Advances in cancer genetics

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Advances in Cancer Genetics

Advances in Cancer Genetics could usher in sophisticated Drugs, but safety is key Concern

Breast Cancers are a diverse and deadly set of diseases that are the most common form of cancer in the UK today1. This is especially significant when you consider that women are the vast majority of sufferers (less than 1% occur in men) 2. Despite improvements over the past few decades, cancer treatments are still disappointingly ineffective, with 45-50% of patients developing resistance to treatments 3 and cancer survival relying largely upon early detection. Current chemotherapies damage healthy as well as cancerous tissue resulting in nasty side effects 3. This has led to a big demand for a new generation of cancer drugs that are more effective at killing cancer cells with out damaging healthy tissue. Herceptin (Trastuzumab), hailed as a ‘wonder drug' by the media, displayed unprecedented cancer killing credentials in clinical trials and the promise of the beginning of the end of breast cancer. Under pressure to get it to the market, NICE (National Institute for Clinical Excellence) ‘fast-tracked' Herceptin through the licensing process 5. However, longer term studies have shown this extremely expensive drug to be less effective than originally perceived and to cause some harmful side effects. Recent advances in genome sequencing of breast cancers could lead to a great increase in drugs like Herceptin, which could improve cancer treatment but pose a danger to patients if not properly tested.

Herceptin is a highly targeted treatment that works by binding to specific molecules on the surface of cancer cells to stop them dividing, ultimately causing them to die (fig.1). These are the HER-2 receptors and there are more of these than normal on cells of 20-25% of breast cancers 4. When used alongside traditional chemotherapy Herceptin can increase the chances of survival by 45-50% in patients with the most HER-2 on their cancer cells 3. This is a vast improvement on existing cancer treatments offering hope to patients, especially those in the advanced stages of the disease who have few treatment options. Based on this initial evidence, NICE approved the drug for use against advanced breast cancer, encouraged by the number of lives that could potentially be saved or prolonged 5. Herceptin has since proven to be effective at prolonging life 3,4 in a number of cases, justifying the fast-track to approval.

Figure 1. How Herceptin attacks cancer cells

However, longer term studies have exposed several problems with Herceptin that cast doubt over its true effectiveness. Most cancers that responded well initially, started growing again within a year 4 and only one trial has shown it to increase survival over four years 6. This resistance is probably due to changes in the interaction between Herceptin and HER-2, or by the cell compensating for the presence of Herceptin by using other signals to cause cell growth 4. On top of this, instances of heart failure of 6-8% occurred in recipients 3, an important risk factor in older patients. When you consider that the Norwich and Norfolk University Hospital would need £1.9 million just to buy the drug for 75 patients (excluding associated treatment costs) 6,7, it starts to represent poor value for money and other cancer sufferers are disadvantaged by the funding gap7.

It is likely that more highly specific drugs like Herceptin will become available as we learn more about the changes in the DNA that cause cells to become cancerous. A recent study used improved techniques to compare the DNA sequence of 24 different breast cancer cells 8. It showed that parts of DNA had been copied many times and/or moved around to other parts of the DNA structure, causing the cells to make too many copies of themselves 8. This work enables scientists to pinpoint what makes cancers different to healthy cells and to each other, providing a new level of detail with which targeted therapies can be developed. In some cancers, certain proteins are produced more than in others so drugs can be designed that exploit these differences to kill the cancer cells and leave the healthy ones. It may also be possible to determine how likely it is that a person will become resistant to a drug like Herceptin as changes in HER-2 will be detected 4.

A complete knowledge of the DNA of an individual patient's cancer cell could soon be a reality 9, allowing tailored cancer treatments that are highly specific to the patient. Although this is an excellent advance for cancer treatment, care must be taken to ensure that the mistakes of Herceptin are not repeated. Organisations like NICE have a responsibility to protect patients by ensuring each new drug produced is put through rigorous testing for safety and not rushed in to use, no matter how promising it initially appears.

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