14 results on '"Bhalla, K N"'
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2. A phase Ib study of oral panobinostat (LBH589) administered with 5-azacitidine (5-Aza) in patients with myelodysplastic syndromes (MDS), chronic myelomonocytic leukemia (CMML), or acute myeloid leukemia (AML).
3. A phase I dose escalation study of AUY922, a novel HSP90 inhibitor, in patients with advanced solid malignancies
4. Nilotinib in patients with imatinib-resistant or -intolerant chronic myelogenous leukemia in chronic phase (CML-CP): Updated phase II results
5. Effect of pan-histone deacetylase inhibitor panobinostat (LBH589) on CXCR4 levels and signaling and on anti-leukemia activity in combination with CXCR4 antagonists
6. Depletion of HDAC7 and de-repression of Nur77: a mechanism for sensitivity of cutaneous lymphoma (CTCL) cells to pan- histone deacetylase inhibitor Panobinostat (LBH589)
7. Novel aurora kinases-targeted combination therapy for breast cancers
8. Minimal cross-intolerance between nilotinib and imatinib in patients with imatinib-intolerant chronic myelogenous leukemia (CML) in chronic phase (CP) or accelerated phase (AP)
9. Nilotinib in chronic myelogenous leukemia patients who failed prior imatinib and dasatinib therapy: Updated results of an open-label phase II study
10. Anti-leukemia activity of histone deacetylase (HDAC) inhibitor LBH589 involves depletion of EZH2 and DNA methyltransferase (DNMT) 1 through disruption of their chaperone association with heat shock protein (hsp) 90
11. Inhibition of histone deacetylase (HDAC) 6 sensitizes human leukemia and breast cancer cells to antagonists of heat shock protein (hsp) 90 and/or bortezomib (BZ)
12. Molecular mechanisms of underlying synergistic effect of combinations of histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) with docetaxel and trastuzumab against human breast cancer cells
13. A combination of histone deacetylase inhibitor LBH589 and the hsp90 inhibitor 17-AAG is highly active against human CML-BC and AML cells with constitutively active mutant FLT-3 tyrosine kinase
14. A combination of histone deacetylase inhibitor LBH589 and the hsp90 inhibitor 17-AAG is highly active against human CML-BC and AML cells with constitutively active mutant FLT-3 tyrosine kinase
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