CANCER

Collaborative Damage

+ See all authors and affiliations

Science  30 Jan 2009:
Vol. 323, Issue 5914, pp. 563
DOI: 10.1126/science.323.5914.563b

The success of cancer as a disease is due in part to a collaborative effort between tumor cells and other populations of nonmalignant cells in the body. These nonmalignant cells, such as stromal fibroblasts and bone marrow-derived cells, have been shown to be capable of promoting tumor growth and metastasis. Tumor growth is fueled by the formation of new blood vessels in a process known as angiogenesis, which is stimulated by secreted peptides such as vascular endothelial growth factor A (VEGF-A). Antibodies to VEGF have been demonstrated to be effective anticancer agents in the clinic; however, tumor resistance arises rapidly, followed by patient relapse.

Crawford et al. looked at tumor-associated fibroblasts (TAFs) from a murine lymphoma model that was resistant to antibodies to VEGF. They found that these TAFs were able to stimulate the growth of anti-VEGF-sensitive tumors in vivo, suggesting that the tumor somehow regulates the tumorigenic properties of TAFs. Notably, this stimulation occurred even when VEGF was inhibited, implying that TAFs can influence how the tumor responds to being deprived of a major angiogenic factor. The authors found that TAFs from anti-VEGF-resistant tumors were also able to support angiogenesis, which was due to elevated expression of VEGF-A and another growth promoter, platelet-derived growth factor C (PDGF-C), pointing toward another target for the treatment of cancers (such as pancreatic cancer) that are relatively unresponsive to anti-VEGF therapies. — HP*

Cancer Cell 15, 21 (2009).

  • *Helen Pickersgill is a locum editor in Science's editorial department.

Navigate This Article