Endogenous oncogenic Nras mutation initiates hematopoietic malignancies in a dose- and cell type-dependent manner. - Wikidata - awgldk - TriplyDB

Endogenous oncogenic Nras mutation initiates hematopoietic malignancies in a dose- and cell type-dependent manner.

Endogenous oncogenic Nras mutation initiates hematopoietic malignancies in a dose- and cell type-dependent manner.

http://www.wikidata.org/entity/Q35112241

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Combined MEK and JAK inhibition abrogates murine myeloproliferative neoplasm.Copy-neutral loss of heterozygosity is prevalent and a late event in the pathogenesis of FLT3/ITD AML Nras overexpression results in granulocytosis, T-cell expansion and early lethality in mice.BRAF kinase domain mutations are present in a subset of chronic myelomonocytic leukemia with wild-type RAS.NRASG12V oncogene facilitates self-renewal in a murine model of acute myelogenous leukemia Distinct requirements of hematopoietic stem cell activity and Nras G12D signaling in different cell types during leukemogenesis.Inhibiting the palmitoylation/depalmitoylation cycle selectively reduces the growth of hematopoietic cells expressing oncogenic Nras An NF-κB pathway-mediated positive feedback loop amplifies Ras activity to pathological levels in mice.Deficiency of β Common Receptor Moderately Attenuates the Progression of Myeloproliferative Neoplasm in NrasG12D/+ Mice.Loss of Dnmt3a and endogenous Kras(G12D/+) cooperate to regulate hematopoietic stem and progenitor cell functions in leukemogenesis PRAK suppresses oncogenic ras-induced hematopoietic cancer development by antagonizing the JNK pathway.Signaling profiling at the single-cell level identifies a distinct signaling signature in murine hematopoietic stem cells Oncogenic NRAS hyper-activates multiple pathways in human cord blood stem/progenitor cells and promotes myelomonocytic proliferation in vivo.Targeting oncogenic Ras signaling in hematologic malignancies.Direct reprogramming by oncogenic Ras and Myc.Loss of CD44 attenuates aberrant GM-CSF signaling in Kras G12D hematopoietic progenitor/precursor cells and prolongs the survival of diseased animals.The IRP1-HIF-2α axis coordinates iron and oxygen sensing with erythropoiesis and iron absorption Activated N-Ras signaling regulates arterial-venous specification in zebrafish Chronic myelomonocytic leukemia: Forefront of the field in 2015.Notch1 gene mutations target KRAS G12D-expressing CD8+ cells and contribute to their leukemogenic transformation.Nras(G12D/+) promotes leukemogenesis by aberrantly regulating hematopoietic stem cell functions miR-340 predicts glioblastoma survival and modulates key cancer hallmarks through down-regulation of NRAS Cancer-associated IDH2 mutants drive an acute myeloid leukemia that is susceptible to Brd4 inhibition.Stat5 is critical for the development and maintenance of myeloproliferative neoplasm initiated by Nf1 deficiency Rasgrp1 mutation increases naive T-cell CD44 expression and drives mTOR-dependent accumulation of Helios⁺ T cells and autoantibodies.Loss of wild-type Kras promotes activation of all Ras isoforms in oncogenic Kras-induced leukemogenesis.The ability of endogenous Nras oncogenes to initiate leukemia is codon-dependent.MEK1 is required for the development of NRAS-driven leukemia.Acute myeloid leukemia with DNMT3A mutations.Ras/Raf/MEK/ERK Pathway Activation in Childhood Acute Lymphoblastic Leukemia and Its Therapeutic Targeting Overcoming inherent resistance to histone deacetylase inhibitors in multiple myeloma cells by targeting pathways integral to the actin cytoskeleton Turning the tide in myelodysplastic/myeloproliferative neoplasms.Dominant role of oncogene dosage and absence of tumor suppressor activity in Nras-driven hematopoietic transformation.p53-/- synergizes with enhanced NrasG12D signaling to transform megakaryocyte-erythroid progenitors in acute myeloid leukemia.Kras is Required for Adult Hematopoiesis.The mystery of oncogenic KRAS: Lessons from studying its wild-type counter part.Juvenile myelomonocytic leukemia-associated variants are associated with neo-natal lethal Noonan syndrome.Constitutional NRAS mutations are rare among patients with Noonan syndrome or juvenile myelomonocytic leukemia.Concurrent juvenile myelomonocytic leukemia and T-lymphoblastic lymphoma with a shared missense mutation in NRAS.Interrogating the protein interactomes of RAS isoforms identifies PIP5K1A as a KRAS-specific vulnerability

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Endogenous oncogenic Nras mutation initiates hematopoietic malignancies in a dose- and cell type-dependent manner.

http://www.wikidata.org/entity/Q35112241

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2011年の論文

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2011年論文

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2011年论文

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Endogenous oncogenic Nras muta ...... nd cell type-dependent manner.

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Endogenous oncogenic Nras muta ...... nd cell type-dependent manner.

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Endogenous oncogenic Nras muta ...... nd cell type-dependent manner.

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Endogenous oncogenic Nras muta ...... nd cell type-dependent manner.

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Endogenous oncogenic Nras muta ...... nd cell type-dependent manner.

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Benjamin Meline

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Erik Ranheim

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Jing Zhang

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Jinyong Wang

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Juan Du

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Ken H Young

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Li Xuan Tan

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Myung-Jeom Ryu

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Qiang Chang

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Yangang Liu

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P2860

Analysis of RAS oncogene mutations in human lymphoid malignancies

Oncogenic Kras initiates leukemia in hematopoietic stem cells

A restricted spectrum of NRAS mutations causes Noonan syndrome

RAS mutation in acute myeloid leukemia is associated with distinct cytogenetic subgroups but does not influence outcome in patients younger than 60 years.

The GTPase superfamily: conserved structure and molecular mechanism

The GTPase superfamily: a conserved switch for diverse cell functions

ras oncogenes in human cancer: a review

Inducible gene targeting in mice

A clonogenic common myeloid progenitor that gives rise to all myeloid lineages

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