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Biomedical subjects

N Wake

Publications and source records attributed to N Wake.

At least 73 records · Page 4Linked to original sources
PubMed1990

[Cytogenetical study on the etiology of partial mole].

The cytogenetical etiology of partial mole (PM) was studied by means of the Q-banding technique in 49 cases during the period between Sep. 1976 and Nov. 1986. Moreover, histological examinations were performed in 39 cases concentrating on the existence of fetal components and trophoblastic hyperplasia, etc. The results were as follows. 1. Karyotype analysis showed triploidy (24 cases), normal diploidy (10 cases), trisomy (9 cases) and other anomalies (mosaic, translocation etc.) (6 cases). These results are quite different from those of many western authors, who reported that most cases of PM are triploidy. 2. The criteria of PM in Japan differ from those of WHO Scientific Group in regard to trophoblastic hyperplasia. 3. Our cases were reclassified on the basis of the definition drawn up by the WHO Scientific Group. Nevertheless, the rate of triploidy was only 54.5%, which is lower than that reported by many western authors. These results show that the development of PM cannot be explained cytogenetically at present, in contrast with complete mole.

Diploidy↗
PubMed1990

Multiple chromosomes carrying tumor suppressor activity for a uterine endometrial carcinoma cell line identified by microcell-mediated chromosome transfer.

Putative tumor suppressor genes can be mapped to specific chromosomes by the introduction of individual chromosomes derived from normal cells via microcell fusion. We have examined whether a highly malignant human uterine endometrial carcinoma cell line, HHUA, can be suppressed by only one normal chromosome or by multiple chromosomes. A library of mouse A9 clones containing different human chromosomes tagged with the pSV2-neo plasmid DNA were constructed. Transfer by microcell fusion of either chromosome 1, 6, 9, 11, or 19 into the HHUA tumor cell line was performed, and the abilities of the microcell hybrids to form tumors in nude mice were examined. The introduction of a chromosome 19 had no effect on the tumorigenicity of the cells, whereas microcell-hybrid clones with an introduced chromosome 1, 6 or 9 were completely suppressed for tumorigenicity. A decrease in tumor-take incidence in some but not all clones was observed following the introduction of a chromosome 11. The nontumorigenic microcell hybrids with an introduced chromosome 1 differed from the nontumorigenic microcell hybrids with an introduced chromosome 6, 9, or 11. A large percentage of hybrids with chromosome 1 senesced and/or showed alterations in cellular morphology and transformed growth properties in vitro. No growth or morphology alterations were observed following transfer of the other chromosomes. These results may indicate that more than one chromosome carries a tumor suppressor gene(s) for this human uterine endometrial carcinoma cell line and support the hypothesis that multiple tumor suppressor genes control the tumorigenic phenotype in the multistep process of neoplastic development.

Cell Fusion↗
PubMed1989

Methotrexate-resistant mechanisms in human choriocarcinoma cells.

Choriocarcinoma cells grown in the presence of methotrexate (MTX) developed resistance in two ways. HCCM-derived sublines (relatively high MTX resistance) produced enhanced levels of dihydrofolate reductase (DHFR) and had impaired transport of MTX. Altered transport was the primary determinant of response in CC1-derived sublines (low MTX resistance). Since the selection procedures used were identical, it was assumed that altered MTX transport was insufficient to account entirely for the various degrees of resistance. An increased level of DHFR activity was necessary for the development of high MTX resistance. The overproduction of DHFR was the consequence of amplification of the DHFR gene sequence. The incidence of double minutes (DMs) in metaphase paralleled the degree of resistance. However, DMs were also present in cells not showing DHFR gene amplification. Mechanisms other than DHFR gene multiplication were responsible for the de novo synthesis of DMs.

Blotting, Southern↗
PubMed1989

[Omentum in the management of thoracic surgery: especially its application to tracheobronchial surgery].

Omentum is now not only policeman of the abdomen but also of the thorax. We applied omental pedicle flap in the management of 14 patients with thoracic surgery including chest wall reconstruction, empyema, thoracic skeletal infection and tracheobronchial problems. Especially, tracheobronchial reconstruction using omental pedicle flap for the patient combined with lung cancer (T4N2M0 STAGE IIIB) and asthma under steroid therapy was reported. The case was 71-year-old man with complaint of hemosputum. He had 5-6 year history of bronchial asthma with disturbed pulmonary function of % VC 44%, FVC1.0% 37%. Bronchoscopic study revealed the tumor invading the right side of trachea originating from right upper bronchus with histological diagnosis of moderately differentiated squamous cell carcinoma. Preoperatively, he experienced a heavy asthma attack which was controlled by steroid administration. Following extended right sleeve upper lobectomy, we applied omental pedicle flap around the reconstructed portion for the protection of infection, impaired wound healing due to postoperative steroid therapy and strong tension at anastomoses. Postoperative course was satisfactory. We suggest omental pedicle flap is an effective surgical armamentarium in the management of tracheobronchial surgery for the patient with strong anastomotic tension, immunocompromised condition, preoperative irradiation at bronchial stump and use of drug causing delayed wound healing (steroid, anticancerous drug etc).

Aged↗
PubMed1989

[Somatic cell hybrids used in cytogenetic analysis of transformation mechanism of uterine endometrial cell].

6-Thioguanine and Neomycin resistant human endometrial carcinoma cells were established from parental HHUA 95 cells in the present study. The karyotype was 46,XX although chromosome abnormalities had been observed occasionally. Cell hybrids between 6-TGr neor 95 and rat immortalized, non-tumorigenic 3Y1 cells were formed to analyze for cosegregation of chromosomes and tumorigenicity. However, the morphology of 3 hybrid clones was a spindle form, similar to the 3Y1 cells. In spite of the consistent presence of human chromosomes, negative anchorage independent growth in these clones suggested that none of the chromosomes involved in fused cells was associated with tumorigenicity of endometrial carcinoma. Loci on a few human chromosomes of a normal cell cause suppression in several hybrid systems. Cell fusion between 6-TGr 95 and normal human fibroblasts (HF) was performed to confirm whether this is also true in endometrial carcinoma. Hybrid cells had four copies of homologous chromosomes (two from each of the parent cells). These had a polygonal appearance, being similar to the HHUA 95 cells. Both anchorage independence and tumorigenesis were negative. Those results suggested that malignant transformation of endometrial cells was the result of multiple genetic changes. In this respect, the loss of genes implicated in the suppression plays an important role in endometrial carcinogenesis.

Adenocarcinoma↗
PubMed1987

Nonsurgical therapy to preserve oviduct function in patients with tubal pregnancies.

Surgical treatment for tubal pregnancies greatly impairs the subsequent fertility of patients because of salpingectomy and its complicated adhesions. Nonsurgical methotrexate therapy was developed to avoid such complications. Although early detection was of prime importance, resolution of ectopic pregnancy was obtained in 22 patients (95.7%) with methotrexate administration alone. Patency of the oviducts was evaluated with hysterosalpingography and/or laparoscopy in 19 patients after termination of methotrexate treatment. In 10 of 19 patients (52.6%), complete patency of the involved oviduct confirmed the validity of this regimen. Severe side effects were not observed in any of the 23 patients.

Adult↗
PubMed1987

Hydatidiform mole: parental chromosome aberrations in partial and complete moles.

The relationship between parental constitutional chromosome abnormalities and the development of hydatidiform mole was evaluated in series from four institutions. Karyotype analysis was performed on blood samples from 237 patients with a pathological diagnosis of complete mole and 217 of their spouses. One patient was found to have a constitutional balanced translocation, t(11;18), while one spouse was found to have a balanced translocation, t(4;20). Among 125 patients with partial mole and 106 of their spouses, one male was found to be a translocation carrier, t(13;14). No significant increase in the frequency of translocations in the parents of complete moles was found in any of the series considered separately or together. Data from the combined series show no evidence of constitutional parental chromosome aberrations as an aetiological factor in the development of molar pregnancies.

Chromosome Aberrations↗
PubMed1987

[MTX resistant mechanisms in human choriocarcinoma cells].

Choriocarcinoma cells grown in the presence of MTX have developed resistance in two ways. The HCCM derived sublines (relatively high MTX resistant) produced enhanced levels of DHFR and had relatively unimpaired transport of MTX, though altered transport was the primary determinant of response in the CC1 derived sublines (low MTX resistant). Since the selection procedure used was identical, it was assumed that altered MTX transport was insufficient to account entirely for various degrees of resistance. Increased DHFR activity was necessary for the development of high MTX resistance. The overproduction of DHFR was the consequence of amplification of the DHFR gene sequence. The incidence of DMs in metaphases paralleled the degree of resistance. Since DMs were also present in the cells not showing DHFR gene amplification, mechanisms other than DHFR gene multiplication were responsible for the de novo synthesis of DMs.

Cells, Cultured↗
PubMed1986

Primary liposarcoma of the mediastinum--a case report and review of the literature.

Liposarcoma of the mediastinum is a rare disease. A 59 year old woman was seen with the complaint of dizziness. A chest radiogram taken during the course of investigation for hypertension revealed a large mass shadow 24 X 18.5 X 12 cm located in the anterior mediastinum. The tumor of the mediastinum was diagnosed as a benign lipoma when it was first resected, but subsequently proved to be a liposarcoma when it re-appeared 2 years and 10 month later. Based on the WHO classification, the mixed type of liposarcoma was diagnosed. The salient and pathological features of mediastinal liposarcoma are reviewed and compared with those nine cases reported in Japan and fifty in North America and European countries. Treatment by simple enucleation or shelling out of the tumor should be discouraged, since this seems to be the main cause of local recurrence. Surgical wide en bloc excision is the treatment of choice.

Female↗
PubMed1986

[Abnormalities of chromosome involving 1q in uterine endometrial carcinomas].

Cytogenetic studies were performed on endometrial specimens from four patients with hyperplasia, six with adenocarcinoma and one with mixed mesodermal tumor. Except for one cell, all 65 cells from the hyperplastic specimens had a normal female karyotype. However, a total of 92 cells from the 5 adenocarcinoma specimens had chromosomal abnormalities, though all 20 cells from a specimen of a well differentiated adenocarcinoma showed a normal karyotype. The chromosome number and morphology of the aneuploid cells had minimal changes. The modal number of chromosomes was pseudodiploid in one case and hyperdiploid in four. Three kinds of structural abnormalities involving chromosomes 1q were identified as of clonal origin: del. 1 (p21) in 2 cases, t. dic (1;16) (p21;q24) in one case and i (1q) markers in 2 cases. Since the carcinoma cells had two chromosomes 1 of normal morphology, the presence of the marker chromosome led to a partial trisomy or tetrasomy of the long arm of a chromosome 1. This involvement of the long arm of chromosome 1, therefore, may be assumed to represent a karyotypic change in the characteristics of adenocarcinoma of the endometrium. Complex karyotypes with many rearranged chromosomes were observed in cells from the mixed mesodermal tumor. The karyotypic differences between endometrial carcinoma and the mixed mesodermal tumor suggest that the genesis (and its mechanism) of the former may differ from that of the latter.

Adenocarcinoma↗
PubMed1986

[Establishment and characterization of the cell line derived from low differentiated adenocarcinoma of the endometrium].

A new human carcinoma cell line (HEC-1), which was derived from low differentiated adenocarcinoma of the endometrium, has been established. Cells from tumor tissues grown in athymic mice were cultured in minimal essential medium supplemented with 20% fetal calf serum. Contaminated mouse fibroblasts were removed from the culture by the absorption of anti-mouse serum. Continuous cell growth (doubling time: 51.6 hrs) could be observed during 64 passages. The cultured cells appeared monolayer and the cellular arrangement was a pavement-like pattern. The morphology of cells was analogous to the one of adenocarcinoma cells. The modal number of chromosomes of the original tumor cells were 46. The t. dic (1; 16)(p21; q24) marker which had been identified as the clonal abnormality in the original tumor cells, was also observed consistently in cultured cells, though the loss of chromosome 19 was disappeared during the passage. This suggested that the rearrangements of the long arm of chromosome 1 played an important role for the endometrial carcinogenesis.

Adenocarcinoma↗
PubMed1986

[Experimental induction and cytogenetic study of yolk sac tumors in Chinese hamsters].

The development of teratomas and yolk sac tumors from displaced yolk sac is well documented in rats and mice. However, the precise mechanisms of induction and pathogeneses of these tumors still remain unknown. The present study was undertaken in order 1) to elucidate whether this phenomenon is common to all rodents, 2) to identify the origin of these tumors and 3) to explore specific chromosomal changes in yolk sac tumors. Ten benign teratomas and two malignant tumors with teratomatous elements were obtained from 33 Chinese hamsters after fetectomy, followed by displacement of yolk sac. The histological characteristics and the presence of laminin in the stroma suggested that the malignant tumors belonged to the category of yolk sac tumors. Similarities in electromicroscopic features observed in the tumor cells and the yolk sac of normal 12-day conceptuses suggested that the tumor originated from yolk sac cells. Chromosomal analyses of in vitro cell lines established from one of the yolk sac tumors disclosed that the tumors was composed of clones with an XX and XY sex chromosome constitution. The 1p + marker was identified as a consistent abnormality, which seemed to play an important role in the development of yolk sac tumors in Chinese hamsters.

Animals↗
PubMed1985

Marker chromosomes of the long arm of chromosome 1 in endometrial carcinoma.

Cytogenetic studies were performed on endometrial specimens of four patients with hyperplasia, six with adenocarcinoma, and one with a mixed mesodermal tumor. Except for one cell, all 65 cells from the hyperplastic specimens had a normal female karyotype. However, a total of 92 cells from the five adenocarcinoma specimens had chromosome abnormalities, though all 20 cells from a specimen of a well differentiated adenocarcinoma showed a normal karyotype. The chromosome number and morphology of the aneuploid cells had minimal changes. The modal number of chromosomes was pseudodiploid in one case and hyperdiploid in four cases. Three kinds of structural abnormalities involving chromosomes #1 were identified to be of clonal origin: del(1p21) in two cases, tdic(1;16)(p21;q24) in one case, and i(1q) markers in two cases. Because the carcinoma cells had two chromosomes #1 of normal morphology, the presence of the marker chromosome led to partial trisomy or tetrasomy of the long arm of chromosome #1. This involvement may be assumed to represent a karyotypic change characteristic of some adenocarcinomas of the endometrium. Complex karyotypes with many rearranged chromosomes were observed in cells from the mixed mesodermal tumor. The karyotypic differences between endometrial carcinoma and the mixed medodermal tumor suggest that the genesis (and its mechanism) of the former may differ from that of the latter.

Adenocarcinoma↗