Loss or Inhibition of Stromal-Derived PlGF Prolongs Survival of Mice with Imatinib-Resistant Bcr-Abl1+ Leukemia

(Cancer Cell 19, 740–753; June 14, 2011) In the originally published version of this article, during final figure preparation the authors inadvertently selected an incorrect western blot image for Figure 3C (lower right; p65 blot for BMSC + CML). The blot image for phospho-p65 was mistakenly copied into the p65 panel. The densitometric quantification of band intensities was based on the correct blot images. The correction to the image in Figure 3C does not affect the conclusions of the paper. The authors apologize for any confusion or inconvenience that this oversight may have caused. Loss or Inhibition of Stromal-Derived PlGF Prolongs Survival of Mice with Imatinib-Resistant Bcr-Abl1+ LeukemiaSchmidt et al.Cancer CellJune 14, 2011In BriefImatinib has revolutionized the treatment of Bcr-Abl1+ chronic myeloid leukemia (CML), but, in most patients, some leukemia cells persist despite continued therapy, while others become resistant. Here, we report that PlGF levels are elevated in CML and that PlGF produced by bone marrow stromal cells (BMSCs) aggravates disease severity. CML cells foster a soil for their own growth by inducing BMSCs to upregulate PlGF, which not only stimulates BM angiogenesis, but also promotes CML proliferation and metabolism, in part independently of Bcr-Abl1 signaling. Full-Text PDF Open Archive