Faculty Profiles - HIRASAWA Akira

Papers - HIRASAWA Akira

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Relationship Between ABCF2 Expression and Response to Chemotherapy or Prognosis in Clear Cell Adenocarcinoma of the Ovary

Hiroshi Tsuda, Kiyoshi Ito, Nobuo Yaegashi, Akira Hirasawa, Tamotsu Sudo, Tsunekazu Kita, Yoshito Terai, Junzo Kigawa, Toru Sugiyama, Daisuke Aoki

INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER 20 ( 5 ) 794 - 797 2010.7

Language：English Publishing type：Research paper (scientific journal) Publisher：LIPPINCOTT WILLIAMS & WILKINS

Objectives: The purpose of this study was to evaluate the association of ABCF2 (adenosine triphosphate-binding cassette superfamily F2) protein expression with response to chemotherapy and prognosis in patients with clear cell adenocarcinoma (CCC) of the ovary.
Methods: One hundred sixty-five patients with CCC were studied, and cytoplasmic ABCF2 expression was detected by immunohistochemical staining. All patients underwent platinum-based primary chemotherapy followed by primary surgery.
Results: Adenosine triphosphate-binding cassette superfamily F2 expression was detected in 118 (71.5%) of 165 patients and was not related to age or clinical stage. The response rate to chemotherapy in 38 patients with measurable disease was 47.3% (18/38). The response rate tended to be higher in patients without ABCF2 expression than in those with ABCF2 expression; however, this difference was not significant (66.7% vs 34.8%, P = 0.096). There was no significant difference in overall survival between ABCF2-positive and ABCF2-negative cases (median survival time, 1175 vs 1257 days; P = 0.24).
Conclusions: Adenosine triphosphate-binding cassette superfamily F2 protein was highly expressed in CCC of the ovary, but expression was not related to age, clinical stage, chemoresponse, or prognosis.

DOI： 10.1111/IGC.0b013e3181a835fc

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家族性乳癌・遺伝性乳癌の現状と課題遺伝相談外来を受診したBRCA1/2遺伝子変異を有する遺伝性乳がん卵巣がん家系の臨床遺伝学的特徴

菅野康吉, 牧島恵子, 友田茉莉, 安藤二郎, 矢崎久妙子, 武田祐子, 平澤晃, 神野浩光, 北川雄光, 和泉秀子, 古賀範子, 木下貴之

日本乳癌学会総会プログラム抄録集 18回 260 - 260 2010.5

ファーマコゲノミクスの臨床応用を目指した簡易迅速な遺伝子多型診断システムの開発.

平沢晃

臨床薬理 41 ( 3 ) 109-110 - 110S 2010

平沢晃, 赤羽智子, 牧田和也, 青木大輔

Osteoporosis Japan 18 ( 3 ) 406-408 - 408 2010

閉経前両側卵巣摘出例における骨密度とFRAXの特徴に関する検討.

堀場裕子, 平沢晃, 牧田和也, 松村聡子, 小川真里子, 岩田卓, 弟子丸亮太, 柳本茂久, 青木大輔

Osteoporosis Japan 18 ( 3 ) 461-465 - 465 2010

月経関連片頭痛に対する呉茱萸湯の周期的投与の試み.

牧田和也, 堀場裕子, 平沢晃, 青木大輔, 吉村泰典

産婦人科漢方研究のあゆみ 27 ( 27 ) 73-75 - 75 2010

ゲノム薬理学の最近の親展とUGT1A1遺伝子多型診断について

AOKI DAISUKE

産婦人科の実際 58 ( 12 ) 2005-2011 - 2011 2009.11

私はこうしている：私の主張週1回のビスフォスフォネート製剤の投与

AOKI DAISUKE

産婦人科治療 99 ( 5 ) 509-511 - 511 2009.11

Analysis of candidate target genes for mononucleotide repeat mutation in microsatellite instability-high (MSI-H) endometrial cancer

Makiko Kawaguchi, Kouji Banno, Megumi Yanokura, Yusuke Kobayashi, Arisa Kishimi, Seiji Ogawa, Iori Kisu, Hiroyuki Nomura, Akira Hirasawa, Nobuyuki Susumu, Daisuke Aoki

INTERNATIONAL JOURNAL OF ONCOLOGY 35 ( 5 ) 977 - 982 2009.11

Language：English Publishing type：Research paper (scientific journal) Publisher：SPANDIDOS PUBL LTD

Microsatellite instability (MSI) is an indicator of DNA instability and is caused by abnormalities in DNA mismatch repair (MMR) genes such as hMLH1, hMSH2 and hMSH6. MSI occurs frequently in endometrial cancer (in approximately 30% of cases), and accumulation of gene mutations due to MSI may therefore have a major role in the mechanism of malignant transformation. However, a responsible target gene has not been identified in endometrial cancer. In this study, we analyzed mutations in 11 cancer-related genes with mononucleotide repeats susceptible to MST in a coding region [hMSH3 (A8), hMSH6 (C8), TGF-beta RII (A10), MBD4 (A10), BAX (G8), PTEN (A6 in exon 7), HDAC2 (A9), EPHB2 (A9), Caspase-5 (A10), TCF-4 (A9) and Axin2 (G7)] in 22 patients with MSI-H sporadic endometrial cancer. Mutations in hMSH6 (C8) and TGF-beta RII (A10) were found most frequently, at rates of 36.3% (8/22) each. Mutations of BAX (G8) and TCF-4 (A9), which are common in MSI-positive colorectal cancer, occurred at rates of 22.7 and 0%, respectively, which suggests that the MSI target gene may differ between endometrial and colorectal cancers. Mutations in hMSH6 (C8) were correlated with reduced protein expression (p=0.042) and patients with these mutations had significantly more mutations in mononucleotide repeats in other cancer-related genes compared to patients without hMSH6 (C8) mutations (p=0.042). This suggests the possibility of a novel cascade in carcinogenesis of endometrial cancer in which MST mutates hMSH6 (C8), increases gene instability, and leads to accumulation of mutations in other cancer-related genes. To our knowledge, this is the first report to show that hMSH6 (C8) has an important role as an MSI target gene in sporadic endometrial cancer.

DOI： 10.3892/ijo_00000411

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Epigenetic DNA hypermethylation: clinical applications in endometrial cancer (Review). International journal

Yuriko Muraki, Kouji Banno, Megumi Yanokura, Yusuke Kobayashi, Makiko Kawaguchi, Hiroyuki Nomura, Akira Hirasawa, Nobuyuki Susumu, Daisuke Aoki

Oncology reports 22 ( 5 ) 967 - 72 2009.11

Language：English Publishing type：Research paper (scientific journal) Publisher：SPANDIDOS PUBL LTD

Improvements in epigenetics have resulted in identification of a number of genes with aberrant hypermethylation associated with systematic occurrence of cancer. It is now evident that aberrant hypermethylation inactivates cancer-related genes including those associated with cell cycle control, apoptosis, and DNA repair. An epigenetic analysis of DNA hypermethylation in type I endometrial cancer has led to a proposed mechanism for endometrial carcinogenesis. Reduced DNA mismatch repair due to loss of hMLH1 expression is thought to have a major role in carcinogenesis and these findings open up approaches to prevention, diagnosis, risk assessment, and treatment of type I endometrial cancer. Aberrant DNA hypermethylation can be detected with high sensitivity for identification of cancer cells in sputum, blood and other biopsy materials, including in endometrial cancer specimens. There have been many attempts to use methylation inhibitors as anticancer agents, and epigenetic abnormalities may be useful as biomarkers of anticancer drug sensitivity and to identify biological characteristics of tumor cells for determination of treatment options based on hypermethylation. For example, aberrant hypermethylation of the CHFR gene is correlated with cellular sensitivity to microtubule inhibitors, and this may be useful in treatment of type I endometrial cancer. An ultimate objective of epigenetics is to identify the type of hereditary methylation responsible for cancer, with the goal of improved diagnosis and treatment based on control of methylation.

DOI： 10.3892/or_00000523

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Epigenetic DNA hypermethylation: Clinical applications in endometrial cancer (Review) Reviewed

Yuriko Muraki, Kouji Banno, Megumi Yanokura, Yusuke Kobayashi, Makiko Kawaguchi, Hiroyuki Nomura, Akira Hirasawa, Nobuyuki Susumu, Daisuke Aoki

ONCOLOGY REPORTS 22 ( 5 ) 967 - 972 2009.11

Language：English Publishing type：Research paper (scientific journal) Publisher：SPANDIDOS PUBL LTD

Improvements in epigenetics have resulted in identification of a number of genes with aberrant hypermethylation associated with systematic occurrence of cancer. It is now evident that aberrant hypermethylation inactivates cancer-related genes including those associated with cell cycle control, apoptosis, and DNA repair. An epigenetic analysis of DNA hypermethylation in type I endometrial cancer has led to a proposed mechanism for endometrial carcinogenesis. Reduced DNA mismatch repair due to loss of hMLH1expression is thought to have a major role in carcinogenesis and these findings open up approaches to prevention, diagnosis, risk assessment, and treatment of type I endometrial cancer. Aberrant DNA hypermethylation can be detected with high sensitivity for identification of cancer cells in sputum, blood and other biopsy materials, including in endometrial cancer specimens. There have been many attempts to use methylation inhibitors as anticancer agents, and epigenetic abnormalities may be useful as biomarkers of anticancer drug sensitivity and to identify biological characteristics of tumor cells for determination of treatment options based on hypermethylation. For example, aberrant hypermethylation of the CHFR gene is correlated with cellular sensitivity to microtubule inhibitors, and this may be useful in treatment of type I endometrial cancer. An ultimate objective of epigenetics is to identify the type of hereditary methylation responsible for cancer, with the goal of improved diagnosis and treatment based on control of methylation.

DOI： 10.3892/or_00000523

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Analysis of candidate target genes for mononucleotide repeat mutation in microsatellite instability-high (MSI-H) endometrial cancer Reviewed

Makiko Kawaguchi, Kouji Banno, Megumi Yanokura, Yusuke Kobayashi, Arisa Kishimi, Seiji Ogawa, Iori Kisu, Hiroyuki Nomura, Akira Hirasawa, Nobuyuki Susumu, Daisuke Aoki

INTERNATIONAL JOURNAL OF ONCOLOGY 35 ( 5 ) 977 - 982 2009.11

Language：English Publishing type：Research paper (scientific journal) Publisher：SPANDIDOS PUBL LTD

DOI： 10.3892/ijo_00000411

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Analysis of candidate target genes for mononucleotide repeat mutation in microsatellite instability-high (MSI-H) endometrial cancer. International journal

Makiko Kawaguchi, Kouji Banno, Megumi Yanokura, Yusuke Kobayashi, Arisa Kishimi, Seiji Ogawa, Iori Kisu, Hiroyuki Nomura, Akira Hirasawa, Nobuyuki Susumu, Daisuke Aoki

International journal of oncology 35 ( 5 ) 977 - 82 2009.11

Language：English Publishing type：Research paper (scientific journal) Publisher：SPANDIDOS PUBL LTD

Microsatellite instability (MSI) is an indicator of DNA instability and is caused by abnormalities in DNA mismatch repair (MMR) genes such as hMLH1, hMSH2 and hMSH6. MSI occurs frequently in endometrial cancer (in approximately 30% of cases), and accumulation of gene mutations due to MSI may therefore have a major role in the mechanism of malignant transformation. However, a responsible target gene has not been identified in endometrial cancer. In this study, we analyzed mutations in 11 cancer-related genes with mononucleotide repeats susceptible to MSI in a coding region [hMSH3 (A8), hMSH6 (C8), TGF-beta RII (A10), MBD4 (A10), BAX (G8), PTEN (A6 in exon 7), HDAC2 (A9), EPHB2 (A9), Caspase-5 (A10), TCF-4 (A9) and Axin2 (G7)] in 22 patients with MSI-H sporadic endometrial cancer. Mutations in hMSH6 (C8) and TGF-beta RII (A10) were found most frequently, at rates of 36.3% (8/22) each. Mutations of BAX (G8) and TCF-4 (A9), which are common in MSI-positive colorectal cancer, occurred at rates of 22.7 and 0%, respectively, which suggests that the MSI target gene may differ between endometrial and colorectal cancers. Mutations in hMSH6 (C8) were correlated with reduced protein expression (p=0.042) and patients with these mutations had significantly more mutations in mononucleotide repeats in other cancer-related genes compared to patients without hMSH6 (C8) mutations (p=0.042). This suggests the possibility of a novel cascade in carcinogenesis of endometrial cancer in which MSI mutates hMSH6 (C8), increases gene instability, and leads to accumulation of mutations in other cancer-related genes. To our knowledge, this is the first report to show that hMSH6 (C8) has an important role as an MSI target gene in sporadic endometrial cancer.

DOI： 10.3892/ijo_00000411

Web of Science

PubMed

researchmap

Epigenetic DNA hypermethylation: Clinical applications in endometrial cancer (Review)

Yuriko Muraki, Kouji Banno, Megumi Yanokura, Yusuke Kobayashi, Makiko Kawaguchi, Hiroyuki Nomura, Akira Hirasawa, Nobuyuki Susumu, Daisuke Aoki

ONCOLOGY REPORTS 22 ( 5 ) 967 - 972 2009.11

Language：English Publishing type：Research paper (scientific journal) Publisher：SPANDIDOS PUBL LTD

Improvements in epigenetics have resulted in identification of a number of genes with aberrant hypermethylation associated with systematic occurrence of cancer. It is now evident that aberrant hypermethylation inactivates cancer-related genes including those associated with cell cycle control, apoptosis, and DNA repair. An epigenetic analysis of DNA hypermethylation in type I endometrial cancer has led to a proposed mechanism for endometrial carcinogenesis. Reduced DNA mismatch repair due to loss of hMLH1expression is thought to have a major role in carcinogenesis and these findings open up approaches to prevention, diagnosis, risk assessment, and treatment of type I endometrial cancer. Aberrant DNA hypermethylation can be detected with high sensitivity for identification of cancer cells in sputum, blood and other biopsy materials, including in endometrial cancer specimens. There have been many attempts to use methylation inhibitors as anticancer agents, and epigenetic abnormalities may be useful as biomarkers of anticancer drug sensitivity and to identify biological characteristics of tumor cells for determination of treatment options based on hypermethylation. For example, aberrant hypermethylation of the CHFR gene is correlated with cellular sensitivity to microtubule inhibitors, and this may be useful in treatment of type I endometrial cancer. An ultimate objective of epigenetics is to identify the type of hereditary methylation responsible for cancer, with the goal of improved diagnosis and treatment based on control of methylation.

DOI： 10.3892/or_00000523

Web of Science

researchmap

ファーマコゲノミクスの現状と課題ファーマコゲノミクスの臨床応用を目指した簡易迅速な遺伝子多型診断システムの開発

平沢晃, 松村聡子, 鶴田智彦, 赤羽智子, 野村弘行, 青木大輔, 谷川原祐介, 杉田哲佳, 緒方是嗣, 花房信博

臨床薬理 40 ( Suppl. ) S138 - S138 2009.11

当科更年期外来受診患者における動脈硬化性疾患の危険因子に関する検討

柳本茂久, 牧田和也, 堀場裕子, 平沢晃, 田島博人, 金田佳史, 伊藤仁彦, 高松潔, 青木大輔

日本更年期医学会雑誌 17 ( Suppl. ) 113 - 113 2009.10

子宮傍結合織炎

AOKI DAISUKE

日本臨床（子宮疾患・子宮内膜症の臨床－基礎・臨床研究のアップデート） 67 ( 増刊号5 ) 327-330 2009.8

イリノテカン

AOKI DAISUKE

小児科 50 ( 7 ) 1227-1232 2009.6

中高年女性と片頭痛

AOKI DAISUKE

産婦人科治療 98 ( 6 ) 971-975 - 975 2009.6

Analysis of a correlation between the BRAF V600E mutation and abnormal DNA mismatch repair in patients with sporadic endometrial cancer. International journal

Makiko Kawaguchi, Megumi Yanokura, Kouji Banno, Yusuke Kobayashi, Yoshiko Kuwabara, Maya Kobayashi, Hiroyuki Nomura, Akira Hirasawa, Nobuyuki Susumu, Daisuke Aoki

International journal of oncology 34 ( 6 ) 1541 - 7 2009.6

Language：English Publishing type：Research paper (scientific journal) Publisher：SPANDIDOS PUBL LTD

Point mutations of KRAS and BRAF genes are thought to be important in carcinogenesis of colon cancer. In particular, gene instability caused by decreased expression of the hMLH1 gene, a DNA mismatch repair (MMR) gene, may be linked to the activating BRAF V600E point mutation in sporadic colon cancer. However, a consensus has not been established regarding the correlation between point mutations of KRAS or BRAF and carcinogenesis in patients with endometrial cancer, which is closely related to colon cancer. Therefore, we analyzed aberrant hypermethylation of the hMLH1 gene, microsatellite instability (MSI), and point mutations of KRAS and BRAF in 44 samples of sporadic endo-metrial cancer, with the aim of examining the mechanism of carcinogenesis in patients with endometrial cancer. Aberrant hMLH1 hypermethylation was found in 17 of the 44 cases (38.6%) and showed a significant positive correlation with MSI (p=0.02). This suggests that an abnormal MMR mechanism plays an important role in carcinogenesis of sporadic endometrial cancer. Point mutation of KRAS was found in 6 of the 44 cases (13.6%), but no BRAF V600E mutation was detected. These data suggest that the BRAF V600E mutation is not the target gene for abnormal MMR in carcinogenesis in patients with sporadic endometrial cancer, unlike in colon cancer. This is supported by the relatively few previous reports indicating a correlation between endometrial cancer and the BRAF V600E mutation. Identification of new candidates for the target gene for abnormal MMR in endometrial cancer requires further work.

DOI： 10.3892/ijo_00000283

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