FLT3 mutations in the activation loop of tyrosine kinase domain are frequently found in infant ALL with MLL rearrangements and pediatric ALL with hyperdiploidy.
about
Downstream molecular pathways of FLT3 in the pathogenesis of acute myeloid leukemia: biology and therapeutic implicationsRevisiting the biology of infant t(4;11)/MLL-AF4+ B-cell acute lymphoblastic leukemiaMutant FLT3 signaling contributes to a block in myeloid differentiationFLT3 mutation incidence and timing of origin in a population case series of pediatric leukemia.Discovery of a Diaminopyrimidine FLT3 Inhibitor Active against Acute Myeloid Leukemia.Childhood B-acute lymphoblastic leukemia: a genetic update.FLT3 Internal Tandem Duplication and D835 Mutations in Patients with Acute Lymphoblastic Leukemia and its Clinical SignificanceThe AML1-ETO fusion gene and the FLT3 length mutation collaborate in inducing acute leukemia in mice.MLL-AF9 and FLT3 cooperation in acute myelogenous leukemia: development of a model for rapid therapeutic assessment.The Biology and Targeting of FLT3 in Pediatric Leukemia.Interleukin-3 receptor in acute leukemia.Identification of somatic and germline mutations using whole exome sequencing of congenital acute lymphoblastic leukemia.Gain-of-function of Stat5 leads to excessive granulopoiesis and lethal extravasation of granulocytes to the lungInhibition of FLT3 expression by green tea catechins in FLT3 mutated-AML cellsKey pathways are frequently mutated in high-risk childhood acute lymphoblastic leukemia: a report from the Children's Oncology Group.A novel somatic mutation in ACD induces telomere lengthening and apoptosis resistance in leukemia cellsUse of Genome Engineering to Create Patient Specific MLL Translocations in Primary Human Hematopoietic Stem and Progenitor Cells.MLL fusions: pathways to leukemiaMolecular genetic analysis of haematological malignancies: I. Acute leukaemias and myeloproliferative disorders.Emerging drugs for adult acute lymphoblastic leukaemia.Prospective tracing of MLL-FRYL clone with low MEIS1 expression from emergence during neuroblastoma treatment to diagnosis of myelodysplastic syndromeTreatment of infant leukemias: challenge and promise.Quizartinib (AC220) is a potent second generation class III tyrosine kinase inhibitor that displays a distinct inhibition profile against mutant-FLT3, -PDGFRA and -KIT isoformsNovel targeted drug therapies for the treatment of childhood acute leukemiaDeep targeted sequencing in pediatric acute lymphoblastic leukemia unveils distinct mutational patterns between genetic subtypes and novel relapse-associated genes.The evolution of clinical trials for infant acute lymphoblastic leukemia.Insights into the cellular origin and etiology of the infant pro-B acute lymphoblastic leukemia with MLL-AF4 rearrangement.FMS-like tyrosine kinase 3 inhibitors: a patent review.Pediatric relapsed or refractory leukemia: new pharmacotherapeutic developments and future directions.Ras/Raf/MEK/ERK Pathway Activation in Childhood Acute Lymphoblastic Leukemia and Its Therapeutic TargetingThe pre-B-cell receptor checkpoint in acute lymphoblastic leukaemia.Genetic aberrations in childhood acute lymphoblastic leukaemia: application of high-density single nucleotide polymorphism array.Prognostic significance of FLT3 mutational status and expression levels in MLL-AF4+ and MLL-germline acute lymphoblastic leukemia.The multikinase inhibitor Sorafenib displays significant antiproliferative effects and induces apoptosis via caspase 3, 7 and PARP in B- and T-lymphoblastic cells.Prognostic and therapeutic role of targetable lesions in B-lineage acute lymphoblastic leukemia without recurrent fusion genes.Combinations of the FLT3 inhibitor CEP-701 and chemotherapy synergistically kill infant and childhood MLL-rearranged ALL cells in a sequence-dependent manner.Silencing of the tumor suppressor gene FHIT is highly characteristic for MLL gene rearranged infant acute lymphoblastic leukemia.Human leukemias with mutated FLT3 kinase are synergistically sensitive to FLT3 and Hsp90 inhibitors: the key role of the STAT5 signal transduction pathway.High PRDM16 expression identifies a prognostic subgroup of pediatric acute myeloid leukaemia correlated to FLT3-ITD, KMT2A-PTD, and NUP98-NSD1: the results of the Japanese Paediatric Leukaemia/Lymphoma Study Group AML-05 trial.Dimerization of MLL fusion proteins and FLT3 activation synergize to induce multiple-lineage leukemogenesis.
P2860
Q29958043-1699B327-1F22-4F04-80BC-3F4F8DDB8A3FQ54749231-215E43A3-BA82-4183-92FD-EE453C7A97BAQ54753062-AA55F4D6-F76A-4023-A1BB-FFFB266A98D4Q54753211-8DA6FFBA-9B5A-46B1-9FE2-9E91FBF1971DQ54798653-A26BE8E8-3703-4829-92CD-89627C605740Q54809037-CB1F4BE1-C0E2-4714-9C05-33E415303EA6Q54813813-D72DBF8A-1B35-4218-A9D9-FE7E30781B7AQ54813866-8E0D1C02-C133-4731-B3EA-5E4A72952E09Q54814772-905C8937-AC56-47F4-9CC2-306439D95346Q54828579-F7FFAABC-6FBD-4B71-9A72-3B42579158C7Q54872387-97783447-DAD1-4B1C-94A8-B9BCF682CEC8Q54882501-2F3CAF45-DFA6-4752-A2DA-78510BE20031Q54897680-2AB5BAA3-946A-4863-92F7-877EBEFD97C3Q54899520-52C26737-D7B5-45C1-B91D-30A6BA7F9F1DQ54899699-4009C737-924C-4D87-9ABE-875525176C70Q54899833-70A046C9-2F0C-457C-B9E5-BA16E06243C4Q54900278-DEE31390-F5E8-4329-898A-16A521D0D844Q54900279-DFFAAF60-D055-4AFB-883E-EAB15E831F51Q54900280-71C7D3BA-9CCE-420E-9758-F376C5DA75FEQ54900281-70BC987E-7834-4388-ADA2-17DF11CA16D4Q54900284-0C933095-8D13-456C-BB44-9F84D68405A4Q54900285-95A0875B-0D94-4251-B28B-6370AB2A52F8Q54900299-70699FDD-AE6F-4EF2-8EB6-5399CB4EADE4Q54900307-041A011C-7AE1-4DBB-9E8C-390A5B3BEE2EQ54902172-90A30E1E-DEC7-4B64-BB4D-E28580ECA16CQ54906316-E6F92559-EFEA-4999-8F88-1FB27318E002Q54906320-ECAA17C8-DE03-4E51-A96C-8073EF30BA4AQ54906330-A942FD44-3AAB-4CA0-8FB8-E34EBE281EEFQ54907109-22098943-164E-4988-847C-875C23B92CB6Q54907398-92D885E0-22DA-42FB-9531-AC35B1B8A139Q54907401-19250099-F3D6-48BB-8F26-256005860638Q54907405-45A700A5-B001-45C1-A593-97B1961F7B1AQ54907408-266FACDF-A117-48B2-987D-6208DF7E1E64Q54907527-B4065FA6-8303-4FEB-ADF4-BBDFB2D860ECQ54932024-8341DD84-C40E-418B-97EB-308265071B18Q54937246-BFECC1D2-6D65-4140-89F6-9FC4C4DE8155Q54952453-D8408817-A66E-4542-976E-9D1DDA3F78ACQ54955009-4FEA95DB-C25E-493B-A4F0-71559AF3BB01Q54973096-FE73A5F0-48CC-44B9-A5F7-ACF52ED61B90Q54992244-B6B97CE3-1806-4036-A2C4-461A7CEAEC71
P1343
Q24617091-2C06E45E-C8AD-4588-A55B-2B6700AF122AQ26783577-7C00B1BB-93C7-434C-8C85-8C024E66A84EQ28279890-8BA39687-17EF-4CE1-91B3-59585E80574EQ33704528-31EC711D-462E-403D-A5DA-A6C7300A6318Q33749036-FDA10EAD-96DF-40FE-A99D-AE915CAED330Q33777616-267C455B-2459-4798-A8BB-F75CD3E93A01Q33778374-DD04E3D2-621A-47A1-B8FE-825D9CF54BD1Q33895709-298497AE-6781-4FFB-BCC2-6CE5C560DA23Q34113855-507A5787-383B-44AC-9E15-FD4DDBD1F324Q34229555-E61E1A1D-0041-48A5-A331-E9E5F207B84BQ34283145-DAF4AE9D-1C76-4A81-8610-270D9B1682C9Q34573775-9130E89F-1DC7-42EC-809E-E02E85000529Q34658643-59C0A47C-7059-4D74-9743-A0FE52F896F6Q34805329-379B7F76-EC28-4868-A0FD-7F99C316A682Q35220417-2E7A67AF-9CBF-4015-81C1-20B0C82C160CQ35765789-6B7EBDE9-6EF2-48D7-9BFA-CB38724A7B45Q35767483-01BE17FE-8EF7-476B-BADC-6FA38BA01F4DQ35788362-B8A53932-67CC-4ACD-B64D-CD82D9B16AA4Q36153422-57039AEC-1D29-44CC-9458-0BEFC27BFFC4Q36219661-EE9C86BF-FF19-41F2-A128-60BE8CD197D8Q36508959-B2EAAC66-580B-4DB0-BBB7-7677E4206E92Q36508988-9245FA02-4D0F-47B8-97FF-C48C37C7BFBAQ36798620-95E8D0C8-8A1A-48A2-A9FE-DBF4624B0951Q37477482-96CC1EA7-14A1-4FC0-AA69-2B63D79C53A2Q37665574-D8E01677-B2BF-4531-B1A8-6A8FDC0DEC7EQ37730023-AE70C74B-570C-45DF-9985-297F8B3D727FQ37816933-19F876F8-2BDC-44CD-BC8C-915AA3F0A610Q37842585-1834E159-ED3C-4615-98F4-04064A728E0BQ38097334-B3F986A2-CBE2-4D9D-98C5-36EFF4B69990Q38227885-F23BA850-0820-4394-9286-8EA85753FB01Q38460308-F7B8BFA8-2DCB-400B-B9D0-5CE2BCACEAC7Q39108890-87520AC7-FF86-4C76-A14E-2ED3445B51B2Q39601375-B7BBE079-6FA2-4BD0-907C-97BB6F483D37Q39643630-1BECBC1F-A911-4D21-A561-B5E874E04502Q39992854-102CEBD8-D0BA-4C00-B021-BA8EEE9C8D1BQ40270156-A038D10F-5379-4C1A-A8BA-EF818FD0364AQ40339478-1864E897-3D33-4DBA-85B3-DD900E900A79Q40395107-8743D87C-A1FC-48BB-BC50-2B0B1F1F4E72Q41036515-59546159-F55E-409E-AC88-2E147EB2F00DQ41976616-C601DD10-97A2-4F3A-85E4-9DFB730D5FAC
P2860
FLT3 mutations in the activation loop of tyrosine kinase domain are frequently found in infant ALL with MLL rearrangements and pediatric ALL with hyperdiploidy.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年論文
@yue
2003年論文
@zh-hant
2003年論文
@zh-hk
2003年論文
@zh-mo
2003年論文
@zh-tw
2003年论文
@wuu
2003年论文
@zh
2003年论文
@zh-cn
name
FLT3 mutations in the activati ...... iatric ALL with hyperdiploidy.
@en
type
label
FLT3 mutations in the activati ...... iatric ALL with hyperdiploidy.
@en
prefLabel
FLT3 mutations in the activati ...... iatric ALL with hyperdiploidy.
@en
P2093
P4510
P1433
P1476
FLT3 mutations in the activati ...... iatric ALL with hyperdiploidy.
@en
P2093
Eiichi Ishii
Kanji Sugita
Kenichi Sugita
Kohmei Ida
Masahiro Tsuchida
Ryoji Hanada
Takeshi Taketani
Tomohiko Taki
Yasuhide Hayashi
Yoshiyuki Furuichi
P304
P356
10.1182/BLOOD-2003-02-0418
P407
P577
2003-09-22T00:00:00Z