2021/08/16 更新

写真a

カトウ アスカ
加藤 あす香
KATO Asuka
所属
大学院医学系研究科 伊藤忠商事次世代がん治療研究講座 特任助教
職名
特任助教

学位 1

  1. 博士(理学) ( 2019年3月   明治大学 ) 

 

論文 11

  1. Altered serum soluble furin and prorenin receptor levels in pregnancies with pre-eclampsia and fetal growth restriction.

    Ohwaki A, Nishizawa H, Kato A, Yoshizawa H, Miyazaki J, Noda Y, Sakabe Y, Sekiya T, Fujii T, Kurahashi H

    Journal of gynecology obstetrics and human reproduction   50 巻 ( 10 ) 頁: 102198   2021年7月

     詳細を見る

    記述言語:英語  

    DOI: 10.1016/j.jogoh.2021.102198

    PubMed

  2. Microbiome, fibrosis and tumor networks in a non-alcoholic steatohepatitis model of a choline-deficient high-fat diet using diethylnitrosamine. 国際誌

    Yamamoto K, Honda T, Yokoyama S, Ma L, Kato A, Ito T, Ishizu Y, Kuzuya T, Nakamura M, Kawashima H, Ishigami M, Tsuji NM, Fujishiro M

    Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver     2021年3月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1016/j.dld.2021.02.013

    PubMed

  3. An aggressive systemic mastocytosis preceded by ovarian dysgerminoma 国際誌

    Tsutsumi Makiko, Miura Hiroki, Inagaki Hidehito, Shinkai Yasuko, Kato Asuka, Kato Takema, Hamada-Tsutsumi Susumu, Tanaka Makito, Kudo Kazuko, Yoshikawa Tetsushi, Kurahashi Hiroki

    BMC CANCER   20 巻 ( 1 ) 頁: 1162 - 1162   2020年12月

     詳細を見る

    記述言語:日本語   掲載種別:研究論文(学術雑誌)   出版者・発行元:BMC Cancer  

    Background: Aggressive systemic mastocytosis (ASM) is a rare malignant disease characterized by disordered mast cell accumulation in various organs. We here describe a female ASM patient with a previous history of ovarian dysgerminoma. Methods: Molecular cytogenomic analyses were performed to elucidate an etiological link between the ASM and dysgerminoma of the patient. Results: This patient was affected by ovarian dysgerminoma which was treated by chemotherapy and surgical resection. Having subsequently been in complete remission for 2 years, she developed symptoms of ASM. A somatic D816A mutation in the KIT gene was detected in her bone marrow, which facilitated the diagnosis of ASM. Unexpectedly, this KIT D816A variant was also detected in the prior ovarian dysgerminoma sample. Whole-exome sequencing allowed us to identify a somatic nonsense mutation of the TP53 gene in the bone marrow, but not in the dysgerminoma. Microarray analysis of the patient’s bone marrow revealed a copy-number-neutral loss of heterozygosity at the TP53 locus, suggestive of the homozygous nonsense mutation in the TP53 gene. In addition, the loss of heterozygosity at the TP53 locus was also detected in the dysgerminoma. Conclusions: These results indicated that either the mast cells causing the ASM in this case had originated from the preceding ovarian dysgerminoma as a clonal evolution of a residual tumor cell, which acquired the TP53 mutation, or that both tumors developed from a common cancer stem cell carrying the KIT D816A variation.

    DOI: 10.1186/s12885-020-07653-z

    Web of Science

    Scopus

    PubMed

  4. AMINO ACID POLYMORPHISM IN HEPATITIS B VIRUS ASSOCIATED WITH NATURAL CLEARANCE OF HBV DNA AND HBsAg

    Honda Takashi, Yamada None, Murayama Asako, Kato Asuka, Ito Takanori, Ishizu Yoji, Kuzuya Teiji, Ishigami Masatoshi, Murakami Yoshiki, Ishikawa Tetsuya, Fujishiro Mitsuhiro, Kato Takanobu

    HEPATOLOGY   72 巻   頁: 508A - 509A   2020年11月

     詳細を見る

    記述言語:日本語  

    Web of Science

  5. The involvement of U-type dicentric chromosomes in the formation of terminal deletions with or without adjacent inverted duplications 国際誌

    Kato Takema, Inagaki Hidehito, Miyai Syunsuke, Suzuki Fumihiko, Naru Yuki, Shinkai Yasuko, Kato Asuka, Kanyama Kazuo, Mizuno Seiji, Muramatsu Yukako, Yamamoto Toshiyuki, Shinya Mitsuhisa, Tazaki Yukiko, Hiwatashi Sayuri, Ikeda Toshiro, Ozaki Mamoru, Kurahashi Hiroki

    HUMAN GENETICS   139 巻 ( 11 ) 頁: 1417 - 1427   2020年11月

     詳細を見る

    記述言語:日本語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Human Genetics  

    An inverted duplication with a terminal deletion (inv-dup-del) is one of the complex constitutional structural rearrangements that can occur in a chromosome. Although breakages of dicentric chromosome have been suggested, the precise mechanism of this is yet to be fully understood. In our present study, we investigated the genomic structure of 10 inv-dup-del cases to elucidate this mechanism. Two recurrent 8p inv-dup-del cases harbored a large copy-number-neutral region between the duplication and deletion in common. Although the other non-recurrent cases did not appear to have this copy-number-neutral region, refined sequencing analysis identified that they contained a small intervening region at the junction between the inverted and non-inverted segment. The size of this small intervening region ranged from 1741 to 3728 bp. Combined with a presence of microhomology at the junction, a resolution of the replication fork stalling through template switching within the same replication fork is suggested. We further observed two cases with mosaicism of the dicentric chromosome and various structural rearrangements related to the dicentric chromosome. Refined analysis allowed us to identify different breakpoints on the same chromosome in the same case, implicating multiple rounds of U-type formation and its breakage. From these results, we propose that a replication-based mechanism generates unstable dicentric chromosomes and that their breakage leads to the formation of inv-dup-dels and other related derivative chromosomes.

    DOI: 10.1007/s00439-020-02186-8

    Web of Science

    Scopus

    PubMed

  6. Placental Genetic Variants in the Upstream Region of the FLT1 Gene in Pre-eclampsia.

    Ohwaki A, Nishizawa H, Kato A, Kato T, Miyazaki J, Yoshizawa H, Noda Y, Sakabe Y, Ichikawa R, Sekiya T, Fujii T, Kurahashi H

    Journal of reproduction & infertility   21 巻 ( 4 ) 頁: 240 - 246   2020年10月

     詳細を見る

    記述言語:英語  

    DOI: 10.18502/jri.v21i4.4325

    PubMed

  7. Potentially effective method for fetal gender determination by noninvasive prenatal testing for X-linked disease. 国際誌

    Noda Y, Kato T, Kato A, Nishizawa H, Miyazaki J, Ito M, Terasawa S, Sekiya T, Fujii T, Kurahashi H

    Congenital anomalies   59 巻 ( 3 ) 頁: 88 - 92   2019年5月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1111/cga.12302

    PubMed

  8. Multiplex PCR in noninvasive prenatal diagnosis for FGFR3-related disorders. 国際誌

    Terasawa S, Kato A, Nishizawa H, Kato T, Yoshizawa H, Noda Y, Miyazaki J, Ito M, Sekiya T, Fujii T, Kurahashi H

    Congenital anomalies   59 巻 ( 1 ) 頁: 4 - 10   2019年1月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1111/cga.12278

    PubMed

  9. Twin pregnancy with chromosomal abnormalities mimicking a gestational trophoblastic disorder and coexistent foetus on ultrasound.

    Ohwaki A, Nishizawa H, Aida N, Kato T, Kambayashi A, Miyazaki J, Ito M, Urano M, Kiriyama Y, Kuroda M, Nakayama M, Sonta SI, Suzumori K, Sekiya T, Kurahashi H, Fujii T

    Journal of obstetrics and gynaecology : the journal of the Institute of Obstetrics and Gynaecology   38 巻 ( 7 ) 頁: 1023 - 1025   2018年10月

     詳細を見る

    記述言語:英語  

    DOI: 10.1080/01443615.2017.1401598

    PubMed

  10. Potential role for nectin-4 in the pathogenesis of pre-eclampsia: a molecular genetic study. 国際誌

    Ito M, Nishizawa H, Tsutsumi M, Kato A, Sakabe Y, Noda Y, Ohwaki A, Miyazaki J, Kato T, Shiogama K, Sekiya T, Kurahashi H, Fujii T

    BMC medical genetics   19 巻 ( 1 ) 頁: 166 - 166   2018年9月

     詳細を見る

    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1186/s12881-018-0681-y

    PubMed

  11. Increased levels of soluble corin in pre-eclampsia and fetal growth restriction.

    Miyazaki J, Nishizawa H, Kambayashi A, Ito M, Noda Y, Terasawa S, Kato T, Miyamura H, Shiogama K, Sekiya T, Kurahashi H, Fujii T

    Placenta   48 巻   頁: 20 - 25   2016年12月

     詳細を見る

    記述言語:英語  

    DOI: 10.1016/j.placenta.2016.10.002

    PubMed

▼全件表示

科研費 1

  1. HBs抗原陰性化に関わるB型肝炎ウイルス変異と腸内細菌叢が及ぼす免疫応答の解明

    研究課題/研究課題番号:20K08382  2020年4月 - 2023年3月

    日本学術振興会  科学研究費助成事業 基盤研究(C)  基盤研究(C)

    本多 隆

      詳細を見る

    担当区分:研究分担者 

    B型肝炎ウイルス(HBV)排除は現在困難でありHBs抗原が陰性化する機能的治癒(Functional Cure: FC)が治療目標となる。一方自然経過でFCが得られる症例も存在するが、FCに関与する因子と詳しいメカニズムは不明である。申請者はHBVコアI97の変異症例では肝炎沈静化及びFC率が高いことを見出しているが、コア変異が起こる機序は不明である。本研究ではB型肝炎の肝炎沈静化及びFCに関連する因子について、コア変異を含むウイルス変異、免疫応答、腸内細菌叢、miRNAの解析を含め、多面的に調べることにより、コア変異と免疫応答の関係、腸内細菌叢を介した免疫応答とFCの関連などを明らかにする。