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Start Over Author "Yinyan Xu" Journal british journal of haematology
6 results on '"Yinyan Xu"'

2. Aldehyde dehydrogenase-2 polymorphism contributes to the progression of bone marrow failure in children with idiopathic aplastic anaemia

Author

Xinan Wang, Hideki Muramatsu, Seiji Kojima, Atsushi Narita, Koji Nakanishi, Asahito Hama, Nozomu Kawashima, Yoshiyuki Takahashi, Yinyan Xu, Sayoko Doisaki, and Hirotoshi Sakaguchi

Subjects
Male, Idiopathic aplastic anaemia, Adolescent, Pancytopenia, Aldehyde dehydrogenase, Bone Marrow, medicine, Humans, Child, ALDH2, Polymorphism, Genetic, biology, business.industry, Aldehyde Dehydrogenase, Mitochondrial, Bone marrow failure, Anemia, Aplastic, Infant, Hematology, Aldehyde Dehydrogenase, medicine.disease, Child, Preschool, Immunology, Disease Progression, biology.protein, Female, business
Published
2014
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3. Clinical utility of next-generation sequencing-based minimal residual disease in paediatric B-cell acute lymphoblastic leukaemia

Author

Xinan Wang, Yuko Sekiya, Atsushi Narita, Nao Yoshida, Yoshiyuki Takahashi, Koji Kato, Hideki Muramatsu, Seiji Kojima, Yinyan Xu, Asahito Hama, Nozomu Kawashima, Kyogo Suzuki, Hirotoshi Sakaguchi, and Yusuke Okuno

Subjects
Male, medicine.medical_specialty, Pediatrics, Neoplasm, Residual, Time Factors, Adolescent, Gastroenterology, Disease-Free Survival, 03 medical and health sciences, 0302 clinical medicine, Maintenance therapy, hemic and lymphatic diseases, Internal medicine, Medicine, Humans, Child, Retrospective Studies, Univariate analysis, B-Lymphocytes, business.industry, Proportional hazards model, Infant, Bone Marrow Examination, Hematology, DNA, Neoplasm, Sequence Analysis, DNA, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Minimal residual disease, Confidence interval, medicine.anatomical_structure, 030220 oncology & carcinogenesis, Relative risk, Child, Preschool, Cohort, Female, Bone marrow, business, 030215 immunology
Abstract

Summary We assessed the clinical utility of next-generation sequencing (NGS)-based monitoring of minimal residual disease (MRD) in a uniformly treated cohort of 79 patients with paediatric B-cell acute lymphoblastic leukaemia. Bone marrow samples were collected at the time of diagnosis, days 33 and 80, pre- (4–5 months) and post- (24 months) maintenance therapy time points, and at relapse. We identified leukaemia-specific CDR3 sequences in 72 of 79 patients (91%) and detected MRD in 59 of 232 samples. Although MRD was detected in 28 of 55 samples (51%) on day 33, the frequencies of MRD detection decreased to 25% (16/65) at day 80, 19% (11/58) at 4–5 months and 7·4% (4/54) at 24 months. In a univariate analysis, positive MRD results on day 80 [relative risk (RR) 95% confidence interval (CI) = 7·438 (2·561–21·6), P

Published
2016

4. Mutation in the THPO gene is not associated with aplastic anaemia in Japanese children

Author

Sayoko Doisaki, Yusuke Tsumura, Makito Tanaka, Hirotoshi Sakaguchi, Akira Shimada, Olfat Ismael, Hideki Muramatsu, Asahito Hama, Yoshiyuki Takahashi, Seiji Kojima, Yinyan Xu, Atsushi Narita, and Xinan Wang

Subjects
Genetics, Adolescent, business.industry, Anemia, Aplastic, Hematology, Polymorphism, Single Nucleotide, Case-Control Studies, Mutation (genetic algorithm), Mutation, Medicine, Humans, Genetic Predisposition to Disease, business, Child, Gene, Receptors, Thrombopoietin
Published
2012

5. Spectrum of molecular defects in juvenile myelomonocytic leukaemia includes ASXL1 mutations

Author

Koji Kato, Hideki Makishima, Jaroslaw P. Maciejewski, Yuka Sugimoto, Atsushi Manabe, Hiroshi Yagasaki, Asahito Hama, Seiji Kojima, Courtney Prince, Yoshiyuki Takahashi, Yinyan Xu, Nobuhiro Nishio, Hideki Muramatsu, Nao Yoshida, and Anna M. Jankowska

Subjects
Neuroblastoma RAS viral oncogene homolog, Male, congenital, hereditary, and neonatal diseases and abnormalities, Chronic myelomonocytic leukemia, Protein Tyrosine Phosphatase, Non-Receptor Type 11, Biology, medicine.disease_cause, Polymorphism, Single Nucleotide, Frameshift mutation, medicine, Humans, Frameshift Mutation, Myeloproliferative neoplasm, Genetics, Mutation, Juvenile myelomonocytic leukemia, Infant, Hematology, medicine.disease, Neoplasm Proteins, PTPN11, Repressor Proteins, Leukemia, Myelomonocytic, Juvenile, Codon, Nonsense, Child, Preschool, Karyotyping, Cancer research, Female, KRAS
Abstract

Summary Mutations in NF1, PTPN11, NRAS, KRAS and CBL have been reported to play a pathogenetic role in juvenile myelomonocytic leukaemia (JMML), a rare myelodyplastic/myeloproliferative neoplasm occurring in children. Recently, mutations in ASXL1 were identified in chronic myelomonocytic leukaemia and other myeloid malignancies. We sequenced exon 12 of ASLX1 in 49 JMML patients, and found 2 novel heterozygous (nonsense and frameshift) mutations, one occurring as a sole lesion, the other was in conjunction with a PTPN11 mutation. ASXL1 cooperates with KDM1A in transcriptional repression and thereby ASXL1 mutations may synergize with or mimic other JMML-related mutations.

Published
2010

6. Spectrum of molecular defects in juvenile myelomonocytic leukaemia includes ASXL1 mutations.

Author

Sugimoto, Yuka, Muramatsu, Hideki, Makishima, Hideki, Prince, Courtney, Jankowska, Anna M., Yoshida, Nao, Yinyan Xu, Nishio, Nobuhiro, Hama, Asahito, Yagasaki, Hiroshi, Takahashi, Yoshiyuki, Kato, Koji, Manabe, Atsushi, Kojima, Seiji, and Maciejewski, Jaroslaw P.

Subjects
LEUKEMIA in children, MOLECULAR diagnosis, MYELOPROLIFERATIVE neoplasms, MYELOID leukemia, REPRESSION (Psychology) in children
Abstract

Mutations in NF1, PTPN11, NRAS, KRAS and CBL have been reported to play a pathogenetic role in juvenile myelomonocytic leukaemia (JMML), a rare myelodyplastic/myeloproliferative neoplasm occurring in children. Recently, mutations in ASXL1 were identified in chronic myelomonocytic leukaemia and other myeloid malignancies. We sequenced exon 12 of ASLX1 in 49 JMML patients, and found 2 novel heterozygous (nonsense and frameshift) mutations, one occurring as a sole lesion, the other was in conjunction with a PTPN11 mutation. ASXL1 cooperates with KDM1A in transcriptional repression and thereby ASXL1 mutations may synergize with or mimic other JMML-related mutations. [ABSTRACT FROM AUTHOR]

Published
2010
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