Crizotinib resistance in acute myeloid leukemia with inv(2)(p23q13)/RAN binding protein 2 (RANBP2) anaplastic lymphoma kinase (ALK) fusion and monosomy 7

Takeoka, Kayo; Okumura, Atsuko; Maesako, Yoshitomo; Ohno, Hitoshi

doi:10.1016/j.cancergen.2015.01.003

Cited by 14 publications

(9 citation statements)

References 18 publications

(28 reference statements)

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“…31,32 Although the blast percentage in ALK rearranged MPD/AML is generally rapidly progressing, singleagent ALK tyrosine kinase inhibitors can achieve hematological remission. 14,32,33 The ROS1 receptor tyrosine kinase is structurally close to ALK, and a ROS1 fusion gene (TBL1XR1-ROS1) was noted in a female adolescent with MPD. 14 MPD with eosinophilia and constitutively activated platelet-derived growth factor receptor a, platelet-derived growth factor receptor b, or fibroblast growth factor receptor 1 are classed in a separate World Health Organization category.…”

Section: Cbl-mutated Jmmlmentioning

confidence: 99%

JMML genomics and decisions

Niemeyer

2018

Hematology

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Juvenile myelomonocytic leukemia (JMML) is a unique clonal hematopoietic disorder of early childhood characterized by hyperactivation of the RAS signal transduction pathway. Approximately 90% of patients harbor molecular alteration in 1 of 5 genes (PTPN11, NRAS, KRAS, NF1, CBL), which define genetically and clinically distinct JMML subtypes. Three subtypes, PTPN11- , NRAS-, and KRAS-mutated JMML, are characterized by heterozygous somatic gain-of-function mutations in non syndromic children, while two subtypes, JMML in neurofibromatosis type 1 and in JMML in children with CBL syndrome, are characterized by germ line RAS disease and acquired biallelic inactivation of the respective tumor suppressor genes in hematopoietic cells. In addition to the initiating RAS pathway lesion, secondary genetic alterations within and outside of the RAS pathway are detected in about half the patients. Most recently, genome-wide DNA methylation profiles identified distinct methylation signatures correlating with clinical and genetic features and highly predictive of outcome. JMML is a stem cell disorder, and most JMML patients require allogeneic stem cell transplantation for long-term survival. However, spontaneous disease regression is noted in the majority of children with CBL-mutated JMML and in some NRAS-mutated cases. In the absence of 1 of the 5 canonical RAS pathway alteration, rare mutations in other RAS genes and non-JMML myeloproliferative disorders need to be excluded. Understanding the genetic basis of myeloproliferative disorders in early childhood will greatly improve clinical decision making.

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Section: Cbl-mutated Jmmlmentioning

confidence: 99%

JMML genomics and decisions

Niemeyer

2018

Hematology

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“…However, resistance to crizotinib due to a secondary ALK kinase domain mutation occurred. 5 , 9 The authors consequently suggested the necessity of consolidation therapy using cytotoxic agents to achieve long-term remission. 5 Allogeneic HCT is also a tolerable and curative option after crizotinib therapy, as reported in a case of refractory anaplastic large cell lymphoma.…”

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confidence: 99%

Crizotinib treatment for refractory pediatric acute myeloid leukemia with RAN-binding protein 2-anaplastic lymphoma kinase fusion gene

Hayashi

Tanoshima

et al. 2016

Blood Cancer Journal

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“…44 Interestingly, crizotinib, an oral ALK inhibitor, is being tested in acute myeloid leukemias (AML) and IMT patients with RANBP2-ALK fusion. 45 RANBP2-ABL1/t(2;9)(q21;q34) was detected in one pediatric case of high-risk B-cell acute lymphoblastic leukemia (B-ALL); and RANBP2-FGFR1/t (2;8)(q12;p11) was found in an adult with myelodysplastic syndrome/ myeloproliferative neoplasm (MDS/MPN; Figure 2c and d). 9,46 Many reports linked NUP214 to hematological malignancies as it participates in several oncogenic translocations 47 (Figure 2e and f), typically associated with a subgroup of MDS/AML in children and adolescents with poor response to therapy is the t(6;9)(p23; q34)/DEK-NUP214.…”

Section: Cardiovascular Disordersmentioning

confidence: 99%

Nucleoporin genes in human diseases

2016

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Nuclear pore complexes (NPCs) are large channels spanning the nuclear envelope that mediate nucleocytoplasmic transport. They are composed of multiple copies of ~30 proteins termed nucleoporins (NUPs). Alterations in NUP genes are linked to several human neoplastic and non-neoplastic diseases. This review focuses on NUPs, their genes, localization, function in the NPC and involvement in human diseases.

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Crizotinib resistance in acute myeloid leukemia with inv(2)(p23q13)/RAN binding protein 2 (RANBP2) anaplastic lymphoma kinase (ALK) fusion and monosomy 7

Cited by 14 publications

References 18 publications

JMML genomics and decisions

JMML genomics and decisions

Crizotinib treatment for refractory pediatric acute myeloid leukemia with RAN-binding protein 2-anaplastic lymphoma kinase fusion gene

Nucleoporin genes in human diseases

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