Biomedical subjects

Teiichi Motoyama

Publications and source records attributed to Teiichi Motoyama.

41 records · Page 3Linked to original sources

PubMed2002

Glassy cell carcinoma of the uterine cervix: histochemical, immunohistochemical, and molecular genetic observations.

Glassy cell carcinoma (GCC) of the uterine cervix is characterized by distinctive cytological features and an aggressive clinical course. Although this tumor has been usually considered a poorly differentiated variety of adenosquamous carcinoma (ASC), a clarification of the phenotype and histogenesis of GCC is still required. We examined three GCCs and four ASCs for histochemical and immunohistochemical phenotypes and molecular genetic status, comparing them with five nonkeratinizing squamous cell carcinomas and five endocervical-type mucinous adenocarcinomas. GCCs had a profile of cytokeratin expression similar to that of reserve cells or immature squamous cells of the cervix. In addition to squamous differentiation, GCCs sporadically produced intestinal-type mucin. HPV 18 was detected in two of three GCCs and two of four ASCs. GCCs may originate from multipotential stem or reserve cells that undergo early squamous differentiation. The presence of HPV 18 might stimulate biphasic squamous and glandular differentiation.

Adenocarcinoma, Mucinous↗

PubMed2002

Molecular and cellular phenotypic profiles of gastric noninvasive neoplasia.

According to the Padova international classification, 52 gastric noninvasive neoplasias (NIN) were classified as follows: 20 low-grade NIN (L-NIN); 9 high-grade NIN including suspicion for carcinoma without invasion (H-NIN); and 23 high-grade NIN including carcinoma without invasion (Ca-NIN). The molecular and cellular phenotypic profiles were investigated and compared. The APC gene was mutated in seven (35%) L-NIN, two (22%) H-NIN, and two (9%) Ca-NIN tumors; APC mutations were significantly more frequent in L-NIN compared with Ca-NIN tumors (p < 0.05). Mutations of the p53 gene were found in five (22%) Ca-NIN tumors but were not observed in L-NIN or H-NIN tumors (p < 0.05). Loss of heterozygosity involving at least one chromosomal locus was detected in 14 (61%) Ca-NIN tumors but was not detected in L-NIN or H-NIN tumors. High-frequency microsatellite instability (MSI-H) was detected in one (5%) L-NIN tumor and in six (26%) Ca-NIN tumors. The frequencies of loss of heterozygosity and MSI-H were significantly higher in Ca-NIN than in L-NIN or H-NIN tumors (p < 0.05). Nuclear accumulation of p53 protein was detected in no L-NIN tumors, 1 (11%) H-NIN tumor, and 10 (44%) Ca-NIN tumors (p < 0.01). All tumors with loss of hMLH1 expression exhibited MSI-H (p < 0.01). Cellular phenotypic analysis revealed that seven (35%) L-NIN tumors and one (4%) Ca-NIN tumor had complete-type intestinal metaplastic phenotype and that one (5%) L-NIN tumor and one (4%) Ca-NIN tumor had a gastric foveolar epithelial phenotype, whereas the remaining tumors exhibited an ordinary phenotype. Thus, the complete-type intestinal metaplastic phenotype was more characteristic of L-NIN tumors than of H-NIN or Ca-NIN tumors (p < 0.01). In summary, the Padova international classification correlated with both the molecular and cellular phenotypic profiles. In practice, p53 and hMLH1 immunohistochemistry discriminated Ca-NIN from L-NIN and H-NIN tumors.

Adaptor Proteins, Signal Transducing↗

PubMed2002

Frequent epigenetic silencing of the p16 gene in non-small cell lung cancers of tobacco smokers.

Epidemiological studies have demonstrated a causal link between tobacco smoking and lung cancer. We investigated the association between inactivation of the p16 gene and tobacco smoking in 51 non-small cell lung cancers (NSCLCs). Aberrations of the p16 gene were studied by PCR single-strand conformation polymorphism analysis, followed by direct sequencing, microsatellite analysis, methylation-specific PCR, and immunohistochemistry. Mutations were detected in 3.9% (2/51) of the tumors; the tumors carrying mutations were from smokers. The incidences of loss of heterozygosity, homozygous deletion, and promoter methylation in 37 smokers vs. 14 non-smokers were; 45.9% vs. 28.6%, 16.2% vs. 7.1%, and 35.1% vs. 7.1%, respectively. Among these, only the association between promoter methylation and tobacco smoking was statistically significant (P < 0.05). Therefore, epigenetic aberration is considered to be a major causative event in p16 silencing by tobacco smoking. Loss of p16 protein expression was apparent in 49% (25/51) of the tumors, and was associated with tobacco smoking (P < 0.05) and with histological type (P < 0.05). These findings suggest that tobacco smoking leads to inactivation of the p16 gene mainly through the epigenetic mechanism, ultimately increasing the risk of NSCLC, especially the squamous cell histological type.

Aged↗

PubMed2002

Hypermethylation of the TSLC1 gene promoter in primary gastric cancers and gastric cancer cell lines.

The TSLC1 (tumor suppressor in lung cancer-1) gene is a novel tumor suppressor gene on chromosomal region 11q23.2, and is frequently inactivated by concordant promoter hypermethylation and loss of heterozygosity (LOH) in non-small cell lung cancer (NSCLC). Because LOH on 11q has also been observed frequently in other human neoplasms including gastric cancer, we investigated the promoter methylation status of TSLC1 in 10 gastric cancer cell lines and 97 primary gastric cancers, as well as the corresponding non-cancerous gastric tissues, by bisulfite-SSCP analysis followed by direct sequencing. Allelic status of the TSLC1 gene was also investigated in these cell lines and primary gastric cancers. The TSLC1 promoter was methylated in two gastric cancer cell lines, KATO-III and ECC10, and in 15 out of 97 (16%) primary gastric cancers. It was not methylated in non-cancerous gastric tissues, suggesting that this hypermethylation is a cancer-specific alteration. KATO-III and ECC10 cells retained two alleles of TSLC1, both of which showed hypermethylation, associated with complete loss of gene expression. Most of the primary gastric cancers with promoter methylation also retained heterozygosity at the TSLC1 locus on 11q23.2. These data indicate that bi-allelic hypermethylation of the TSLC1 promoter and resulting gene silencing occur in a subset of primary gastric cancers.

Adult↗

PubMedDate not supplied

Clear cell carcinoma arising in a cesarean section scar. Report of a case with fine needle aspiration cytology.

BACKGROUND: Clear cell carcinoma arising in a cesarean section scar is an extremely rare disease. To the best of our knowledge, there is no published report on the aspiration cytology. CASE: A 56-year-old woman presented with a mass in a cesarean section scar. Initially an abdominal desmoid was considered, but the features of fine needle aspiration (FNA) cytology suggested an adenocarcinoma. The resected tumor was histologically composed of clear cell carcinoma showing cystic, solid and papillary patterns. CONCLUSION: FNA cytology of masses arising in a surgical scar can be a useful tool in obtaining an accurate pathologic diagnosis of a malignant neoplasm.

Abdominal Wall↗