No abstract available.

Unstable microsatellite repeat sequences or DNA replication errors(RER) due to defective mismatch repair genes have been reported in a subset of sporadic colorectal tumors and in most tumors of patients of hereditary nonpolyposis colorectal carcinoma(HNPCC). To elucidate the clinicopathological correlation of these RER-positive cancers, we examined 16 cases of colorectal carcinoma of different histologic subtypes(6 cases of carcinoma with no gland formation, 5 cases of mucinous carcinoma and 5 cases of gland forming carcinoma). We detected RER in five cases. The patients with RER-positive cancers had a marked preponderance of carcinoma with no gland formations out of 6 carcinomas with no gland formation were RER-positive cancers) and of cancers proximal to splenic flexure(all of the RER-positive cases were proximal colon carcinomas). We conclude that RER-positive cancers have wiique pathologic features that may be useful for the screening and counselling of patients with hereditary colon cancers.

No abstract available.
Diagnosis*

Dieulafoy's vascular malformation is a rare cause of massive gastrointestinal bleeding. Most often it occurs in stomach within 6 cm from the gastroesophageal junction. Only a few cases have been reported to occur in the small intestine and colon. Occasionally, Dieulafoy's lesion of small intestine is difficult to recognize because of rarity, a paucity of symptoms and negative findings on barium studies. Therefore, this lesion needs to be considered in a patient with massive lower gastrointestinal bleeding. We report a case of Dieulafoy's vascular malformation in ileum 2 m proximal to ileocecal value in a 41-year-old woman who visited emergency clinic because of hematemesis, dizziness and vomiting. Small intestine revealed a wide-caliber artery within the submucosa showing intimal thickening, medial muscular hypertrophy and thrombosis.
Adult ; Arteries ; Barium ; Colon ; Dizziness ; Emergencies ; Esophagogastric Junction ; Female ; Hematemesis ; Hemorrhage* ; Humans ; Hypertrophy ; Ileum* ; Intestine, Small ; Stomach ; Thrombosis ; Vascular Malformations* ; Vomiting

Ovarian endometrioid adenofibroma is rare and characterized by prominent stroma. Its histologic classification is controversial but the malignant counterpart is distinguished from the borderline by the presence of confluent growth pattern of epithelium with invasion of the stroma by the endometrioid cells. A fifty-year-old woman was admitted with one month history of abdominal enlargement. Total abdominal hysterectomy with bilateral salpingo-oophorectomy was performed under the clinical diagnosis of ovarian malignancy. Grossly, the righy ovary had round, encapsulated, solid and whitish gray mass which measured 9 cm in the greatest dimension and showed peripheral small cysts. Microscopic examination revealed that the tumor consisted of endometria type glands set in fibrous stroma. The glands varied from tubules to cysts and the lining cells showed complicated architectural pattern with occasional papillary infoldings, atypical mitosis and malignant nuclear characteristics. Some cysts of glands showed intraluminal mucin products. Stromal invasions by individual epithelial cells showing malignant characteristics were often found. A brief summary of the histopathologic aspect of this tumor is presented together with review of literatures.
Female ; Humans ; Cysts

Ovarian endometrioid adenofibroma is rare and characterized by prominent stroma. Its histologic classification is controversial but the malignant counterpart is distinguished from the borderline by the presence of confluent growth pattern of epithelium with invasion of the stroma by the endometrioid cells. A fifty-year-old woman was admitted with one month history of abdominal enlargement. Total abdominal hysterectomy with bilateral salpingo-oophorectomy was performed under the clinical diagnosis of ovarian malignancy. Grossly, the righy ovary had round, encapsulated, solid and whitish gray mass which measured 9 cm in the greatest dimension and showed peripheral small cysts. Microscopic examination revealed that the tumor consisted of endometria type glands set in fibrous stroma. The glands varied from tubules to cysts and the lining cells showed complicated architectural pattern with occasional papillary infoldings, atypical mitosis and malignant nuclear characteristics. Some cysts of glands showed intraluminal mucin products. Stromal invasions by individual epithelial cells showing malignant characteristics were often found. A brief summary of the histopathologic aspect of this tumor is presented together with review of literatures.
Female ; Humans ; Cysts

A case of primary malignant melanoma of the larynx is reported. The patient, a 41-year-old Korean man, presented with dyspnea and blood tinged sputum. Physical examination showed blackish necrotic mass involving right side of the larynx. The mass proved to be malignant melanoma containing many melanin pigments. A description of the lesion and a review of literature are given.
Adult ; Aged ; Female ; Human ; Laryngeal Neoplasms/pathology* ; Larynx/pathology* ; Male ; Melanoma/pathology* ; Middle Age ; Necrosis

The molecular genetics of colorectal carcinomas are among the best understood of common human cancers. Three inter-related molecular pathways are involved. The chromosomal instability pathway begins with inactivation of the APC/beta-catenin genes followed by activation of oncogenes and inactivation of additional suppressor genes, commonly with high frequency of allelic losses, cytogenetic abnormalities. The microsatellite instability pathway begins with inactivating one of a group of genes responsible for DNA nucleotide mismatch repair leading to extensive mutations in both repetitive and non-repetitive DNA sequences with low frequencies of allelic losses and rare alteration of tumor DNA content. Finally, the CpG island methylation pathway involves inactivation of genes by methylation of cytosines in promoter regions to silence gene expression without DNA sequence alterations. Molecular genetics have the potential for clinical applications. Combination of genetic classification of high levels of microsatellite instability (MSI-H), gene expression analysis of mismatch repair genes and subsequent mutation analysis of inactivated genes can be used as an effective method for the identification of hereditary nonpolyposis colorectal carcinoma patients. Molecular genetic alterations have been proposed to be of prognostic value, including allelic deletion on chromosome 18q, and on chromosome 17p. MSI-H has been reported as a marker for better prognosis. Individualizing chemoradiation by use of predictive markers for response or resistance to therapy is important in patients with advanced disease or candidacy for adjuvant therapy.
Chromosomal Instability ; Colorectal Neoplasms/diagnosis/*genetics/pathology ; English Abstract ; Humans ; Microsatellite Repeats

ln an attempt to clarify the dual origin histiocytes and to reclassify histiocytic proliferative disorders according to their immunohistochemical properties, normal histiocytes and histiocytes in selected proliferative disorders were stained using the peroxidase-antiperoxidase method for lysozyme, 1-antichymotrypsin and for S-100 protein. The proliferated histocytes of cosinophilic granutoma and Letterer-siwe disease were strongly immunoreactive for S-100 protein. In histiocytic medullary reticulosis (HMR) and in histiocytic lymphoma, all three markers were found within the tumor cells. ln fibrous histiocytoma and in juvenile xanthogranuloma, only a few weakly immunoreactive cells for S-100 protein were observed. lnflammatory malignant fibrous histiocytoma(MFH) (Xanthosarcoma) and xanthoma were immunoreactive for 1-antichymotrypsin and lysozyme respectively. ln MFH of the storiform -pleomorphic type and in atypical fibroxanthoma, stains using all of the histiocytic markers were negative. These results suggest that eosinophilic granuloma. Letterer-Siew disease, fibroxanthoma and juvenile xanthogranloma are proliferative disorder of T-zone histiocytes; HMR and histiocytic lymphoma are those of pluripotential stem cells capable of dual histiocytic differentiation; xanthoma and xanthosarcoma are monocytic proliferative disease; and MFH of the storiform-pleomorphic type and atypical fibroxanthoma are not true histiocytic diseases.
Histiocytes/*metabolism ; Human ; Immunohistochemistry ; Reticuloendotheliosis/classification/*metabolism/pathology ; S100 Proteins/metabolism ; Support, Non-U.S. Gov't

Microsatellite mutator phenotype (MMP) tumors were reported in a subset of gastrointestinal carcinomas. The molecular pathogenesis of MMP tumors shows defects in the DNA mismatch repair genes, and also many germline and somatic mutations were reported in the MMP tumors. However, the detection of genetic defects in the MMP tumors is very difficult, mainly because many genes are included in the DNA mismatch repair genes. This study was undertaken to determine the best strategy for detecting defects in the DNA mismatch repair genes in gastrointestinal carcinomas. One of the effective ways for detecting defects in DNA mismatch repair genes is to screen the MMP tumors and evaluate the products of DNA mismatch repair genes by performing the multiplex RT-PCR method. We have screened the MMP tumors by using 5 microsatellite markers in the 12 cancer cell lines, 120 colon carcinomas and 99 gastric carcinomas and found 6 MMP cell lines, 10 MMP colon cancers, and 9 MMP gastric carcinomas. In addition, we evaluated 6 DNA mismatch repair gene products (hMSH2, hMSH3, hMSH6, hMLH1, hPMS1 and hPMS2) by multiplex RT-PCR analysis and found decreased expression of the DNA mismatch repair genes in 5 (hMSH6 in DLD-1 and HCT-15; hMSH2 in LoVo; hMLH1 and hMSH3 in HCT-116; hMLH1 in SNU-638) out of 6 MMP cell lines. We also found a decreased expression of hMLH1 in 3 out of 10 MMP colon carcinomas, and in 6 out of 9 MMP gastric carcinomas. Our results indicate that the expression analysis of the DNA mismatch repair genes by multiplex RT-PCR method can reduce the number of genes subjected to mutational analysis and is convenient for screening the responsible DNA mismatch repair genes.
Cell Line ; Colon ; Colonic Neoplasms ; DNA Mismatch Repair* ; DNA* ; Mass Screening ; Microsatellite Repeats* ; Phenotype*