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. Author manuscript; available in PMC: 2013 Jul 2.
Published in final edited form as: Br J Haematol. 2010 Jul 7;151(1):3–15. doi: 10.1111/j.1365-2141.2010.08262.x

Fig 1.

Fig 1

Multiple myeloma targets. New biological therapies may target extracellular ligands or other elements of the tumour microenvironment, cell surface or transmembrane receptors, or components of the intracellular signalling cascades. APAF-1, apoptotic protease activating factor 1; ERK, extracellular regulated kinase; FKHR, forkhead in rhabdomyosarcoma; HAT, histone acetyltransferase; HDAC, histone deacetylase; HSP90, heat shock protein 90; IAP, inhibitor of apoptosis protein; IGF-1, insulin-like growth factor-1; IL-6, interleukin-6; IRS-1, Insulin receptor substrate 1; MAPK, mitogen-activated protein kinase; MEK, mitogen-activated protein kinase kinase; TNF, tumour necrosis factor; TNFR1, tumour necrosis factor receptor 1; VEGF, vascular endothelial growth factor; JAK, Janus kinase; PI3K, phosphoinositol-3 kinase; NFKB, nuclear factor kappa B; STAT3, signal transducer and activator of transcription 3; mTOR, mammalian target of rapamycin; PKC, protein kinase C; PKD, protein kinase D.