Loss of Imprinting of Human Insulin-like Growth Factor II Gene, IGF2, in Acute Myeloid Leukemia

1997 ◽  
Vol 231 (2) ◽  
pp. 466-472 ◽  
Author(s):  
Hua-Kang Wu ◽  
Rosanna Weksberg ◽  
Mark D. Minden ◽  
Jeremy A. Squire
Keyword(s):  
Acute Myeloid Leukemia ◽  
Growth Factor ◽  
Human Insulin ◽  
Myeloid Leukemia ◽  
Insulin Like Growth Factor ◽  
Loss Of Imprinting ◽  
Factor Ii ◽  
Acute Myeloid

scholarly journals Concordant Loss of Imprinting of the Human Insulin-like Growth Factor II Gene Promoters in Cancer

1995 ◽  
Vol 270 (47) ◽  
pp. 27983-27986 ◽  
Author(s):  
Shili Zhan ◽  
David Shapiro ◽  
Shixing Zhan ◽  
Lijuan Zhang ◽  
Steven Hirschfeld ◽  
...  
Keyword(s):  
Growth Factor ◽  
Human Insulin ◽  
Gene Promoters ◽  
Insulin Like Growth Factor ◽  
Loss Of Imprinting ◽  
Factor Ii

Impact of insulin-like growth factor 1 and insulin-like growth factor binding proteins on outcomes in acute myeloid leukemia

2015 ◽  
Vol 56 (11) ◽  
pp. 3135-3142 ◽  
Author(s):  
Reem Karmali ◽  
Melissa L. Larson ◽  
Jamile M. Shammo ◽  
Sanjib Basu ◽  
Kent Christopherson ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Growth Factor ◽  
Myeloid Leukemia ◽  
Binding Proteins ◽  
Insulin Like Growth Factor ◽  
Factor Binding ◽  
Acute Myeloid

Mammalian target of rapamycin (mTOR) inhibition activates phosphatidylinositol 3-kinase/Akt by up-regulating insulin-like growth factor-1 receptor signaling in acute myeloid leukemia: rationale for therapeutic inhibition of both pathways

Blood ◽  
2008 ◽  
Vol 111 (1) ◽  
pp. 379-382 ◽  
Author(s):  
Jerome Tamburini ◽  
Nicolas Chapuis ◽  
Valérie Bardet ◽  
Sophie Park ◽  
Pierre Sujobert ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Growth Factor ◽  
Myeloid Leukemia ◽  
Insulin Like Growth Factor ◽  
Phosphatidylinositol 3 Kinase ◽  
Akt Phosphorylation ◽  
Akt Activation ◽  
Blast Cells ◽  
Acute Myeloid ◽  
Phosphatidylinositol 3

The phosphatidylinositol 3-kinase (PI3K)/Akt and mTORC1 pathways are frequently activated, representing potential therapeutic targets in acute myeloid leukemia (AML). In 19 AML samples with constitutive PI3K/Akt activation, the rapamycin derivative inhibitor everolimus (RAD001) increased Akt phosphorylation. This mTOR C1-mediated Akt up-regulation was explained by an insulin-like growth factor-1 (IGF-1)/IGF-1 receptor autocrine loop: (1) blast cells expressed functional IGF-1 receptors, and IGF-1-induced Akt activation was increased by RAD001, (2) a neutralizing anti-IGF-1R α-IR3 monoclonal antibody reversed the RAD001-induced Akt phosphorylation, and (3) autocrine production of IGF-1 was detected in purified blast cells by quantitative reverse transcription-polymerase chain reaction and immunofluorescence. This RAD001-induced PI3K/Akt up-regulation was due to an up-regulated expression of the IRS2 adaptor. Finally, we observed that concomitant inhibition of mTORC1 and PI3K/Akt by RAD001 and IC87114 induced additive antiproliferative effects. Our results suggest that dual inhibition of the mTORC1 complex and the IGF-1/IGF-1R/PI3K/Akt pathway in AML may enhance the efficacy of mTOR inhibitors in treatment of this disease.

Impact of circulating members of the insulin-like growth factor receptor (IGF-1R) axis on outcomes in acute myeloid leukemia.

2014 ◽  
Vol 32 (15_suppl) ◽  
pp. 7069-7069 ◽  
Author(s):  
Reem Karmali ◽  
Jeffrey Allen Borgia ◽  
Melissa L. Larson ◽  
Jamile M. Shammo ◽  
Sanjib Basu ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Growth Factor ◽  
Myeloid Leukemia ◽  
Growth Factor Receptor ◽  
Insulin Like Growth Factor ◽  
Acute Myeloid

SUMOylation of insulin-like growth factor 1 receptor, promotes proliferation in acute myeloid leukemia

2015 ◽  
Vol 357 (1) ◽  
pp. 297-306 ◽  
Author(s):  
Jian Zhang ◽  
Fang-Fang Huang ◽  
Deng-Shu Wu ◽  
Wen-Jin Li ◽  
Hui-En Zhan ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Growth Factor ◽  
Myeloid Leukemia ◽  
Insulin Like Growth Factor ◽  
Acute Myeloid
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