JaLCDOI 10.18926/AMO/52408
FullText URL 68_2_119.pdf
Author Takeda, Akiko| Shimada, Akira| Hamamoto, Kazuko| Yoshino, Syuuji| Nagai, Tomoko| Fujii, Yousuke| Yamada, Mutsuko| Nakamura, Yoshimi| Watanabe, Toshiyuki| Watanabe, Yuki| Yamamoto, Yuko| Sakakibara, Kanae| Oda, Megumi| Morishima, Tsuneo|
Abstract Acute megakaryocytic leukemia (AMKL) with t(1;22)(p13;q13) is a distinct category of myeloid leukemia by WHO classification and mainly reported in infants and young children. Accurate diagnosis of this type of AMKL can be difficult, because a subset of patients have a bone marrow (BM) blast percentage of less than 20% due to BM fibrosis. Therefore, it is possible that past studies have underestimated this type of AMKL. We present here the case of a 4-month-old female AMKL patient who was diagnosed by presence of the RBM15-MKL1 (OTT-MAL) fusion transcript by RT-PCR. In addition, we monitored RBM15-MKL1 fusion at several time points as a marker of minimal residual disease (MRD), and found that it was continuously negative after the first induction chemotherapy even by nested RT-PCR. Detection of the RBM15-MKL1 fusion transcript thus seems to be useful for accurate diagnosis of AMKL with t(1;22)(p13;q13). We recommend that the RBM15-MKL1 fusion transcript be analyzed for all suspected AMKL in infants and young children. Furthermore, monitoring of MRD using this fusion transcript would be useful in treatment of AMKL with t(1;22)(p13;q13).
Keywords AMKL infant RBM15-MKL1 OTT-MAL
Amo Type Case Report
Publication Title Acta Medica Okayama
Published Date 2014-04
Volume volume68
Issue issue2
Publisher Okayama University Medical School
Start Page 119
End Page 123
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2014 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 24743787
Web of Science KeyUT 000334652700007
JaLCDOI 10.18926/AMO/54815
FullText URL 70_6_503.pdf
Author Kanazawa, Yui| Yamashita, Yuka| Fujiwara, Mitsuhiro| Muraoka, Michiko| Washio, Kana| Kanamitsu, Kiichiro| Ishida, Hisashi| Nakano, Takae| Yamada, Miho| Horibe, Keizo| Tanaka, Takehiro| Yoshino, Tadashi| Shimada, Akira|
Abstract Childhood anaplastic large cell lymphoma (ALCL) accounts for approx. 10–30 of cases of non-Hodgkin lymphoma, and the ALCL99 study reported 60–75 disease-free survival; however, a relatively high relapse rate was observed (25–30 ). We report 2 patients with Stage III ALCL who relapsed 6–18 months after the end of ALCL99 chemotherapy. A retrospective molecular analysis identified the nucleophosmin (NPM)-anaplastic lymphoma kinase (ALK) fusion gene in the first diagnostic bone marrow samples taken from both patients. However, antibodies against the ALK protein appeared to be relatively low in the serum of both patients (×100 and ×750). An increase in chemotherapy intensity may be beneficial if Stage III ALCL patients are shown to be NPM-ALK chimera-positive in the first diagnostic bone marrow sample.
Keywords ALCL NPM-ALK fusion lymphoma
Amo Type Case Report
Publication Title Acta Medica Okayama
Published Date 2016-12
Volume volume70
Issue issue6
Publisher Okayama University Medical School
Start Page 503
End Page 506
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2016 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 28003677
JaLCDOI 10.18926/AMO/55208
FullText URL 71_3_249.pdf
Author Washio, Kana| Muraoka, Michiko| Kanamitsu, Kiichiro| Oda, Megumi| Shimada, Akira|
Abstract  We diagnosed a female infant with Langerhans cell histiocytosis (LCH) who was refractory to conventional chemotherapy. She showed refractory inflammation that was complicated with hemophagocytic lymphohistiocytosis (HLH) during LCH chemotherapy; therefore, we changed the protocol to HLH2004 (dexamethasone, cyclosporine A and VP16). However, there were no signs of hematological recovery. We therefore performed cord blood transplantation with reduced-intensity conditioning, and she achieved complete remission for over 2 years. As salvage therapy for refractory LCH, hematopoietic stem cell transplantation may be a good therapeutic choice, especially when LCH is complicated with HLH.
Keywords langerhans cell histiocytosis (LCH) hemophagocytic lymphohistiocytosis (HLH) hematopoietic stem cell transplantation (HSCT) reduced-intensity conditioning (RIC) refractory
Amo Type Case Report
Publication Title Acta Medica Okayama
Published Date 2017-06
Volume volume71
Issue issue3
Publisher Okayama University Medical School
Start Page 249
End Page 254
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2017 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 28655945
Author Iwasaki, Yuka| Nishiuchi, Rituo| Aoe, Michinori| Takahashi, Takahide| Watanabe, Hirokazu| Tokorotani, Chiho| Kikkawa, Kiyoshi| Shimada, Akira|
Published Date 2017-02
Publication Title Acta Medica Okayama
Volume volume71
Issue issue1
Content Type Journal Article
JaLCDOI 10.18926/AMO/54829
JaLCDOI 10.18926/AMO/61215
FullText URL 74_6_545.pdf
Author Tatebe, Yasuhisa| Kanamitsu, Kiichiro| Kanzaki, Hirotaka| Ishida, Hisashi| Fujiwara, Kaori| Washio, Kana| Kitamura, Yoshihisa| Sendo, Toshiaki| Shimada, Akira| Tsukahara, Hirokazu|
Abstract Polymorphisms in methotrexate transporter pathways have been associated with methotrexate toxicities and clearance. Recent genome-wide association studies have revealed that the SLCO1B1 T521C variant is associated with methotrexate elimination. We present a case of a pediatric patient with acute lymphoblastic leukemia who suffered from persistently high plasma methotrexate concentrations and acute kidney injuries after the admin-istration of a medium dose of methotrexate. Subsequent genetic analysis showed that he was a carrier of dys-functional genetic variants associated with methotrexate clearance. This case highlights that polymorphisms of methotrexate transporter pathways can adversely affect methotrexate elimination in a clinically significant manner.
Keywords methotrexate polymorphism drug elimination acute kidney injury acute lymphoblastic leukemia
Amo Type Case Report
Publication Title Acta Medica Okayama
Published Date 2020-12
Volume volume74
Issue issue6
Publisher Okayama University Medical School
Start Page 545
End Page 550
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2020 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 33361876
Web of Science KeyUT 000601203600012
NAID 120006948942
FullText URL fulltext.pdf
Author Ishida, Hisashi| Iguchi, Akihiro| Aoe, Michinori| Nishiuchi, Ritsuo| Matsubara, Takehiro| Keino, Dai| Sanada, Masashi| Shimada, Akira|
Keywords leukemia pediatric acute myeloid leukemia molecular genetics precision medicine
Published Date 2020-11
Publication Title Biomedical Reports
Volume volume13
Issue issue5
Publisher Spandidos Publications
Start Page 46
ISSN 2049-9434
NCID AA12610729
Content Type Journal Article
language English
OAI-PMH Set 岡山大学
File Version publisher
PubMed ID 32934818
DOI 10.3892/br.2020.1353
Web of Science KeyUT 000606302400012
Related Url isVersionOf https://doi.org/10.3892/br.2020.1353
FullText URL fulltext20210428_3.pdf
Author Shimada, Akira|
Keywords Down syndrome Acute myeloid leukemia Acute megakaryoblastic leukemia Transient abnormal myelopoiesis Acute lymphoblastic leukemia Solid tumor Cancer predisposition syndrome GATA1 Down syndrome critical region 1
Published Date 2021-01-21
Publication Title Pediatric Hematology Oncology Journal
Publisher Elsevier
ISSN 24681245
Content Type Journal Article
language English
OAI-PMH Set 岡山大学
File Version author
DOI 10.1016/j.phoj.2021.01.001
Related Url isVersionOf https://doi.org/10.1016/j.phoj.2021.01.001
FullText URL fulltext20211004-1.pdf
Author Fukui, Yuko| Hayano, Satoru| Kawanabe, Noriaki| Wang, Ziyi| Shimada, Akira| Saito, Megumu K.| Asaka, Isao| Kamioka, Hiroshi|
Keywords iPS cell RPL5 cleft lip and palate chondrocyte Diamond-Blackfan Anemia
Note This is an Accepted Manuscript of an article published by Wiley.
This is the peer reviewed version of the following article: [Fukui, Y, Hayano, S, Kawanabe, N, Wang, Z, Shimada, A, Saito, MK, et al. Investigation of the molecular causes underlying physical abnormalities in Diamond-Blackfan anemia patients with RPL5 haploinsufficiency. Pathology International. 2021; 1-11. https://doi.org/10.1111/pin.13168], which has been published in final form at [https://doi.org/10.1111/pin.13168]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-ArchivedVersions. This article may not be enhanced, enriched or otherwise transformed into a derivative work, without express permission from Wileyor by statutory rights under applicable legislation. Copyright notices must not be removed, obscured or modified. The article must be linked toWiley’s version of record on Wiley Online Library and any embedding, framing or otherwise making available the article or pages thereof bythird parties from platforms, services and websites other than Wiley Online Library must be prohibited.|
Published Date 2021-9-29
Publication Title Pathology International
Volume volume2021
Publisher Wiley
Start Page 1
End Page 11
ISSN 1320-5463
Content Type Journal Article
language English
OAI-PMH Set 岡山大学
Copyright Holders © 2021 Japanese Society of Pathology and John Wiley & Sons Australia, Ltd
File Version author
DOI 10.1111/pin.13168
Related Url isVersionOf https://doi.org/10.1111/pin.13168
FullText URL fulltext.pdf
Author Oyama, Takanori| Noda, Takuo| Washio, Kana| Shimada, Akira|
Keywords growing teratoma syndrome immature teratoma ovarian tumor pediatric
Published Date 2020-09-18
Publication Title Medicine
Volume volume99
Issue issue38
Publisher Lippincott, Williams & Wilkins
Start Page e22297
ISSN 0025-7974
NCID AA00728867
Content Type Journal Article
language English
OAI-PMH Set 岡山大学
Copyright Holders © 2020 the Author(s).
File Version publisher
PubMed ID 32957389
DOI 10.1097/MD.0000000000022297
Web of Science KeyUT 000579298600086
Related Url isVersionOf https://doi.org/10.1097/MD.0000000000022297