Search PubMedSearch

Biomedical subjects

Y Kaneko

Publications and source records attributed to Y Kaneko.

At least 19 recordsLinked to original sources

Consistent disruption of the AML1 gene occurs within a single intron in the t(8;21) chromosomal translocation.

The AML1 gene on chromosome 21 was rearranged by the t(8;21) chromosomal translocation in acute myeloid leukemia (AML). Southern blot analysis of 21 AML patients with t(8;21), including three with complex translocations, t(8;V;21), demonstrated that all the breakpoints occurred at random within a single intron between two coding exons of AML1. Clustering of the breakpoints in the restricted intron suggests the formation of a unique fusion gene between the AML1 gene and a presumable counterpart gene on chromosome 8. Nucleotide sequencing of the breakpoint region revealed that the translocation event was accompanied by deletion of a short stretch of nucleotides.

Base Sequence

Co-ordinate expression of c-fos, p53 and cytokeratin genes during the alteration of growth of human hepatoma cells. mRNA levels measured by reverse transcription and polymerase chain reaction.

Teleocidin, a tumor promoter, inhibited the proliferation, enhanced cytokeratin assembly and increased the type III procollagen production of PLC/PRF/5 hepatoma cells. Teleocidin transiently increased the levels of c-fos and p53 mRNAs measured by reverse transcription and polymerase chain reaction. This was followed by a reduction of c-myc mRNA and an increase of cytokeratin mRNA. The level of p120 mRNA was not remarkably altered. Sequential alterations of the expression of c-fos, p53, c-myc and cytokeratin genes induced by teleocidin may be responsible for the morphological and functional changes of hepatoma cells induced by this tumor promoter.

Base Sequence

An immunohistochemical study of regenerating newt retinas.

Light-microscopical examination was carried out to investigate the emergence and development of several classes of immunoreactive cells in regenerating retinas of the adult newt (Triturus pyrrhogaster) after total retinal ablation. Immunoreactive proliferating cell nuclear antigen (ir-PCNA, a marker for replicating cells) was present in nuclei of all neuroblasts in the early mono-layered to several-layered stages (15-20 days after retinal ablation; days 15-20), but was lost progressively in an intermediate-to-central/peripheral order as cells and layers increased (days 20-25). Cells, which had lost ir-PCNA, began to separate to form the outer nuclear, inner nuclear and ganglion cell layers around days 25-30 (the cell separation stage). Finally, the location of ir-PCNA was restricted to a band of neuroblast cells at the retinal margin (days 30-35) as seen in intact adult retinas. Visinin-immunoreactive (ir) cells, mainly destined to be cones, appeared first singly or as clusters at the most distal layer in the intermediate region of retinas multi-layered with PCNA-ir neuroblasts, which was followed by appearance of opsin-ir rod outer segments and tyrosine hydroxylase-ir amacrine cells around the cell separation stage. Shortly later, cells respectively immunoreactive to glutamic acid decarboxylase, neuropeptide Y, serotonin, glucagon, glutamine synthetase, glial fibrillary acidic protein, substance P and protein kinase C were found to emerge also in an intermediate-to-central/peripheral sequence. Some of the glucagon-ir cells appeared to be of an interplexiform type.

Animals

Cerebral neurocytoma. A new subset of benign neuronal tumors of the cerebrum.

Three cases of patients with unusual neuronal tumors in the cerebral hemisphere are reported. All were associated with long-standing epileptic seizures. Computed tomography disclosed low-density lesions without contrast enhancement, which were interpreted as either arachnoid cysts or a cerebral infarction at initial diagnosis. Magnetic resonance imaging scans, however, revealed the lesions to be solid tumors. At surgery, the tumors were found to be relatively well demarcated, soft, and gelatinous. Histologically, all tumors were composed of small uniform stellate cells, which proliferated in a loose myxoid fibrillary matrix and resembled either oligodendroglial or astrocytic tumors. Ultrastructurally, however, all tumors showed neuronal differentiation, including numerous clear and occasional dense-core vesicles, microtubules, and a number of synapses. A review of the literature uncovered no other such cases, and therefore it was decided to classify these tumors as a distinct group of benign neuronal tumors, designated as "cerebral" neurocytoma compared with "intraventricular" neurocytoma. Related nosologic problems of neuronal tumors of the central nervous system and their possible histogenesis are also discussed.

Adult

Increased assembly of cytoskeletal proteins associated with the transformation of human liver cells into fibroblast-like cells.

A topoisomerase II inhibitor, novobiocin, and a deacetylase inhibitor, butyrate, synergistically transformed human liver cells into fibroblast-like cells. This morphological change was associated with an increased production of procollagen type III peptide and a simultaneous assembly of actin, tubulin, vimentin and cytokeratin. Novobiocin and butyrate had no marked effect on the phosphorylation state of cytokeratin proteins, but synergistically enhanced [3H]acetate uptake. From these results, it can be speculated that protein acetylation plays an important role in inducing the assembly of cytoskeletal proteins and the morphological transformation of human liver cells.

Acetylation

Allelotype analysis in osteosarcomas: frequent allele loss on 3q, 13q, 17p, and 18q.

We have investigated the involvement of tumor suppressor genes in the genesis of osteosarcoma by analyzing allele losses at polymorphic loci in tumor tissues. Genotypes of DNA from primary osteosarcoma tissue and corresponding normal cells from 37 patients were analyzed at 58 polymorphic loci representing each autosomal chromosome arm except 5p and 20q. Allele losses were found at polymorphic loci on 36 of 37 chromosome arms analyzed. In particular, four of them showed frequencies of allele loss higher than 60%: 3q (75%); 13q (68%); 17p (72%); and 18q (64%). This result suggests that, in addition to the RB (retinoblastoma) gene on 13q and the p53 gene on 17p, at least two more tumor suppressor genes located on 3q and 18q are frequently involved in the development of osteosarcoma. The extent of allele losses as defined by fractional allelic loss among 36 tumors was diverse, from 0 to 0.64. The median fractional allelic loss value of 0.32 was much higher than those previously reported in colorectal carcinoma and breast carcinoma. Although no definite association of fractional allelic loss value to clinical prognosis of each case was found in osteosarcoma, tumors with 17p loss were more prone to the early onset of lung metastasis than tumors without 17p loss, indicating that allele loss on chromosome 17p can be a useful measure of prognosis.

Adolescent

Two cell lines established from mixed müllerian tumors of the uterus. Morphologic, immunocytochemical, and cytogenetic analyses.

To clarify the cellular origin and characteristics of malignant mixed müllerian tumor (MMMT), the authors investigated two cell lines (designated as FU-MMT-1 and FU-MMT-2) established from two patients with heterologous MMMT of the uterus. Both cell lines propagated continuously for 83 and 55 serial passages over 1.5 years, respectively. Morphologically, FU-MMT-2 was a mixture of carcinoma cells and sarcoma cells with predominance of carcinoma cells; FU-MMT-1 only had a sarcomatous element with distinct rhabdomyoblastic differentiation. Immunocytochemically, the sarcoma cells of each cell line expressed, not only myogenic and mesenchymal antigens (desmin, myoglobin, and vimentin), but also epithelial antigens, including epithelial membrane antigen and keratin. The carcinoma cells in FU-MMT-2 were positive for the epithelial antigens and vimentin and negative for desmin and myoglobin. Both lines had abnormal karyotypes; the modal chromosome numbers of FU-MMT-1 and FU-MMT-2 were 47 and 80, respectively. In addition, FU-MMT-1 had trisomy 8, and FU-MMT-2 had complex structural abnormalities. When transplanted into nude mice, FU-MMT-1 reproduced and maintained the characteristics of the original tumor. These cell lines and xenografts appear to provide a useful system for studying the biologic behavior, cytogenetic features, and histogenesis of MMMT. In conclusion, the presence of epithelial antigens in the sarcomatous and carcinomatous elements seemed to support the hypothesis that both elements are derived from a common stem cell.

Aged

Chromosome abnormalities in adult T-cell leukemia/lymphoma: a karyotype review committee report.

Karyotypes of 107 cases with adult T-cell leukemia/lymphoma (58 male, 49 female; 81 acute or lymphoma type, 26 chronic or smoldering type) were reviewed by a panel of cytogeneticists and were correlated with the subtypes of the disease. Clonal chromosome abnormalities were found in 103 (96%) cases, of which four had hypotetraploidy. Of 184 numerical abnormalities in the remaining 99 cases with near- or pseudodiploidy, trisomies for chromosomes 3 (21% of cases), 7 (10%), and 21 (9%), monosomy for X chromosome (38%) in the female, and loss of a Y chromosome (17%) in the male were more frequent than expected (P less than 0.01). Of 373 structural abnormalities in all the 103 aneuploid cases, translocations involving 14q32 (28%) or 14q11 (14%) and deletion of 6q (23%) were most frequent, followed by deletion of 10p (9%), 3q (8%), 5q, 9q, and 13q (7% each), and 1p and 7p (6% each). The proportion of cases with aneuploid clones (with greater than or less than 46 chromosomes), the average numbers per case of both numerical and structural abnormalities, and marker chromosomes were larger in the aggressive acute or lymphoma type than in the nonaggressive chronic or smoldering type (P less than 0.01). The combination of rearrangement in 14q32 and monosomy X (seven cases) or deletion of 10p (six cases), and that of trisomy 3 and deletion in 6q21 (six cases), occurred only in the acute or lymphoma type and may be associated with the aggressiveness in adult T-cell leukemia/lymphoma.

Adult

Cloning and characteristics of a positive regulatory gene, THI2 (PHO6), of thiamin biosynthesis in Saccharomyces cerevisiae.

A thi2(pho6) mutant of Saccharomyces cerevisiae, defective in the expression of structural genes for thiamin-repressible acid phosphatase and enzymes involved in thiamin biosynthesis, was found to retain sufficient thiamin transport activity. The transport activity was repressed by thiamin in growth medium. We isolated from a S. cerevisiae genomic library two hybrid plasmids, pTSR1 and pTSR2, containing 10.2- and 12.0-kilobase (kb) DNA fragments, respectively, which complement the thi2(pho6) mutation of S. cerevisiae. This gene was localized on a 6.0-kb ClaI-ClaI fragment in the subclone pTSR3. Complementation of the enzyme activities for thiamin metabolism in the thi2(pho6) mutant transformed by some plasmids with the TH12(PHO6) gene was also examined.

Cloning, Molecular

Long-distance restriction mapping of the proximal long arm of human chromosome 21 with Not I linking clones.

Human chromosome 21 is the smallest of the 22 autosomes and 2 sex chromosomes. Hybridization of the human repetitive sequence Alu to pulsed-field gel-fractionated Not I-digested genomic DNA from a human-mouse hybrid cell line containing chromosome 21 as the sole human component identified chromosome 21 Not I restriction fragments. A Not I restriction map of regions of the chromosome was constructed, by identifying neighboring Alu bands with Not I linking clones. This approach simplifies the task of physical mapping and avoids ambiguities in Not I fragment assignments that arise from gel-to-gel mobility variations. A contiguous map was constructed with six Not I linking clones that covers at least the proximal one-third of the long arm of chromosome 21 and spans 20 megabases. A more detailed restriction map revealed 11 likely CpG islands in this region and localized 11 additional DNA markers.

Chromosomes, Human, Pair 21

Acute megakaryoblastic leukemia with translocation t(1;22)(p13;q13) in a 10-week-old infant.

A 10-week-old girl without Down syndrome developed an acute megakaryoblastic leukemia (AMKL). Bone marrow aspirates and biopsy showed megakaryoblastic infiltration with myelofibrosis. The diagnosis was made based on the findings that the positive reactions of leukemic cells to platelet peroxidase and to monoclonal antibodies which recognize platelet-specific surface glycoprotein (GP) IIb/IIIa and GP78. The blasts also showed myeloid and monocytoid differentiation antigens. The leukemic cells had a karyotype of 46,XX,t(1;22)(p13;q13). Our case and two other infantile cases reported by other investigators establish the novel association of the t(1;22) with AMKL.

Antibodies, Monoclonal

Appearance and maturation of voltage-dependent conductances in solitary spiking cells during retinal regeneration in the adult newt.

Electrical membrane properties of solitary spiking cells during newt (Cynops pyrrhogaster) retinal regeneration were studied with whole-cell patch-clamp methods in comparison with those in the normal retina. The membrane currents of normal spiking cells consisted of 5 components: inward Na+ and Ca++ currents and 3 outward K+ currents of tetraethylammonium (TEA)-sensitive, 4-aminopyridine (4-AP)-sensitive, and Ca(++)-activated varieties. The resting potential was about -40 mV. The activation voltage for Na+ and Ca++ currents was about -30 and -17 mV, respectively. The maximum Na+ and Ca++ currents were about 1057 and 179 pA, respectively. In regenerating retinae after 19-20 days of surgery, solitary cells with depigmented cytoplasm showed slow-rising action potentials of long duration. The ionic dependence of this activity displayed two voltage-dependent components: slow inward Na+ and TEA-sensitive outward K+ currents. The maximum inward current (about 156 pA) was much smaller than that of the control. There was no indication of an inward Ca++ current. During subsequent regeneration, the inward Ca++ current appeared in most spiking cells, and the magnitude of the inward Na+, Ca++, and outward K+ currents all increased. By 30 days of regeneration, the electrical activities of spiking cells became identical to those in the normal retina. No significant difference in the resting potential and the activation voltage for Na+ and Ca++ currents was found during the regenerating period examined.

Action Potentials

Establishment and characterization of a cell line of congenital primitive neuroectodermal tumor of soft tissue.

A new human cell line, termed Muraoka, has been established from the recurrent tumor of a case of congenital primitive neuroectodermal tumor (PNET) arising at the temporofacial region of a male infant. The microscopic findings of this cell line were epithelioid, and the xenografted tumor in a nude mouse consisted of the malignant epithelioid cells. Immunohistochemically, the cells were positive for neuron-specific enolase, S-100 protein, carcinoembryonic antigen, cytokeratin, epithelial membrane antigen, and glial fibrillary acidic protein. These findings were quite similar to those of the epithelioid cells in the original tumor and of the xenografted tumor cells. Neither chromosomal abnormalities nor N-myc amplification were observed. Morphological differentiation after treatment with N6-2'-O-dibutyryladenosine 3':5'-cyclic monophosphate (Bt2-cAMP), all-trans-retinoic acid (RA), prostaglandin E1 (PGE1), and 5-bromo-2'-deoxyuridine (BrdU) showed two different results. Bt2-cAMP and PGE1 induced neuronal differentiation with the extension of neurites, whereas RA and BrdU predominantly induced Schwannian differentiation (flat cells). In these respects, the cell line Muraoka seems to be useful for studying characteristics of PNET as well as for developing the new treatments against such tumors.

Animals

A case of lipoblastoma with t(3;8)(q12;q11.2).

We studied a single case of lipoblastoma in a 4-year-old boy. Cytogenetic analysis of the tumor cells showed two abnormal clones: 47,XY,t(3;8)(q12;q11.2),+mar, and 46,XY,t(3;8)(q12;q11.2). To our knowledge, this is the second report of chromosome findings in this rare tumor. Although lipoblastomas are frequently confused with myxoid liposarcomas, breakpoints in our patient were different from those of myxoid liposarcoma.

Child, Preschool

Chromosome abnormalities in liposarcomas.

We performed a cytogenetic study of short-term cultures from fresh surgical specimens obtained from four patients with liposarcoma. Myxoid liposarcomas (cases 1-3) were associated with a specific translocation between chromosomes 12 and 16. Trisomy 8, a nonrandom secondary aberration in myxoid liposarcoma, was observed in the third case as the only additional change. Round cell liposarcoma (case 4) showed complex chromosomal aberrations affecting chromosomes 1, 2, 5, 6, 7, 13, 14, 17, 19, and 22. Neither band 12q13 nor 16p11 was visibly rearranged. Three subgroups of liposarcomas are proposed. The first group is characterized by t(12;16)(q13;p11), the second group by ring chromosomes, telomeric associations, and giant markers, and the last by complex numerical and structural aberrations.

Adult

Stimulation of microbicidal host defence mechanisms against aerosol influenza virus infection by lentinan.

The ability of polysaccharide immunomodulator lentinan to stimulate non-specific resistance against respiratory viral infections was investigated. Significant protection was conferred by lentinan administered intranasally before lethal influenza virus infection and could be corroborated by a reduction of the lung virus titres. Since the lung is the target organ of influenza virus infection, lentinan was also administered by the intravenous route. Lentinan conferred complete protection against a LD75 challenge dose of virulent influenza virus and significantly prolonged the survival time after a LD100 challenge. The effect on respiratory burst of broncho-alveolar macrophages was investigated by luminol-dependent chemiluminescence (CL) in response to stimulation by zymosan. Enhanced CL activity was present at an early stage in groups receiving lentinan. Significant nitric oxide activity could also be stimulated by culturing broncho-alveolar macrophages in the presence of lentinan. TNF activity could not be detected in lung lavage but measurable IL-6 was produced already after 6 h in animals administered lentinan alone and in lentinan-pretreated influenza virus-infected mice. Influenza virus alone did not induce measurable IL-6 at 6 h but high activity was present at later time periods.

Aerosols