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MDM2 antagonists induce p53-dependent apoptosis in AML: implications for leukemia therapy.
No induction of apoptosis was observed in AML samples harboring mutant p53, and p53 activation by targeting the p53-MDM2 interaction might offer a novel therapeutic strategy for AML that retain wild-type p53. Expand
UHRF1 overexpression drives DNA hypomethylation and hepatocellular carcinoma.
It is proposed that UHRF1 overexpression is a mechanism underlying DNA hypomethylation in cancer cells and that senescence is a primary means of restricting tumorigenesis due to epigenetic disruption. Expand
Results of the Phase I Trial of RG7112, a Small-Molecule MDM2 Antagonist in Leukemia
This phase I study of RG7112 provides proof-of-concept that MDM2 inhibition restores p53 function and generates clinical responses in hematologic malignancies and demonstrates clinical activity against relapsed/refractory AML and CLL/sCLL. Expand
Mdm2 inhibitor Nutlin-3a induces p53-mediated apoptosis by transcription-dependent and transcription-independent mechanisms and may overcome Atm-mediated resistance to fludarabine in chronic…
- K. Kojima, M. Konopleva, T. McQueen, S. O’Brien, W. Plunkett, M. Andreeff
- Biology, Medicine
- 1 August 2006
Results suggest that the nongenotoxic activation of p53 by targeting the Mdm2-p53 interaction provides a novel therapeutic strategy for CLL. Expand
Prognostic impact and targeting of CRM1 in acute myeloid leukemia.
Data suggest that CRM1 exerts an antiapoptotic function and is highly prognostic in AML, and a novel combinatorial approach is proposed aimed at maximal activation of p53-mediated apoptosis by concomitant MDM2 andCRM1 inhibition. Expand
The Novel Tryptamine Derivative JNJ-26854165 Induces Wild-Type p53- and E2F1-Mediated Apoptosis in Acute Myeloid and Lymphoid Leukemias
- K. Kojima, J. Burks, J. Arts, M. Andreeff
- Biology, Medicine
- Molecular Cancer Therapeutics
- 24 August 2010
The data suggest that JNJ-26854165 may provide a novel therapeutic approach for the treatment of acute leukemias because it synergizes with 1-β-arabinofuranosylcytosine or doxorubicin to induce p53-mediated apoptosis and may prevent the selection of p53 mutant subclones during therapy. Expand
Decreases in Ikaros activity correlate with blast crisis in patients with chronic myelogenous leukemia.
It is suggested that a reduction of Ikaros activity may be an important step in the development of blast crisis in CML and further evidence that mutations that alter Ikaro expression may contribute to human hematological malignancies is provided. Expand
FLJ10849, a septin family gene, fuses MLL in a novel leukemia cell line CNLBC1 derived from chronic neutrophilic leukemia in transformation with t(4;11)(q21;q23)
The results suggest that FLJ10849 might define a new septin family particularly involved in the pathogenesis of 11q23-associated leukemia, and the established cell line, CNLBC1, could provide a useful model for analyzing the pathogenic of MLL-septin leukemias and chronic neutrophilic leukemia. Expand
ATF4 induction through an atypical integrated stress response to ONC201 triggers p53-independent apoptosis in hematological malignancies
The results suggest that by inducing an atypical ISR and p53-independent apoptosis, ONC201 has clinical potential in hematological malignancies. Expand
The dual PI3 kinase/mTOR inhibitor PI-103 prevents p53 induction by Mdm2 inhibition but enhances p53-mediated mitochondrial apoptosis in p53 wild-type AML
It is suggested that PI-103 actively enhances downstream p53 signaling and that a combination strategy aimed at inhibiting PI3K/Akt/mTOR signaling and activating p53 signaled is potentially effective in AML, where TP53 mutations are rare and downstream p 53 signaling is intact. Expand