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Biomedical subjects

A Horii

Publications and source records attributed to A Horii.

At least 91 records · Page 5Linked to original sources
PubMed1998

Detailed deletion mapping on chromosome 1p32-p36 in human colorectal cancer: identification of three distinct regions of common allelic loss.

Recent studies have suggested the existence of one or several tumor-suppressor genes on chromosome arm 1p in colorectal tumors. To determine the localization of the putative tumor suppressor genes, we performed LOH analysis in 1p in colorectal tumors. A total of 48 paired normal and tumor DNAs of 46 colorectal tumor patients and 21 microsatellite markers on 1p32.1-p36.3 were used for PCR-LOH analysis. Three commonly deleted regions were found: i) 1p36.3 (10-cm); ii) 1p35.1-p36.3 (2-cm); and iii) 1p34.2-p35 (1-cm). These regions overlapped with those reported in several types of tumor. No significant associations were found between LOH and clinicopathologic features. The regions identified in the present study could harbor tumor suppressor genes that would also be associated with several types of human cancer.

Adult↗
PubMed1998

[Clinical features in patients with delayed endolymphatic hydrops].

We report clinical features in patients with delayed endolymphatic hydrops (DEH) with juvenile unilateral deafness. Among 23 patients with DEH, 15 cases were diagnosed as ipsilateral DEH and 8 cases as contralateral DEH. The distribution of onset age showed two peaks at ages of < 30 years and > 40 years. In 80% of the ipsilateral DEH cases, the onset of episodic vertigo was at younger ages. On the other hand, in 75% of the contralateral DEH cases, the onset of fluctuation hearing loss of the contralateral ear was at older ages. Ispilateral DEH and Meniere's disease may show different pathophysiologies. The incidence of dominant negative summating potential in the better-hearing ear was 20% in the ispilateral DEH cases and 60% in the contralateral DEH cases. It is suggested that endolymphatic hydrops is in the better-hearing ear of contralateral DEH.

Adult↗
PubMed1998

[Flow cytometric DNA analysis and MR imaging of salivary gland tumors].

We correlated the histopathology of 32 cases of salivary gland tumors with MR imaging and flow cytometric DNA analysis. All malignant tumors were invasive and/or had an ill-defined margin. Fifty-seven percent of the pleomorphic adenomas were shown as a high signal intensity area on T2 weighted images. Fifty-six percent of Warthin tumors were shown as a low or iso signal intensity area on T2 weighted images associated with the cystic portion. Sixty-seven percent of malignant tumors were characterized by DNA aneuploidy and/or a total percentage of the S-phase fraction plus the G2 + M fraction higher than 10%. It was less than 10% and the Ki-67 positive fraction was higher than 20% in all pleomorphic adenomas. The Ki-67 positive fraction was less than 20% in 78% of Warthin tumors. The histopathology of all malignant tumors, 86% of the pleomorphic adenomas, and 89% of Warthin tumors was correctly predicted by the combination of MR images and flow cytometry. We suggest that the MR images combined with flow cytometric analysis of fine needle aspiration-derived materials is useful in the pre-operative histopathologic diagnosis of salivary gland tumors.

Adenolymphoma↗
PubMed1998

Papillary thyroid carcinoma: MR diagnosis of lymph node metastasis.

PURPOSE: The purpose of this study was to ascertain the usefulness of MR imaging in the diagnosis of nodal metastasis of papillary thyroid carcinoma and to establish the most indicative MR criteria of metastasis. METHODS: Pathologic records and MR images in 50 patients with papillary thyroid carcinoma were reviewed. Each neck was divided into four nodal levels, so that 200 nodal levels were assessed in all. The maximum of the minimum transverse diameters of the lymph nodes on each nodal level measured on MR images and the certainty of metastasis as determined by a head and neck radiologist on the basis of morphologic aspects were compared with the pathologic findings by using receiver operating characteristic curves. The presence or absence of cystic nodes on each nodal level was also evaluated. RESULTS: Metastasis was found on 87 (44%) of the nodal levels in 34 (68%) of the patients. A cystic node was identified on 33 (17%) of the nodal levels in 13 (26%) of the patients and was seen only on positive nodal levels. Morphologic diagnosis by the radiologist was better than that obtained by measurement. With the combined criteria of a cystic node or a node of 13 mm or more for the maximum of the minimum transverse diameters, specificity was 100% with an 82% accuracy and always indicated metastasis (100% positive predictive value). However, 41% of the metastatic nodes were missed with this criterion (59% sensitivity). CONCLUSION: MR imaging was useful for diagnosing metastatic nodes; a nodal diameter threshold of 13 mm or the presence of a cystic node strongly indicated metastasis from papillary thyroid carcinoma.

Adult↗
PubMed1998

The BAX gene, the promoter of apoptosis, is mutated in genetically unstable cancers of the colorectum, stomach, and endometrium.

Disruption of the DNA mismatch repair system, characterized by microsatellite instability (MI), plays an important role in the course of human carcinogenesis by increasing the rate of mutations of genes associated with cancers. However, it is not clear which genes are the target genes for mutation in the course of carcinogenesis. Microsatellites within the coding region of the transforming growth factor beta receptor type II (RII) and insulin-like growth factor II receptor (IGF-IIR) genes were reported to be targets for mutation during the course of carcinogenesis in MI+ tumors. Recently, somatic mutations were found in a poly(G)8 tract in the BCL-2-associated X protein (BAX) gene, one of the essential players in apoptosis, in some MI+ tumors. We examined mutations of BAX in MI+ cancers of various organs and found frameshift mutations at the poly(G)8 tract in 5 of 15 (33%) gastric cancers, 3 of 26 (12%) endometrial cancers, and 9 of 22 (41 %) colorectal cancers. In contrast, no such mutations were found in pancreatic cancer. These results suggest that mutations of BAX play an important role in the course of carcinogenesis in the stomach, colorectum, and endometrium.

Apoptosis↗
PubMed1998

[Frequent loss of heterozygosity on the long arm of chromosome 21 in human esophageal, squamous cell carcinoma].

We investigated human esophageal squamous cell carcinoma using microsatellite markers on the long arm of chromosome 21 (21q) and found frequent loss of heterozygosity (LOH). The frequency of LOH was more than 50% in most of the microsatellite markers examined. Whole chromosome deletion suspected cases were observed in 25% of all cases. No case with microsatellite instability was found. Three common regions of allelic loss were identified. The frequent LOH was observed from early stage in pTNM classification. An unknown tumor suppressor gene in the genesis of esophageal squamous cell carcinoma may exist in 21q.

Carcinoma, Squamous Cell↗
PubMed1998

Identification of a 910-kb region of common allelic loss in chromosome bands 16q24.1-q24.2 in human lung cancer.

To understand the molecular pathogenesis of human lung cancer, we analyzed allelic deletions on the long arm of chromosome 16 by PCR amplification of microsatellite markers. A total of 203 lung cancer specimens (78 squamous cell carcinomas and 125 adenocarcinomas) were analyzed. In both cell types, a common region of allelic loss was identified in 16q24.1-q24.2; it is flanked by the two markers D16S534 and D16S422 that spanned at most 910 kb. These results were confirmed by fluorescence in situ hybridization. There was no correlation between allelic loss and histopathologic diagnosis or clinical stage. These results suggest the existence of a tumor-suppressor gene that plays an important role in the course of carcinogenesis in both squamous cell carcinoma and adenocarcinoma of the lungs.

Adult↗
PubMed1998

Chromosome bands 3p14.2, 9p21, and 13q14 are frequently deleted in roentgenographically occult bronchogenic squamous cell carcinoma of the lung.

Roentgenographically occult bronchogenic squamous cell carcinomas are early lung cancers that localize mainly within the bronchial wall and are thought to be a good model for elucidating chromosomal alterations during lung cancer progression. In this study, we analyzed allelic losses on chromosome regions 1p36, 3p14.2, 9p21, 10q25.3-q26.1, 13q14.12-q14.2, and 16q24.1-q24.2, in which there are putative tumor suppressor genes that may play roles in lung carcinogenesis. Forty-five cases with roentgenographically occult bronchogenic squamous cell carcinoma (ROC) and 47 cases of bronchogenic carcinoma with abnormal shadows (roentgenographically nonoccult bronchogenic squamous cell carcinoma [RNOC]) were examined. Highly frequent LOHs in both ROCs and RNOCs were observed in chromosome regions 3p14.2, 9p21, and 13q14.1-q14.2. LOHs were more frequently observed in RNOCs than in ROCs at two loci: 10q25.3-q26.1 and 16q24.1-q24.2. These results suggested that (1) putative tumor suppressor genes exist on 3p14.2, 9p21, 10q25.3-q26.1, 13q14.12-q14.2, and 16q24.1-q24.2, which may play important roles in lung carcinogenesis; (2) mutations in genes at 3p14.2, 9p21, and 13q14.12-q14.2 represent rather early events in lung carcinogenesis; and (3) mutations in genes on 10q25.3-q26.1 and 16q24.1-q24.2 represent rather late events.

Aged↗
PubMed1997

Alternative splicing of GTBP in normal human tissues.

GTBP is one of the functional homologues of the bacterial mismatch repair gene mutS, whose product forms a heterodimer with hMSH2 to bind to the mismatched region of double-stranded DNA. We determined the expression of the GTBP gene and found that two forms of the transcripts were ubiquitously expressed in normal human tissues. These transcripts, termed GTBP-N and GTBP-ALT, were generated by the alternative splicing machinery. These two transcripts share 3172 bp from the translation initiation codon that codes for 1057 amino acids. GTBP-ALT lacked a region that codes for a highly conserved region between GTBP-N, hMSH2, and hMSH3 in their C-termini.

Actins↗
PubMed1997

The insulin-like growth factor II receptor gene is mutated in genetically unstable cancers of the endometrium, stomach, and colorectum.

Disruption of the DNA mismatch repair system, characterized by microsatellite instability (MI), plays an important role in the course of human carcinogenesis. Repetitive sequences constitute targets for mutation in MI+ cells, and frequent mutations have indeed been reported in such regions within the transforming growth factor beta receptor II (RII) gene in genetically unstable colorectal and gastric cancers. However, other genes that are targets for mutations in MI+ cells during the course of carcinogenesis have proven elusive. Because the insulin-like growth factor II receptor (IGFIIR) gene contains several repetitive sequences within its coding region, we examined mutations of this gene in MI+ cancers occurring at various primary sites. We found frameshift mutations in the poly(G)8 tract of IGFIIR in eight tumors, all of which were MI+: 4 of 26 (15%) MI+ endometrial cancers, 3 of 12 (25%) MI+ gastric cancers, and 1 of 18 (6%) MI+ colorectal cancers. In contrast, no mutation was found in 51 pancreatic cancers, 7 of which (14%) were MI+. These results implicate abnormal IGFIIR-mediated growth control in carcinogenesis involving the endometrium, stomach, and colorectum but not the pancreas.

Breast Neoplasms↗
PubMed1997

Identification of a 790-kilobase region of common allelic loss in chromosome 10q25-q26 in human endometrial cancer.

We previously identified two commonly deleted regions on chromosome bands 10q25-q26 in endometrial cancer: an 8-cM region and a 12-cM region. In the present study, we further studied the 8-cM region with 83 endometrial cancer specimens and 14 microsatellite markers and narrowed it down to a 1-cM region between D10S587 and D10S1723. This result was confirmed by two-color fluorescence in situ hybridization analysis. An association between histopathologically lower grade tumor and allelic loss (P = 0.03 by Fisher's exact test) was also observed. We also constructed a yeast artificial chromosome (YAC) contig and found that one YAC clone, which was 790 kb in size, harbored the whole 1-cM region of common allelic loss.

Alleles↗
PubMed1997

Granulocyte colony stimulating factor-producing tongue carcinoma.

BACKGROUND: Leukocytosis without infection in patients with malignancies is known as the leukemoid reaction. The mechanisms involved in this phenomenon remain uncertain. METHODS: We describe the clinical, biochemical and immunohistochemical findings in a patient with recurrent tongue carcinoma accompanied by marked leukocytosis as high as 96200/ mm3. RESULTS: The serum granulocyte colony stimulating factor (G-CSF) concentration was increased to 204 (normal: < 30) pg/ml, which paralleled to the elevation of white blood cell (WBC) count and the tumor growth. The G-CSF content of the tumor tissue was also elevated (131 pg/mg protein) compared to that in control patients (6.63 +/- 2.63 pg/mg protein). Production of G-CSF from the tumor was evidenced by immunohistochemical staining with monoclonal antibody against human recombinant G-CSF. CONCLUSIONS: We suggest that the G-CSF production of the tumor participates in the mechanisms of the leukemoid reaction.

Aged↗
PubMed1997

Frequent gain of copy number on the long arm of chromosome 20 in human pancreatic adenocarcinoma.

We have used comparative genomic hybridization (CGH) to survey genomic regions with aberrant copy numbers of DNA sequences in pancreatic adenocarcinoma. In 12 cell lines and 6 primary tumors from 18 patients with pancreatic adenocarcinomas, highly frequent losses (> 60%) were observed on chromosome arms 6q, 9p, and 18q and the Y chromosome. Moderately frequent losses (40-60%) were observed on chromosome arms 3p, 4q, 8p, and 21q. Interestingly, these samples showed extremely high frequencies of increases in copy numbers of DNA sequences on the long arm of chromosome 20 (15/18, 83%). We further analyzed five cell lines by fluorescence in situ hybridization (FISH) with probes on chromosome 20 to define the increase in copy number more accurately, and we found that 20q was increased to between 5 and 8 copies per cell. These results suggest the existence of an oncogene or oncogenes in 20q that play a role in the development and/or the progression of pancreatic carcinogenesis.

Adenocarcinoma↗
PubMed1997

Alternative splicing of hMSH2 in normal human tissues.

hMSH2 is a homolog of bacterial mutS and yeast Msh2, a member of the group of mismatch repair genes whose products bind to mismatched regions of double-stranded DNA. We analyzed expression of hMSH2 in normal human organs by the polymerase chain reaction coupled with reverse transcription and found two novel types of alternatively spliced mRNAs that were expressed in normal human organs. One lacked exon 13, and the other lacked a portion from the second nucleotide of codon 633 to the second nucleotide of codon 719. In the latter transcript, intro 12 started with TA and ended with TT (TA-TT intron) which did not meet the GT-AG rule. Both types of transcript resulted in frameshifts which generated truncated hMSH2 proteins lacking the main part of the highly conserved region. The biological significance of the alternative splicing remains to be elucidated.

Adenosine Triphosphatases↗
PubMed1997

Frequent gains on chromosome arms 1q and/or 8q in human endometrial cancer.

Comparative genomic hybridization (CGH) was employed to survey genomic regions with increased and decreased copy number of the DNA sequence in 15 endometrial cancers [10 cases with microsatellite instability positive (MI+) and 5 cases with MI-]. Twelve of these 15 tumors (80%) showed abnormalities in copy number at one or more of the chromosomal regions. There were no regions with frequent chromosomal losses. Conversely, 11 of 15 cases (73%) showed gains on chromosome arms 1q (8/15; 53%) and/or 8q (6/15; 40%). Concordant gains of both chromosome arms 1q and 8q were observed in all three endometrial cancers of histological grade 3. These results suggest that these two chromosomal regions may contain genes whose increased expression contributes to development and/or progression of endometrial carcinogenesis. Two cases were further analyzed by fluorescence in situ hybridization (FISH) using three probes on chromosome 1 and two probes on chromosome 8 to more accurately determine increases in copy number. We found gains of chromosome 1q to 2.9-3.6 copies per cell and on 8q to 4.4 copies per cell.

Chromosome Aberrations↗
PubMed1997

Histamine release from the hypothalamus induced by gravity change in rats and space motion sickness.

Freely moving rats were exposed to 2 g hypergravity in an animal centrifuge device to produce motion sickness. Histamine release from the anterior hypothalamus of the rats was measured in vivo with a microdialysis technique. After a 2-h load of 2 g hypergravity, rats ate kaolin. Because pica, eating a nonnutritive substance such as kaolin, is a behavioral index of motion sickness in rats, this finding indicates that the rats suffered from motion sickness. During 2 g hypergravity for 2-h, histamine release from the hypothalamus was transiently increased. In contrast, neither the transient increase of histamine release nor the kaolin consumption were induced by 2 g hypergravity in bilaterally labyrinthectomized rats. Pretreatment with alpha-fluoromethylhistidine, an inhibitor of histamine-synthesizing enzyme, decreased both the basal and hypergravity-induced releases of histamine from the hypothalamus and suppressed the kaolin consumption induced by hypergravity. Taken together, these findings suggest that the vestibular information of changes in gravity activate the histaminergic neuron system, resulting in the development of motion sickness. More prolonged stimulation, a 4-h load of 2 g hypergravity, induced significant increase of kaolin consumption on postdays 1-3, though rats ate kaolin on postdays 1-2 after 2 g hypergravity for 2 h. During 2 g hypergravity for 4 h, the initial transient increase of histamine release was followed by the gradual increase of histamine release after the end of centrifugation. It is suggested that rats adapted to the hypergravity environment after centrifugation for 4 h, but not 2 h, so that the change in gravity from 2 g to 1 g became a provocative stimulation. We, therefore, concluded that motion sickness in rats induced by a negative change in gravity can be used as a simulation of space motion sickness, which is induced by exposure to microgravity. Histaminergic activation in the development of motion sickness induced by negative change in gravity might be an underlying mechanism of space motion sickness.

Animals↗
PubMed1997

Accessory parotid gland tumor: a case report.

We report a case of pleomorphic adenoma which was assessed pre-operatively as arising from the accessory parotid gland. Computed tomography (CT)-sialography provided information about the relationship between the tumor and the remaining normal accessory parotid tissue, and fine-needle aspiration of the tumor provided additional information as to the histologic features of the tumor, i.e. it was identified as of salivary origin. Zygomatic and buccal branches of the facial nerve extended over the accessory parotid gland tumor and the parotid duct was located just beneath the tumor. Therefore, pre-operative assessment of the tumor's nature was important for prevention of facial nerve damage and salivary fistula. The normal accessory parotid gland tissue associated with the accessory parotid tumor was histologically different from that of normal parotid gland tissue dissected in other patients with pleomorphic adenoma of the parotid gland. It is suggested that the difference in cell composition between these glands affects the development of the associated tumors.

Adenoma, Pleomorphic↗