Young Kim, Sug Hyung Lee, Won Sang Park, Nam Jin Yoo; Korean J Pathol. 1998;32(5):321-327.

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Abstract: RNA fingerprinting using on arbitrary primed polymerase chain reaction (RAP-PCR) was carried out to identify differentially expressed genes in HL-60 cell after treatment of methylmethane sulfonate (MMS). Twenty differentially expressed PCR products were cloned and analyzed. We have successfully obtained eight partial cDNA sequences by TA cloning method. Among these, six cDNAs were up-regulated and two cDNAs were down-regulated after the MMS treatment. Of these six up-regulated cDNAs, 3 cDNAs were equivalent to known genes in the GenBank/EMBL databases with 98~100% homology searched by BLAST program: genomic DNA fragment containing CpGg island (clone 26h8), Human Rev interacting protein-1 (RIP-1), and human zinc finger protein-4 (HZF4). The sequences of the three remaining cDNA were entirely new genes, but we didn't try to identify a full cDNA sequence. Two clones called KIAA0060 and KIAA0065, were down-regulated in HL-60 cells after the MMS treatment. These findings suggest that the RNA fingerprinting method using RAP-PCR is an effective method which can identify and separate the differentially expressed cDNAs and that the isolated cDNAs might involve in regulation mechanism of apoptosis and/or cell cycle delay, especially a p53-independent pathway, in the cells after DNA damage. But the nature of cDNAs that we have isolated remains to be elucidated.

Identification of Zinc Finger Genes that are Differentially Expressed upon Apoptosis of Ramos B Cells.: Min Sun Shin, Su Young Kim, Seung Myung Dong, Eun Young Na, Sug Hyung Lee, Won Sang Park, Jung Young Lee, Nam Jin Yoo; Korean J Pathol. 1998;32(12):1043-1048.

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Abstract: Typical programmed cell death requires de novo macromolecular synthesis and shares common morphological changes referred to as apoptosis. To elucidate the molecular mechanism of apoptosis, we isolated 13 cDNA clones of zinc finger genes that are differentially expressed in calcium ionophore-induced apoptosis of Ramos human B cell by 'targeted RNA fingerprinting' protocol (Stone & Wharton, 1993). According to DNA sequence analysis of the 13 cDNA clones, three clones are identical with ZNF7, ZNF143 and MTB-Zf, respectively, and 8 out of the other 10 clones showed partial homology to known zinc finger genes. Differential expression was confirmed in the three known zinc finger genes by ribonuclease protection assay. ZNF7 and ZNF143 are up-regulated after induction of apoptosis, and, in contrast, MTB-Zf is down-regulated. According to the previous reports on these three genes, all of the three genes have been suspected to be tumor suppressor genes, but their functions have not been identified yet. Taken together, our results suggest that many of the novel and known zinc finger genes might play important roles in regulation of apoptosis and that these findings also provide clues as to the functions of the three putative tumor suppressor genes, ZNF7, ZNF143 and MTB-Zf in terms of apoptosis. In addition, the isolation of zinc finger genes by targeted RNA fingerprinting could be a straightforward approach for the identification of novel candidate genes associated with apoptosis.

Loss of Heterozygosity at VHL, FHIT, and p16 Loci in Nonpapillary Renal Cell Carcinoma.: Won Sang Park, Seung Myung Dong, Yong Hyun Cho, Tae Gon Hwang, Su Young Kim, Min Sun Shin, Jae Ho Pi, Suk Hyung Lee, Nam Jin Yoo, Jung Young Lee; Korean J Pathol. 1999;33(1):8-14.

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Abstract PDF: The objectives of this study were to characterize the alterations of 3p and 9p in sporadic renal cell carcinomas (RCC) and to assess the relationship between the clinical stages or tumor size and the alteration of these chromosomes. Thirty eight archival, paraffin embedded tissue sections from 38 patients with RCC were analyzed for loss of heterozygosity (LOH) at 3p and 9p with 11 microsatellite markers. LOH was detected in 81.6% (31/38) and 37.8% (14/37) at 3p and 9p, respectively. The frequencies of LOH at VHL and FHIT locus were 75.6% and 72.2%, respectively. Twelve cases out of 38 showed LOH at both 9p21 and 3p. The loss of 3p in the samples tested was not related to clinical stages and tumor size, but that of 9p21 was significantly associated with advanced stage and larger tumor size. These results support that 3p deletion, including VHL and FHIT gene, play a critical role in the tumorigenesis of sporadic RCC, especially at early stage, and that 9p21 may contribute to the progression of sporadic RCC.

Ethnic Differences of the p53 Genetic Alteration in Cutaneous Malignant Melanoma.: Won Sang Park, Eun Young Na, Sang Kyu Lee, Sug Hyung Lee, Su Young Kim, Seok Jin Kang, Kye Yong Song, Suk Woo Nam, Nam Jin Yoo, Jung Young Lee; Korean J Pathol. 2001;35(2):158-164.

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Abstract PDF: BACKGROUND
There are significant differences in the clincopathologic pattern including the incidence, favor site, and histopathologic type between cutaneous malignant melanomas arising from whites, asians and blacks. These differences might suggest that there is a racial difference in the molecular tumorigenesis mechanism of malignant melanoma.
METHODS
To determine the ethnic differences in tumorigenesis of malignant melanoma, we performed loss of heterozygosity (LOH) and sequencing analyses of the p53 gene in cutaneous malignant melanomas arising from 22 white American, 30 Korean and 15 black African patients.
RESULTS
The frequency of LOH of the p53 gene is only 12.5% in white American patients, but the frequency is significantly higher in Korean (42.1%) and black African (61.5%) patients. We also detected 17 mutations (nonsense: 1, missense: 16) of the p53 gene in the cutaneous malignant melanomas of Koreans and black Africans, but none in those of white Americans: among the 16 missense mutations, 10 mutations were C:G to T:A transitional mutations. Of these, we also detected one GG (CC) to AA (TT) tandem mutation at the pyrimidine sequence.
CONCLUSION
These results strongly suggest that there might be a racial difference in molecular carcinogenesis mechanisms among the cutaneous malignant melanomas occurring in white American, Korean and black African patients. But the role of the p53 genetic alteration in the genesis of melanomas in Korean and black African patients is subject to further evaluation.

Mutational Analysis of Proapoptotic bcl-2 Family genes in Colon Carcinomas.: Young Hwa Soung, Jong Woo Lee, Su Young Kim, Suk Woo Nam, Won Sang Park, Jung Young Lee, Nam Jin Yoo, Sug Hyung Lee; Korean J Pathol. 2005;39(3):168-171.

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Abstract PDF: BACKGROUND
Several lines of evidence have indicated that the deregulation of apoptosis is involved in the mechanisms of cancer development, and somatic mutations of the apoptosisrelated genes have been reported in human cancers. Members of the bcl-2 family proteins regulate the intrinsic apoptosis pathway mainly in the mitochondria. The aim of this study was to explore whether the somatic mutation of the proapoptotic bcl-2 family genes, one of the mechanisms that prolong the survival of cancer cells, occurred in colorectal carcinomas.
METHODS
In the current study, to detect the somatic mutations in the DNA sequences encoding the bcl-2 homology 3 (BH3) domain of the human bak, bid, bik, bim, PUMA, bcl-rambo, bcl-G, and bmf genes in 98 colon adenocarcinomas, we used polymerase chain reaction (PCR), single strand conformation polymorphism (SSCP), and DNA sequencing.
RESULTS
The SSCP analysis detected no evidence of somatic mutations of the genes in the coding regions of the BH3 domain in the cancers.
CONCLUSIONS
The data presented here indicate that the proapoptotic bcl-2 family genes, bak, bid, bik, bim, PUMA, bcl-rambo, bcl-G and bmf may not be somatically mutated in human colorectal carcinomas, and suggest that the colorectal cancers may not utilize mutational events of these proapoptotic bcl-2 family genes in the mechanisms for evading apoptosis.

Case Report

Acardiac Fetus with Encephalocele: A case report.: Seong Beom Lee, Won Sang Park, Ki Hwa Yang, Jong Chul Shin, Jung Yong Lee, Sang Ho Kim, Choo Soung Kim; Korean J Pathol. 1994;28(6):678-681.

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Abstract PDF: The acardiac fetus is a rare type of fetal monster in which, as the name implies, the heart is completely absent. Acardius occurs only in a pair monozygotic twin, and shows various other defects in addition to the absence of the heart. Our autopsy case is acardiac anceps. He weighed 1,980 gm and the height was 33 cm. The brain is poorly developed, 60 gm in weight and similar to reversed snowman (3.5x2.8x2.8, 1.5x1.5x1.3 cm). Encephalocele, 6 cm in diameter, was communicated with the brain by a tract which contains nervous tissue and primitive choroid plexus. The upper extremities were absent, while the vertebrae and lower extremities were relatively well developed. The heart, lungs, stomach, liver, and spleen were absent, but the kidney, genital organs and urinary bladder were present. The intestine was seperated into two segments which were blindly ended, 32 cm and 15 cm in length, respectively.

Original Article

Mutation of Adenomatous Polyposis Coli Gene in Human Stomach Cancer.: Won Sang Park, Mun Gan Rhyu, Sug Hyung Lee, Yun Jun Chung, Gum Ryong Kim, Choo Soung Kim; Korean J Pathol. 1993;27(1):34-39.

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Abstract PDF: Recently the adenomaatous polyposis coli(APC) gene, a tumor suppressor gene, was identified and the cDNA was cloned from chromosome 5q21. Allelic deletion or point mutation of tumor suppressor genes(TSGs) has been considered as an important mechanism in development of human tumor. Point mutations affecting APC gene are seen in the hereditary syndrome, adenomatous polyposis and spordic colon cancer. However, the mutation of APC gene and other TSGs have not been described in gastric cancer. In order to identify the mutation of exon 11 of APC gene for gastric cancer, we amplified DNA extracted from paraffin-embedded tissues by polymerase chain reaction(PCR) and digested the PCR products with restriction enzyme Rsa I. We examined the DNA extracted from paraffin-embedded 44 gastric cancer tissues with lymph nodes. Eighteen(41%) among 44 were informative for the study exon 11 of the APC gene, and we found loss of heterozygosity(LOH) for APC in 6/18(33.3%). These data suggest that the point mutation or the base change of APC gene commonly occurs in gastric cancer. We conclude that the mutation of APC gene is strongly connected with development of human gastric cancer.

Case Report

Carcinosarcoma of the Esophagus: A report of case.: Sug Hyung Lee, Won Sang Park, Young Jin Choi, An Hee Lee, Sun Moo Kim; Korean J Pathol. 1992;26(2):191-196.

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Abstract PDF: Carcinosarcoma of the esophagus is a rare neoplasm composed of both carcinoma and spindle sarcomatous area. Usually the carcinoma component is a squamous cell carcinoma but rarely adenocarcinoma or undifferentiated carcinoma is found. The histogenesis of the sarcomatous component is still unknown. A case of ulcerated polypoid lesion with a stalk in esophagus was reported. Microscopically it was composed of spindle shaped cells interminled with squamous cell carcinoma and small cell carcinoma nests. No distinct transition between spindle shaped cells and carcinoma are was observed. Immunoreactivity to cytokeratin was observed in both carcinomatous and spindle cell component, but electron microscopic examination failed to demonstrated desmosome or tonofilaments in spindle cells. Undifferentiated small cell nests were reactive to neuron specific enolase and contained membrane bounded secretory granule in electron microscopy.

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