Flies help understand why cancer patients waste away
Cancer is one of the main causes of death in industrialized societies. With a lifetime risk of a cancer diagnosis of around 40% in the US, cancer affects every one of us. More than 80% of terminal cancer patients develop a form of tissue wasting called cachexia, which amounts to 20% of total cancer deaths. Cachexia results in a loss of muscles and fat in patients. This loss makes the patients weaker and results in increased risk of respiratory failure and susceptibility to chemotherapy toxicity.
The underlying mechanism of cachexia is still not understood, but it is more often associated with certain cancers. Simply boosting dietary intake is not enough to avoid cachexia-induced wasting and thus it is not easily reversable.
In a recently published study (Figueroa-Clarevega and Bilder, 2015) from the laboratory of David Bilder at the University of California, Berkeley, USA, Figueroa-Clarevega and colleagues investigated the mechanisms inducing cachexia in flies. The authors transplanted different kinds of tumors into healthy flies and noticed cachexia occurred only upon transplanting of cancerous, but not benign tumors. This phenomenon was independent of the implanted tumor size, suggesting cachexia is controlled by intrinsic properties of the tumor rather than by the sheer size of the tumor itself.
The authors compared the genetic activity of cancerous versus benign tumors and noticed that cancerous ones had increased levels of a protein called Impl2. Impl2 is known to downregulate insulin signaling and is conserved in humans. The authors induced production of Impl2 independently of tumors and found that cachexia affected these flies. The authors also blocked Impl2 in the transplanted tumors and found that this prevented cachexia.
Overall, this study provided a functional example of how cachexia develops in flies, paving a direction for further studies in humans. A simple model animal like Drosophila can be very useful for quickly characterizing these disease mechanisms and facilitates research in human health.
Citation: Figueroa-Clarevega, A. and Bilder, D. (2015) ‘Malignant drosophila tumors interrupt insulin signaling to induce cachexia-like wasting’, Developmental Cell. Elsevier Inc., 33(1), pp. 47–56. doi: 10.1016/j.devcel.2015.03.001.
The underlying mechanism of cachexia is still not understood, but it is more often associated with certain cancers. Simply boosting dietary intake is not enough to avoid cachexia-induced wasting and thus it is not easily reversable.
In a recently published study (Figueroa-Clarevega and Bilder, 2015) from the laboratory of David Bilder at the University of California, Berkeley, USA, Figueroa-Clarevega and colleagues investigated the mechanisms inducing cachexia in flies. The authors transplanted different kinds of tumors into healthy flies and noticed cachexia occurred only upon transplanting of cancerous, but not benign tumors. This phenomenon was independent of the implanted tumor size, suggesting cachexia is controlled by intrinsic properties of the tumor rather than by the sheer size of the tumor itself.
The authors compared the genetic activity of cancerous versus benign tumors and noticed that cancerous ones had increased levels of a protein called Impl2. Impl2 is known to downregulate insulin signaling and is conserved in humans. The authors induced production of Impl2 independently of tumors and found that cachexia affected these flies. The authors also blocked Impl2 in the transplanted tumors and found that this prevented cachexia.
Overall, this study provided a functional example of how cachexia develops in flies, paving a direction for further studies in humans. A simple model animal like Drosophila can be very useful for quickly characterizing these disease mechanisms and facilitates research in human health.
Citation: Figueroa-Clarevega, A. and Bilder, D. (2015) ‘Malignant drosophila tumors interrupt insulin signaling to induce cachexia-like wasting’, Developmental Cell. Elsevier Inc., 33(1), pp. 47–56. doi: 10.1016/j.devcel.2015.03.001.