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Article: [Molecular mechanisms of pediatric intractable leukemia].

Takita, Junko

Rinsho ketsueki] The Japanese journal of clinical hematology

2023 Volume 64, Issue 8, Page(s) 810–815

Abstract: Recent advances in intensive treatment strategies have resulted in an overall treatment rate of approximately 70% for pediatric cancers. The most notable improvement in clinical outcomes has been observed for acute lymphocytic leukemia, with the cure ... ...

Abstract	Recent advances in intensive treatment strategies have resulted in an overall treatment rate of approximately 70% for pediatric cancers. The most notable improvement in clinical outcomes has been observed for acute lymphocytic leukemia, with the cure rate increasing from approximately 10% 50 years ago to 90% at present. However, relapsed and refractory cases of childhood leukemia continue to have a poor prognosis, and there is no standard treatment strategy for many cases. Moreover, even in cases with favorable outcomes, growth retardation and endocrine disorders are major complications. To improve the cure rate of pediatric cancers, we have focused on the molecular mechanisms of leukemia, the most common type of pediatric cancer. In this symposium, recent findings on T-cell acute lymphocytic leukemia will be outlined.
MeSH term(s)	Humans ; Child ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
Language	Japanese
Publishing date	2023-08-10
Publishing country	Japan
Document type	English Abstract ; Journal Article
ZDB-ID	390900-1
ISSN	0485-1439
ISSN	0485-1439
DOI	10.11406/rinketsu.64.810
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Article ; Online: Molecular Basis and Clinical Features of Neuroblastoma.

Takita, Junko

JMA journal

2021 Volume 4, Issue 4, Page(s) 321–331

Abstract: Neuroblastoma, a neoplasm of the sympathetic nervous system, originates from neuroblastoma stem cells during embryogenesis. It exhibits unique clinical features including a tendency for spontaneous regression of tumors in infants and a high frequency of ... ...

Abstract	Neuroblastoma, a neoplasm of the sympathetic nervous system, originates from neuroblastoma stem cells during embryogenesis. It exhibits unique clinical features including a tendency for spontaneous regression of tumors in infants and a high frequency of metastatic disease at diagnosis in patients aged over 18 months. Genetic risk factors and epigenetic dysregulation also play a significant role in the development of neuroblastoma. Over the past decade, our understanding of this disease has advanced considerably. This has included the identification of chromosomal copy number aberrations specific to neuroblastoma development, risk groups, and disease stage. However, high-risk neuroblastoma remains a therapeutic challenge for pediatric oncologists. New therapeutic approaches have been developed, either as alternatives to conventional chemotherapy or in combination, to overcome the dismal prognosis. Particularly promising strategies are targeted therapies that directly affect cancer cells or cancer stem cells while exhibiting minimal effect on healthy cells. This review summarizes our understanding of neuroblastoma biology and prognostic features and focuses on novel therapeutic strategies for this intractable disease.
Language	English
Publishing date	2021-09-01
Publishing country	Japan
Document type	Journal Article ; Review
ZDB-ID	3053329-6
ISSN	2433-3298 ; 2433-328X
ISSN (online)	2433-3298
ISSN	2433-328X
DOI	10.31662/jmaj.2021-0077
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Article: [Precision medicine and molecular target drugs in pediatric hematologic malignancies: acute lymphoblastic leukemia].

Takita, Junko

Rinsho ketsueki] The Japanese journal of clinical hematology

2020 Volume 61, Issue 6, Page(s) 657–664

Abstract: Recent advances in genomic analysis technology have revolutionized precision medicine, especially with respect to the diagnosis, prognosis, and treatment of pediatric cancers. Pediatric acute lymphoblastic leukemia (ALL) is the most common pediatric ... ...

Abstract	Recent advances in genomic analysis technology have revolutionized precision medicine, especially with respect to the diagnosis, prognosis, and treatment of pediatric cancers. Pediatric acute lymphoblastic leukemia (ALL) is the most common pediatric cancer; genetic abnormalities associated with ALL are useful for the diagnosis and risk stratification in patients with ALL. Thus, genomic medicine (clinical sequencing) in pediatric ALL at diagnosis would help in the improvement of prognostic prediction and risk stratification. Recently, integrated genetic analysis using next generation sequencing technology revealed the full genetic landscape of pediatric ALL. These studies disclosed that in addition to fusion genes, aberrations of cell proliferation pathways and epigenetic regulations are also involved in the pathogenesis of pediatric ALL. Therefore, the realization of genomic medicine is an urgent necessity for improving the outcomes of pediatric patients diagnosed with ALL.
MeSH term(s)	Child ; High-Throughput Nucleotide Sequencing ; Humans ; Molecular Targeted Therapy ; Precision Medicine ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy ; Prognosis
Language	Japanese
Publishing date	2020-07-06
Publishing country	Japan
Document type	Journal Article
ZDB-ID	390900-1
ISSN	0485-1439
ISSN	0485-1439
DOI	10.11406/rinketsu.61.657
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Zs.A 1175: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: [Genetic basis of pediatric T-cell acute lymphoblastic leukemia and its clinical impact].

Takita, Junko

Rinsho ketsueki] The Japanese journal of clinical hematology

2018 Volume 59, Issue 7, Page(s) 953–959

Abstract: Despite an improvement in the prognosis of pediatric T-cell acute lymphoblastic leukemia (T-ALL), the outcome of patients with relapse or refractory T-ALL remains dismal. Activating mutations of the NOTCH pathway and the loss-of-function mutations of ... ...

Abstract	Despite an improvement in the prognosis of pediatric T-cell acute lymphoblastic leukemia (T-ALL), the outcome of patients with relapse or refractory T-ALL remains dismal. Activating mutations of the NOTCH pathway and the loss-of-function mutations of CDKN2A are frequent genetic alterations in T-ALL; however, these changes exert no prognostic impact. Furthermore, several gene fusions, including STIL-TAL1, were recently detected in T-ALL; however, other genetic events are necessary for the development of T-ALL. Recently, we detected novel recurrent SPI1 fusions in T-ALL by RNA sequencing using next-generation sequencing technology. Patients with SPI1 fusions revealed highly poor prognosis, suggesting that these fusions would be useful prognostic markers in T-ALL. Furthermore, the intensification of treatment of patients with SPI1 fusions may contribute to the improvement of the outcome of patients with T-ALL.
MeSH term(s)	Child ; High-Throughput Nucleotide Sequencing ; Humans ; Mutation ; Oncogene Proteins, Fusion/genetics ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Prognosis ; Proto-Oncogene Proteins/genetics ; Trans-Activators/genetics
Chemical Substances	Oncogene Proteins, Fusion ; Proto-Oncogene Proteins ; Trans-Activators ; proto-oncogene protein Spi-1
Language	Japanese
Publishing date	2018-08-02
Publishing country	Japan
Document type	Journal Article ; Review
ZDB-ID	390900-1
ISSN	0485-1439
ISSN	0485-1439
DOI	10.11406/rinketsu.59.953
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Article ; Online: The role of anaplastic lymphoma kinase in pediatric cancers.

Takita, Junko

Cancer science

2017 Volume 108, Issue 10, Page(s) 1913–1920

Abstract: The anaplastic lymphoma kinase (ALK) gene was initially identified as a fusion partner of the nucleophosmin gene in anaplastic large-cell lymphoma with t(2;5)(p23;q35) translocation, and then described with different genetic abnormalities in a number of ... ...

Abstract	The anaplastic lymphoma kinase (ALK) gene was initially identified as a fusion partner of the nucleophosmin gene in anaplastic large-cell lymphoma with t(2;5)(p23;q35) translocation, and then described with different genetic abnormalities in a number of tumors. Although ALK is known to be involved in the pathogenesis of neuroblastoma through activating mutations or gene amplification, its role in the pathogenesis of other pediatric cancers is still elusive. In addition to neuroblastoma, the high-grade amplification of ALK has been described in a subset of rhabdomyosarcoma cases. Normal ALK protein expression is restricted to the nervous systems of adult mammals, but the aberrant expression of ALK has been observed in a variety of pediatric cancers, including glioma and Ewing sarcoma. The discovery of oncogenic activation of ALK in neuroblastoma suggests that this cancer could be potentially treated with an ALK inhibitor, as could other cancers, such as non-small-cell lung cancer and anaplastic large-cell lymphoma. However, cellular responses to mutant ALK are complex when compared to rearranged ALK, and treatment remains a challenge. This review focuses on the biology of ALK in pediatric cancers and possible therapeutic strategies for ALK-associated tumors.
MeSH term(s)	Anaplastic Lymphoma Kinase ; Animals ; Carcinoma, Non-Small-Cell Lung/genetics ; Child ; Enzyme Activation ; Gene Amplification ; Genetic Predisposition to Disease ; Glioma/genetics ; Humans ; Lung Neoplasms/genetics ; Lymphoma, Large-Cell, Anaplastic/genetics ; Mutation ; Neoplasms/genetics ; Neoplasms, Muscle Tissue/genetics ; Neuroblastoma/genetics ; Receptor Protein-Tyrosine Kinases/genetics ; Receptor Protein-Tyrosine Kinases/metabolism ; Sarcoma, Ewing/genetics ; Signal Transduction ; Translocation, Genetic
Chemical Substances	ALK protein, human (EC 2.7.10.1) ; Anaplastic Lymphoma Kinase (EC 2.7.10.1) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	2017-08-24
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2115647-5
ISSN	1349-7006 ; 1347-9032
ISSN (online)	1349-7006
ISSN	1347-9032
DOI	10.1111/cas.13333
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Article: Genetic and epigenetic aberrations of pediatric leukemia and clinical applications.

Takita, Junko

Rinsho ketsueki] The Japanese journal of clinical hematology

2016 Volume 57, Issue 10, Page(s) 2294–2300

Abstract: Pediatric acute lymphoblastic leukemia (ALL) is the most common pediatric cancer. Although fusion genes generated by chromosomal rearrangements are the most frequent genetic alterations in pediatric ALL, fusions are insufficient for the development of ... ...

Abstract	Pediatric acute lymphoblastic leukemia (ALL) is the most common pediatric cancer. Although fusion genes generated by chromosomal rearrangements are the most frequent genetic alterations in pediatric ALL, fusions are insufficient for the development of this disease, and thus, cannot serve as therapeutic targets for ALL. Recently, integrated genetic analysis using next generation sequencing technology has revealed the genetic landscapes of pediatric ALL. These studies disclosed that in addition to fusion genes, aberrations of cell proliferation pathways and epigenetic regulations are also involved in the pathogenesis of pediatric ALL. On the other hand, more recently, abnormalities of supper enhancer regions of TAL1 have been detected as a novel oncogenic mechanism of pediatric T cell ALL. Furthermore, germline mutations of ARID5B, PAX5, and GATA3 have been found to be involved in the genetic risk of developing ALL. Therefore, currently, the molecular mechanisms of pediatric ALL have been fully disclosed.
MeSH term(s)	Child ; Epigenesis, Genetic ; Gene Expression Regulation, Leukemic ; Genetic Testing ; Genome, Human ; Humans ; Leukemia/genetics ; Mutation ; Ploidies
Language	Japanese
Publishing date	2016
Publishing country	Japan
Document type	Journal Article
ZDB-ID	390900-1
ISSN	0485-1439
ISSN	0485-1439
DOI	10.11406/rinketsu.57.2294
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Article ; Online: Neuropsychological outcome after frontal surgery for pediatric-onset epilepsy with focal cortical dysplasia in adolescent and young adult.

Kimura, Nobusuke / Takahashi, Yukitoshi / Usui, Naotaka / Matsuda, Kazumi / Otani, Hideyuki / Kasai, Yoshinobu / Kondo, Akihiko / Imai, Katsumi / Takita, Junko

Epilepsy & behavior : E&B

2024 Volume 153, Page(s) 109687

Abstract: Objective: We investigated neuropsychological outcome in patients with pharmacoresistant pediatric-onset epilepsy caused by focal cortical dysplasia (FCD), who underwent frontal lobe resection during adolescence and young adulthood.: Methods: Twenty- ... ...

Abstract	Objective: We investigated neuropsychological outcome in patients with pharmacoresistant pediatric-onset epilepsy caused by focal cortical dysplasia (FCD), who underwent frontal lobe resection during adolescence and young adulthood. Methods: Twenty-seven patients were studied, comprising 15 patients who underwent language-dominant side resection (LDR) and 12 patients who had languagenondominant side resection (n-LDR). We evaluated intelligence (language function, arithmetic ability, working memory, processing speed, visuo-spatial reasoning), executive function, and memory in these patients before and two years after resection surgery. We analyzed the relationship between neuropsychological outcome and resected regions (side of language dominance and location). Results: Although 75% of the patients showed improvement or no change in individual neuropsychological tests after surgical intervention, 25% showed decline. The cognitive tests that showed improvement or decline varied between LDR and n-LDR. In patients who had LDR, decline was observed in Vocabulary and Phonemic Fluency (both 5/15 patients), especially after resection of ventrolateral frontal cortex, and improvement was observed in WCST-Category (7/14 patients), Block Design (6/15 patients), Digit Symbol (4/15 patients), and Delayed Recall (3/9 patients). In patients who underwent n-LDR, improvement was observed in Vocabulary (3/12 patients), but decline was observed in Block Design (2/9 patients), and WCST-Category (2/9 patients) after resection of dorsolateral frontal cortex; and Arithmetic (3/10 patients) declined after resection of dorsolateral frontal cortex or ventrolateral frontal cortex. General Memory (3/8 patients), Visual Memory (3/8 patients), Delayed Recall (3/8 patients), Verbal Memory (2/9 patients), and Digit Symbol (3/12 patients) also declined after n-LDR. Conclusion: Postoperative changes in cognitive function varied depending on the location and side of the resection. For precise presurgical prediction of neuropsychological outcome after surgery, further prospective studies are needed to accumulate data of cognitive changes in relation to the resection site.
MeSH term(s)	Child ; Humans ; Adolescent ; Young Adult ; Adult ; Focal Cortical Dysplasia ; Treatment Outcome ; Epilepsy/etiology ; Epilepsy/surgery ; Epilepsy/psychology ; Frontal Lobe/diagnostic imaging ; Frontal Lobe/surgery ; Memory, Short-Term ; Neuropsychological Tests ; Epilepsy, Temporal Lobe/surgery ; Retrospective Studies
Language	English
Publishing date	2024-02-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	2010587-3
ISSN	1525-5069 ; 1525-5050
ISSN (online)	1525-5069
ISSN	1525-5050
DOI	10.1016/j.yebeh.2024.109687
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Article ; Online: Chloroquine decreases cardiac fibrosis and improves cardiac function in a mouse model of Duchenne muscular dystrophy.

Hirata, Takuya / Baba, Shiro / Akagi, Kentaro / Matsuda, Koichi / Umeda, Katsutsugu / Adachi, Souichi / Heike, Toshio / Takita, Junko

PloS one

2024 Volume 19, Issue 1, Page(s) e0297083

Abstract: Background: Duchenne muscular dystrophy (DMD), a severe degenerative skeletal and cardiac muscle disease, has a poor prognosis, and no curative treatments are available. Because decreased autophagy has been reported to contribute to skeletal muscle ... ...

Abstract	Background: Duchenne muscular dystrophy (DMD), a severe degenerative skeletal and cardiac muscle disease, has a poor prognosis, and no curative treatments are available. Because decreased autophagy has been reported to contribute to skeletal muscle degeneration, therapies targeting autophagy are expected to improve skeletal muscle hypofunction. However, the role of this regulatory mechanism has not been evaluated clearly in DMD cardiomyocytes. Methods: In this present study, we evaluated myocardial fibrosis and its mechanism in mdx mice, a model of DMD, and also evaluated changes in cardiac function. Results: As assessed by LC3 immunohistochemistry, a small number of autophagosomes were detected in cardiomyocytes of both mdx mice and control wild-type (WT) mice. The number of autophagosomes was significantly enhanced by 4 weeks of isoproterenol-induced cardiac stress in cardiomyocytes of mdx but not WT mice. Simultaneously, isoproterenol increased cardiomyocyte fibrosis in mdx but not WT mice. Administration of chloroquine significantly decreased cardiomyocyte fibrosis in mdx mice, even after isoproterenol treatment. Left ventricle size and function were evaluated by echocardiography. Left ventricular contraction was decreased in mdx mice after isoproterenol treatment compared with control mice, which was alleviated by chloroquine administration. Conclusions: Heart failure in DMD patients is possibly treated with chloroquine, and the mechanism probably involves chloroquine's anti-inflammatory effects.
MeSH term(s)	Humans ; Mice ; Animals ; Muscular Dystrophy, Duchenne/pathology ; Mice, Inbred mdx ; Isoproterenol/pharmacology ; Cardiomyopathies ; Muscle, Skeletal ; Myocytes, Cardiac/pathology ; Fibrosis ; Disease Models, Animal ; Dystrophin
Chemical Substances	Isoproterenol (L628TT009W) ; Dystrophin
Language	English
Publishing date	2024-01-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0297083
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Article ; Online: Alemtuzumab-based reduced-intensity conditioning for XIAP deficiency.

Kobushi, Hirokazu / Umeda, Katsutsugu / Hiejima, Eitaro / Kato, Kentaro / Sugimoto, Mayumi / Kanegane, Hirokazu / Takita, Junko

Pediatrics international : official journal of the Japan Pediatric Society

2023 Volume 65, Issue 1, Page(s) e15576

MeSH term(s)	Humans ; Alemtuzumab/therapeutic use ; Lymphoproliferative Disorders ; Genetic Diseases, X-Linked ; Hematopoietic Stem Cell Transplantation ; Transplantation Conditioning ; Graft vs Host Disease ; X-Linked Inhibitor of Apoptosis Protein
Chemical Substances	Alemtuzumab (3A189DH42V) ; XIAP protein, human ; X-Linked Inhibitor of Apoptosis Protein
Language	English
Publishing date	2023-12-23
Publishing country	Australia
Document type	Journal Article
ZDB-ID	1470376-2
ISSN	1442-200X ; 1328-8067
ISSN (online)	1442-200X
ISSN	1328-8067
DOI	10.1111/ped.15576
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Zs.A 848: Show issues

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Article ; Online: Juvenile xanthogranuloma manifesting with LCH-associated neurodegenerative disease-like radiological findings.

Daifu, Tomoo / Umeda, Katsutsugu / Yokoyama, Atsushi / Yoshida, Takeshi / Saida, Satoshi / Kato, Itaru / Hiramatsu, Hidefumi / Kudo, Ko / Higuchi, Yoshihisa / Takita, Junko

Pediatric blood & cancer

2024 , Page(s) e31043

Abstract: Here, we describe two patients with juvenile xanthogranuloma (JXG) manifesting with Langerhans cell histiocytosis (LCH)-associated neurodegenerative disease (ND)-like radiological findings. One patient showed typical radiological abnormalities at onset, ... ...

Abstract	Here, we describe two patients with juvenile xanthogranuloma (JXG) manifesting with Langerhans cell histiocytosis (LCH)-associated neurodegenerative disease (ND)-like radiological findings. One patient showed typical radiological abnormalities at onset, which worsened with progressing central nervous system symptoms 7 years after LCH-oriented chemotherapy. Another showed spontaneous regression of clinical symptoms, with a transient radiological change 1 year after salvage chemotherapy for recurrence of JXG. These data regarding JXG-associated ND will facilitate future investigation of the disease, as well as development of therapeutic interventions.
Language	English
Publishing date	2024-04-28
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.31043
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