Herceptin was supposed to be the miracle cure for breast cancer. Women have been willing to sell their houses in order to get hold of this vastly expensive drug. But behind the hype, the statistics tell another story. Herceptin kills more than cures and certainly fares poorly against a natural competitor: mistletoe.
The champagne corks were popping in Switzerland on 9 June, when the National Institute for Health and Clinical Excellence (NICE), the official British drug appraisal agency, announced that Herceptin (trastuzumab) would soon be approved for use in early-stage breast cancer. For Swiss pharmaceutical giant Roche, the incorporation of Herceptin into the British NHS system will be the final crowning glory of one of the most successful marketing campaigns in medical history.
In 1998, Roche bought the international marketing rights to Herceptin from the drug’s US manufacturer, Genentech. Over the last eight years, the orchestration of their joint public relations has been masterful—with newspaper headlines of a “wonder drug”,“a breakthrough treatment” and even a “cure”, and stories of people so desperate to get hold of Herceptin that they’ll sell the roof over their head to pay for it, and High Court battles to get the drug prescribed on the NHS.
How does it work?
So what’s so special about Herceptin; what’s all the fuss about?
The headlines have got it right in one respect. Herceptin is indeed a breakthrough in chemotherapy, but it could be argued that it’s about time we had one. The vast majority of chemo drugs are simply poisons, whose mode of action is to try and kill cancer cells before killing the rest of the healthy cells in the patient. Hardly 21st-century medicine.
Herceptin is different from a poison in that it’s claimed to specifically target breast cancer cells, by blocking some of the chemical signals they need in order to grow. There’s good evidence that some cancers, breast cancer in particular, are related to a gene called HER2. The term HER has nothing to do with the female gender; it stands for Human Epidermal growth factor Receptor, with the 2 meaning it’s the second one to be discovered.
Some breast cancers have been found to be correlated with an abnormally high level of HER2 genes in the body. When that happens, the gene “orders” an excess production of receptors on the surface of cancer cells. The receptors are the “ears” of the cell, picking up chemical signals from the rest of the body, and adjusting the cell’s growth accordingly. However, if there are too many receptors, as is the case in some breast cancers, the cells pick up too many growth signals, and start to multiply uncontrollably.
Herceptin works by attaching itself to the receptor “ears”, thus effectively blocking them up, and preventing the chemical “grow” signals from getting through. Roche’s marketing has stressed that, because Herceptin only attaches itself to HER2 breast cancer cells, it can’t theoretically affect other cells in the body. Thus it’s a true “breakthrough” in chemotherapy.
Targets other cells
So far so good. The problem, though, is that in practice Herceptin is not that specific. It turns out that other receptors besides breast cancer cells can get blocked by the drug. So far, the receptors that have been found to be damaged are those in the heart and lungs. Researchers at the prestigious Salk Institute have shown that Herceptin damages a gene called erbB2, which is intimately connected with heart and lung function. Interference with this gene can cause breathing problems, and damage heart muscle to the extent of actually compromising the pumping action, leading to heart failure (Recent Prog Horm Res, 2004; 59: 1–12).