Autocrine insulin-like growth factor-I signaling promotes growth and survival of human acute myeloid leukemia cells via the phosphoinositide 3-kinase/Akt pathway (Q40117414)

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English	Autocrine insulin-like growth factor-I signaling promotes growth and survival of human acute myeloid leukemia cells via the phosphoinositide 3-kinase/Akt pathway	scientific article

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scholarly article

1 reference

Europe PubMed Central

PubMed publication ID

17 September 2017

Autocrine insulin-like growth factor-I signaling promotes growth and survival of human acute myeloid leukemia cells via the phosphoinositide 3-kinase/Akt pathway (English)

1 reference

Europe PubMed Central

PubMed publication ID

17 September 2017

acute myeloid leukemia

1 reference

based on heuristic

inferred from title

author name string

Doepfner KT

1

1 reference

Europe PubMed Central

PubMed publication ID

17 September 2017

Spertini O

2

1 reference

Europe PubMed Central

PubMed publication ID

17 September 2017

Arcaro A

3

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Europe PubMed Central

PubMed publication ID

17 September 2017

publication date

21 June 2007

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Europe PubMed Central

PubMed publication ID

17 September 2017

1 reference

Europe PubMed Central

PubMed publication ID

17 September 2017

21

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Europe PubMed Central

PubMed publication ID

17 September 2017

9

1 reference

Europe PubMed Central

PubMed publication ID

17 September 2017

1921-1930

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Europe PubMed Central

PubMed publication ID

17 September 2017

Genetics of myeloid leukemias

1 reference

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Prognostic factors and risk-based therapy in pediatric acute myeloid leukemia

1 reference

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FLT3 ligand causes autocrine signaling in acute myeloid leukemia cells

1 reference

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The roles of FLT3 in hematopoiesis and leukemia

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Inhibition of the transforming activity of FLT3 internal tandem duplication mutants from AML patients by a tyrosine kinase inhibitor

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SU11248 is a novel FLT3 tyrosine kinase inhibitor with potent activity in vitro and in vivo

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FLT3 inhibitors: a paradigm for the development of targeted therapeutics for paediatric cancer

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Inhibition of the insulin-like growth factor receptor-1 tyrosine kinase activity as a therapeutic strategy for multiple myeloma, other hematologic malignancies, and solid tumors

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Phosphoinositide 3-kinases: A conserved family of signal transducers

1 reference

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Cellular function of phosphoinositide 3-kinases: implications for development, homeostasis, and cancer.

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Mutational analysis of the tumour suppressor gene MMAC1/PTEN in malignant myeloid disorders

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The tumor suppressor, PTEN/MMAC1, dephosphorylates the lipid second messenger, phosphatidylinositol 3,4,5-trisphosphate

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Phosphatidylinositol 3-kinase mutations identified in human cancer are oncogenic

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High frequency of mutations of the PIK3CA gene in human cancers

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Mutation analysis of PTEN/MMAC1 in acute myeloid leukemia

1 reference

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Survival of acute myeloid leukemia cells requires PI3 kinase activation

1 reference

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Alteration of phosphatidylinositol 3-kinase cascade in the multilobulated nuclear formation of adult T cell leukemia/lymphoma (ATLL)

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In vivo antitumor activity of NVP-AEW541-A novel, potent, and selective inhibitor of the IGF-IR kinase

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Tolerance of human MSH2+/- lymphoblastoid cells to the methylating agent temozolomide

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A large-scale RNAi screen in human cells identifies new components of the p53 pathway

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Protein kinase B modulates the sensitivity of human neuroblastoma cells to insulin-like growth factor receptor inhibition.

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PI 3-kinase p110beta: a new target for antithrombotic therapy

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Essential role of phosphoinositide 3-kinase delta in neutrophil directional movement

1 reference

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Sensitivity toward tyrosine kinase inhibitors varies between different activating mutations of the FLT3 receptor.

1 reference

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Patients with acute myeloid leukemia and an activating mutation in FLT3 respond to a small-molecule FLT3 tyrosine kinase inhibitor, PKC412.

1 reference

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Analysis of FLT3-activating mutations in 979 patients with acute myelogenous leukemia: association with FAB subtypes and identification of subgroups with poor prognosis

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The insulin-like growth factor system in regulation of normal and malignant hematopoiesis

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Synergy between an IGF-1R antibody and Raf/MEK/ERK and PI3K/Akt/mTOR pathway inhibitors in suppressing IGF-1R-mediated growth in hematopoietic cells.

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The insulin-like growth factor-I receptor kinase inhibitor, NVP-ADW742, sensitizes small cell lung cancer cell lines to the effects of chemotherapy

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Phosphoinositide 3-kinase/Akt signaling pathway and its therapeutical implications for human acute myeloid leukemia.

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Essential role for the p110 isoform in phosphoinositide 3-kinase activation and cell proliferation in acute myeloid leukemia

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Critical role for the p110alpha phosphoinositide-3-OH kinase in growth and metabolic regulation

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A pharmacological map of the PI3-K family defines a role for p110alpha in insulin signaling

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The effects of insulin-like growth factors on tumorigenesis and neoplastic growth

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Characterization of insulin-like growth factor I receptors on human erythroleukemia cell line (K-562 cells)

1 reference

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Decrease in IGF-I binding sites on human promyelocytic leukemia cell line (HL-60) with differentiation

1 reference

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Absence of hot spot mutations of the PIK3CA gene in acute myeloid leukaemia

1 reference

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based on heuristic

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PI3-kinase/Akt is constitutively active in primary acute myeloid leukaemia cells and regulates survival and chemoresistance via NF-kappaB, Mapkinase and p53 pathways

1 reference

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7 January 2021

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Insulin-like growth factor-I can mediate autocrine proliferation of human small cell lung cancer cell lines in vitro

1 reference

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7 January 2021

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Changes of serum growth factors (IGF-I,-II and IGFBP-2,-3) prior to and after stem cell transplantation in children with acute leukemia

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A selective inhibitor of the p110delta isoform of PI 3-kinase inhibits AML cell proliferation and survival and increases the cytotoxic effects of VP16

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10.1038/SJ.LEU.2404813

1 reference

Europe PubMed Central

PubMed publication ID

17 September 2017

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PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

17 September 2017

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