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Biomedical subjects

Y Sameshima

Publications and source records attributed to Y Sameshima.

At least 19 recordsLinked to original sources
PubMed1996

[Acute myelogenous leukemia with ins(21;8) expressing AML-1-MTG8 fusion transcript].

Here we report a case of acute myelogenous leukemia (M2, FAB classification) presenting with cytogenetic abnormalities of ins(21;8), +del(8) without t(8;21). A 8;21 chromosome translocation is frequently found in acute myelogenous leukemia, especially in the M2 subtype. The translocation results in a fusion transcript between AML1 and MTG8 (ETO), assigned on chromosomes 21 and 8, respectively. Among patients with a t(8;21) abnormality, solid leukemic tumor deposits outside the marrow or good response to chemotherapy are observed frequently. Decrease in neutrophil alkaline phosphatase score and positive rate, and eosinophilia in bone marrow or the blast cells with Auer rods expressing CD19, CD56 antigens occur at a relatively high rate. Although our case lacked these clinical, cytological and cytochemical features, expression of chimeric AML1-MTG8 mRNA was detected. AML1-MTG8 fusion transcript may play a critical role in leukemogenesis of AML M2. Studies on this case may help to reveal the oncogenic function of the AML1-MTG8 fusion gene in AML M2.

Adult↗
PubMed1995

Effects of auricular acupuncture stimulation on nonobese, healthy volunteer subjects.

Effects of auricular acupuncture stimulation on nonobese healthy volunteers were investigated. Subjects (n = 35) averaged 34.5 years old, and BMI was 25.3 kg/m2. Small (0.15 x 2.0 mm) auricular needles were applied intracutaneously into the bilateral cavum conchae that was identified by having less than 100 k omega resistance. Body weight was measured four times a day and charted by the subjects themselves. Results showed that, in the period 11-2, in which only body weight was measured, without auricular acupuncture stimulations, 57.1% of the subjects reduced their body weight. This indicates that charting body weight themselves might be useful to maintain their weight. In the auricular acupuncture treated period, 19 (70.4%) out of 27 decreased (p < 0.01), 5 (18.5%) was increased, and 3 (11.1%) had no change in body weight. In conclusion, the results suggest that success in maintaining weight reduction can be attributed to graphic illustration of one's weight pattern. Bilateral auricular acupuncture stimulation can also reduce body weight of healthy non-obese subjects. This is consistent with the suggestion that it might be effective in the treatment of obese patients.

Acupuncture Points↗
PubMed1995

Effects of auricular stimulation on feeding-related hypothalamic neuronal activity in normal and obese rats.

It is known that auriculotherapy occasionally affects dramatic body weight reduction for obese patients, although the physiological and anorexigenic functions are not clear. Effects of auricular stimulation on feeding-related lateral (LHA) and ventromedial (VMH) hypothalamic neuronal activity in normal and experimental (hypothalamic and dietary) obese rats were investigated. The LHA and/or VMH neuronal activity were recorded from feeding-related regions in Wistar SPF/VAF male and experimental (hypothalamic and dietary) obese rats, anesthetized with urethane-chloralose, under stereotaxic coordination. Recording was through 3 M KCI glass microelectrodes, while stimulating the ipsilateral vagal innervated region of the auricle. This is equivalent to the cavum conchae in the human, and was identified by resistance less than 10-50 k omega. The stimulating electrode was a stainless steel ear acupuncture (0.12 x 2.0 mm). The latency of potentials evoked in the LHA by unilateral stimulation of a specific site in the ear was 28.1 +/- 3.3 ms (8-92, n = 41). LHA neuronal activity was depressed 45.6% (n = 12, p < 0.01), and VMH activity was excited (60.5%, n = 18, p < 0.01). The auricular acupuncture stimulation clearly modulates feeding-related hypothalamic neuronal activity of experimental (both hypothalamic and dietary) obese rats. These auricle acupuncture stimulation effects were correlated to the degree of obesity. In conclusion, the results suggest that auricular acupuncture stimulation may not reduce appetite, but is more likely concerned with satiation formation and preservation. Thus, auricular acupuncture should be more effective on obese rats than on normal rats.

Acupuncture Therapy↗
PubMed1995

Effects of hypothalamic paraventricular nucleus: electrical stimulation produce marked analgesia in rats.

The effect of the electrical simulation induced analgesia (ESIA) on the hypothalamic paraventricular nucleus (PVN) was investigated by the paw pressure test, which was used to avoid any tissue damage to the paw of Wistar-SPF/VAF male rats. A stimulating electrode was chronically implanted in the parvocellular (PVN-prv) or magnocellular (PVN-mgn) divisions of the PVN. The ESIA was examined at least 10 days after surgery. The electrical stimulation of the PVN markedly showed analgesia (ESIA), but stimulation of most locations outside the PVN did not produce ESIA. Stimulation threshold for the ESIA was lower from PVN-prv than from PVN-mgn, but neither region was affected by naloxone administration (10 mg/kg, i.p.). These results indicate that the PVN is a part of the pain inhibitory system in the CNS, and show that PVN-ESIA might not be mediated either by opioids or by neuropeptides such as vasopressin.

Analgesia↗
PubMed1994

Frequent allelic losses on chromosomes 2q, 18q, and 22q in advanced non-small cell lung carcinoma.

Although it is widely accepted that tumor suppressor genes play an important role in the genesis and progression of human cancer, little is known about genetic events that accumulate during multistage lung carcinogenesis. Thus, to determine a subset of tumor suppressor genes that are involved in the genesis and progression of non-small cell lung carcinoma (NSCLC), 22 brain metastases and 23 stage I primary lung tumors were examined for allelic losses at 40 loci on 10 chromosomes including the loci of 5 tumor suppressor genes, APC, WT1, RB, p53, and DCC. The incidence of allelic losses on chromosomes 3p, 13q, and 17p was high (> 60%) in both primary tumors and brain metastases. In brain metastases, a high incidence of allelic losses (> 60%) was also observed at loci on chromosomes 2q, 18q, and 22q, and the incidence of allelic losses on these chromosomes in brain metastases was significantly higher than that in primary tumors (P < 0.05). In two cases of brain metastases with corresponding primary lung tumors, sequential accumulation of allelic losses during progression of primary lung tumors was observed on several chromosomes including chromosomes 2q and 18q. These results indicate that, besides loss of heterozygosity for chromosomes 3p, 13q, and 17p, loss of heterozygosity for chromosomes 2q, 18q, and 22q also occurs frequently in advanced NSCLCS. Thus, it is possible that loss of heterozygosity on chromosomes 2q, 18q, and 22q occurs late in the progression of NSCLC and/or causes phenotypic alterations of NSCLC cells into more aggressive ones.

Base Sequence↗
PubMed1993

Germ-line p53 mutation is uncommon in patients with triple primary cancers.

We examined five patients with multiple primary cancers who had a history of three different types of primary cancers for germ-line p53 mutations. The germ-line p53 mutation was detected in a patient who conformed to the Li-Fraumeni syndrome, but not in the other four patients. The diagnosis of these four patients did not fall in the category of Li-Fraumeni syndrome. This result indicates that germ-line p53 mutations are uncommon even in patients with triple primary cancers.

Female↗
PubMed1992

Detection of novel germ-line p53 mutations in diverse-cancer-prone families identified by selecting patients with childhood adrenocortical carcinoma.

BACKGROUND: Germ-line p53 mutations appear to be inherited among the members of families diagnosed with Li-Fraumeni syndrome (LFS). The mutations detected in those families to date have been clustered in exon 7 of the p53 gene and, typically, have been single-base substitutions resulting in amino acid changes. PURPOSE: Our aim was to define the spectrum of p53 mutations associated with LFS. METHODS: From seven cancer-prone families identified by selecting members with childhood adrenocortical carcinoma as probands, we chose two families, each of which had two members from whom specimens could be obtained for genetic analysis. To detect germ-line p53 gene mutations in these individuals, we performed polymerase chain reaction (PCR)-single-strand conformation polymorphism analysis with Taq polymerase and oligonucleotide primers specific for p53 gene sequences. Genomic DNA extracted from fresh tissue samples and paraffin-embedded tumor samples was amplified, denatured, and electrophoresed on neutral polyacrylamide gels. PCR amplification was also carried out using total RNA from adrenocortical carcinoma samples of the proband in family 1. PCR products were purified, subcloned, and sequenced. RESULTS: We detected novel germ-line p53 mutations in affected members of both cancer-prone families. In the proband of family 1, a single-base deletion was detected at the first nucleotide of codon 307 in exon 8 of the p53 gene, resulting in a premature stop codon in exon 10. In family 2, we detected an A to C transversion at the second nucleotide of codon 286 in exon 8, both in DNA isolated from the adrenocortical tumor of the proband and in DNA isolated from the astrocytoma of the proband's father. This single-base substitution resulted in an amino acid substitution of alanine for glutamic acid. Both of these mutations are located outside the highly conserved region of the p53 gene where mutations in patients with LFS have been reported previously. CONCLUSION: Our results indicate that a wide range of germ-line p53 mutations is inherited in members of diverse-cancer-prone families.

Adrenal Cortex Neoplasms↗
PubMed1992

Appearance of the tumor marker CA 19-9 in liver transplant patients during rejection episodes.

The tumor marker CA 19-9 was shown to be elevated in liver transplant patients, particularly during rejection. Serial serum samples taken from 24 patients after liver transplantation were examined for tumor markers CA 19-9, SLEX, CEA, and TNF-alpha. During rejection, 85% of the patients had elevated levels of CA 19-9. Patients with early rejection had persistently higher levels than patients without rejection. The serum levels were low in nonrejecting patients compared with those with rejection. Thus, the CA 19-9 marker cannot be considered a specific tumor marker. It may, however, be an indicator of an immune response or it may be a byproduct of an inflammatory reaction to a tumor or a transplant.

Antigens, Tumor-Associated, Carbohydrate↗
PubMed1992

Alterations of the p53 gene are common and critical events for the maintenance of malignant phenotypes in small-cell lung carcinoma.

To clarify the incidence, timing and pathogenetic significance of p53 gene alterations in the progression of small-cell lung carcinoma (SCLC), 17 primary tumors, 13 metastases and nine cell lines from 27 patients were analysed by a polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) analysis. Allelic losses and mutations of the p53 gene were detected in 24 out of 25 informative cases (96%) and 23 out of 27 cases (85%) respectively. Simultaneous losses and mutations were detected in all 16 stage III-IV tumors, while these alterations were detected only in 3 of 6 stage I-II tumors. When allelic losses and/or mutations were detected in the primary tumors, the same alterations were always maintained in the process of metastasis. In three cases, identical p53 alterations were detected among different organ metastases. The mutations detected in five cell lines were also detected in the corresponding original tumors. These results suggest that the alterations of the p53 gene are common and early events, but probably not the first events, in the development of SCLC, and that these alterations are essential for the maintenance of malignant phenotypes in the progression of SCLC.

Base Sequence↗
PubMed1991

Adult T-cell leukemia: structures and expression of the p53 gene.

Experiments were undertaken to investigate a genetic event involved in leukemogenesis in adult T-cell leukemia (ATL). For this purpose, the p53 gene was chosen for study, since alteration of the gene has been found in a wide variety of human cancers. Structures and expression of the p53 gene in ATL cells were investigated by Southern and Northern blot analyses and a polymerase-chain-reaction single-strand conformation-polymorphism (PCR-SSCP) analysis. Either subtle alterations of the p53 gene or the absence of detectable level of p53 mRNA were found in 2 of 3 acute ATL cell lines and 2 of 12 acute ATL fresh samples. In contrast, no mutation was detected in 4 cases with less aggressive types of ATL (3 chronic and 1 smoldering ATL cases). Mutations found in acute ATL cells occurred in regions highly conserved in evolution and all the cells carrying p53 mutation showed loss of the other p53 allele. These results suggests that alteration of the p53 gene may contribute to progression of the disease in some cases of ATL.

Adult↗
PubMed1991

Allelic loss on chromosome 17p and p53 mutations in human endometrial carcinoma of the uterus.

To understand the involvement of allelic losses and inactivation of tumor suppressor genes for the development of endometrial carcinoma of the uterus (EC), 24 cases of EC were examined for loss of heterozygosity (LOH) using a total of 57 polymorphic DNA markers covering all 23 pairs of chromosomes. LOH was observed at 27 loci on 10 different chromosomes, i.e., chromosomes 1, 3, 6, 11, 13, 15, 17, 18, 20, and 21, but was not detected at loci on chromosomes 4, 5, 7, 9, 10, 12, 14, 16, and X. It was observed only in seven of 24 cases, and the other 19 cases did not show LOH at any loci examined, including five cases of tumors with a high proportion of adenomatous hyperplasia. Among seven tumors with LOH at one or more loci, five tumors showed LOH at loci on the short arm of chromosome 17. Furthermore, mutations of the p53 gene, which is located on the short arm of chromosome 17, were detected in three of these 24 tumors by a polymerase chain reaction-single strand conformation polymorphism analysis and subsequent DNA sequencing. In two of these three tumors, p53 mutations were accompanied by the loss of wild-type p53 alleles. These results suggest that inactivation of the p53 gene is involved in the development of EC as in the case of several other types of human cancers.

Alleles↗
PubMed1991

Frequent allelic losses and mutations of the p53 gene in human ovarian cancer.

The p53 gene on chromosome 17p is considered to be a tumor suppressor gene, and frequent mutations of the p53 gene have been found in a wide variety of human cancers. We examined 31 ovarian cancers for allelic losses and mutations of the p53 gene by polymerase chain reaction-single strand conformation polymorphism analysis as well as restriction fragment length polymorphism analysis. Allelic loss of the p53 gene was detected in 16 of 20 cases (80%). Mutations were detected in 9 of 31 cases (29%): 2 cases in exon 4; 5 cases in exons 5-6; and 2 cases in exons 7-8. In 8 of 9 cases, p53 mutations were accompanied by losses of the normal allele. These alterations of the p53 gene were commonly detected from stage I to stage IV. These results suggest that alterations of the p53 gene play an important role in the development of human ovarian cancers.

Base Sequence↗
PubMed1991

Prognosis of unresectable hepatocellular carcinoma: an evaluation based on multivariate analysis of 90 cases.

A multivariate analysis of data from 90 patients with unresectable hepatocellular carcinoma was performed using Cox's regression model to identify factors possibly affecting their prognoses. Thirty-one patients underwent arterial anticancer chemotherapy, and the remaining 59 patients received transcatheter arterial embolization with anticancer agents. Four of 27 variables tested for all the patients (i.e., encapsulation [p less than 0.05], gross appearance of hepatocellular carcinoma [p less than 0.01], clinical stage [p less than 0.01] and therapy [p less than 0.01]) were found to be prognostically significant. Five of 27 variables tested were prognostically significant for the transcatheter arterial embolization group; they were an extension rate of hepatocellular carcinoma (p less than 0.01), encapsulation (p less than 0.01), alpha-fetoprotein (p less than 0.01), prothrombin time (p less than 0.01) and serum sodium (p less than 0.01). Regression equations were used to describe a prognostic index. A prognostic index was defined as the regression equation derived from the results of a total of 90 patients; PI-1 = eY, where PI-1 = prognostic index 1 Y = 1.549 (gross appearance of hepatocellular carcinoma - 1.344) + 0.778 (encapsulation - 1.622) + 0.818 (clinical stage - 1.800) + 1.760 (therapy - 1.344) and prognostic index 2, the regression equation derived from the results of the transcatheter arterial embolization group of patients; PI-2 = eY, where PI-2 = prognostic index 2 Y = 1.210 (extension rate of hepatocellular carcinoma - 1.576) + 1.179 (encapsulation - 1.475) + 0.0001277 (alpha-fetoprotein - 1420.792) -0.039 (prothrombin time - 72.237) - 0.214 (serum sodium - 138.427).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Tumor suppressor genes involved in metastasis of lung and colorectal carcinomas.

Inactivation of tumor suppressor genes is now believed to play an important role in various progression stages of human cancers. To clarify the possible involvement of tumor suppressor gene inactivation in the acquisition of metastatic potential in lung and colorectal carcinoma cells, we examined various genetic alterations in both primary tumors and metastases obtained from patients with lung and colorectal carcinomas. In lung carcinoma, loss of heterozygosity on chromosomes 3p, 13q, and 17p is a common genetic alteration, and both RB and p53 genes are inactivated as a result of chromosome 13q and 17p losses. In some cases, allelic loss on chromosome 11p and amplification of myc family oncogenes occur during tumor progression. In colorectal carcinoma, p53 and DCC alterations were detected in 100% of metastases, and sequential accumulation of allelic losses on chromosomes 13q, 14q, and 18q in the process of metastasis was observed. These results indicate that a subset of tumor suppressor genes is involved in metastasis of lung and colorectal carcinomas.

Colorectal Neoplasms↗