Primary cutaneous meningiomas are extremely rare tumors found in the cutis or subcutis, and generally have a benign course. The tend to be located on the scalp, face, neck. or paravertebral area. The primary cutaneous meningioma bears similarities to developmental defects and probably originates from arachnoid cell rests in the skin, although diverse groups of cutaneous meningiomas seem to arise from several different sources. A case of primary cutaneous meningioma occuring in the scalp of left parietal area of a 27-year-old female is presented. Clinically the lesion appeared as indolent, slow growing cutaneous mass and has no connection with underlying brain tissue, as determined by examination of the roentgenographs. The definite diagnosis was made after pathological examination. Microscopically the tumor is composed of sheets and nests of meningothelial cells. Immunohistochemical and electron microscopic studies reveal the typical findings of meningioma.
Female ; Humans ; Meningioma

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.
Adenocarcinoma

This experiment is designed to find differentially expressed genes in p388D1 cells that are specific for the serum deprived state. Serum starvation induces cells to enter the quiscent state in the cell cycle and is used to arrest cell growth or synchronize the cell cycle. Differential display and ribonuclease protection assay were used to identify quantitative change in gene expression. Nineteen genes that showed a differential expression in the differential display were cloned and 7 clones were verified by a ribonuclease protection assay. Among the 7 clones clone-16 showed same expression pattern in comparison with the differential display. Deduced amino acid sequences of clone-16 had N-glycosylation motif and seems to be a secretory protein. Getting a full sequence of clone-16 is critical for the characterization of it.
Amino Acid Sequence ; Cell Cycle ; Clone Cells ; Gene Expression ; Ribonucleases ; Starvation

PURPOSE : Cell death deregulation is a hallmark of human cancers. BNIP3, which was initially identified as a pro-apoptotic member of the Bcl-2 family, plays an important role in apoptosis, necrosis and autophagy. This study was conducted to explore whether mutation of the BNIP3 gene is a characteristic of human non-small cell lung cancers (NSCLC). MATERIALS AND METHODS : In the current study, we used polymerase chain reaction (PCR), single-strand conformation polymorphism (SSCP), and DNA sequencing to detect somatic mutations in the DNA sequences encoding the BH3 (Bcl-2 homology3) and TM (transmembrane) domains that are important to the cell death function of BNIP3 in 48 NSCLCs. RESULTS : SSCP analysis revealed no evidence of somatic mutation in the DNA sequences encoding the BH3 and TM domains of the human BNIP3 gene in the 48 NSCLCs evaluated in this study. CONCLUSION : The data presented here indicate that the pro-apoptotic BNIP3 gene may not be somatically mutated in human NSCLCs, which suggests that mutational events of the BNIP3 gene may not be involved in the mechanisms by which NSCLCs evade cell death
Apoptosis ; Autophagy ; Base Sequence ; Carcinoma, Non-Small-Cell Lung ; Cell Death ; Humans ; Lung Neoplasms* ; Lung* ; Necrosis ; Polymerase Chain Reaction ; Polymorphism, Single-Stranded Conformational ; Sequence Analysis, DNA

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.
Humans ; Genes, Tumor Suppressor ; Stomach Neoplasms

PURPOSE: Several lines of evidence have indicated that the deregulation of apoptosis is involved in the mechanisms of cancer development, and somatic mutations of the apoptosis-related genes have been reported in human cancers. In addition to its role in oxidative phosphorylation, release of cytochrome c from the mitochondrial intermembrane space results in nuclear apoptosis. The aim of this study was to explore whether alteration of cytochrome c gene mutation is a characteristic of human non-small cell lung cancers (NSCLC). MATERIALS AND METHODS: In the current study, to detect the somatic mutations in the DNA sequences encoding cytochrome c in 48 NSCLCs, we used polymerase chain reaction (PCR), single-strand conformation polymorphism (SSCP), and DNA sequencing. RESULTS: The SSCP analysis revealed no mutation in the entire coding regions and all splice sites of human cytochrome c gene in the 48 NSCLCs. CONCLUSION: The data presented here indicate that the pro-apoptotic cytochrome c may not be somatically mutated in human NSCLCs, and suggest that NSCLCs may not utilize mutational events of cytochrome c gene in the mechanisms for evading apoptosis.
Apoptosis ; Base Sequence ; Carcinoma, Non-Small-Cell Lung ; Clinical Coding ; Cytochromes c* ; Cytochromes* ; Humans ; Lung Neoplasms* ; Lung* ; Oxidative Phosphorylation ; Polymerase Chain Reaction ; Polymorphism, Single-Stranded Conformational ; Sequence Analysis, DNA

No abstract available.
Frameshift Mutation ; Microsatellite Instability ; Microsatellite Repeats

Apoptosis is a principal type of cell death, and it has a profound effect on the development of cancer. It is also well known that anti-cancer agents induce apoptosis, and defects in the apoptosis pathways reduce the treatment sensitivity. Of the many pathways that induce apoptosis, the mechanisms of the intrinsic and extrinsic apoptosis pathways are well established. Non-small cell lung cancer (NSCLC) is a leading cause of cancer death worldwide, yet the exact molecular mechanisms of its development remain unclear. Apoptosis deregulations may underlie the development and pathogenesis of NSCLC. This review discusses the general mechanisms of apoptosis, the constituents of the apoptosis machinery and the alterations of the apoptosis-related genes in NSCLC
Apoptosis ; Carcinoma, Non-Small-Cell Lung ; Cell Death

PURPOSE: Mounting evidence indicates that perturbation of tyrosine phosphorylation is implicated in the development of many human diseases, including cancers. Docking proteins (DOKs) are tyrosine-phosphorylated proteins that negatively regulate tyrosine kinase signaling and they are considered to be tumor suppressors. Deletion and the altered expression of the DOK2 gene have been studied in leukemias and lung cancers. However, the somatic mutation status of the DOK2 gene has not been studied in lung cancers. The aim of this study was to see whether alterations of DOK2 protein expression and somatic mutation of the DOK2 gene are present in human non-small cell lung cancer (NSCLC). MATERIALS AND METHODS: We analyzed DOK2 somatic mutation in 45 NSCLCs (23 adenocarcinomas (AD) and 22 squamous cell carcinomas (SCC) by single-strand conformation polymorphism (SSCP). We examined the DOK2 protein expression in 45 NSCLCs by immunohistochemistry. RESULTS: SSCP analysis revealed no evidence of somatic mutation in the DNA sequences encoding the DOK2 gene in the 45 NSCLCs. Among the informative cases, 27% and 21% of the ADs and SCCs showed allelic loss in the DOK2 locus, respectively. On the immunohistochemistry, DOK2 protein was expressed in the normal bronchial epithelial cells, while it was lost in 10 (22%) of the NSCLCs. CONCLUSION: Our data indicates that DOK2 is altered in NSCLC at the expressional level, but not at the mutational level. The data also suggests that loss of the expression of DOK2 might play roles in NSCLC development by possibly altering tyrosine kinase signaling.
Adenocarcinoma ; Base Sequence ; Carcinoma, Non-Small-Cell Lung ; Carcinoma, Squamous Cell ; Epithelial Cells ; Gene Expression ; Humans ; Immunohistochemistry ; Leukemia ; Loss of Heterozygosity ; Lung ; Lung Neoplasms ; Phosphorylation ; Polymorphism, Single-Stranded Conformational ; Protein-Tyrosine Kinases ; Proteins ; Tyrosine

PURPOSE: Several lines of evidence have indicated that perturbations of autophagy are involved in the development of many human diseases, including cancer. The autophagy-related genes (ATG) encode proteins that play important roles in autophagic processes. The aim of this study was to see whether alterations of the ATG5 protein expression and somatic mutations of the ATG5 gene are present in human non-small cell lung cancers (NSCLCs). MATERIALS AND METHODS: We analyzed the ATG5 somatic mutations in 45 NSCLCs by performing single-strand conformation polymorphism (SSCP). We examined the ATG5 protein expression in 45 NSCLCs by performing immunohistochemistry. RESULTS: The SSCP analysis revealed no evidence of somatic mutation in the DNA sequences encoding the ATG5 gene in the 45 NSCLCs. On the immunohistochemistry, ATG5 protein was expressed in the normal bronchial epithelial cells, while it was lost in 9 (20%) of the NSCLCs. CONCLUSION: Our data indicates that ATG5 is altered in NSCLC at the expressional level, but not at the mutational level. The data also suggests that the loss of expression of ATG5 might play a role in the pathogenesis of NSCLC by altering autophagic and apoptotic cell death.
Autophagy ; Base Sequence ; Carcinoma, Non-Small-Cell Lung ; Cell Death ; Epithelial Cells ; Humans ; Immunohistochemistry ; Lung ; Lung Neoplasms ; Polymorphism, Single-Stranded Conformational ; Proteins