Summary
Angiogenesis research is being translated to the clinic. Certain guidelines may facilitate
this effort. Recruitment of endothelial cells by a tumor is an early event in angiogenesis,
a process regulated at genetic and epigenetic levels. The microvascular endothelial
cell has become an important second target in cancer therapy. Angiogenesis inhibitors
are either “direct” or “indirect” and their optimal dosing depends on a different
logic than conventional chemotherapy. Conversely, antiangiogenic scheduling of chemotherapy
can by-pass drug resistance. Like all solid tumors, hematologic malignancies are angiogenesis-dependent.
Further, angiogenesis is modulated by proteins and cells from the hematopoietic and
hemostatic systems. Clinical testing of angiogenesis inhibitors has accentuated the
need for surrogate markers of tumor angiogenesis activity. Microvessel density, so
valuable as a prognostic indicator of metastatic risk, cannot determine efficacy of
an angiogenesis inhibitor. In the future, angiogenesis inhibitors may be added to
chemotherapy or to radiotherapy, or to other modalities. Also, combinations of angiogenesis
inhibitors may be administered together.
Key words
Angiogenesis - leukemia - antiangiogenic therapy - angiogenesis inhibitor