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T Taki

Publications and source records attributed to T Taki.

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

Ongoing prospective study of segmentectomy for small lung tumors. Study Group of Extended Segmentectomy for Small Lung Tumor.

BACKGROUND: Lesser resection for small lung tumors remains an unresolved problem. This study was conducted to see whether this type of operation is acceptable or not. METHODS: From 1992 to 1994, 55 patients were enrolled in a multicenter trial of limited surgical resection for peripheral tumors of less than 2 cm diameter. The procedure consisted of segmentectomy with exploration of lymph nodes by examining frozen sections. The operation was modified if the report was positive. The intersegmental plane was identified by keeping the resected segments inflated and the preserved segments collapsed. To divide the plane, stapling or electrocauterization on the edge of the collapsed area was used. In this way the resection line was delivered beyond the burdened segment; this was called extended segmentectomy. RESULTS: There were no perioperative deaths, but there were eight postoperative deaths. In 1 patient who died because of local recurrence, it had been known that the margin to the lesion had been narrow (15 mm); 1 had bilateral intrapulmonary nodules, 1 had nodules in the side that was not operated on, and another succumbed to a second neoplasm of small cell lung cancer 4 years after the first operation. The remaining 4 died of nonpulmonary diseases. Almost all other patients are alive and free from recurrence, except for 1 in whom N2 disease was not detected intraoperatively but was confirmed after the operation. CONCLUSIONS: The interim results suggest that extended segmentectomy is applicable in patients with a small peripheral lung cancer. However, a wide margin and aggressive intraoperative pathologic examinations are mandatory.

Adenocarcinoma↗
PubMed1998

In vivo etoposide-resistant C6 glioma cell line: significance of altered DNA topoisomerase II activity in multi-drug resistance.

We have established an in vivo etoposide-resistant glioma cell line (C6/VP) from C6 rat glioma cells by stepwise exposure to increasing doses of etoposide. The C6/VP cells were 10 times more resistant to etoposide than the parental C6 cells. In addition C6/VP cells demonstrated cross-resistance to vincristine and vinblastine, but not to ADM or m-AMSA. Interestingly, the cells had collateral sensitivity to ACNU, cisDDP and Ara-C. The C6/VP cells did not express the MDR gene or p-glycoprotein, while they showed 16 times less topoisomerase II catalytic activity compared to the C6 cells. Although there was no significant difference between C6 and C6/VP cells in amounts of topoisomerase II in nuclear extracts, the C6/VP cells had 2.9 times higher amounts of the enzyme than C6 cells in nuclear scaffold prepared from a relatively low-salt buffer (0.5 M NaCl). Northern blot analysis demonstrated that mRNAs of topoisomerase IIalpha isoforms were expressed both in C6 and C6/VP cells, and that the amounts of topoisomerase IIalpha in C6/VP cells were 14 times greater than in C6 cells. The total uptake of etoposide in tumor tissues derived from C6/VP cells was 3 times less than those derived from parental C6 cells. These results indicate that the C6/VP acquired a multi-drug resistance phenotype by a reduction of the catalytic activity of topoisomerase II and/or diminished accumulation of drugs. This phenotype did not involve the p-glycoprotein. Alterations of topoisomerase II in the C6/VP cells also were accompanied by an increased amount of the topoisomerase IIalpha isoform, most of which was localized in the nuclear scaffold (matrix). This suggests that altered binding of topoisomerase II to topologically organized DNAs in the nuclear scaffold may be the molecular basis of this multi-drug resistance phenotype.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1998

Analysis of glycosphingolipids of human head and neck carcinomas with comparison to normal tissue.

Glycosphingolipids of head and neck carcinomas from six tumor-bearing patients were analyzed and compared to those of normal tissue from similar areas. The total glycosphingolipid content and the lipid-bound sialic acid were much higher in carcinomas than in normal tissue. Major neutral glycolipids were glucosylceramide, lactosylceramide, trihexosylceramide and paragloboside. Sulfatides were seen only in extracts from normal tissue which also showed a rather simple ganglioside pattern with #GM3 and GD3 as major species, whereas tumors showed additional species such as GM2 and GD2, along with a strong increase in LM1, GM1, GD1a and GT1b.

Biomarkers, Tumor↗
PubMed1998

Colour Doppler-guided spectral analysis of gall-bladder wall flow.

For the purpose of the present study to diagnose gall-bladder cancers, which cannot be detected or are only partly visible by conventional ultrasonography (US), we attempted differential diagnoses of 69 patients with gall-bladder diseases (12 with gall-bladder cancer, five with acute cholecystitis, 11 with chronic cholecystitis, 27 with cholesterol polyp and 14 with adenomyomatosis) using the evaluation of gall-bladder wall blood flow (GWBF). GWBF was evaluated by colour Doppler-guided spectral analysis (CDSA). Thirty-three healthy volunteers were selected as controls at random. Two parameters of GWBF, namely flow velocity and resistive index (RI), were compared between patients with gall-bladder diseases and healthy volunteers. GWBF could be ultrasonically evaluated in 92 (90%) of 102 subjects. All 12 patients with gall-bladder cancer had a significantly rapid blood flow value compared with other patients and healthy volunteers. There was no significant difference in RI among patients and healthy volunteers. When cut-off level of the flow velocity was set at 30 cm/s, gall-bladder cancer could be diagnosed by flow velocity with 100% sensitivity (12/12) and 96% specificity (50/52). Using the same cut-off level of the flow velocity, 17 patients were analysed prospectively. In four asymptomatic gall-bladder cancers and two acute cholecystitis cases with some symptoms, the flow velocity was over 30 cm/s. In two of four patients with gall-bladder cancer, only a part of the tumour was visualized on conventional abdominal US. In conclusion, CDSA was more useful for diagnosing gall-bladder lesions than the conventional abdominal US due to estimation of arterial flow velocity in the gall-bladder wall.

Blood Flow Velocity↗
PubMed1998

Reduced integrin alpha3 expression as a factor of poor prognosis of patients with adenocarcinoma of the lung.

PURPOSE: We investigated the possible association between integrin alpha3 and motility-related protein (MRP-1), cluster of differentiation antigen 9 (CD9) gene expression in non-small-cell lung cancer (NSCLC) and evaluated the prognostic significance of integrin alpha3 expression. PATIENTS AND METHODS: We performed a retrospective study of integrin alpha3 and MRP-1/CD9 expression in resected tumor tissues from 151 NSCLC patients using quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) and immunohistochemistry. RESULTS: The ratio of integrin alpha3/beta-actin expression ranged from 0 to 5.87 (mean was 0.80; median, 0.70). Using the cutoff value of 0.7, there were 78 (52%) integrin alpha3-positive tumors and 73 (48%) tumors with reduced integrin alpha3 expression. The immunohistochemical results agreed well with those of the RT-PCR assays, and 88% had no discrepancy. In case of discrepancy, the results of RT-PCR were used in specimen classification. Integrin alpha3 gene expression was independent from MRP-1/CD9 gene expression. No significant association was found between integrin alpha3 expression and the patients' clinical characteristics. The overall survival rate of patients with integrin alpha3-positive NSCLCs was only slightly better than that of individuals whose tumors had reduced integrin alpha3 expression (55.9% v 47.1%; P = .085). By comparison, the overall survival rate of patients with integrin alpha3-positive adenocarcinomas was strikingly greater than in those whose tumors had reduced gene expression (54.4% v 35.2%; P = .004). Multivariate analysis with the Cox regression model of NSCLC and adenocarcinoma indicated that integrin alpha3 expression correlated better (P = .0188 and P = .0008, respectively) with the overall survival rate than other variables, except lymph node status. CONCLUSION: No significant association was found between integrin alpha3 and MRP-1/CD9 gene expression in lung cancer. However, reduced integrin alpha3 expression is a poor prognosis factor in patients with adenocarcinomas.

Adenocarcinoma↗
PubMed1998

Novel staging protocol for non-small-cell lung cancers according to MRP-1/CD9 and KAI1/CD82 gene expression.

PURPOSE: The transmembrane-4 superfamily (TM4SF) is a recently discovered family of genes. Of the TM4SF members, MRP-1/CD9, KAI1/CD82, and ME491/CD63 have been reported to modulate tumor progression or metastasis. In this study, we investigated the relationships between these three genes, MRP-1, KAI1, and ME491, in patients with non-small-cell lung cancers (NSCLCs). Moreover, we assessed the prognostic value of evaluating the expressions of MRP-1, KAI1, and ME491 simultaneously in NSCLCs. PATIENTS AND METHODS: One hundred seventy-two patients up to stage IIIB NSCLC underwent radical surgery during the period of January 1991 through June 1994. Using a quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) analysis, we studied the expression of MRP-1, KAI1, and ME491 genes in these patients. RESULTS: We found that 109 patients (63.4%) had MRP-1-positive tumors and 42 patients (24.4%) had KAl1-positive tumors. Conversely, all 172 patients expressed ME491. No relationship was found between MRP-1 expression and KAI1 expression. We classified these patients into three groups. The 36 patients who were positive for both MRP-1 and KAI1 were defined as group A; the 79 patients with reduced expression of either MRP-1 or KAI1 were defined as group B, and the remaining 57 patients with reduced expression of both MRP-1 and KAI1 were defined as group C. This new classification was correlated with nodal status, tumor status, and pathologic stage (P = .0056, P = .0003, and P < .0001, respectively). In NSCLC patients, the 5-year survival rate of group A patients was significantly better than that of group B patients and much better than that of group C patients (86.8%, 53.9%, and 31.5%, respectively; P < .0001). Cox multivariate regression analysis showed that this new classification in NSCLCs was a significant prognostic factor, as was the nodal status (P < .0001). CONCLUSION: Our results suggest that a low MRP-1 and KAI1 expression by tumors of the lung may be associated with poor prognosis. It is conceivable that the evaluation for MRP-1 and KAI1 expression may identify node-negative lung cancer patients who are at high risk for early disease recurrence, and thus need intensive adjuvant therapy.

Adult↗
PubMed1998

Mutations of p53 and K-ras genes as prognostic factors for non-small cell lung cancer.

To evaluate the importance of mutations of p53 and K-ras genes in the prognosis of patients with non-small cell lung cancer, one hundred and forty-four patients who underwent surgery were studied. DNA was extracted from frozen specimens. Polymerase chain reaction-single strand conformation polymorphism and sequencing were performed to investigate mutations of p53 from exon 5 to 8, and mutations of exon 1 of K-ras. Mutations of p53 gene occurred in 35. 4% of patients, and mutations of the K-ras gene in 8.3%. The overall survival rate of non-small cell lung cancer patients with wild-type K-ras was better than that of patients whose tumors had mutations of K-ras (P=0.0330). Among patients with adenocarcinoma of the lung, the overall survival rate of patients with wild-type p53 was strikingly better than that of patients whose tumors had mutations of p53 (P=0.0234). Multivariate analysis with the Cox regression model of all patients with non-small cell lung cancer and those with adenocarcinoma indicated that mutations of K-ras best correlated with the overall survival rate (P=0.0005 and P=0.0361, respectively). In conclusion, evaluation of mutations of both the p53 and K-ras genes in the lung tumors might be useful for assessing the prognosis, especially in patients with adenocarcinoma.

Adenocarcinoma↗
PubMed1998

Therapy-related leukemia and myelodysplasia following oral administration of etoposide for recurrent breast cancer.

We report a high risk of therapy-related acute myeloid leukemia and myelodysplastic syndrome (t-AML/MDS) in patients receiving oral administration of etoposide for recurrent breast cancer. We examined 119 patients with recurrent disease. Patients were initially treated with anthracyclines, cyclophosphamide, or cisplatin with or without radiation before etoposide treatment. Etoposide was used as the final drug in most cases. Twenty-four patients were treated with the oral administration of etoposide (50 or 100 mg/day for 5-7 days at 4-week intervals). Three cases of t-AML/MDS developed among those 24 patients exposed to etoposide. In contrast, the development of t-AML/MDS was not observed in the other 95 patients not treated with etoposide. Our data suggest that there is a substantial risk of secondary leukemia with oral administration of etoposide for a prolonged period as well as i.v. schedules.

Administration, Oral↗
PubMed1998

Usefulness of intraductal ultrasonography in gallbladder disease.

This study was designed to compare intraductal ultrasonography of the gallbladder wall with histopathologic findings and to assess the clinical usefulness of this imaging method in gallbladder disease. Thirty-one gallbladder specimens were examined by intraductal ultrasonography retrospectively. The gallbladder is composed of three layers: an innermost hyperechoic layer, a middle hypoechoic layer, and an outermost hyperechoic layer. The second layer on ultrasonograms corresponds to the muscle layer plus the fibrous tissue of the superficial perimuscular connective tissue layer. In cases in which the thickness of the second layer was 500 microns or less, little fibrous tissue was seen and the second layer was approximately identical to the muscle layer on sonograms. Clinical study was performed on 22 gallbladders. The use of a guidewire through the papilla facilitated intraductal ultrasonographic examination. The intraductal sonographic probe could be inserted into the gallbladder fundus in 13 of 22 cases. In nine unsuccessful cases, technical difficulties were as follows: sharply angulated gallbladder (four cases), stenosis of the gallbladder (two cases), difficulty in transmitting power in the correct direction (three cases). With regard to the area visualized in 13 successful cases, in three cases the area visualized was 100%, in seven cases it was 75%, and three cases it was 50%. Intraductal ultrasonographic images could be obtained in 83.3% (10 of 12) of elevated lesions of the gallbladder. The indications for intraductal ultrasonography will be cases in which an abnormality was detected by transabdominal ultrasonography or other modalities in which the physician does not know whether or not to operate. In conclusion, we defined the intraductal sonographic images of gallbladder wall and clarified the clinical indications for use of this imaging method.

Gallbladder↗
PubMed1998

[A case of asynchronous renal cell carcinoma, hepatocellular carcinoma and residual ureteral cancer].

A case of asynchronous triple cancer in an 88-year-old male is reported. Six years ago, he had received left radical nephrectomy for renal cell carcinoma, and 2 years ago partial hepatectomy for hepatocellular carcinoma detected by follow-up computed tomography (CT). During the post-operative follow-up, no metastasis of either the renal or hepatic carcinoma was detected. On February 12, 1997 he presented with macroscopic hematuria. Cystoscopy revealed a tumor emerging from the left ureteral orifice, while CT and magnetic resonance imaging (MRI) revealed a tumor mass in the left exterior of bladder. Diagnosis of residual ureter tumor, we performed both left ureterectomy and partial cystectomy. Histological diagnosis revealed transitional cell carcinoma of the residual ureter (G2 > G3, pT1, pV0, pL0, pR0). Convalescence was uneventful and 10 months after the operation, he is alive with no recurrence or metastasis. We stress the importance of careful follow-up not only to perceive the recurrence or metastasis of renal cancer but also to detect cancer in other parts of the body.

Aged↗
PubMed1997

Adenoviral E1A-associated protein p300 is involved in acute myeloid leukemia with t(11;22)(q23;q13).

p300, which was originally cloned as a nuclear binding target of the adenovirus E1A oncoprotein, forms a family with cyclic-AMP response element binding protein (CREB)-binding protein (CBP). p300/CBP are considered to be transcriptional coactivators that connect the basal transcriptional machinery to various DNA-binding transcriptional factors. p300/CBP are implicated in both cell differentiation and regulation of cell-cycle. We identify here that the p300 gene is fused to the MLL gene and that in-frame MLL-p300 fusion protein is generated in acute myeloid leukemia (AML) with t(11; 22)(q23; q13). These findings suggest that the basis for the leukemogenesis of t(11; 22)-AML is the inability of p300 to regulate cell-cycle and cell differentiation after fusion with MLL.

Amino Acid Sequence↗
PubMed1997

Preparation of peptides which mimic glycosphingolipids by using phage peptide library and their modulation on beta-galactosidase activity.

We describe the use of a phage-displayed random pentadecamer peptide library for searching glycosphingolipid mimicking peptides. Two phage clones (AD-1 and AD-2) were selected by biopanning using monoclonal antibody AD117m, directed to lactotetraosylceramide (Lc4Cer). The amino acid sequences of the selected clones showed high homology (VPPXFXXXY) in 9-mer. Three phage clones were selected by using monoclonal antibody H11, directed to neolactotetraosylceramide (nLc4Cer), the linkage isomer of Lc4Cer, and the displayed amino acid sequences were compared. One of these peptides showed the same amino acid sequence as that of AD-2 except for one amino acid substitution. Pentadecamer, 9-mer and point mutated 9-mer peptides were synthesized on the basis of the displayed amino acid sequences. Binding activity of the peptides to the monoclonal antibodies or Ricinus communis lectin showed that 9-mer peptides are enough to mimic the epitope carbohydrate structure. Furthermore, six of the synthesized peptides inhibited Jack bean beta-galactosidase activity towards nLc4Cer at a high concentration of the enzyme, whereas at lower enzyme concentrations some peptides showed potent activation of the enzyme activity. This is the first report of carbohydrate mimicking peptides which modulate glycosidase activity.

Amino Acid Sequence↗
PubMed1997

Structure of a novel phosphocholine-containing aminoglycoglycerolipid of Mycoplasma fermentans.

Mycoplasma fermentans is thought to be a pathogen of rheumatoid arthritis or a cofactor of AIDS (acquired immunodeficiency syndrome). To elucidate the possible involvement of membrane constituents in the pathogenesis of these diseases, we studied its lipid components. Several alkali labile glycophospholipids were detected and named glycoglycerophospholipids (GGPLs). Previously, we purified and determined the structure of one of them as 6'-O-phosphocholine-alpha-glucopyranosyl-(1'-3)-1,2-diacyl-sn-glycerol (GGPL-I). The present paper describes the purification and structural characterization of GGPL-III, the major GGPL of M. fermentans using 1H-, 13C- and 31P-nuclear magnetic resonance spectroscopy, and mass-spectroscopy as 1"-phosphocholine,2"-amino dihydroxypropane-3"-phospho-6'-alpha-glucopyranosyl-(1'-3)-1,2-dia cyl-glycerol.

Glycolipids↗
PubMed1997

TLC blotting: application to microscale analysis of lipids and as a new approach to lipid-protein interaction.

A simple method for the transfer of phospholipids and glycosphingolipids from a high-performance thin-layer chromatography (HPTLC) plate to a polyvinylidene difluoride (PVDF) membrane, called thin-layer chromatography (TLC) blotting, and its application in lipid research are described. Most of the lipids developed on the HPTLC plate are blotted quantitatively. Detection of the lipids on the membrane is done by chemical and immunological staining. This method makes it possible to purify individual lipid components separated on an HPTLC plate and to determine the structures of lipids in limited biological samples when combined with direct mass spectrometric analysis (TLC blotting/MS). A binding assay and the identification of ligands for microorganisms can be made using TLC blotting/MS. In addition, simple methods for the detection of enzymes on a substrate-immobilized PVDF membrane are described.

Animals↗
PubMed1997

Identification of translocational breakpoints within the intron region before the last coding exon (exon 12) of the EVI1 gene in two cases of CML-BC with inv(3)(q21q26).

We have previously shown that the EVI1 gene at chromosome 3q26 is transcriptionally activated by chromosomal rearrangements in acute myelogenous leukemias (AMLs) with inv(3)(q21q26) or t(3;3)(q21;q26). The breakpoints in t(3;3) cases were 15 to 330 kb upstream of the EVI1 gene, while those in inv(3) cases were 150 to 200 kb downstream and outside of the EVI1 coding region. The EVI1 gene is also activated in chronic myelogenous leukemia-blastic crisis (CML-BC) with inv(3)(q21q26); however, the molecular mechanism of EVI1 activation in CML-BC is still unclear. In this paper, we have analyzed chromosomal rearrangements in two leukemia cell lines derived from CML-BC with inv(3)(q21q26) and have identified the breakpoints within the EVI1 coding area. The EVI1 gene spans over 100 kb with 12 exons (10 coding exons), and the chromosomal breakpoints are clustered in the intron region before the last coding exon (exon 12). The nucleotide sequence of EVI1 cDNA clones from MOLM-1 cells was truncated at exon 11, and a novel sequence of 681 nucleotides was added at the 3' end of the EVI1 transcripts. The novel sequence was derived from a readthrough intron sequence 3' to the coding exon 11 adjacent to the breakpoint. The breakpoints at 3q21 were within the breakpoint cluster area downstream of the ribophorin I gene, suggesting that the activation mechanism of the EVI1 gene in CMLs with inv(3) is the same as that in AMLs with inv(3). These results indicate that expression of a truncated EVI1 gene is an important factor in the progression of CML.

Amino Acid Sequence↗
PubMed1997

The t(11;16)(q23;p13) translocation in myelodysplastic syndrome fuses the MLL gene to the CBP gene.

The recurrent translocation t(11;16)(q23;p13) has been reported to be associated with therapy-related acute leukemia. The MLL gene involved in other 11q23 abnormalities was also rearranged by this translocation. We analyzed two patients with myelodysplastic syndrome with t(11;16) and showed that the MLL gene on 11q23 was fused with CREB-binding protein (CBP) gene on 16p13 in these patients. The CBP gene encodes a transcriptional adaptor/coactivator protein and it is mutated in patients with Rubinstein-Taybi syndrome. The CBP gene is also involved in acute myeloid leukemia (AML) with t(8;16)(p11;p13). In-frame MLL-CBP fusion transcripts combine the MLL AT-hook motifs and DNA methyltransferase homology region with a largely intact CBP. Our results combined with the finding of the MOZ-CBP fusion in t(8;16)-AML suggest that the CBP gene may be associated with leukemogenesis through translocations.

Amino Acid Sequence↗
PubMed1997

Ganglioside GD1alpha functions in the adhesion of metastatic tumor cells to endothelial cells of the target tissue.

We studied the role of glycosphingolipids expressed on the cell surfaces of a metastatic tumor cell line. Glycosphingolipid compositions of the low-metastatic murine lymphosarcoma cell line RAW117-P and its sub-line, RAW117-H10, which shows higher metastatic potential for the liver than P cells, were compared. Both types of cells had LacCer, Gg3Cer, and Gg4Cer as the major neutral glycosphingolipids and GM1b and GD1alpha as the gangliosides. There are differences in glycosphingolipid contents, the neutral glycosphingolipid contents in the parental cells being 1.5-fold higher than that in the variant ones. In contrast, the level of GD1alpha in H10 cells was twice as much as that in the P cells; however, the expression of other gangliosides was down-regulated. On the basis of the results of glycosphingolipid analysis, we investigated the functional role of GD1alpha in H10 cells in the adhesion of the tumor cells to the target tissue by using hepatic sinusoidal endothelial (HSE) cells. GD1alpha and GM1b inhibited the adhesion when HSE cells were incubated prior to coculture with the tumor cells. This inhibitory effect by GD1alpha and GM1b was observed within 30 min after addition of H10 cells to HSE cells and was dose dependent. GD1alpha showed a higher inhibitory effect on the adhesion than GM1b, whereas other glycosphingolipids showed no inhibitory effect. Anti-GD1alpha monoclonal antibody also inhibited the adhesion between the H10 and HSE cells. When cultured without fetal bovine serum for 30 min in a various glycosphingolipids-coated dish for bacterial culture, HSE cells adhered to the area coated with GD1alpha but not to areas coated with other glycosphingolipids. HSE cell adhesion depended on the amount of GD1alpha coated on the plate. These data indicate that GD1alpha functions as an adhesion molecule in the process of metastasis of H10 cells.

Animals↗