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O Tanizawa

Publications and source records attributed to O Tanizawa.

At least 37 records · Page 2Linked to original sources
PubMed1994

Detection of high-risk human papillomavirus in the cervix and semen of sex partners.

To investigate the possibility of sexual transmission of human papillomavirus (HPV), 53 married couples were examined for the presence of HPV-16 and -18 DNAs in the uterine cervix and semen using the polymerase chain reaction method. Twenty-three of the 53 women and 12 of the 53 male partners were positive for HPV-16 DNA. No HPV-18 DNA was detected in samples from any of the partners. In 27 pairs, both partners were negative for HPV DNA in cervix or semen; in the remaining 26 pairs, at least 1 of the partners was HPV-16-positive. In 9 (35%) of these 26 pairs, both partners were infected. Furthermore, 9 (75%) of the 12 women with HPV-positive partners were HPV-positive, while 9 (39%) of the 23 men with HPV-positive female partners were HPV-positive. These findings suggest an increased risk of HPV transmission via sexual intercourse, thereby underscoring the importance of preventive care against HPV infection during intercourse.

Adult↗
PubMed1994

Analysis of clonality by amplification of short tandem repeats. Carcinomas of the female reproductive tract.

The clonal composition of cancers of the female reproductive tract was evaluated by analysis of patterns of X-chromosome inactivation. Using DNA extracted from frozen tissues or paraffin-embedded archival specimens as template, polymerase chain reaction (PCR) was performed to generate amplified DNA fragments of exon 1 of the X-linked androgen receptor gene, which contains a highly polymorphic trinucleotide repeat. Predigestion of tumor DNA with methylation-sensitive restriction endonuclease Hha I or Hpa II permitted selective PCR amplification from the methylated (uncleaved) allele. Of a total of 54 tumors analyzed, 50 cases showed heterozygosity (93%) and were therefore informative for clonal analysis. Monoclonal composition of the tumors was suggested in a total of 49 of 50 cases, including 12 adenocarcinomas of the uterine endometrium, 13 squamous cell carcinomas of the uterine cervix, 6 adenocarcinomas of the uterine endocervix, and 18 epithelial tumors of the ovary. However, polyclonal composition was observed in one mucinous carcinoma of the ovary, in which we previously showed that both GGT-->GAT and GGT-->GTT mutations are present in > 20% of total K-ras copies in the tissue. Our studies demonstrate the utility of PCR amplification of highly polymorphic repetitive sequences for analysis of patterns of X-chromosome inactivation. This approach is practical for the analysis of clonal cell composition in a high proportion of both formalin-fixed and frozen archival tissues.

Carcinoma↗
PubMed1994

A case-control study on risk factors for uterine endometrial cancer in Japan.

A case-control study of 143 Japanese women with uterine endometrial cancer and 143 individually age-matched controls was conducted to assess the risk factors for endometrial cancers in Japan. Among the characteristics studied, the following factors were significantly greater in the cases than in the controls: nulliparity (odds ratio for parity 1-3 and > or = 4 versus nullipara are 0.40 and 0.02, respectively), obesity (odds ratio: 2.73), hypertension (odds ratio: 2.4), diabetes mellitus (odds ratio: 6.30), and a personal medical history of cancer (odds ratio: 3.06). The present study showed that Japanese women have the same risk factors for endometrial cancer as those reported in Western countries. The recent increase in the incidence of endometrial cancer in Japan may be largely attributed to the decrease in parity.

Adenocarcinoma↗
PubMed1994

Alteration of the p53 tumor suppressor gene occurs independently of K-ras activation and more frequently in serous adenocarcinomas than in other common epithelial tumors of the human ovary.

To clarify the role of the p53 tumor suppressor gene in the development of human ovarian epithelial tumors and to study the association of p53 alterations with K-ras activation, a series of 70 common epithelial ovarian tumors from Japanese patients was studied. These included 31 serous adenocarcinomas, 12 mucinous adenocarcinomas, 5 mucinous tumors of borderline malignancy, 13 endometrioid adenocarcinomas, and 9 clear cell carcinomas. Allelic loss, recognized at the polymorphic site in codon 72 of the p53 gene, was detected in 14 of 36 (39%) informative cases by restriction fragment length polymorphism analysis and by single-strand conformation polymorphism (SSCP) analysis of polymerase chain reaction (PCR)-amplified DNA fragments. Mutations in the highly conserved regions of the p53 gene were detected by SSCP analysis of PCR-amplified fragments. Mutations were found in 22 of 70 (31%) ovarian tumors, including 1 of 5 mucinous tumors of borderline malignancy. Mutations were subsequently characterized by direct sequencing. Single missense base substitutions were detected in 13 ovarian carcinomas and in one case of mucinous tumor of borderline malignancy. Short (1-8 bp) deletions and insertions were found in 8 cases. Mutations in the p53 gene occurred more frequently in serous adenocarcinomas (14/31, 45%) than in all nonserous types of malignant epithelial tumors combined (7/34, 21%; P = 0.032). Point mutations in K-ras were identified by dot blot hybridization analysis of PCR-amplified fragments with mutation-specific oligonucleotides and by direct sequencing. The overall frequency of K-ras mutations was 19/70 (27%). K-ras mutations were found in 12 of 17 (71%) mucinous tumors (8/12 mucinous carcinomas [67%] and 4/5 mucinous tumors of borderline malignancy [80%]), and occurred more frequently than in serous carcinomas (4/31, 13%; P = 0.00009) or in all nonmucinous types of ovarian epithelial tumors combined (7/53, 13%; P = 0.00002). These data suggest that different combinations of oncogenes and/or tumor suppressor genes may be involved in the genesis and development of histologically distinct categories of common epithelial tumors of the human ovary.

Adenocarcinoma, Clear Cell↗
PubMed1994

An experimental model for ovarian tumor invasion of cultured mesothelial cell monolayer.

BACKGROUND: Peritoneal spread of tumor cells is one of the characteristic features of biologic behavior of ovarian cancers. To understand the mechanism by which human tumor cell invasion takes place, we have tried to establish an in vitro experimental model for ovarian tumor cell invasion of the mesothelial cell monolayer. EXPERIMENTAL DESIGN: Mesothelial cells were isolated from normal rat mesentery by trypsin digestion and the cells (1 x 10(5)/dish) were cultured in Eagle's minimum essential medium supplemented with 10% fetal calf serum. Cultured mesothelial cells (M cells) grew forming a pavement-like monolayer. When M cells grew to a confluent state, tumor cells (1 x 10(5)/dish) were seeded on M cell monolayers and cultured. Four tumor cell lines derived from human ovarian cancers were tested for their invasive behaviors. The penetration of M cell monolayers by the tumor cells was confirmed by a perpendicular section of the cell layers. The number of penetrated single tumor cells and colonies/cm2 was counted under a phase contrast microscope after the tumor cell seeding. RESULTS: Several hours after the tumor cell seeding, the cells adhered to M cell monolayers and started to penetrate by extending pseudopodia-like cytoplasmic processes through junctional margins of neighboring M cells, resulting in the formation of penetrated single tumor cells that then proliferated to form colonies under the monolayer. The number of penetrated single tumor cells and colonies/cm2 increased up to 24 hours after the tumor cell seeding, and thereafter stayed almost constant. The number increased with the number of tumor cells seeded, when counted at 48 hours, and therefore was taken to be the number of tumor cells invaded. The in vitro invasiveness of tumor cells varied with the tumor cell lines examined. CONCLUSIONS: Application of this system appears to provide rapid determinations of the invasive potential of ovarian tumor cells and to make it easy to screen substances that modify the invasion of mesothelial cells.

Adenocarcinoma↗
PubMed1993

High magnesium concentration inhibits ligand-stimulated calcium influx and hormone secretion in rat pituitary lactotropes with involvement of intracellular free magnesium.

The effects of extracellular magnesium concentration ([Mg2+]ex) on thyrotropin-releasing hormone (TRH)-stimulated intracellular free calcium mobilization and prolactin secretion were investigated concomitantly with measurement of the intracellular free magnesium concentration ([Mg2+]i). TRH-stimulated intracellular free calcium mobilization was significantly inhibited when the medium was replaced by high Mg2+ medium ([Mg2+]ex = 10 mM) in normal Ca2+ medium. The inhibitory effects of high Mg2+ became apparent concomitantly with an increase in [Mg2+]i from 0.7 to 1.3 mM. High Mg2+ significantly inhibited TRH-induced PRL secretion in a dose-dependent manner in normal Ca2+ medium. TRH-stimulated inositol triphosphate (IP3) production was rather augmented by the replacement with high Mg2+ medium. In summary, high Mg2+ inhibits Ca2+ influx stimulated by TRH in the rat pituitary lactotropes, possibly with the involvement of [Mg2+]i increase. These results have general importance in relation to high Mg(2+)-induced suppression of the biological functions of cells.

Animals↗
PubMed1993

Dynamics of exocytosis, endocytosis and recycling in single pituitary gonadotropes.

The dynamic changes in exocytosis, endocytosis and recycling in single gonadotropes induced by gonadotropin-releasing hormone (GnRH) were visualized and estimated with an impermeable fluorescent membrane probe, 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatrien (TMA-DPH), using a digital imaging and confocal laser scanning microscope. 10(-7) M GnRH induced exocytosis and endocytosis within 10 sec and 60 sec, respectively. Recycling of the plasma membrane started at 180-300 sec. Exocytosis and endocytosis in purified gonadotropes changed dose-dependently with 10(-10)-10(-7) M GnRH. These results show that GnRH-induced exocytosis, endocytosis and recycling in gonadotropes maintain dynamic equivalence. The procedure we established will be very useful in studies of the function of secretory cells.

Animals↗
PubMed1993

Autocrine growth mechanism by transforming growth factor (TGF)-beta 1 and TGF-beta 1-receptor regulation by epidermal growth factor in a human endometrial cancer cell line IK-90.

Transforming growth factor-beta 1 (TGF-beta 1) enhanced cell proliferation in a concentration-dependent manner in a human endometrial cancer cell line, IK-90. Scatchard analysis of TGF-beta 1 receptor in IK-90 cells, using 125I-TGF-beta 1 as a ligand, revealed the presence of a class of high-affinity TGF-beta 1 receptors (2,000 sites per cell, KD = 74pM). Moreover, IK-90 cells produced and secreted TGF-beta 1: TGF-beta 1 messenger RNA was detected at 2.5 and 4.0 kb by Northern-blot analysis using 32P-labeled TGF-beta 1 cDNA as a probe, and TGF-beta 1 activity in conditioned medium by the inhibition of 3H-thymidine uptake into CCl 64 mink lung epithelial cells. We investigated the regulation of TGF-beta 1 receptor by 4 kinds of growth factor: epidermal growth factor (EGF) but not TGF-beta 1, insulin or insulin-like growth factor-1 increased the level of TGF-beta 1 binding sites in a concentration- and time-dependent manner. These findings suggest that TGF-beta 1 may be a potential autocrine growth factor in a human endometrial cancer cell line IK-90 and that this autocrine mechanism may be affected by EGF.

Adult↗
PubMed1993

Alterations of the p53 tumor suppressor gene and its association with activation of the c-K-ras-2 protooncogene in premalignant and malignant lesions of the human uterine endometrium.

We previously reported (T. Enomoto et al., Cancer Res., 50: 6139-6145, 1990; T. Enomoto et al., Cancer Res., 51: 5308-5314, 1991) a significant frequency of activating point mutations in codon 12 of the c-K-ras-2 protooncogene in endometrial adenocarcinoma and its premalignant precursor lesions (series 1 and 2). To reveal the role of the p53 tumor suppressor gene in the development of endometrial adenocarcinoma and to study the association of p53 alterations with K-ras activation, an additional 28 endometrial adenocarcinomas and an additional 11 premalignant atypical uterine hyperplasias (series 3), as well as 12 cases of endometrial adenocarcinoma (10 having K- or N-ras activation) and 2 cases of atypical hyperplasia from series 1 and 2, were screened for the presence of p53 alterations. Allelic loss, recognized at the polymorphic site in codon 72 of the p53 gene, was detected in 6 of 19 (32%) informative cases of endometrial adenocarcinoma and 1 of 4 (25%) informative cases of endometrial atypical hyperplasia by restriction fragment length polymorphism analysis and by single-strand conformation polymorphism analysis of polymerase chain reaction (PCR)-amplified DNA fragments. Mutations in the highly conserved regions of the p53 gene were detected by single-strand conformation polymorphism analysis of PCR-amplified DNA fragments. Mutations were found in 9 of 40 (23%) endometrial adenocarcinomas and 1 of 13 (8%) atypical hyperplasias that were studied. Mutations in p53 were significantly more frequently found in clinical grade 3 (G3) cancers (6 of 14, 43%) than in G1-G2 cancers (3 of 26, 12%) (P = 0.033). Mutations were subsequently confirmed by direct sequencing. Single missense base substitutions were detected in 6 cases of endometrial carcinoma and in one case of atypical hyperplasia. Deletions of a single base and of 2 bases were each detected in single cases of endometrial carcinoma, and a single base insertion was found in a third case. Point mutations in K-ras were also identified in tumors of series 3 by direct sequencing of PCR-amplified DNA fragments of exons 1 and 2. Point mutations in codons 12 and 13 in K-ras were detected by direct sequencing of PCR-amplified DNA in 7 of 28 adenocarcinomas in series 3, but none were found in exon 2 (codons 59.63. The spectrum of point mutations in p53 in endometrial adenocarcinomas was almost identical to what we found in K-ras in series 1 and 2 and in series 3, suggesting the possible role of a mutagen that might be responsible for mutations in both K-ras and p53.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenocarcinoma↗
PubMed1993

Alterations of the Rb gene and its association with Ki-ras activation and p53 inactivation in endometrial adenocarcinoma.

Alterations of the retinoblastoma (Rb) gene were evaluated in nine primary endometrial adenocarcinomas that we had previously analyzed for the presence of Ki-ras activations and p53 alterations and in three endometrial carcinoma cell lines. Loss of mRNA expression in the Rb gene was detected in two of the 12 tumors. Internal deletions of Rb cDNA were observed in two tumors; one was a deletion of exon 21 in a primary carcinoma, and the other was a deletion of exon 8 in one allele in one cell line. Loss of heterozygosity of the Rb gene, which was detectable by polymorphisms in introns 1 and 17, was analyzed using polymerase chain reaction-restriction fragment length polymorphism analysis in 29 endometrial carcinomas. Of 13 heterozygous cases, two cases (15%) showed loss of heterozygosity. We therefore suggest that alteration of the Rb gene, as well as activation of the Ki-ras gene and alterations of the p53 gene, plays a significant role in the etiology of endometrial adenocarcinoma.

Adenocarcinoma↗
PubMed1993

Adenocarcinoma in a benign cystic teratoma of the ovary: report of a case with a long survival period.

We report a case of adenocarcinoma associated with benign cystic teratoma (dermoid cyst) of the ovary in which the patient has survived for a long time. A 62-year-old woman underwent abdominal total hysterectomy with bilateral salpingo-oophorectomy on March 16, 1976 because of a large left ovarian tumor. There were no pathologic findings in other intra-abdominal organs. The tumor was cystic, contained dark and mucinous sebaceous material with hair, and weighed 15 kg. Papillary growths protruded into the cavity in some areas of the wall. Microscopically and immunohistochemically, the tumor was characterized as a mucinous adenocarcinoma associated with dermoid cyst, suggesting a possible gastrointestinal origin. After the surgery, she was treated with chemotherapy and is alive and well more than 15 years later. Our review of the literature indicates that, while it is widely held that patients with adenocarcinoma associated with dermoid cyst do not survive, many in fact do survive for a long period after surgery.

Adenocarcinoma, Mucinous↗
PubMed1993

Immunohistochemical study of proliferating cell nuclear antigen (PCNA) in endometrial carcinoma with argyrophil cells.

We performed an immunohistochemical study of argyrophil cells in 10 endometrial carcinomas using the monoclonal antibody PC 10 to detect proliferating cell nuclear antigen (PCNA). Formalin-fixed, paraffin-embedded sections of 10 endometrial carcinomas containing argyrophil cells which are chromogranin positive (four containing type I cells, two type II, and four mixed-type I and type II) were stained with monoclonal antibody PC 10. In addition, one of the tumors with mixed-type cells was transplanted into nude mice, and the tumors which developed in subpassages were also analyzed for PCNA. Argyrophil cells in 10 endometrial carcinomas were found to be negative immunohistochemically for PCNA, regardless of their type, suggesting that they are not proliferating. Surprisingly, however, all subpassaged tumors contained argyrophil cells which were also negative for PCNA. From these results, it may be postulated that argyrophil cells were induced through differentiation to neuroendocrine direction of neoplastic cells.

Adenocarcinoma↗
PubMed1993

Immunohistochemical study of cytokeratin 7 for the differential diagnosis of adenocarcinomas in the ovary.

Mucinous adenocarcinomas of the ovary were studied immunohistochemically for cytokeratins 7 and 18, either to determine whether the ovarian tumor was primary or a metastasis or to establish the histogenetic origin of the tumor. Primary ovarian tumors were strongly positive for both cytokeratins, while ovarian metastases from colonic cancers were negative for cytokeratin 7, as were the colonic cancers. Three of four ovarian tumors complicated by pseudomyxoma peritonei were negative for cytokeratin 7, indicating appendiceal origin. Two of seven mucinous tumors associated with dermoid cysts were negative for cytokeratin 7, suggesting gastrointestinal origin.

Adenocarcinoma, Mucinous↗
PubMed1993

Ovariectomy increases the level of estrogen receptor mRNA and estrogen receptor binding sites in female rat adipose tissue.

The roles of estrogen in the changes in estrogen receptor (ER) mRNA and ER binding sites in rat adipose tissue were studied in female rats. To elucidate the mechanism(s) behind ovariectomy (OVX)-induced obesity, the levels of ER mRNA and ER binding sites in adipose tissue were analyzed three weeks after OVX using Northern blot analysis of ER mRNA and the [3H]E2 binding assay, respectively. OVX induced an increase in body weight, and replacement of estradiol (E2) prevented that increase. Significant increases in the amounts of ER mRNA and in [3H]E2-specific binding were observed after OVX, and E2 replacement reduced both of those increases. These results suggest that E2 may regulate rat obesity directly through ER in adipose tissues.

Adipose Tissue↗
PubMed1993

Magnesium sulfate inhibits oxytocin-induced calcium mobilization in human puerperal myometrial cells: possible involvement of intracellular free magnesium concentration.

OBJECTIVE: Our purpose was to elucidate the mechanisms of the tocolytic action of Mg2+ on the human myometrium. STUDY DESIGN: The effects of extracellular Mg2+ on oxytocin-induced increases in the intracellular free Ca2+ concentration in human puerperal myometrial cells were examined by means of indo-1-AM. The changes in the intracellular free Mg2+ concentration under various conditions were also measured with Mg(2+)-fura-2-AM. RESULTS: The increase in intracellular free Ca2+ concentration induced by oxytocin was reduced to 26% of that in the normal solution 20 minutes after replacement of the normal solution with an extracellular Mg2+ solution, 10 mmol/L. When extracellular Ca2+ was removed, the increase in intracellular free Ca2+ concentration was not suppressed even 20 minutes after the replacement. A solution of extracellular Mg2+ concentration, 10 mmol/L, raised the intracellular free Mg2+ concentration gradually, by approximately 150% in 20 minutes, concomitant with the suppression of the response to oxytocin in the intracellular free Ca2+ concentration. CONCLUSION: High intracellular free Mg2+ concentration, caused by high extracellular Mg2+, is essential for suppression of oxytocin-induced Ca2+ influx across the cell membrane; this presumably results in inhibition of uterine contractions.

Calcium↗
PubMed1993

Fetal mononuclear cells show a comparable capacity with maternal mononuclear cells to produce IL-8 in response to lipopolysaccharide in chorioamnionitis.

IL-8 is a chemotactic and activating cytokine for neutrophils which eliminate invading bacteria by releasing bactericidal metabolites. Cord blood mononuclear cells (CBMCs) obtained from neonates born to mothers with chorioamnionitis actively produced a significantly higher amount of IL-8 than those of neonates without chorioamnionitis, suggesting that the mononuclear cells of fetuses with chorioamnionitis had been activated in utero. As lipopolysaccharide (LPS) can often be detected in the uteroplacental space in chorioamnionitis, the LPS-mediated activation mechanism of neonatal mononuclear cells was analyzed in vitro to produce IL-8. Neonatal mononuclear cells stimulated with LPS increased IL-8 production in a time- and dose-dependent manner. The ability of term or preterm neonatal mononuclear cells to produce IL-8 was comparable with that of adult (maternal) mononuclear cells, suggesting functional maturity of the neonatal or fetal mononuclear cells to produce IL-8. However, IL-8 production by neonatal CBMCs was down-regulated by dexamethasone, a glucocorticoid which is clinically administered to mothers to promote fetal lung maturity in preterm delivery. Our present study revealed a regulatory mechanism of fetal IL-8 production, suggesting that functionally mature fetal mononuclear cells produce IL-8 in response to LPS in chorioamnionitis and activate the fetal defense mechanism against infection.

Cells, Cultured↗