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Article ; Online: An infantile case of hereditary folate malabsorption with sudden development of pulmonary hemorrhage: a case report.

Sakurai, Yukari / Toriumi, Naohisa / Sarashina, Takeo / Ishioka, Toru / Nagata, Marino / Kobayashi, Hiroya / Azuma, Hiroshi

Journal of medical case reports

2022 Volume 16, Issue 1, Page(s) 268

Abstract: Background: Hereditary folate malabsorption-a rare disorder caused by impairment of the folate transporter-can develop into severe folate deficiency manifesting as megaloblastic anemia and occasionally thrombocytopenia. Reportedly, megaloblastic anemia ... ...

Abstract	Background: Hereditary folate malabsorption-a rare disorder caused by impairment of the folate transporter-can develop into severe folate deficiency manifesting as megaloblastic anemia and occasionally thrombocytopenia. Reportedly, megaloblastic anemia can manifest with hemorrhagic episodes, possibly due to ineffective platelet production and platelet dysfunction. However, life-threatening hemorrhage events in hereditary folate malabsorption have not been well investigated. Case presentation: A 3-month-old Japanese boy was transferred to our hospital due to thrombocytopenia and severe megaloblastic anemia. During a thorough examination of hematopoietic abnormalities, the patient suddenly went into cardiac arrest due to pulmonary hemorrhage. Although intravenous folate supplementation was started soon after the identification of folate deficiency, the patient died of circulatory defect and multiple organ failure. The cause of pulmonary hemorrhage, such as respiratory infection, could not be confirmed. Genetic investigation revealed a mutation in the SLC46A1 gene to be the cause of the hereditary folate malabsorption. Conclusion: We report an infantile case of hereditary folate malabsorption that progressed to lethal pulmonary hemorrhage before folate deficiency was identified. Clinicians should consider that megaloblastic anemia could lead to severe bleeding without warning, and that nutrient supplementation should be initiated as soon as possible.
MeSH term(s)	Anemia, Megaloblastic/etiology ; Folic Acid/therapeutic use ; Folic Acid Deficiency ; Hemorrhage/etiology ; Humans ; Infant ; Malabsorption Syndromes ; Male ; Proton-Coupled Folate Transporter/genetics ; Thrombocytopenia/complications
Chemical Substances	Proton-Coupled Folate Transporter ; SLC46A1 protein, human ; Folic Acid (935E97BOY8)
Language	English
Publishing date	2022-06-30
Publishing country	England
Document type	Case Reports ; Journal Article
ZDB-ID	2269805-X
ISSN	1752-1947 ; 1752-1947
ISSN (online)	1752-1947
ISSN	1752-1947
DOI	10.1186/s13256-022-03448-x
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Metronomic Chemotherapy for Pediatric Refractory Solid Tumors: A Retrospective Single-Center Study.

Sakurai, Yukari / Iwasaki, Fuminori / Hirose, Ayana / Matsumoto, Naoya / Miyagawa, Naoyuki / Keino, Dai / Yokosuka, Tomoko / Hamanoue, Satoshi / Yanagimachi, Masakatsu / Shiomi, Masae / Goto, Shoko / Tanaka, Mio / Tanaka, Yukichi / Nozawa, Kumiko / Goto, Hiroaki

Journal of pediatric hematology/oncology

2024

Abstract: Metronomic chemotherapy (MC) is based on chronic administration of chemotherapeutic agents at minimally toxic doses without prolonged drug-free breaks, that inhibits tumor angiogenesis and induces tumor dormancy. This study aimed to determine the ... ...

Abstract	Metronomic chemotherapy (MC) is based on chronic administration of chemotherapeutic agents at minimally toxic doses without prolonged drug-free breaks, that inhibits tumor angiogenesis and induces tumor dormancy. This study aimed to determine the efficacy of MC for pediatric refractory solid tumors. We retrospectively analyzed the data of pediatric patients with relapsed/refractory solid tumors who received treatment, including low-dose continuous administration of anticancer drugs, at our institute. Of the 18 patients, the disease statuses at the initiation of MC were complete remission (n=2), partial remission/stable disease (n=5), and progressive disease (n=11). The overall survival rate was 61% at 12 months and 34% at 24 months, and the progression-free survival rate was 21% at 12 and 24 months. Although only 5 of the 18 patients showed certain tumor regression or maintained remission, tumors that stabilized, maintained remission/stable disease, and showed certain advantages in terms of overall survival rate, even if limited to progressive disease. Approximately half of the patients demonstrated temporal tumor stabilization and improved survival time. Overall, previous reports and the present study support the conclusion that MC has the potential to play an important role in pediatric cancer treatment during the advanced stage.
Language	English
Publishing date	2024-04-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	1231152-2
ISSN	1536-3678 ; 1077-4114 ; 0192-8562
ISSN (online)	1536-3678
ISSN	1077-4114 ; 0192-8562
DOI	10.1097/MPH.0000000000002870
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Article: A case of cervical schwannoma with upper tracheal stenosis followed up as asthma for 4 years.

Naomi, Akira / Hujiwara, Hideyuki / Koizumi, Tatsuhiko / Sakurai, Yukari / Kohashi, Yasuo / Yoneda, Yukiko / Kitamura, Yuka / Hattori, Yoshinobu / Saitou, Yuji

Respirology case reports

2022 Volume 10, Issue 8, Page(s) e01005

Abstract: Cases of upper tracheal stenosis due to cervical schwannoma are fairly rare; therefore, no treatment has been determined. In this case, our patient had been treated for asthma for 4 years and was admitted to our hospital because of exacerbation. Computed ...

Abstract	Cases of upper tracheal stenosis due to cervical schwannoma are fairly rare; therefore, no treatment has been determined. In this case, our patient had been treated for asthma for 4 years and was admitted to our hospital because of exacerbation. Computed tomography showed a tracheal stenosis lesion just below the vocal cords, and a biopsy revealed schwannoma. Conservative therapy was preferred rather than tumour resection by surgery. Follow-up for 5 years showed no changes on imaging. Conservative treatment is considered as an option if the extratracheal tumour does not grow.
Language	English
Publishing date	2022-07-07
Publishing country	United States
Document type	Case Reports
ZDB-ID	2750180-2
ISSN	2051-3380
ISSN	2051-3380
DOI	10.1002/rcr2.1005
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Article ; Online: B-Cell Precursor-Acute Lymphoblastic Leukemia With EBF1-PDGFRB Fusion Treated With Hematopoietic Stem Cell Transplantation and Imatinib: A Case Report and Literature Review.

Sakurai, Yukari / Sarashina, Takeo / Toriumi, Naohisa / Hatakeyama, Naoki / Kanayama, Takuyo / Imamura, Toshihiko / Osumi, Tomoo / Ohki, Kentaro / Kiyokawa, Nobutaka / Azuma, Hiroshi

Journal of pediatric hematology/oncology

2020 Volume 43, Issue 1, Page(s) e105–e108

Abstract: A 9-year-old girl was diagnosed with B-cell precursor-acute lymphoblastic leukemia (BCP-ALL). Although she entered remission after induction therapy, she relapsed 15 months after maintenance therapy cessation. Since further investigation revealed EBF1- ... ...

Abstract	A 9-year-old girl was diagnosed with B-cell precursor-acute lymphoblastic leukemia (BCP-ALL). Although she entered remission after induction therapy, she relapsed 15 months after maintenance therapy cessation. Since further investigation revealed EBF1-PDGFRB fusion, her condition was treated as BCR-ABL1-like acute lymphoblastic leukemia. She was started on a tyrosine kinase inhibitor, imatinib, and chemotherapy and underwent umbilical cord blood transplantation following reduced intensity conditioning. She has remained in complete remission for 36 months after cord blood transplantation. This case demonstrates the successful use of a tyrosine kinase inhibitor to treat BCP-ALL with a fusion transcript and highlights the need for a standardized treatment protocol.
MeSH term(s)	Child ; Combined Modality Therapy ; Female ; Hematopoietic Stem Cell Transplantation/methods ; Humans ; Imatinib Mesylate/therapeutic use ; Oncogene Proteins, Fusion/genetics ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/pathology ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/therapy ; Prognosis ; Protein Kinase Inhibitors/therapeutic use ; Receptor, Platelet-Derived Growth Factor beta/genetics ; Trans-Activators/genetics
Chemical Substances	EBF1 protein, human ; Oncogene Proteins, Fusion ; Protein Kinase Inhibitors ; Trans-Activators ; Imatinib Mesylate (8A1O1M485B) ; PDGFRB protein, human (EC 2.7.10.1) ; Receptor, Platelet-Derived Growth Factor beta (EC 2.7.10.1)
Language	English
Publishing date	2020-02-21
Publishing country	United States
Document type	Case Reports ; Journal Article ; Review
ZDB-ID	1231152-2
ISSN	1536-3678 ; 1077-4114 ; 0192-8562
ISSN (online)	1536-3678
ISSN	1077-4114 ; 0192-8562
DOI	10.1097/MPH.0000000000001743
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Article ; Online: Correction to: Aurora B kinase as a therapeutic target in acute lymphoblastic leukemia.

Goto, Hiroaki / Yoshino, Yuki / Ito, Mieko / Nagai, Junichi / Kumamoto, Tadashi / Inukai, Takesi / Sakurai, Yukari / Miyagawa, Naoyuki / Keino, Dai / Yokosuka, Tomoko / Iwasaki, Fuminori / Hamanoue, Satoshi / Shiomi, Masae / Goto, Shoko

Cancer chemotherapy and pharmacology

2021 Volume 88, Issue 6, Page(s) 1055–1056

Language	English
Publishing date	2021-07-17
Publishing country	Germany
Document type	Published Erratum
ZDB-ID	6820-2
ISSN	1432-0843 ; 0344-5704 ; 0943-9404
ISSN (online)	1432-0843
ISSN	0344-5704 ; 0943-9404
DOI	10.1007/s00280-021-04321-2
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Article ; Online: A case of primary familial congenital polycythemia with a novel EPOR mutation: possible spontaneous remission/alleviation by menstrual bleeding.

Toriumi, Naohisa / Kaneda, Makoto / Hatakeyama, Naoki / Manabe, Hiromi / Okajima, Kazuki / Sakurai, Yukari / Yamamoto, Masayo / Sarashina, Takeo / Ikuta, Katsuya / Azuma, Hiroshi

International journal of hematology

2018 Volume 108, Issue 3, Page(s) 339–343

Abstract: A 10-year-old girl with persistent erythrocytosis and ruddy complexion was diagnosed with primary familial congenital polycythemia (PFCP) involving a novel heterozygous mutation of c.1220C>A, p.Ser407X in exon 8 of the erythropoietin receptor gene (EPOR). ...

Abstract	A 10-year-old girl with persistent erythrocytosis and ruddy complexion was diagnosed with primary familial congenital polycythemia (PFCP) involving a novel heterozygous mutation of c.1220C>A, p.Ser407X in exon 8 of the erythropoietin receptor gene (EPOR). This mutation causes truncation of EPOR, resulting in loss of the cytoplasmic region, which is necessary for negative regulation of erythropoietin signal transmission. Genetic analysis showed that the mutated EPOR was inherited from her mother. Her mother had polycythemia and had undergone venesection several times when she was young, but her polycythemic state appeared to have resolved. Venesection was not needed to maintain Hct levels within normal range. For the case reported here, venesection was also conducted to maintain the blood Hct level below 50%. We observed that after the patient experienced menarche, the volume and frequency of venesection needed to maintain Hct level < 50% were clearly reduced compared with those before menarche. These findings suggest that, in female patients with this type of EPOR mutation, menstruation might reduce blood volume in a manner similar to venesection. Spontaneous remission of erythrocytosis may thus occur after the start of menstrual bleeding.
MeSH term(s)	Blood Volume ; Child ; Exons/genetics ; Female ; Hemorrhage ; Humans ; Menstruation/physiology ; Mutation/genetics ; Peptide Fragments/genetics ; Phlebotomy ; Polycythemia/congenital ; Polycythemia/diagnosis ; Polycythemia/genetics ; Polycythemia/therapy ; Receptors, Erythropoietin/genetics ; Remission, Spontaneous
Chemical Substances	Peptide Fragments ; Receptors, Erythropoietin ; erythropoietin receptor (1-225)
Language	English
Publishing date	2018-04-05
Publishing country	Japan
Document type	Case Reports ; Journal Article
ZDB-ID	1076875-0
ISSN	1865-3774 ; 0917-1258 ; 0925-5710
ISSN (online)	1865-3774
ISSN	0917-1258 ; 0925-5710
DOI	10.1007/s12185-018-2435-1
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Article ; Online: Aurora B kinase as a therapeutic target in acute lymphoblastic leukemia.

Cancer chemotherapy and pharmacology

2020 Volume 85, Issue 4, Page(s) 773–783

Abstract: Purpose: Acute lymphoblastic leukemia (ALL) is curable with standardized chemotherapy. However, the development of novel therapies is still required, especially for patients with relapsed or refractory disease. By utilizing an in vitro drug screening ... ...

Abstract	Purpose: Acute lymphoblastic leukemia (ALL) is curable with standardized chemotherapy. However, the development of novel therapies is still required, especially for patients with relapsed or refractory disease. By utilizing an in vitro drug screening system, active molecular targeting agents against ALL were explored in this study. Methods: By the in vitro drug sensitivity test, 81 agents with various actions were screened for their cytotoxicity in a panel of 22 ALL cell lines and ALL clinical samples. The drug effect score (DES) was calculated from the dose-response of each drug for comparison among drugs or samples. Normal peripheral blood mononuclear cells were also applied onto the drug screening to provide the reference control values. The drug combination effect was screened based on the Bliss independent model, and validated by the improved isobologram method. Results: On sensitivity screening in a cell line panel, barasertib-HQPA which is an active metabolite of barasertib, an aurora B kinase inhibitor, alisertib, an aurora A kinase inhibitor, and YM155, a survivin inhibitor, were effective against the broadest range of ALL cells. The DES of barasertib-HQPA was significantly higher in ALL clinical samples compared to the reference value. There were significant correlations in DES between barasertib-HQPA and vincristine or docetaxel. In the drug combination assay, barasertib-HQPA and eribulin showed additive to synergistic effects. Conclusion: Aurora B kinase was identified to be an active therapeutic target in a broad range of ALL cells. Combination therapy of barasertib and a microtubule-targeting drug is of clinical interest.
MeSH term(s)	Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Aurora Kinase A/antagonists & inhibitors ; Cell Cycle ; Cell Proliferation ; Docetaxel/administration & dosage ; Drug Therapy, Combination ; Furans/administration & dosage ; High-Throughput Screening Assays ; Humans ; Ketones/administration & dosage ; Phosphorylation ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/enzymology ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/pathology ; Prognosis ; Quinazolines/pharmacology ; Tumor Cells, Cultured ; Vincristine/administration & dosage
Chemical Substances	Furans ; Ketones ; Quinazolines ; Docetaxel (15H5577CQD) ; AZD 1152-HQPA (29P8LWS24N) ; Vincristine (5J49Q6B70F) ; AURKA protein, human (EC 2.7.11.1) ; Aurora Kinase A (EC 2.7.11.1) ; eribulin (LR24G6354G)
Language	English
Publishing date	2020-03-06
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	6820-2
ISSN	1432-0843 ; 0344-5704 ; 0943-9404
ISSN (online)	1432-0843
ISSN	0344-5704 ; 0943-9404
DOI	10.1007/s00280-020-04045-9
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Article ; Online: Using the in vitro drug sensitivity test to identify candidate treatments for transient abnormal myelopoiesis.

British journal of haematology

2021 Volume 196, Issue 3, Page(s) 764–768

Abstract: Approximately 20% of patients with transient abnormal myelopoiesis (TAM) die due to hepatic or multiorgan failure. To identify potential new treatments for TAM, we performed in vitro drug sensitivity testing (DST) using the peripheral blood samples of ... ...

Abstract	Approximately 20% of patients with transient abnormal myelopoiesis (TAM) die due to hepatic or multiorgan failure. To identify potential new treatments for TAM, we performed in vitro drug sensitivity testing (DST) using the peripheral blood samples of eight patients with TAM. DST screened 41 agents for cytotoxic properties against TAM blasts. Compared with the reference samples of healthy subjects, TAM blasts were more sensitive to glucocorticoids, the mitogen-activated protein kinase kinase (MAP2K) inhibitor trametinib, and cytarabine. Our present results support the therapeutic potential of glucocorticoids and the role of the RAS/MAP2K signalling pathway in TAM pathogenesis.
MeSH term(s)	Adult ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Biomarkers ; Cell Culture Techniques ; Cells, Cultured ; Drug Screening Assays, Antitumor/methods ; Female ; Gene Expression Regulation/drug effects ; High-Throughput Nucleotide Sequencing ; High-Throughput Screening Assays ; Humans ; Immunohistochemistry ; Leukemoid Reaction/drug therapy ; Leukemoid Reaction/etiology ; Leukocytes, Mononuclear/drug effects ; Male ; Middle Aged ; Myelopoiesis/drug effects
Chemical Substances	Antineoplastic Agents ; Biomarkers
Language	English
Publishing date	2021-11-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80077-6
ISSN	1365-2141 ; 0007-1048
ISSN (online)	1365-2141
ISSN	0007-1048
DOI	10.1111/bjh.17970
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Article ; Online: Pilot study of the combination of sorafenib and fractionated irinotecan in pediatric relapse/refractory hepatic cancer (FINEX pilot study).

Keino, Dai / Yokosuka, Tomoko / Hirose, Ayana / Sakurai, Yukari / Nakamura, Wataru / Fujita, Sachio / Hayashi, Akiko / Miyagawa, Naoyuki / Iwasaki, Fuminori / Hamanoue, Satoshi / Yanagimachi, Masakatsu / Shiomi, Masae / Goto, Shoko / Kitagawa, Norihiko / Tanaka, Mio / Nozawa, Kumiko / Tanaka, Yukichi / Goto, Hiroaki

Pediatric blood & cancer

2020 Volume 67, Issue 11, Page(s) e28655

Abstract: Background: Preclinical observations suggested a synergistic effect of sorafenib (SFN) and irinotecan (CPT-11) in hepatoblastoma (HB). Thus, we conducted a feasibility study of fractionated CPT-11 combined with SFN to develop a new therapy against ... ...

Abstract	Background: Preclinical observations suggested a synergistic effect of sorafenib (SFN) and irinotecan (CPT-11) in hepatoblastoma (HB). Thus, we conducted a feasibility study of fractionated CPT-11 combined with SFN to develop a new therapy against relapsed/refractory pediatric hepatic cancer (HC). Procedure: The study was originally designed as a phase I, standard 3+3 dose-finding study to evaluate dose-limiting toxicities (DLTs) for the regimen and the optimal CPT-11 dose in combination with SFN against relapsed/refractory pediatric HC, including HB and hepatocellular carcinoma (HCC). The enrolled patients received SFN at 200 mg/m Results: Six patients with HB (n = 4) or HCC (n = 2) were enrolled and treated with CPT-11 dose level 1. The median age at enrollment was 8.7 (6.2-16.3) years. All patients received platinum-containing chemotherapy, and five or two patients received CPT-11 or SFN before enrollment, respectively. Regimen toxicities were evaluable in all patients. One of six patients experienced a grade 4 transaminase levels increase, which was defined as a DLT per protocol. Grade 3/4 neutropenia and a grade 3 transaminase level increase occurred in three patients and one patient, respectively. All patients reported grade 1/2 toxicities such as anemia, skin toxicity, gastrointestinal symptoms, and hypoalbuminemia. Conclusions: Although the study was terminated before determining the maximum-tolerated CPT-11 dose, SFN and CPT-11 at the level 1 dose were concluded to be tolerable in pediatric patients with HC.
MeSH term(s)	Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/pathology ; Child ; Child, Preschool ; Drug Resistance, Neoplasm ; Female ; Follow-Up Studies ; Humans ; Infant ; Irinotecan/administration & dosage ; Liver Neoplasms/drug therapy ; Liver Neoplasms/pathology ; Male ; Neoplasm Recurrence, Local/drug therapy ; Neoplasm Recurrence, Local/pathology ; Pilot Projects ; Prognosis ; Salvage Therapy ; Sorafenib/administration & dosage ; Survival Rate
Chemical Substances	Irinotecan (7673326042) ; Sorafenib (9ZOQ3TZI87)
Language	English
Publishing date	2020-08-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2131448-2
ISSN	1545-5017 ; 1545-5009
ISSN (online)	1545-5017
ISSN	1545-5009
DOI	10.1002/pbc.28655
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