Liquid tumors need blood

It is a widely accepted principle that angiogenesis is required for new tissue growth.  This is particularly true in cancer where numerous therapeutic approaches have been used to target tumor angiogenesis, thus effectively choking the tumor.  An interesting take on blocking angiogesis is that the endothelial cells, which are responsible for angiogenesis do not mutate, therefore drug resistance would not be a problem the way it is in the tumor which is always mutating. 

While it is conceptually easy to understand that solid tumors require angiogenesis, the question of "liquid tumors", such as leukemias requiring angiogenesis is interesting.  In a recent paper (Zhelyalzkova et al. Prognostic significance of hepatocyte growth factor and microvessel bone marrow density in patients with chronic myeloid leukaemia. Scand J Clin Lab Invest. 2008 Feb 18:1-9) the issue of angiogenesis in chronic myeloid leukemia (CML) was addressed. 

The investigators found that in contrast to healthy controls, patients with CML had higher density of microvessels in the bone marrow, and that bone marrow microvessel density correlated with stage of the disease.  Correlating with microvessel density was expression of the angiogenic molecule HGF.  Interestingly plasma VEGF was not associated with microvessel density or disease progression. 

Other studies have demonstrated that HGF is a potent angiogenic factor, with some level of therapeutic activity in critical limb ischemia and cardiac ischemia. 

It will be interesting to see what other molecules are associated with angiogenesis and stromal alterations in CML.  It may be that targeting of leukemia is more effective if the microenvironment is therapeutically modified.