研究者詳細 - 大内田　守

論文 - 大内田　守

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Significant correlation of the SCN1A mutations and severe myoclonic epilepsy in infancy.

Iori Ohmori, Mamoru Ouchida, Yoko Ohtsuka, Eiji Oka, Kenji Shimizu

Review Series Neurology, 2, 14-17 2003年

難治性リンパ腫発症関連遺伝子SHP1に関する最新知見

岡剛史, 大内田守

日本臨床 61(11): 2025-2032 2003年

Gene silencing of the tyrosine phosphatase SHP1 gene by aberrant methylation in leukemias/lymphomas. 国際誌

Takashi Oka, Mamoru Ouchida, Maho Koyama, Yoichiro Ogama, Shinichi Takada, Yoko Nakatani, Takehiro Tanaka, Tadashi Yoshino, Kazuhiko Hayashi, Nobuya Ohara, Eisaku Kondo, Kiyoshi Takahashi, Junjiro Tsuchiyama, Mitsune Tanimoto, Kenji Shimizu, Tadaatsu Akagi

Cancer research 62 ( 22 ) 6390 - 4 2002年11月

記述言語：英語掲載種別：研究論文（学術雑誌）

High-frequent silencing of hematopoietic cell-specific protein-tyrosine phosphatase SHP1 gene by promoter methylation was detected in various kinds of leukemias and lymphomas, as well as in many hematopoietic cell lines, which is supported by our previous observation of strong decrease of SHP1 mRNA and protein. The promoter methylation of the SHP1 gene was clearly correlated with the clinical stage. Loss of heterozygosity with microsatellite markers near the SHP1 gene was shown in 79% of informative acute lymphoblastic leukemia cases. These results suggest that functional loss of SHP1 is associated with the pathogenesis of leukemias/lymphomas.

Prognostic value of loss of heterozygosity around three candidate tumor suppressor genes on chromosome 10q in astrocytomas 国際誌

K Terada, T Tamiya, S Daido, H Kambara, H Tanaka, Y Ono, K Matsumoto, S Ito, M Ouchida, T Ohmoto, K Shimizu

JOURNAL OF NEURO-ONCOLOGY 58 ( 2 ) 107 - 114 2002年6月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：KLUWER ACADEMIC PUBL

We thoroughly examined loss of heterozygosity (LOH) around three candidate tumor suppressor genes on chromosome 10q to determine whether LOH of each tumor suppressor gene is associated with the previously defined clinical prognostic indices. We also examined whether LOH can help predict prognostic variables in astrocytomas.
We selected samples from 40 astrocytomas (grades 2-4), performed Ki-67 immunostaining, and counted positive cells. Using DNA from aliquots of tumor blocks and leukocytes, we investigated LOH around the PTEN, NEURL, and DMBT1 genes (10q23.3-26.1) with the silver staining procedure. We then statistically evaluated the relationship among histological features, regional LOH on chromosome 10q, and survival. The mean survival period for patients with LOH around PTEN was 7.2 months after surgery, while that for patients without LOH around PTEN was 21.4 months. Thus, LOH around PTEN was closely associated with a reduced overall survival (p = 0.0020) but LOH at NEURL or DMBT1 was not (p > 0.05).
The combined features of an increase in histological grading and Ki-67-positive cells and the presence of LOH around PTEN significantly correlated with poor prognosis. These factors may be useful predictors of survival, and LOH analysis of tumor suppressor genes on chromosome 10q can contribute greatly to the treatment of patients with astrocytoma.

DOI： 10.1023/A:1016017711033

Allelic loss and reduced expression of the ING3, a candidate tumor suppressor gene at 7q31, in human head and neck cancers 国際誌

M Gunduz, M Ouchida, K Fukushima, S Ito, Y Jitsumori, T Nakashima, N Nagai, K Nishizaki, K Shimizu

ONCOGENE 21 ( 28 ) 4462 - 4470 2002年6月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：NATURE PUBLISHING GROUP

Loss of heterozygosity (LOH) has been frequently detected at chromosome 7q31 region in human head and neck squamous cell carcinomas (HNSCC) and many other cancers, suggesting the existence of tumor suppressor genes (TSG). We analysed LOH at 7q3I region in 49 HNSCC by using six polymorphic microsatellite markers and found allelic deletion in 48% (22/46) of the informative cases. We detected two preferentially deleted regions, one is around D7S643 and the other around D7S486. When we redefined the map of 7q31 region according to the contiguous sequences, a recently identified gene, ING3, was found in the proximity of D7S643. ING3 protein harbors the PHD domain highly homologous among ING family proteins, in which we previously found mutations in a related gene, ING1. As only one missense mutation of the ING3 gene was found in HNSCC, we examined the expression level. Reverse-transcription-PCR analysis demonstrated decreased or no expression of ING3 mRNA in 50% of primary tumors as compared with that of matched normal samples. Especially, about 63% of tongue and larynx tumors showed the decrease and a tendency of higher mortality was observed in cases with decreased ING3 expression. All these findings suggest a possibility that the ING3 gene functions as a TSG in a subset of HNSCC.

DOI： 10.1038/sj.onc.1205540

Astrocytomaにおける10番染色体長腕遺伝子異常と悪性度との関連

大同茂, 田宮隆, 小野恭裕, 大塚真司, 松下博和, 黒住和彦, 大本尭史, 伊藤佐智夫, 大内田守, 清水憲二

Brain Tumor Pathology 19 ( Suppl. ) 96 - 96 2002年5月

Reduced expression of the REIC/Dkk-3 gene by promoter-hypermethylation in human tumor cells 国際誌

K Kobayashi, M Ouchida, T Tsuji, H Hanafusa, M Miyazaki, M Namba, N Shimizu, K Shimizu

GENE 282 ( 1-2 ) 151 - 158 2002年1月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：ELSEVIER SCIENCE BV

The human REIC gene is a recently found mortalization-related gene and a candidate tumor suppressor gene expression of which is largely attenuated in many immortalized and tumor-derived cell lines (Biochem. Biophys. Res. Commun. 268 (2000) 20-24). To gain insight into the mechanisms of the down-regulation, we investigated the genomic structure and promoter activity of the human REIC gene. The gene, identical with the DKK-3 gene, resides on chromosome 11pl5.1, consists of nine exons, and has two promoters. Methylation in the main promoter region was detected in I I out of 21 cell lines tested (52%) derived from a variety of human tumors, in which the expression of the REIC gene was decreased, In ten of these 11 cell lines the minor promoter was also methylated. Similarly, the REIC gene expression was decreased in 14 of 24 fresh non-small cell lung cancer specimens (58%) compared to that in corresponding non-cancerous tissue, though allelic loss and tumor-specific mutation were rare. Of these 14 tumors, at least five tumors exhibited heavy methylation of the REIC promoter region. These results indicate that the down-regulation of the REIC gene expression is ascribed to the aberrant promoter p hyper-methylation at least in a subset of human tumors. The expression was restored upon treatment of SQ5 cells with 5-aza-deoxycytidine, confirming DNA methylation as the mode of downregulation. A notable single nucleotide polymorphism in the coding region (cSNP) with an amino acid substitution of glycine (GGG) to arginine (AGG) was found at codon 335 of the REIC gene. However, the distribution of the cSNP showed no significant difference between lung cancer patients and healthy population. (C) 2002 Elsevier Science B.V. All rights reserved.

DOI： 10.1016/S0378-1119(01)00838-1

Effect of naturally occurring E2F-4 alterations on transcriptional activation and proliferation in transfected cells

H Takashima, Y Matsumoto, N Matsubara, Y Shirakawa, R Kawashima, M Tanino, S Ito, H Isozaki, M Ouchida, SJ Meltzer, K Shimizu, N Tanaka

LABORATORY INVESTIGATION 81 ( 11 ) 1565 - 1573 2001年11月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：LIPPINCOTT WILLIAMS & WILKINS

E2F is a family of transcription factors implicated in the regulation of gene expression required for progression through the G(1)-S transition. We have previously detected tumor-specific mutations at a trinucleotide repeat coding sequence of E2F-4 gene in a subset of human sporadic colorectal cancers. The purpose of this study was to investigate the potential functional consequences of these E2F-4 mutations. We transfected NIH3T3 fibroblasts with expression constructs containing wild-type as well as mutant E2F-4 cDNA, and the effect of the E2F-4 mutations on proliferation was examined. Alteration in transactivation of the E2F consensus promoter sequence was also examined by transient cotransfection of a E2F-4 with a DP-2 construct into cultured human cells. Transfected cell clones overexpressing mutant E2F-4 grew more rapidly and showed higher proliferative activity by increased immunohistochemical staining for proliferating cell nuclear antigen (PCNA). All three mutant forms of E2F-4 showed elevated transactivation of the E2F consensus promoter sequence. Thus, expression of mutant E2F-4s confers a growth advantage in vivo, and this effect may be related to the acquisition of a neoplastic phenotype.

A novel WD40 repeat protein, WDC146, highly expressed during spermatogenesis in a stage-specific manner

S Ito, A Sakai, T Nomura, Y Miki, M Ouchida, J Sasaki, K Shimizu

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 280 ( 3 ) 656 - 663 2001年1月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：ACADEMIC PRESS INC ELSEVIER SCIENCE

We have cloned a novel cDNA encoding a protein with eight WD repeat motifs and a domain similar to collagen. As the predicted size of the protein was 146 kDa, the gene was named WDC146. Here, we characterized the genomic structure, gene products, and the expression profiles. The human WDC146 gene had 22 exons spanning over 105 kb, and these exons were distributed in three islands intervened by two long introns of around 40 kb. A minimum promoter region was identified within a 0.5 kb 5'-upstream region of exon 1. WDC146 mRNA was most highly expressed in human testis on Northern blot analysis. In mouse tissues, the highest expression was also observed in testis. By in situ hybridization on rat tissues, WDC146 mRNA was detected preferentially in the pachytene stage of spermatocytes in testis, and weakly in white pulp/marginal band of spleen and in cortex of thymus. WDC146 protein was found to be localized in nucleus. These data implied that WDC146 protein may play important roles in the mechanisms of cytodifferentiation and/or DNA recombination. (C) 2001 Academic Press.

DOI： 10.1006/bbrc.2000.4163

HD-PTP: A novel protein tyrosine phosphatase gene on human chromosome 3p21.3

S Toyooka, M Ouchida, Y Jitsumori, K Tsukuda, A Sakai, A Nakamura, N Shimizu, K Shimizu

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 278 ( 3 ) 671 - 678 2000年11月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：ACADEMIC PRESS INC

A human cDNA encoding a novel protein tyrosine phosphatase has been isolated. The phosphatase has unique features in its domain structure: a "Zn-hand" domain containing several SH3-binding motifs, a tyrosine phosphatase domain, a C-terminal PEST motif, and an N-terminal domain similar to yeast BRO1, an apoptosis-related mammalian AIP1 and to a RHO-binding protein, Rhophilin. The gene is located at chromosome 3p21.3, an area frequently deleted in many types of cancer, especially within the functionally defined narrow region. The gene may be a human homolog of the rat PTP-TD14 gene reported by others, which can suppress H-ras-mediated transformation. We identified a hemizygous missense mutation in a lung cancer cell line. Thus, the phosphatase gene may be a candidate for one of the tumor suppressor genes located on 3P21.3. (C) 2000 Academic Press.

DOI： 10.1006/bbrc.2000.3870

A reverse transcriptase-polymerase chain reaction assay in the diagnosis of soft tissue sarcomas

N Naito, A Kawai, M Ouchida, T Dan'ura, Y Morimoto, T Ozaki, K Shimizu, H Inoue

CANCER 89 ( 9 ) 1992 - 1998 2000年11月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：WILEY-LISS

BACKGROUND. Many types of sarcomas are characterized by specific chromosomal translocations that result in the production of novel chimeric genes. Detection of these fusion genes could be a sensitive molecular diagnostic assay. However, to the authors' knowledge there have been few systemic comparisons between the current histopathologic diagnosis and the presence or absence of particular fusion genes in patients with adult soft tissue sarcomas (STSs).
METHODS. Total RNA was extracted from 75 cases of STS and analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) assay for the detection of a variety of fusion transcripts. The results of the molecular assay were compared with standard histopathologic diagnoses.
RESULTS. Of the 18 tumors diagnosed as synovial sarcoma, 17 (94%) expressed SYT-SSX chimeric transcripts. AU nine myxoid liposarcomas were positive for FUS-CHOP fusion transcripts. Of the four cases of Ewing sarcoma, two had an EWS-FLI1 fusion transcript and one had an EWS-ERG fusion transcript. A clear cell sarcoma had a EWS-ATF1 fusion transcript. None of 19 cases of malignant fibrous histiocytoma nor 3 leiomposarcomas contained a fusion transcript. Three cases with an initial diagnosis other than synovial sarcoma expressed a SYT-SSX fusion transcript. A review of the slides and additional examination showed that a diagnosis of synovial sarcoma was appropriate for these cases. There was a trend for biphasic synovial sarcoma to contain the SYT-SSX1 fusion.
CONCLUSIONS, The authors believe RT-PCR assay for the detection of a specific fusion gene provides a useful tool for confirmation of the diagnosis of adult STS in diagnostically difficult cases and in retrospective studies. (C) 2000 American Cancer Society.

DOI： 10.1002/1097-0142(20001101)89:9<1992::AID-CNCR16>3.0.CO;2-R

グリオーマの悪性度と10番染色体遺伝子異常との関連性に関する検討

大同茂, 寺田欣矢, 神原啓和, 小野恭裕, 田宮隆, 松本健五, 大本尭史, 伊藤佐智夫, 大内田守, 清水憲二

日本脳神経外科学会総会抄録集 59回 221 - 221 2000年10月

Genomic structure of the human ING1 gene and tumor-specific mutations detected in head and neck squamous cell carcinomas

M Gunduz, M Ouchida, K Fukushima, H Hanafusa, T Etani, S Nishioka, K Nishizaki, K Shimizu

CANCER RESEARCH 60 ( 12 ) 3143 - 3146 2000年6月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：AMER ASSOC CANCER RESEARCH

We characterized the genomic structure of the human ING1 gene, a candidate tumor suppressor gene, and found that the gene has three exons, We also demonstrated that four mRNA variants Here transcribed from three different promoter regions. Of 34 informative cases of head and neck squamous cell carcinoma, 68% of tumors showed loss of heterozygosity at chromosome 13q33-34, where the ING1 gene is located, Here we present the first report that three missense mutations and three silent changes were detected in the ING1 gene in 6 of 23 tumors with allelic loss at the 13q33-34 region. These missense mutations were found within the PHD finger domain and nuclear localization motif in ING1 protein, probably abrogating the normal function.

Functional mutation of DNA polymerase β found in human gastric cancer - Inability of the base excision repair in vitro

Akinari Iwanaga, Mamoru Ouchida, Kohji Miyazaki, Katsuji Hori, Tsunehiro Mukai

Mutation Research - DNA Repair 435 ( 2 ) 121 - 128 1999年10月

記述言語：英語掲載種別：研究論文（学術雑誌）

DNA polymerase β (polβ) is one of mammalian DNA polymerases and is known to be involved in a G:T/G:U mismatch repair. In order to investigate an involvement of this enzyme in a base excision repair, we searched a mutation of human polβ in human gastric cancer and studied a function of the mutation. We observed cancer-specific missense mutations in 6 of 20 samples. All of these mutations were, however, heterozygous. We further analyzed the base excision repair activity of these mutants to know whether these mutants cause an error of mismatch repair. One of these mutants, which resulted in an amino acid substitution of Glu for Lys at codon 295, showed an inhibitory effect by in vitro base excision repair assay, suggesting that this mutation might play some role in carcinogenesis of the gastric mucosa.

DOI： 10.1016/S0921-8777(99)00036-1

Osteoclast-derived zinc finger (OCZF) protein with POZ domain, a possible transcriptional repressor, is involved in osteoclastogenesis 査読

A Kukita, T Kukita, M Ouchida, H Maeda, H Yatsuki, O Kohashi

BLOOD 94 ( 6 ) 1987 - 1997 1999年9月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：AMER SOC HEMATOLOGY

The differentiation of osteoclasts is regulated by transcription factors expressed in cells of osteoclast lineage. We isolated here a potential transcription factor from a cDNA library of an enriched population of preosteoclasts and osteoclasts, The cDNA encodes a protein with hi-terminal POZ domain and C-terminal Kruppel-like zinc fingers, We designate this protein as osteoclast-derived zinc finger (OCZF), OCZF was found to be rat homologue of mouse leukemia/lymphoma-related factor (LRF), Northern blot and in situ hybridization analysis showed OCZF mRNA at a high level in osteoclasts and kidney cells. OCZF had a nuclear targeting sequence and was localized in the nucleus of transfected cells. In addition, OCZF specifically bound to the guanine-rich consensus sequences of Egr-1 and c-Krox. Transient transfection assays indicate that OCZF can repress transcription activity like other POZ domain proteins. Furthermore, antisense but not sense phosphorothioate oligodeoxynucleotides (ODNs) for OCZF cDNA suppressed the formation of osteoclast-like multinucleated cells (MNCs) in bone marrow culture, whereas the same ODNs did not significantly affect the formation of macrophage polykaryons and mononuclear preosteoclast-like cells (POCs), These results suggest that OCZF is a unique transcription factor that plays an important role in the late stage of osteoclastogenesis, (C) 1999 by The American Society of Hematology.

Osteoclast-derived zinc finger (OCZF) protein with POZ domain, a possible transcriptional regulator, is involved in osteoclastogenesis.

Kukita A, Kukita T, Maeda H, Ouchida M, Yatsuki H, Kohashi O

Blood 1999年

Transforming activity of the RL-akt gene, a c-akt gene activated by long terminal repeat insertion in murine leukemia RL♂1 cells

Motohiko Tanino, Mitsutoshi Matsuo, Akiko Uenaka, Kazunori Tsukuda, Mamoru Ouchida, Eiichi Nakayama, Kenji Shimizu

Molecular Carcinogenesis 26 ( 4 ) 286 - 297 1999年

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Wiley-Liss Inc.

The unique antigen peptide pRL1 on BALB/c radiation-induced leukemia RL♂1 cells is derived from the normally untranslated 5' region of the mouse c-akt gene. Insertion of an endogenous long terminal repeat into the first coding exon of the gene resulted in the enhanced production of an altered akt protein, RL-akt, and creation of the tumor rejection antigen peptide pRL1. In this study, we constructed an RL-akt-expressing vector to investigate the transforming ability and anti-apoptotic activity of RK-akt in NIH/3T3 cells. RL-akt-expressing clones formed more colonies than did c-akt-expressing clones in soft agar and exhibited increased saturation density, a lower serum requirement for growth, and tumorigenicity on athymic nude mice. Immunoblot analysis of subcellular protein distribution showed that a considerable proportion of RL-akt was distributed in the membrane fraction. Thus, RL-akt expressed in NIH/3T3 cells appeared to behave like the v-akt oncoprotein. Furthermore, the RL-akt gene conferred resistance to the apoptosis induced by the calcium ionophore A23187 and by ultraviolet irradiation of NIH/3T3 cells. These findings indicate that the RL-akt gene is able to transform cells and exerts an anti-apoptotic effect on recipient cells, thereby implicating the gene in leukemogenesis of RL♂1 cells.

DOI： 10.1002/(SICI)1098-2744(199912)26:4<286::AID-MC7>3.0.CO;2-U

Cloning of the Xenopus laevis aldolase C gene and analysis of its promoter function in developing Xenopus embryos and A6 cells

Hitomi Yatsuki, Mamoru Outida, Yasuo Atsuchi, Tunehiro Mukai, Koichiro Shiokawa, Katsuji Hori

Biochimica et Biophysica Acta - Gene Structure and Expression 1442 ( 2-3 ) 199 - 217 1998年11月

記述言語：英語掲載種別：研究論文（学術雑誌）

A Xenopus aldolase C gene (XACλ3-1), much longer (9.6 kb) than human and rat genes (3.7-3.6 kb), was isolated and characterized, and expression studies were performed using Xenopus embryos and A6 cells, a kidney cell line constitutively expressing aldolase C gene. The Xenopus gene contained nine exons, and in its proximal 5'-upstream region a GC box and a 16 bp long aldolase C-specific element (ACSE), and in addition, a CCAAT box and a TATA- like element, both missing in mammalian genes. The lacZ gene connected to the 5'-upstream region (1.6 kb) of the aldolase gene containing many potentially regulative sequence elements was expressed in embryos temporally and spatially like the endogenous aldolase C gene. Deletion experiments using embryos and A6 cells suggested that this 5'-upstream DNA contained in its distal part a region which negatively affected on its expression in embryos, but not in A6 cells. The proximal-most region contained a basal promoter (68 bp) essential for expression in both embryos and A6 cells. Deletion experiments using A6 cells failed to detect such regulative regions within the first intron (spanning ca. 4 kb). Analyses with mutated promoters in A6 cells revealed that the GC box was the crucial element in the basal promoter, although the TATA-like element appeared to have a slightly stimulative effect on the GC box functioning. Gel retardation and foot-printing assays revealed the occurrence in A6 cells of a nuclear factor(s) that binds specifically to the GC box. Since Xenopus aldolase C gene has several unique structural features, we expect that it will provide an interesting material for studying the evolution and developmental control of the aldolase C gene.

DOI： 10.1016/S0167-4781(98)00165-1

Inhibition of apoptosis by normal and aberrant Fli-1 and erg proteins involved in human solid tumors and leukemias. 国際誌

H Yi, Y Fujimura, M Ouchida, D D Prasad, V N Rao, E S Reddy

Oncogene 14 ( 11 ) 1259 - 68 1997年3月

記述言語：英語掲載種別：研究論文（学術雑誌）

Two ets family members, namely erg and Fli-1 are fused with two EWS family members namely EWS and TLS/FUS as a result of chromosome translocation in human solid tumors and leukemias. EWS-erg and EWS-Fli-1, which are involved in greater than 95% of Ewing family of tumors, were shown to function as transcriptional activators. TLS/FUS-erg, which is involved in human myeloid leukemias also functions as a transcriptional activator. Expression of these fusion proteins (EWS-erg and EWS-Fli-1) are shown to be essential for maintaining the oncogenic and tumorigenic properties of tumor cells. Cancer is thought to be caused not only by uncontrolled cell proliferation but also by deregulation of programmed cell death. Therefore, we have studied the role of normal (Fli-1 and erg) and aberrant fusion proteins (EWS-erg, EWS-Fli-1 and TLS/FUS-erg) in apoptosis. We have found that expression of normal (Fli-1 and erg) and aberrant fusion proteins inhibit the apoptosis of NIH3T3 cells induced by either serum deprivation or by treatment with calcium ionophore. We have also observed similar suppression of apoptosis in Ewing's sarcoma cells expressing EWS-Fli-1 and EWS-erg proteins suggesting that these fusion proteins may be responsible for the decreased ability of these tumor cells to undergo apoptosis. Inhibition of the expression of these aberrant fusion proteins by antisense RNA technique resulted in increased susceptibility to apoptosis leading to the death of tumor cells. Therefore, our results suggest that one can use therapeutic agents which can down regulate the expression of fusion proteins in combination with chemotherapeutic agents as an effective treatment for these human solid tumors and leukemias.

DOI： 10.1038/sj.onc.1201099

Telomerase activity in gynecologic tumors

Peng-Sheng Zheng, Tsuyoshi Iwasaka, Fumio Yamasaki, Mamoru Ouchida, Masatoshi Yokoyama, Yoshifumi Nakao, Koichi Fukuda, Toshitake Matsuyama, Hajime Sugimori

Gynecologic Oncology 64 ( 1 ) 171 - 175 1997年

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Academic Press Inc.

The standard telomeric repeat assay protocol (TRAP) was used to examine telomerase activity in 16 ovarian tumors, 16 cervical carcinomas, 4 uterine tumors, and 3 vaginal tumors. Telomerase activity was detected in 95% of these tumors, 88% of ovarian malignancies, and 100% of cervical, endometrial, and vaginal malignancies. In contrast, telomerase activity was not evident in normal tissues or in benign proliferative lesions, such as leiomyomas, condyloma acuminata, and simple endometrial hyperplasia. These results suggest that telomerase activation is associated with immortalization or malignant transformation of gynecologic tumors.

DOI： 10.1006/gyno.1996.4523

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