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Review
. 2007 Jan;76(1):8-17.

Chronic Myeloid Leukaemia in The 21st Century

Rachel Frazer  1 , Alexandra E Irvine, Mary Frances McMullin
Affiliations
Review

Chronic Myeloid Leukaemia in The 21st Century

Rachel Frazer et al. Ulster Med J. 2007 Jan.
No abstract available

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Figures

Figure 1
Figure 1
Molecular events leading to the expression of CML disease phenotype.
Figure 2
Figure 2
BCR-ABL signalling pathways.
Figure 3
Figure 3
Defining response to treatment and minimal residual disease, for patients diagnosed with chronic phase CML, treated with imatinib.
Fig 4
Fig 4
Comparing the mode of action of BCR-ABL and imatinib in CML pathogenesis.
Fig 5
Fig 5
Src signalling pathways. The Src protein has three functioning molecular domains. SH2 (SRC homology 2) and SH3 are involved in protein-protein interactions. The third, SH1 is a kinase catalytic domain. Src can transfer from inactive to active state through control of its phosphorylation state, or via protein-protein interactions. FAK (focal adhesion kinase) and PDGF (platelet derived growth factor) are capable of rendering Src active by binding to its SH2 domain. GPCR: G-protein coupled receptors EGF: epidermal growth factor
Figure 6
Figure 6
Targets for CML therapy.
Figure 7
Figure 7
CML therapeutic algorithm.
See this image and copyright information in PMC

References

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