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K Sugio

Publications and source records attributed to K Sugio.

At least 91 records · Page 5Linked to original sources
PubMed1992

Adenosquamous carcinoma of the lung. Clinicopathologic and immunohistochemical features.

Adenosquamous carcinomas (ASC) of the lung comprise only 1.8% of all pulmonary cancers. Eleven patients with this disease (6 men and 5 women; mean age, 62 years [range, 51 to 78 years]) were treated. On the basis of pathologic and immunohistochemical evidence, the tumors were separated into three groups: five ASCs of predominantly glandular type, which may originate from squamous metaplasia in a preexisting adenocarcinoma; three mixed type ASCs, possibly derived from the transition of undifferentiated carcinoma to two different elements; and three predominantly squamous type ASCs resembling high-grade muco-epidermoid carcinoma. The 5-year survival rate of 35% for patients with ASCs was the same as that for patients with other nonsmall cell carcinomas. For two patients with ASCs of the predominantly glandular type and for one with the mixed type, resection was incomplete because of extensive local disease. All tumors of the predominantly squamous type could be excised completely. However, differences in the malignant potential of these three types of ASCs are still controversial.

Adenocarcinoma↗
PubMed1992

Carcinoid tumor of the lung: clinicopathological and immunohistochemical studies.

Carcinoid tumors of the lung in 10 patients were treated surgically and both the clinicopathological manifestations and immunohistochemistry were examined in detail. Five were central carcinoid tumors, located in the main, lobar or segmental bronchus and five were peripheral carcinoid tumors, located in the subsegmental bronchus or beyond. Histologically, eight of the tumors were typical carcinoid tumors, one was an atypical carcinoid tumor, and one a carcinoid tumorlet. Three growth types were also established: polypoid type, iceberg type and intrapulmonary type. The central carcinoid tumors belonged either to the polypoid type or iceberg type, while the peripheral carcinoid tumors were of the intrapulmonary type. Both the iceberg and intrapulmonary types may invade the peribronchial or parenchymal tissues more frequently than does the polypoid type. Immunohistochemically, argyrophilia and neuron-specific enolase (NSE) were detected in all the tumors examined and six stained for polypeptide hormones such as adrenocorticotropic hormone (ACTH) and/or pancreatic polypeptide (PP). Of these, five had epithelial markers such as keratin, epithelial membrane antigen (EMA) and/or carcino-embryonic antigen (CEA). These findings suggest that a carcinoid tumor of the lung originates from primitive multipotential stem cells such as those of a neuroendocrine or epithelial nature.

Adrenocorticotropic Hormone↗
PubMed1991

Nucleolar organizer regions as a prognostic indicator for stage I non-small cell lung cancer.

When the number of silver-stained nucleolar organizer regions (Ag-NORs) was counted in 274 patients with non-small cell lung cancer, the mean number per nucleus in patients overall was 5.07 +/- 1.92 (SD). With the use of the tumor (T)-nodes (N)-metastasis (M) classification, the mean Ag-NOR count for patients with T1 and T2 disease was statistically lower than that for those with T3 and T4 disease (P less than 0.01). The mean Ag-NOR counts were lower in patients with N0 disease than in those with N1 and N2 disease (P less than 0.01); lower in patients with stage I disease than in those with stage II, IIIA, IIIB, or IV disease (P less than 0.01); and lower in patients with adenocarcinoma than in those with squamous cell carcinoma (P less than 0.01) or large-cell carcinoma (P less than 0.05). In 131 patients with stage I disease, the mean Ag-NOR count was 3.80 +/- 1.32, and the 5-year survival rates of patients with Ag-NOR counts of less than 3.80 and greater than or equal to 3.80 were 78 and 44%, respectively, including 78% and 25% for adenocarcinoma, respectively (P less than 0.01). However, there was no statistically significant difference for those in stage II, IIIA, IIIB, or IV, and in stage I (without an adenocarcinoma). Because patients with stage I non-small cell lung cancer and a high number of Ag-NORs had a poor prognosis, Ag-NORs can serve as a pertinent marker of an early recurrence.

Carcinoma, Non-Small-Cell Lung↗
PubMed1991

Association of expression between N-myc gene and major histocompatibility complex class I gene in surgically resected human neuroblastoma.

Amplification of the N-myc gene in neuroblastoma correlates with advanced stage and poor prognosis. Association of the expression between N-myc and major histocompatibility complex (MHC) class I genes in 33 neuroblastomas obtained from Japanese children was investigated. Amplification of the N-myc gene was observed in two of five cases in Stage III, six of 11 cases in Stage IV, and one of five cases in Stage IV-S. In each case, the expression of N-myc gene was significantly increased. The expression was also increased in cases without amplification of the N-myc gene, the origin being from the suprarenal region. Expression of the MHC class I gene was significantly decreased in five of these nine with a high level of N-myc expression with amplification. These results suggest that the down-modulation of the MHC class I expression may be associated with the high level of expression and amplification of N-myc gene in the advanced stage of neuroblastoma.

Child↗
PubMed1991

Subpleural silicotic nodule radiographically resembling to small bronchial carcinoma.

A 65-year-old woman had a solitary nodule radiologically appearing as a coin lesion with pleural indentation, suggesting primary lung cancer. Operative findings and histological examination revealed it to be a silicotic nodule. Despite the rarity of this condition, silicotic nodules should be considered among the causes of solitary or small numbers of peripheral pulmonary nodules in adults.

Aged↗
PubMed1991

[Immunohistochemical evidences of prognostic parameters associated with tumor development of pulmonary adenocarcinoma].

We immunohistochemically examined 186 lung adenocarcinomas for the presence of prognostic indicators of local growth of tumor, invasiveness and metastasis. Of the examined tumors, 67% showed a high expression of transforming growth factor alpha (TGF alpha); 50% for epidermal growth factor (EGF), 45% for EGF receptor (EGFR), and 30% for urokinase type plasminogen activator (uPA). In the EGFR-high cases, the 5-year survival rates of patients with high TGF alpha and low TGF alpha were 36% and 85%, respectively. In the EGFR-low cases, there was no statistical difference between the two groups. These findings suggested the presence of autocrine growth mechanisms. On the other hand, the high expression of uPA was modulated by TGF alpha and/or EGF. The 5-year survival rates of patients with high uPA and low uPA were 20% and 51%, respectively. The tumors with high expression of uPA showed degradation of the matrix components, including laminin and fibronectin. These findings suggested that uPA played a role to break through the surrounding basement membrane of blood and lymphatic vessels, and connective tissue for their growth and metastasis. We wish to emphasize the usefulness of the immunohistochemical evidences, such as autocrine growth mechanism and breakdown of extracellular matrix, as a possible parameters of tumor development, invasiveness and metastasis.

Adenocarcinoma↗
PubMed1990

K-ras activation in colorectal tumors from patients with familial polyposis coli.

K-ras gene mutation in colorectal tumors from patients with familial polyposis coli were investigated using oligonucleotide probes specific for a mutation at codon 12, 13, or 61 of the K-ras gene. The authors examined 22 colorectal carcinomas and 51 colorectal adenomas from 41 familial polyposis coli patients and observed mutations at codons 12 and 13 in eight of 22 colorectal carcinomas (36%) and six of 51 colorectal adenomas (12%). Thus, the frequency and sites of K-ras gene mutation in colorectal carcinoma from familial polyposis coli patients are similar to those in cases of sporadic colorectal carcinoma and may not be the first genetic event linked to the tumorigenesis.

Adenomatous Polyposis Coli↗
PubMed1990

Long-term results of operation for non-small cell lung cancer in the elderly.

We surgically treated 185 patients with non-small cell lung cancer who were 70 years old or older. The operative mortality rate was 3%, and the 5-year survival rate was 48%. The mortality and prognosis were similar to those in younger patients. The number of elderly patients who smoked heavily or who had ventilatory defects was high, but the incidence of pneumonectomy was low. There were no differences based on age in regard to histological type, TNM classification, and curability. Pulmonary complications occurred in 21% of the elderly patients and were correlated with preoperative pulmonary function and smoking habits. When the elderly are to undergo elective pulmonary resection for lung cancer, the preoperative evaluation of pulmonary function should be thorough, and both preoperative and postoperative physical therapy should be given. If postoperative pulmonary function is predicted to be less than 0.8 L/m2 of vital capacity and 0.6 L/m2 of forced expiratory volume in 1 second, a limited resection or nonsurgical therapy should be considered.

Adult↗
PubMed1989

Loss of constitutional heterozygosity in colorectal tumors from patients with familial polyposis coli and those with nonpolyposis colorectal carcinoma.

Familial polyposis coli (FPC) is an autosomal dominant tumorigenic disorder, the major gene of which is mapped to chromosome 5q. We searched for a gene loss in colorectal tumors from FPC patients, as related to tumorigenesis by inactivation of tumor suppression genes, using restriction fragment length polymorphism analysis. The findings were compared with those in the case of nonpolyposis colorectal carcinomas (NPCC). We examined specimens from 39 FPC patients, including 21 adenocarcinomas and 49 adenomas, and 23 colorectal carcinomas from 22 NPCC patients. For this, we used 53 polymorphic DNA markers on all autosomes. Frequent loss of heterozygosity in colorectal carcinoma from FPC patients was observed on chromosomes 5 (24%), 14 (20%), 17 (31%), 18 (40%), and 22 (35%) and also on chromosomes 5 (32%), 14 (30%), 17 (27%), 18 (20%), and 22 (19%) in NPCC. Although loss of heterozygosity in adenoma from FPC patients was observed on nine chromosomes, the frequencies were less than 7%. As we fractionated tumors only macroscopically, actual frequencies of loss of heterozygosity are probably somewhat higher. However, these results do suggest that tumor suppression genes for colorectal carcinoma may locate on chromosomes 5, 14, 17, 18, and 22 and that they may play a critical role in carcinogenesis in both FPC and NPCC patients.

Adenoma↗
PubMed1988

Differential expression of c-myc gene and c-fos gene in premalignant and malignant tissues from patients with familial polyposis coli.

The expression of 8 oncogenes and the structures of 19 oncogenes were analyzed in 15 adenocarcinomas (12 primary and 3 metastatic), 18 adenomatous polyps, and 18 normal colonic mucosae derived from 19 patients with familial polyposis coli. The expression of c-myc gene was most elevated in carcinoma, and moderately elevated in adenoma, compared with corresponding normal colonic mucosa. In contrast, the expression of c-fos gene was markedly decreased in all samples of adenoma and carcinoma, compared with that of normal colonic mucosa. These characteristic expression patterns of c-myc and c-fos genes were revealed not only in familial polyposis coli but also in cases of nonhereditary colon carcinoma. Structures of the 19 oncogenes were not modified in either adenoma or carcinoma, except for amplification of the c-myc gene detected in one carcinoma, but not in adenoma, from the same patient. Analyses of the amplified c-myc gene suggest that gene duplication may relate to the mechanism of gene amplification. Thus, the enhanced expression of c-myc gene in adenoma and carcinoma may reflect the proliferative activity, while the c-fos gene may be a prerequisite to stabilize the state of terminal differentiation of colonic epithelial cells.

Adenomatous Polyposis Coli↗
PubMed1988

Loss of constitutional heterozygosity in colon carcinoma from patients with familial polyposis coli.

Recent studies have suggested a critical role of specific gene loss in several embryonic tumours and certain adult cancers. In retinoblastoma, hemizygosity or homozygosity of a recessive mutant allele results in the loss of normal gene product, and this seems to cause the manifestation of the disorder. Familial polyposis coli (FPC) is a human autosomal dominant trait characterized by numerous adenomatous polyps of the colon and rectum, and a high incidence of colon carcinoma. Karyotype analyses have failed to detect specific deletion or translocation. We report the use of polymorphic DNA markers to look for the somatic loss of heterozygosity at specific loci. Investigation of 38 tumours from 25 FPC patients, and 20 sporadic colon carcinomas from 19 patients, revealed frequent occurrence of allele loss on chromosome 22, with some additional losses on chromosomes 5, 6, 12q and 15. The FPC gene-linked DNA probe C11p11 also detected frequent allele loss in both familial and sporadic colon carcinomas but not in benign adenomas. These results suggest the possible involvement of more than one chromosomal locus in the development of familial and sporadic colon carcinomas.

Adenoma↗
PubMed1988

Increase in vascular permeability of rat and guinea pig skin by T-kinin.

The vascular permeability-increasing response to T-kinin in rat and guinea pig skin was investigated. The vascular permeability was measured with 125I-labeled bovine serum albumin [( 125I]BSA) as a tracer. Plasma exudation rapidly occurred 0-15 min after the intradermal injection of T-kinin. T-kinin in doses of 0.3, 1, and 3 nM/spot significantly increased the vascular permeability in a dose-dependent manner. The vascular response of T-kinin is similar to that of bradykinin. On the other hand, T-kinin analogs, D-Ile-Ser-bradykinin and Ile-D-Ser-bradykinin only weakly enhanced the vascular permeability. Prostaglandin E1, forskolin, and the angiotensin-converting enzyme inhibitor, SQ-14225, potentiated the T-kinin-induced plasma exudation. Cyproheptadine and indomethacin did not affect the T-kinin-induced response. The results suggest that T-kinin will play an important role in increasing vascular permeability associated with inflammation.

Alprostadil↗
PubMed1988

Effects of pentobarbital and cyproheptadine on brain ischemia induced by bilateral occlusions of carotid arteries and vertebral arteries of second cervical vertebra in rats.

The bilateral hemispheric ischemia in rats was induced by the occlusion of bilateral common carotid arteries after permanent electrocauterization of bilateral vertebral arteries at the level of the second cervical vertebra. In ischemic rats, (a) electroencephalograms became flat immediately after occlusion of carotid arteries, and (b) mortalities reached maximum levels at day 3 after recirculation. These results suggested that a constant level of cerebral ischemia was produced in this rat model. Pentobarbital markedly inhibited the mortality in these ischemic rats, whereas cyproheptadine did not.

Animals↗