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T Yasutake

Publications and source records attributed to T Yasutake.

At least 73 records · Page 4Linked to original sources
PubMed1997

Aneusomy of chromosome 18 is associated with the development of colorectal carcinoma.

Specific loss of heterozygosity of chromosome 18 has been observed frequently in advanced colorectal carcinoma and is closely associated with its development. We investigated the prevalence of numerical aberrations of chromosome 18 in 44 specimens of colorectal carcinomas, using fluorescence in situ hybridization. We also examined the relationship between aneusomy of chromosome 18 and the clinicopathological features of these tumors. Aneusomy of the specimens (monosomy and polysomy) was determined when the same aneusomic population was detected in more than 15% of the nuclei. The frequency of monosomy and polysomy of chromosome 18 in colorectal carcinomas was 43% (19/44) and 29% (12/44), respectively. The prevalence of monosomy and polysomy 18 was significantly higher in cancers with invasion exceeding category T2 compared with T1 (P < 0.01), and with tumor size exceeding 20 mm in diameter compared with tumors less than 20 mm (P < 0.05). However, the prevalence of aneusomy 18 was not associated with other clinico-pathological features. The mean survival period and the 5-year survival rate after operation in patients with aneusomy 18 was not different from findings for those with disomy 18. Our results indicate that aneusomy of chromosome 18 is associated with the development of colorectal carcinoma; however, it is not a useful indicator of postoperative prognosis.

Adult↗
PubMed1997

Gain of chromosome 20 is a frequent aberration in liver metastasis of colorectal cancers.

To investigate the characteristics of the numerical chromosome aberrations in liver metastasis of colorectal cancers, fluorescence in situ hybridization (FISH) for chromosomes 8, 18, 14/22, and 20 was performed in 18 specimens of primary regions and 18 of metastatic regions in liver metastasis of colorectal cancers compared with 15 of non-liver metastatic cancers. Among these numerical aberrations, the gain of chromosome 20, especially copy numbers exceeding three, was frequently observed in primary and metastatic cancers. Among these numerical aberrations, the gain of chromosome 20, especially copy numbers exceeding three, was frequently observed in primary and metastatic regions of liver metastasis groups compared with that of the non-liver metastasis group (P < 0.05). The incidences of gain of chromosome 20 in both regions of the liver metastasis group were higher than that of the non-liver metastasis group (P < 0.05). The gain of chromosome 20 is a frequent aberration in primary and metastatic regions in patients with liver metastatic colorectal cancers and may be available as a genetic marker for the diagnosis or prediction of liver metastasis.

Case-Control Studies↗
PubMed1997

Deletion of chromosome 11 and development of colorectal carcinoma.

The deletion of chromosome 11q is observed frequently in tumors of the large intestine. To investigate the relationship between aberrations of chromosome 11 and histopathological features of colorectal carcinoma, we examined the frequency of chromosome aberrations using fluorescence in situ hybridization to 29 short-term cultured cells from surgical specimens. Numerical aberrations were not related to any factors. The deletion of chromosome 11 was frequently observed in larger (> or = 5 cm) and more invasive tumors (> or = T3 category) (p < 0.05). Furthermore, the incidence of aberrations tended to increase in Dukes' B. Although translocation of chromosome 11 was also found in 17% of cases, it was not associated with histopathological features. Our findings indicate that the deletion of chromosome 11 is closely related to the progression of colorectal carcinoma.

Chromosome Aberrations↗
PubMed1997

[p53 alterations and chromosome 17 aberrations in non-small cell lung cancer].

We studied the relationship between DNA index, numerical abberation of chromosome 17 and alterations of the p53 gene in 23 non-small cell lung cancers. Diploid and aneuploid cells from 23 non-small cell lung cancer with DNA aneuploidy were flow sorted into each cell population using FACStar(plus). They were examined by PCR-SSCP analysis for p53 mutation and by microsatellite analysis for loss of heterozygosity at TP53 locus (17p13.1). They were also analyzed by FISH for copy number of chromosome 17. p53 mutations were found in aneuploid cells from the 11 cases (48%). Among them, 8 cases were informative at TP53 locus, and all showed loss of heterozygosity. Aneuploid cells from 16 cases exhibited gain of chromosome 17 copy number in FISH analysis. DNA index was significantly associated with th mean copy number of chromosome 17, suggesting that the number of chromosome 17 changed with DNA index. There were no associations between p53 mutation and DNA index or mean copy number of chromosome 17. In some cases, we also analyzed structural abberation of short arm of chromosome 17 by FISH using p53-cosmid (17p13.1) and Distal 17p (17p13.3-ptel) probes. The p53 gene located on the increased chromosome 17 was lost due to point mutation or deletion of 17p.

Aneuploidy↗
PubMed1997

[Numerical aberration of chromosome 17 is correlated with multiple primary cancer in colorectal carcinoma].

Numerical aberration of chromosome 17 of 14 cases of colorectal carcinoma with multiple primary cancer (: multiple cancer) was compared with that of 35 cases of colorectal carcinoma without any other cancer (: single cancer). Fluorescence in situ hybridization with p17H8 was performed on touch smear from fresh materials. The proportion of aneusomy 17 (NCAI: numerical chromosome aberration index) in multiple cancers was significantly higher than that of single cancers (37.7 +/- 10.5% VS 46.1 +/- 8.0%; p < 0.01). Although NCAI of single cancers conformed to cancer progression (26.1 +/- 4.7% in Dukes A, 33.1 +/- 7.1% in Dukes B, 39.9 +/- 6.9% in Dukes C, and 45.7 +/- 12.0% in Dukes D), that of multiple cancers was high in all stages (44.7 +/- 7.3%, 44.4 +/- 6.8%, 50.4 +/- 11.2%, and 49.6 +/- 5.6%, respectively). Furthermore, the multiple numerical aberration of chromosome 17 in multiple cancers was more often than that of single cancers (64.3% VS 22.9%; p < 0.01).

Aged↗
PubMed1997

[Flow cytometric quantification of numerical chromosome aberrations in non-small cell lung carcinomas using formalin-fixed paraffin-embedded tissue].

Fluorescence in situ hybridization with biotinylated repetitive DNA probe specific for the centromeric region of chromosome 17 (p17H8: Oncor) was applied to suspended nuclei which were isolated by Shutte's method from formalin-fixed paraffin-embedded tissue. The tissues were obtained from surgically resected specimens from nine patients with non-small cell lung carcinoma. The isolated nuclei were prepared with 0.05% pepsin/0.1NHCl for 15 minutes at 37 degrees C. Subsequently, these were immersed in 70% acetic acid for 10 seconds at room temperature. After heat denature with hybridization mixture which contained 3 mu 1 DNA probe for 10 minutesat 70 degrees C, 1 x 10(6) nuclei were incubated overnight at 37 degrees C. After washing with 60% formamide/2 x SSC, the hybridized probes were labeled by FITC conjugated avidin. A number of centromeric signals of chromosome 17 wasevaluated by fluorescence microscopy (BH-2, Olympus). Furthermore, a probe-related FITC intensity was quantified using flow cytometry (FACScan, Becton Dickinson). As the results, there was good correlation between a relative fluorescence intensity determined by flow cytometry and a relative fluorescence signal by fluorescence microscopy (p < 0.05).

Aged↗
PubMed1997

Clinical and pathological significance of numerical aberrations of chromosomes 11 and 17 in colorectal neoplasms.

Numerical chromosome aberrations by interphase cytogenetic analysis have been reported in a few samples of colorectal neoplasms. No studies have defined a distinct relationship between these aberrations and clinicopathological features. To investigate the chromosome aberrations as a marker of invasiveness or prognosis, we conducted an interphase cytogenetic study using fluorescence in situ hybridization and examined 142 colorectal neoplasms consisting of 15 adenomas and 127 cancers. The target chromosomes were chromosomes 11 and 17. We also evaluated the nuclear DNA content as detected by flow cytometry, analyzed the relationship between the frequency of aneusomy and clinicopathological features, and examined the survival rate in these patients. The loss of chromosome 11 was observed in 31% of adenomas, whereas in cancers DNA aneuploidy was observed in 63% of cases, a gain of chromosome 17 was observed in 63% of cases, and a gain of chromosome 11 was observed in 42% of cases. Numerical chromosome aberrations in diploid DNA were also observed. Increased depth of invasion (>/=T3) and advanced Dukes' stage (>/=B) of malignant tumors were associated with a higher frequency of a gain of chromosome 11 (P < 0.01 and P < 0.05, respectively). Increased depth of invasion (>/=T2) in cancers was associated with a higher frequency of a gain of chromosome 17 (P < 0.05). Multivariate analysis of postoperative survival showed that a loss or gain of chromosome 11 was independently associated with a poor prognosis (P < 0.05). Numerical chromosome aberrations appear prior to the alteration of nuclear DNA content as detected by flow cytometry and influence the progression of colorectal cancers. Aneusomy of chromosome 11 is associated with poor postoperative prognosis of primary colorectal cancers.

Adenocarcinoma↗
PubMed1996

Numerical aberrations of chromosomes 11 and 17 in colorectal adenocarcinomas.

Fluorescence in situ hybridization (FISH) is an easy and efficient means of measuring numerical chromosome aberrations in the interphase nuclei of solid tumors; however, the correlation between numerical chromosome aberrations and the clinical stage of solid tumors remains unknown. Thus, in the present study, we investigated the relationship between numerical chromosome aberrations and clinicopathologic features in colorectal adenocarcinomas. FISH was applied to surgically resected colorectal cancer samples from 45 patients to evaluate the numerical aberrations of chromosomes 11 and 17. The mean age of the patients was 65.1 years, and they comprised 13 women and 32 men. According to Dukes' classification, 5 patients were categorized as stage A, 21 as stage B, 10 as stage C, and 9 as stage D. Histologically, 18 of the samples were lymph node metastasis-positive. FISH revealed numerical aberrations of chromosome 11 in 27 out of the 45 patients (60%), and those with a lower chromosome 11 number had a significantly lower incidence of lymph node metastasis (P < 0.05). Chromosome 17 proved to have numerical abnormalities in 33 of the 45 patients (73%), and those with a higher chromosome 17 number had more DNA aneuploidy (P < 0.005). This is the first report to reveal the relationship between monosomy 11 and lymph node metastasis in colorectal adenocarcinomas.

Adenocarcinoma↗
PubMed1996

[A case of solitary splenic metastasis from colon cancer].

A 58-year-old male who had a left hemicolectomy for descending colon cancer on July 1, 1993 was admitted to our hospital. A CT scan revealed a homogeneous low-density mass in the inferior portion of the spleen. Under the diagnosis of solitary splenic metastasis, a splenectomy was performed on August 10, 1995. Histologically, splenic tumor revealed moderately differentiated adenocarcinoma consistent with the primary tumor. Flow cytometric analysis revealed DNA diploidy in the primary tumor, and DNA aneuploidy (DNA index = 1.76) in the metastatic tumor. Using fluorescence in situ hybridization with p17 H8, numerical aerrations of chromosome 17 were observed in the primary tumor.

Adenocarcinoma↗
PubMed1995

Molecular analysis of X-linked adrenoleukodystrophy patients.

A molecular analysis of 4 Japanese adrenoleukodystrophy (ALD) patients was carried out, according to the recently published report on ALD gene cDNA. In a Southern blot analysis, we were not able to detect a large deletion in all patients. In a Northern blot analysis, no mRNA was detected in one patient, while the others had normal mRNA in both size and amount. Three patients had missense mutations including; 534Pro-->Leu (1987C-->T), 660Arg-->Trp (2364C-->T), and 512Gly-->Ser (1920G-->A), respectively. These mutations existed in the C-terminal region conserved in the ATP-binding cassette superfamily of transporters. In a Western blot analysis using polyclonal antibodies against the C-terminal peptide as well as the whole peptide of ALD protein, no 80 kDa protein was found in any of the 4 patients, which was observed in the control cells. The ALD protein in 3 patients with a missense mutation might be degraded immediately after translation because of the unstable higher structure or by the disruption of the hitherto unknown targetting signal to the peroxisome. The molecular analysis of the ALD gene as done in this study is thus considered to be the first step to further elucidate the pathogenic mechanism of ALD.

Adrenoleukodystrophy↗
PubMed1994

Adrenoleukodystrophy gene encodes an 80 kDa membrane protein.

An antibody against the synthetic C-terminal peptides deduced from the cDNA of the gene responsible for X-linked adrenoleukodystrophy (ALD) was produced to characterize the product of the ALD gene. The antibody reacted with the 80 kDa band protein in control fibroblasts, while no bands were detected in the fibroblasts from a patient with ALD (#163), in which mRNA of the ALD gene was undetectable based on Northern blot analysis. The 293T cells transfected with the full-coding cDNA inserted in the expression vector produced a new 80 kDa protein, as detected by Western blot. In an immunocytological study, the staining was in a punctate pattern, in the normal fibroblasts. However, there was no punctate staining in the #163 cells. These data thus indicate that the ALD gene encodes an 80 kDa membrane protein.

Adrenoleukodystrophy↗
PubMed1994

[Detection of chromosomal numerical aberration in early colorectal carcinomas using fluorescence in situ hybridization].

The authors have performed fluorescence in situ hybridization (FISH) in tissue sections of archival paraffin-embedded blocks of seven cases in adenoma and ten cases in carcinoma in order to clarify which chromosomal aberration occurred in association with multi-step carcinogenesis in colorectal carcinomas, using alpha-satellite DNA probes to chromosome 11 and 17, D11Z1 and D17Z1, respectively. Monosomy of chromosome 11 was most frequented (5/7, 71.4%) in adenoma, and trisomy of chromosome 17 was predominant (9/10, 90.0%) in carcinoma. The numerical chromosomal aberrations can be already detected at the stage of adenoma, and monosomy of chromosome 11 was mainly observed in adenoma. Furthermore, malignant transformation arising from adenoma accounted for most of the trisomic change in chromosome 17. Consequently, applying the FISH technique to tissue sections from archival paraffin embedded specimen, it would be possible to distinguish between the cancerous and non-cancerous regions in view of chromosomal numerical aberrations. The authors emphasized that intratumoral heterogeneity could be elucidated at the chromosomal level.

Adenoma↗
PubMed1993

Comparison of pepsin and trypsin digestion on paraffin-embedded tissue preparation for DNA flow cytometry.

Preparation with enzymes plays an important part in obtaining good results in cellular DNA content measurements from paraffin-embedded tissue using flow cytometry. Therefore, we have compared two groups of DNA histograms obtained with pepsin (Hedley method) and trypsin digestion (Schutte method). Samples of five tumor types were compared: eight lung, seven breast, five thyroid, seven stomach, and six colon cancer cases. All samples were stained with propidium iodide (PI). The incidence of DNA aneuploidy determined by the Schutte method indicated a higher ratio in four tumor types than that determined by the Hedley method. Concerning the coefficient of variation (CV) used to estimate the quality of the DNA histogram, the diploid G1 peak determined by the Schutte method produced a smaller CV in five tumor types than did the Hedley method. This Schutte method had especially good results in lung and thyroid cancer. Furthermore, the amount of debris (background) determined by the Schutte method indicated a decrease in four tumor types compared with the Hedley method. In cell-cycle analysis of ten DNA diploid cases, DNA histograms by the Hedley method showed an increased S-phase fraction due to an overlapping of debris and aggregated cells. These results indicate that preparation by trypsin digestion is a method superior to pepsin digestion when the sample from paraffin-embedded tissue is stained with PI for the purpose of DNA content measurement.

Breast Neoplasms↗
PubMed1993

Effect of various vehicles on ketoprofen permeation across excised hairless mouse skin.

The effects of glycerides, short-chain alcohols, and their binary vehicles as donor components on the permeation of ketoprofen (KP) across the excised hairless mouse skin were evaluated with the modified LOVEDAY-type diffusion cell. Among single vehicles, Panasate 800 as tricaprylin appeared to be the most favorable lipophilic vehicle, with no toxicity and with a short lag time (0.9 h), and methanol (MeOH) or ethanol (EtOH) as hydrophilic single vehicles showed the highest KP permeation flux (244.1 and 134.1 micrograms/cm2/h, respectively). Furthermore, KP permeation was enhanced remarkably by the combination of EtOH and Panasate 800 compared with each single vehicle as reflected in the decreased lag time and increased flux. The greatest enhancement was observed in the EtOH/Panasate 800 (40/60) binary vehicle (permeation ratio at 24 h, 40.0%; steady-state flux, 314.0 micrograms/cm2/h; lag time, 3.7 h). Further investigations involving stripping studies and KP accumulation within the skin were performed to explain the mechanism of enhancement caused by the above binary vehicle. It was suggested that the mutual enhancement effect of EtOH/Panasate 800 (40/60) binary vehicle is due to decreasing the barrier ability of the stratum corneum by EtOH and the viable skin by Panasate 800.

Alcohols↗