De-amping the HER2 environment

A team from theUniversity of Pennsylvania School of Medicine and another from the Massachusetts General Hospital Cancer Centerand Cyclacel Pharmaceuticals Inc.have independently identified strategies to improve clinical outcomes for patients with HER2-positive breast cancers refractory to marketed drugs. The UPenn team is tackling a target called HUNK that is downstream of HER2,1 while the MGH group is blocking cyclin E, an amplified target in a related pathway.2

Amplification of HER2 (EGFR2; ERBB2; neu) occurs in about 20% of breast cancers and is associated with aggressive disease and decreased survival.3 In addition, many such tumors acquire-or start out with-resistance to HER2 inhibitors such as Herceptin trastuzumab, from the Genentech Inc. unit of Roche, and Tykerb lapatinib, a small molecule fromGlaxoSmithKline plc.

Lewis Chodosh and colleagues at UPenn have shown that an inhibitor of HUNK (hormonally up-regulated Neu-associated kinase; B19) might increase susceptibility to existing anti-HER2 therapeutics or could itself be an effective single agent.

The team also found that HUNK is required for the development and maintenance of tumors driven by HER2.

Chodosh is chairman of the Department of Cancer Biology at the

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