Technology

Fingerprinting the circulating repertoire of antibodies from cancer patients. Mintz, P.J. et al. Nat. Biotechnol. 21 57–63 (2003)

The identification of molecular targets for use in anticancer therapy is an important goal. One approach to achieve this has been described in Nature Biotechnology. The authors used a phage display system to isolate peptides that are recognized by antibodies purified from the serum of patients with prostate cancer. A consensus motif from the GRP78 protein was shown to selectively bind to antibodies from cancer patients; this was also linked to disease progression and shorter survival of patients.

Oncogenes

Conditional activation of Neu in the mammary epithelium of transgenic mice results in reversible pulmonary metastasis. Moody, S.E. et al. Cancer Cell 2, 451–461 (2002)

Whether tumour progression can be reversed by inhibition of a single oncogene is an important question that is under debate. Moody et al. have investigated this with the Neu oncogene in transgenic mice, and show that even after mammary tumours have metastasized to the lungs, they can still be reversed by switching off the oncogene. However, following regression, most mice develop tumours that have progressed to a Neu-independent state, showing, yet again, the resilience of cancer.

Therapeutics

Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors. Casanova, M.L. et al. J. Clin. Invest. 111, 43–50 (2003)

Cannabinoids have previously been shown to inhibit the growth of gliomas, so Casanova et al. investigated whether they could have a similar effect on non-melanoma skin cancer — one of the most common tumour types. The cannabinoid receptors CB1 and CB2 are expressed in the skin, and their activation by a CB1/CB2 agonist results in apoptosis of tumorigenic skin cells, and growth inhibition and impaired angiogenesis of malignant tumours in nude mice.

Chemoprevention

Essential role of phosphatidylinositol 3-kinase-dependent CCAAT/enhancer binding protein-β activation in the induction of glutathione S -transferase by oltipraz. Kang, K.W. et al. J. Natl Cancer Inst. 95, 53–66 (2003)

The chemopreventive agent oltipraz acts by inducing glutathione S-transferase (GST), a detoxifying enzyme, but what mediates its transcription? The authors investigated the role of C/EBP in this, and found that oltipraz induces expression of GSTA2 by causing translocation of C/EBPβ to the nucleus and its binding to response elements in the promoter, in a PI3K-dependent manner.