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Goetz MP, Toft DO, Ames MM, Erlichman C: The Hsp90 chaperone complex as a novel target for cancer therapy. Ann Oncol 2003, 14:1169-1176.
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Ann Oncol
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Goetz, M.P.1
Toft, D.O.2
Ames, M.M.3
Erlichman, C.4
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50
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A high-affinity conformation of Hsp90 confers tumour selectivity on Hsp90 inhibitors
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Kamal A, Thao L, Sensintaffar J, et al.: A high-affinity conformation of Hsp90 confers tumour selectivity on Hsp90 inhibitors. Nature 2003, 425:407-410.7 This report provides an interesting explanation as to why tumors might be particularly susceptible to Hsp90 inhibitors.
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(2003)
Nature
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Kamal, A.1
Thao, L.2
Sensintaffar, J.3
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51
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0141925960
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FLT3 expressing leukemias are selectively sensitive to inhibitors of the molecular chaperone heat shock protein 90 through destabilization of signal transduction-associated kinases
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Yao Q, Nishiuchi R, Li Q, et al.: FLT3 expressing leukemias are selectively sensitive to inhibitors of the molecular chaperone heat shock protein 90 through destabilization of signal transduction-associated kinases. Clin Cancer Res 2003, 9:4483-4493. A different avenue of attack on aberrant FLT3 signaling is outlined here. This may represent a means to overcoming resistance to FLT3 kinase inhibitors.
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(2003)
Clin Cancer Res
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Yao, Q.1
Nishiuchi, R.2
Li, Q.3
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52
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Cotreatment with 17-allylaminodemethoxygeldanamycin and FLT-3 kinase inhibitor PKC412 is highly effective against human acute myelogenous leukemia cells with mutant FLT-3
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George P, Bali P, Cohen P, et al.: Cotreatment with 17- allylaminodemethoxygeldanamycin and FLT-3 kinase inhibitor PKC412 is highly effective against human acute myelogenous leukemia cells with mutant FLT-3. Cancer Res 2004, 64:3645-3652. Two small-molecule inhibitors of different proteins converge on the same target: FLT3.
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(2004)
Cancer Res
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George, P.1
Bali, P.2
Cohen, P.3
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53
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Superior activity of the combination of histone deacetylase inhibitor LAQ824 and the FLT-3 kinase inhibitor PKC412 against human acute myelogenous leukemia cells with mutant FLT-3
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Bali P, George P, Cohen P, et al.: Superior activity of the combination of histone deacetylase inhibitor LAQ824 and the FLT-3 kinase inhibitor PKC412 against human acute myelogenous leukemia cells with mutant FLT-3. Clin Cancer Res 2004, 10:4991-4997. Yet another means of molecularly targeting FLT3, by inducing its acetylation, is synergistic in vitro with an FLT3 kinase inhibitor.
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(2004)
Clin Cancer Res
, vol.10
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Bali, P.1
George, P.2
Cohen, P.3
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54
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Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell
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Bonnet D, Dick JE: Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell. Nat Med 1997, 3:730-737.
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Nat Med
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Bonnet, D.1
Dick, J.E.2
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55
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Stem cells, cancer, and cancer stem cells
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Reya T, Morrison SJ, Clarke MF, Weissman IL: Stem cells, cancer, and cancer stem cells. Nature 2001, 414:105-111.
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(2001)
Nature
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Reya, T.1
Morrison, S.J.2
Clarke, M.F.3
Weissman, I.L.4
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56
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Acute myeloid leukemia originates from a hierarchy of leukemic stem cell classes that differ in self-renewal capacity
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Hope KJ, Jin L, Dick JE: Acute myeloid leukemia originates from a hierarchy of leukemic stem cell classes that differ in self-renewal capacity. Nat Immunol 2004, 5:738-743. This report does not describe an inhibitor but rather the problem in AML, ie, of the existence of heterogeneous leukemia stem cells within a given patient. Any targeted approach in AML therapy will likely have to impact this cell population in order to be successful.
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(2004)
Nat Immunol
, vol.5
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Hope, K.J.1
Jin, L.2
Dick, J.E.3
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