Fine Needle Aspiration Cytology of Extranodal Marginal Zone B cell Lymphoma with Abundant Plasma Cells and Eosinophilic Histiocytes in Parotid Gland / 대한세포병리학회지

The authors present the fine needle aspiration cytology (FNAC) cytologic findings of a case of extranodal marginal zone B cell lymphoma (MZBCL), which featured abundant plasma cells and eosinophilic histiocytes arising in both parotid glands. A 49-year-old female presented with palpable masses in both parotid glands. She had been suffering from systemic lupus erythematosus and rheumatoid arthritis. The lesions were evaluated by FNAC and smears showed a small number of clusters of oncocytic cells with abundant eosinophilic granular cytoplasm and small nuclei, intermixed with small to medium-sized lymphoid cells containing round to lobulated nuclei, which suggested Warthin's tumor. Some of lymphoid cells had a plasmacytoid appearance, and some scattered large cells contained a large amount of eosinophilic cytoplasm. Bilateral superficial parotidectomy was performed and a histopathologic study indicated MZBCL with abundant plasma cells, intermixed with eosinophilic histiocytes. The presence of oncocytic cells and a mixture of lymphoid and plasma cells indicates Warthin's tumor, but the cytologic features of a relatively monotonous small to medium-sized lymphoid infiltrate suggest the possibility of MZBCL in the clinical setting of an FNAC study performed on a patient suffering from a connective tissue disease.

Genetic and Epigenetic Alterations of the Wnt/beta-catenin Signaling Pathway in Cancer of the Ampulla of Vater

BACKGROUND: Carcinoma of the ampulla of Vater is rare and its pathogenesis is unclear. The role of epigenetic changes in the APC or CDH1, in the Wnt pathway, has not been reported in ampullary carcinomas. METHODS: We performed immunohistochemistry on 73 sporadic ampullary carcinomas to identify Wnt-related molecules (APC, beta-catenin, E-cadherin, c-erbB2, cyclin D1) and examined mutations in the CTNNB1, loss of heterozygosity of 5q21, and the methylation status of the CpG island of APC and CDH1. RESULTS: Thirteen tumors (17.8%) showed abnormal nuclear localization of beta-catenin; this was more prominent in the intestinal type than in the pancreaticobiliary type (p=0.01). The loss of APC correlated with the loss of beta-catenin or c-erb B2 (p<0.01). The prognosis was worse in the group with APC loss than when APC was maintained (p<0.05). There was no mutation identified in CTNNB1. Six (24%) out of 25 informative cases had 5q21 allelic loss. CpG island methylation in APC and CDH1 was detected in 33 (45.2%) and 29 (31.5%) cases, respectively. CONCLUSIONS: The absence of mutations in CTNNB1 and the epigenetic alteration of APC and CDH1, might be characteristic changes in the Wnt/beta-catenin signaling pathway during the carcinogenesis of ampullary carcinomas.

Metastatic Medullary Carcinoma of Thyroid to Breast; A Case Initially Diagnosed as Primary Invasive Lobular Carcinoma: A Case Report

Metastasis to the breast from medullary carcinoma of the thyroid is extremely rare. We report a case of metastatic medullary carcinoma of the thyroid which presented as multiple breast masses with ipsilateral axillary lymphadenopathy in a 48-year-old woman. Six years ago, she underwent total thyroidectomy and neck dissection because of palpable neck masses, with a diagnosis of medullary thyroid carcinoma. Histological features of breast masses showed single- file or linear-cord arrangements, with plasmacytoid appearance, and the initial diagnosis was invasive lobular carcinoma. She underwent modified radical mastectomy. The tumor cells were diffusely positive for E-cadherin, calcitonin and thyroid transcription factor-1 (TTF-1) and were metastatic medullary carcinoma of thyroid. In the patients with a history of medullary carcinoma of the thyroid, a careful examination is necessary for a breast mass composed of solid and cord-like clusters of small round to ovoid cells with plasmacytoid appearance. Immunohistochemical staining for E-cadherin, calcitonin and TTF-1 could be helpful for differential diagnosis.

Follicular Lymphoma with Monoclonal Plasma Cell Differentiation: A Case Report

We present a case of recurrent follicular lymphoma with an extensive plasma cell component involving infra-auricular lymph nodes in a 64 year-old woman. Immunohistochemical staining showed a strongly positive reaction of the follicles with CD20, bcl-2, bcl-6, CD10 and CD21 on the first biopsy specimen. The intrafollicular and interfollicular plasma cells showed monoclonality for IgG heavy chain and lambda light chain. The histological and immunohistochemical findings in the recurrent tumor were identical with those of the original. Discussion is focused on the importance of the differential diagnosis between reactive lymphoid hyperplasia and other lymphomas having plasmacytic differentiation.

Liposclerosing Myxofibrous Tumor in Tibia: A Case Report and Review of the Literature

Liposclerosing myxofibrous tumor (LSMFT) is a benign fibro-osseous lesion that is characterized by a complex mixture of histologic elements, including its fibrous dysplasia-like features and its lipoma, myxofibroma, xanthoma and pseudo-Paget's bone patterns. However, this lesion is considered by some researchers as a variant of fibrous dysplasia or as the non-specific end result of degenerative change, while it is considered by others as a definite clinicopathologic entity. Here, we report on a case of LSMFT occurring in tibia, which is a very uncommon location for this tumor, and we review the related literatures. The case presented here shares features with those described for LSMFT, except for the location of this tumor. We believe that more studies on a larger scale that compare LSMFT with other benign bone lesions, including fibrous dysplasia, are required to clarify the origin and behavior of this lesion.

The Expressions of Tyrosine Kinase Receptors, EphA2, c-met and c-erbB-2 in the Human Breast

BACKGROUND: Tyrosine kinase receptor (TKR) is an important protein for normal-development, growth and tumorigenesis in human tissues. The purpose of this study was to evaluate the effect of TKR in the progression of breast cancer. METHODS: The expressions of EphA2, c-met and c-erbB-2 were examined, by using immunohistochemical methods and RT-PCR, in samples of breast tissue that included 111 samples of normal epithelium, 34 samples of ductal carcinoma in situ (DCIS), and 109 samples of invasive ductal carcinomas (IDC). The results were compared with the prognostic parameters of breast cancer including the tumor grade, growth pattern, lymph node metastasis and the expressions of ER, PR, p53 and Ki-67. RESULTS: The protein expressions of the three TKRs were higher in DCIS and IDC than in normal epithelium. The protein expression of EphA2 was correlated with a tumor grade, a labeling index of Ki-67, and the protein expression of c-met. Overexpression of c-erbB-2 was correlated with lymph node metastasis. The mRNA levels of the three TKRs were correlated with each other in normal tissue and IDC. The level of c-met mRNA was higher in the low grade tumors. CONCLUSIONS: The three TKRs may play roles in the tumorigenesis of human breast cancer. The overexpressions of EphA2 and c-erbB-2 may be a poor prognostic parameter in breast cancers.

Comparative Analysis of Serum Mannose-Binding Lectin in Normal Population and Patients with Different Types of Cancer

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.

Microsatellite Alterations of Chromosome 9p, 13q, 16q in Hepatocellular Carcinoma

PURPOSE: Hepatocellular carcinoma (HCC) patients are asymptomatic and the tumor remains in an unresectable state until the tumor progresses. Recently much efforts for elucidation of the early hepatocarcinogenesis have been made, and for this purpose it is very crucial to investigate the genetic abnormalities. We evaluated microsatellite alterations of five markers from chromosome 9, 13, 16 and investigated the relationships with the clinicopathological parameters in HCC. METHODS: The microsatellite alteration analysis was performed using polymerase chain reaction with five polymorphic microsatellite markers (D9S171, D9S1747, D13S156, D16S419, D16S3106) in 40 surgically resected HCCs and their respective non-tumorous counterparts. RESULTS: D9S171, D9S1747, D13S156, D16S419, D16S3106 abnormalities were detected in 20.0%, 14.3%, 50.0%, 32.4% and 22.6%, respectively. Loss of heterozygosity (LOH) of D9S171 correlated well with higher tumor histologic grade and LOH of D13S156, D16S419 and D16S3106 correlated well with increased tumor size. Microsatellite instability (MSI) was found in two markers, D13S156, D16S419. CONCLUSION: As a result, we concluded that alterations in microsatellites of various chromosomes may contribute to the hepatocarcinogenesis and tumor progression. Especially LOH of chromosome 13 and 16 are considered to correlate with tumor progression.

K-ras Gene Mutations and Expression of K-ras, p16, Cyclin D1 and p53 in Synchronous Lesions of The Colon Adenoma-Carcinoma Sequences

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.

Association between the Expresson of MMP-2 and TIMP-2, and Growth Pattern of Tumor Border, Lymph Node Metastasis, and Estrogen Receptor in the Invasive Ductal Carcinoma of the Breast

The most important prognostic factor of breast cancer is the status of lymph node or distant metastasis, which is resisted by basement membrane and stromal matrix. MMP (matrix metalloproteinase)-2 is a 72-kilodalton type IV collagenase/ gelatinase and degrades the type IV collagen which is a main component of the basement membrane. Therefore, MMP-2 is believed to be one of the key molecule for cancer invasion and metastasis. Enzymatic activity of MMP is inhibited by TIMPs (tissue inhibitors of metalloproteinase). TIMP-2 forms a complex with latent pro-MMP-2 and inhibits the active forms of MMP-2. The balance of MMPs and TIMPs is suspected as the important factor of invasion and metastasis of the tumor cells. We studied the association between the expression of MMP-2/TIMP-2 and growth pattern of tumor border, lymph node metastasis, and estrogen receptor expression in the 57 cases of invasive ductal carcinoma of the breast using immunohistochemical staining methods. The results revealed increased expression of MMP-2 in the infiltrating tumor border and tumors with positive lymph node metastasis and negative estrogen receptor with no statistical significance (p>0.05). But the expression of TIMP-2 was increased in expanding tumor border and tumors with positive lymph node metastasis and negative estrogen receptor without statistical significance (p>0.05).

Growth Factor mRNA Expression in Intimal Hyperplasia after Endothelial Denudation

Intimal hyperplasia is the universal response to endothelial denudation and occur after a variety of vascular procedures. In a proportion of cases the smooth muscle cell proliferation may lead to stenosis of the blood vessels. The precise pathophysiologic pathways leading to the development of intimal hyperplasia have not been characterized. This study was undertaken to examine the effect of drugs on the development of proliferative intimal lesion after experimental arterial injury in a rat model. Aortic denudation was performed by balloon catheter in 20 rats. The rats were divided into three group: 1) control group, normal feeding, 2) heparin group, heparin 1200 U/kg/day subcutaneously, 3) ACE inhibitor group, ramipril 10 mg/kg/day subcutaneously. The rat were sacrificed and aortas were perfused and fixed at 21 days after denudation. Microscopic findings were observed and cross sectional intima-to-media ratio were calculated. To evaluate the effects of various drugs on gene expression of aortic smooth muscle cell, semiquantitative reverse transcription polymerase chain reaction(RT-PCR) was done. After reverse transcription, PCR was done to evaluate the change of gene expression in platelet-derived growth factor(PDGF-B), transforming growth factor-beta(TGF-beta). The results were as follows: 1) Normal aorta with intima to media ratio was 0.38+/-0.06. 2) Marked intimal thickening with a mean I-M ratio of 1.35+/-0.45 in the control group. 3) In contrast, the I-M ratio in the heparin group was 0.54+/-0.23, ramipril group was 0.71+/-0.27(P<0.05). 4) mRNA expression of PDGF-B did show significantly increased in control group compared to normal group(0.97+/-0.34 vs 1.60+/-0.21), treatment with heparin and ACE inhibitor shows a tendency to downregulation of mRNA expression to control group(1.04+/-0.31 in heparin group, 1.23+/-0.41 in ACE inhibitor treated group). 5) mRNA expression of TGF-beta was decreased in control group compared to normal group(2.80+/-0.74 vs 1.97+/ 0.24), treatment with heparin and ACE inhibitor shows a tendency to downregulation of mRNA expression to control group(1.36+/-0.40 in heparin group, 1.65+/- 0.45 in ACE inhibitor treated group). In summary, this study shows that repair in even the simplest model of vascular injury is an exceedingly complex, including upregulation of PDGF gene expression. Treatment with heparin and ACE inhibitor revealed a downregulation of each mRAN expression to control group. There results suggest that dysregulation of there gene expression may be involved in the pathogenesis of intimal hyperplasia after endothelial injury.

Angiogenesis and Basic Fibroblast Growth Factor Expression of Intervertebral Disc in the Patients with Back Pain / 대한정형외과학회잡지

In the normal disc tissue, the blood vessles have not been observed. It has been suggested that the vascular ingrowth promotes the granulation tissue formation in the herniated disc tissue. The origin of capillaries observed in the herniated disc tissue has remained unclear, but basic fibroblast growth factor(bFGF) may be the important inducer of capillary ingrowth. The purpose of this study is to evaluate the neovascularization in the intervertebral disc without rupture of annulus fibrosus, not being exposed to epidural fat. The disc tissues including nucleus pulposus and annulus fibrosus were obtained at anterior interbody fusion from 30 patients with back pain. All specimens were immediately frozen and stored at -70degrees C. Hematoxylin-eosin stain, polyclonal von Willebrand factor(FVIII) antibody, smooth muscle actin antibody and anti-human endothelial cell antibody(CD31) were used to confirm the blood vessel. Polyclonal bFGF antibody expression was evaluated in the disc tiussues. All of the blood vesseles were observed in the inner portion of annulus fibrosus and the transitional zone. The blood vesseles were observed in 96.7% with hematoxylin-eosin stain, 83.3% with smooth muscle actin antiboy stain, 90% with FVIII, 86.7% with CD31 and the immunopositive blood vesseles were observed in 83.3% with bFGF immunostain. The neovascularization of disc was frequently found in the annulus fibrosus and the transitional zone. The neovasuarlization of intervertebral disc was present in the intervertebral disc without rupture of annulus fibrosus.

p53 Mutation and Expression of Rb Protein in Germ Cell Tumors

We investigated the role of the tumor suppressor genes in the germ cell tumor. Immunohistochemistry (IHC) and polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP) for p53 mutation were done in 46 cases of the germ cell tumor with paraffin embedded tissue. The immunohistochemical staining for Rb protein was also performed in the same specimens. The following results were obtained. The overexpression of the p53 protein was detected in 7 of 46 cases (15%). p53 mutation by PCR-SSCP was detected in 1 of 46 cases (2.2%). Expression of Rb protein was negative in 19 cases (41%). These results suggest that p53 mutation does not play an important role in the initiation and progression of germ cell tumors.

A Comparative Study of Immunohistochemical Expression of p53, bcl-2, c-erbB-2, and MIB-1 in Polypoid and Infiltrative Colorectal Carcinomas

Almost all colorectal carcinomas have been thought to develop from pre-existing adenomas. However, some colorectal carcinomas can arise directly from normal flat mucosa, and usually form infiltrative mass at the early stage. The carcinogenesis of this infiltrative carcinoma may be different from the well-known adenoma-carcinoma sequence, which usually forms a polypoid mass. The purpose of this study is to investigate the different expression of various oncogenes in polypoid carcinoma and infiltrative carcinoma. We performed immunohistochemical staining on p53, bcl-2, c-erbB-2 and MIB-1 in 29 polypoid carcinomas arised from adenomas, and 21 infiltrative carcinomas. The average tumor size of infiltrative carcinomas (5.5 cm) was larger than that of polypoid carcinomas (3.1 cm), and the polypoid carcinomas were differentiated more than the infiltrative carcinomas. The results of p53, bcl-2, c-erbB-2, and MIB-1 antisera immunoreactivity in the polypoid carcinoma were 79%, 17%, 21%, and 100%, and those in the infiltrative carcinoma were 71%, 29%, 29%, and 100%, respectively. However the diffuse positivities of p53 and MIB-1 antisera were slightly higher in the infiltraive carcinomas (62%, 76%) than in the polypoid carcinomas (55%, 41%) (p=0.63, 0.01). And the results of p53 and c-erbB-2 immunoreactivity in the adenomas were 52% and 17%, respectively, which is significantly lower than that in the polypoid carcinoma(p=0.03, 0.74). The immunoreactivty of bcl-2 in the adenoma was 72%, which was significantly higher than that in the polypoid carcinoma (17%) (p<0.01). In summary, we did not show the significant difference in expression of p53, bcl-2, c-erbB-2, and MIB-1 proteins between polypoid and infiltrative carcinomas. However, the tendency of infiltrative carcinomas having a more aggressive nature suggests another carcinogenetic mechanism is involved in the colorectal carcinogenesis.

Drugs in Reducing the Development of Rat Intimal Hyperplasia after Endothelial Denudatiotn

Intimal hyperplasia is the universal response to endothelial denudation and occur after a variety of vascular procedures. In a proportion of cases the smooth muscle cell proliferation may lead to stenosis of the blood vessels. The precise pathophysiologic pathways leading to the development of intimal hyperplasia have not been characterized. Once the surface has been denuded of endothelium, a stereotyped sequence of events ensues and leads to intimal thickening. The denuded regions are immediately covered by a carpet of platelets. SMC in the media begin to proliferate. They then migrate into the intima and continue to proliferate as well as to synthesize and secrete large amounts of extracellular matrix. This study was undertaken to examine the effect of drugs on the development of proliferative intimal lesion after experimental arterial injury in a rat model. Aortic denudation was performed by balloon catheter in 30 rats. The rats were divided into five group: control group, normal feeding; heparin group, heparin 1200 U/kg/day subcutaneously; steroid group, dexamethasone 0.1 mg/kg/day; CsA group, CsA 3 mg/kg/day subcutaneously; ACE inhibitor, ramipril 10 mg/kg/day subcutaneously. The rat were sacrified and aortas were perfused and fixed at 21 days after denudation. Microscopic findings were observed and cross sectional intima-to-media ratio were calculated. The results were as follows: 1) Normal aorta with intima to media ratio was 0.38+/-0.06 2) Marked intimal thickening with a mean I-M ratio of 1.35+/-0.45 in the control group. 3) In contrast, the I-M ratio in the heparin group was 0.54+/-0.23, steroid group was 0.48+/-0.21, CsA group was 0.64+/-0.12, ramipril group was 0.71+/-0.27(P<0.05). In summary, this study shows that repair in even the simplest model of vascular injury is an exceedingly complex process and further studies are required.

The Immunohistochemical Study of Oncogene and Tumor Suppressor Gene Proteins on Bone Tumor / 대한정형외과학회잡지

The discovery of oncogenes and tumor suppressor genes have made it possible to partly understand the mechanism of cancer development. It is generally accepted that the cancer development is caused by specific gene alterations and now more than 100 oncogenes and suppressor genes are known to be involved in human carcinogenesis. However, there are only a few reports about oncogene expression on bone tumors. The author carried out an immunohistochemical study to reveal the oncogene and suppressor genes on carcinogenesis of bone tumors using antibodies against c-myc, c-H-ras, p53 and EGF. In 32 cases of osteochondrorma, EGF, p53 and c-myc antisera revealed positive reaction in 4 (12.5%), 2 (6.3%) and 7 (21.9%) cases, and, in 4 cases of chondrosarcoma, c-myc antisera revealed positive reaction in 2 (50%) cases. In 21 cases of osteosarcoma, the positive reaction of p53 was noted in 10 (47.6%) cases and that of c-myc in 3 (14.3%) cases. In 14 cases of fibrous bone tumors, there are only 2 (14.3%) cases of positive reaction with p53. These results suggest some roles of the p53 and c-myc genes in osteosarcoma development and c-myc gene in osteochondroma and chondrosarcoma development.

Expression of TGF-alpha, p53 and PCNA in Laryngeal Dysplasia / 대한이비인후과학회지

BACKGROUND: Transforming growth factor(TGF-alpha) is a polypeptide which is structurally related to epidermal growth factor(EGF) and binds to the epidermal growth factor receptor(EGFR). TGF-alpha utilizes EGFR to increase the activation of tyrosine kinase to involve in signal transduction of cellular growth. TGF-alpha synthesis occurs in a variety of neoplastic cells. p53 is a tumor-suppressor gene. There is a strong corrleation between immunohistochemical p53 positivity and p53 mutations in lung and laryngeal carcinoma. PCNA is expressed by cycling cells in late G1, S and G2 phase, and may be used to indicate the degree of cellular proliferation. OBJECTIVES: To evaluate whether TGF-alpha, p53 and PCNA can be used as an indicator to malignant transformation of dysplasia in larynx or not. MATERIALS AND METHODS: The authors investigated the TGF-alpha score, p53 immunoreactivity and PCNA proliferating index by immunohistochemical staining in 30 laryngeal dysplasia from 1992 to 1995. RESULTS: Dysplasia with malignant transformation showed values of 5.46 for TGF-alpha, 29.2 for PCNA proliferating index and 37.5 for p53 immunoreactivity. Dysplasia without malignant transformation showed values of 1.88 for TGF-alpha, 8.6 for PCNA proliferating index and 4.5 for p53 immunoreactivity. Conclusions: The results suggest that TGF-alpha, p53 and PCNA could be an useful indicator to predict the progression of laryngeal dysplasia.

Cytologic Features of Medullary Carcinoma of the Thyroid Occurring in a Child: A Case Report / 대한세포병리학회지

Medullary carcinoma of the thyroid gland is a malignant neuroendocrine tumor arising from calcitonin producing-parafollicular cells. The tumor is clinically divided into sporadic and familial form, constituting about 80% and 20%, respectively. Recently, we experienced a case of unilateral and solitary sporadic medullary carcinoma of the left thyroid gland. The patient was a 9 year-old female, who presented with a palpable mass on the anterior lateral neck of 8 months duration without any familial and personal history of neuroendocrine disease. The cytopathologic findings showed spindle cells and plasmacytoid cells in the background of colloid-like materal. The nuclei were eccentrically located, mildly hyperchromatic and pleomorphic, showing speckled chromatin pattern without nuclear inclusion or prominent nucleoli. The cytoplasm was abundant and had a pale granular cyanophilic appearance. No amyloid materal could be identified.

An Immunohistochemical study on distribution of natural killer(NK) cell in patients with cervical dysplasia and cervical cancer / 대한부인종양콜포스코피학회잡지

Natural Killer (NK) cells are a subpopulation of in vivo activated lymphocytes that display spontaneous cytotoxicity against a variety of targets as virus-infeeted, and transformed neoplastic cells, in major histocompatibility-unrestricted fashion. Depression of the NK aetivity in patients with advanced stages of various types of solid neopls,sms appears to be dependent upon the prcgressive growth and metastatic spread of the tumor. There are many reports that different distribution of subpopulations of lymphocytes in neopiastic tissue may influence the prognosis of the patients, In this study, we have performed immunohistochemieal study with Leu-7, MT1, LN2, and antilysozyrne antiserum on the tissue of uterine cervieal dysplasia and cancer to investigate the distribution of the NK cell, T cell, B cell, and macrophage. The results were as follows ; 1. The major subpopulation of lymphocytes infiltrating the lesion of intraepithelial neoplasia and squamous cell carcinama was T cell. 2. The number of infiltrated. lymphocytes was layer in the lesion of keratinzing type than in that of non keratinizing and small cell earcinorna of the uterine cervix. 3. NK cell was more frequently noted in the malignant lesion than the dysplastic lesion.

A Case of Unilateral Lung Agenesis (Right) Associated with Skeletal Anomalies

No abstract available.