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New hope for setback-dogged cancer treatment
Date:11/26/2012

Several drugs companies have ineffectively tried to produce antibodies that bind to the IGF-1 receptor on the cell surface, which has a critical part to play in the development of cancer. Scientists at Karolinska Institutet in Sweden have now ascertained how these antibodies work, and can explain why only some cancer patients are helped by IGF-1 blockers during clinical tests. The researchers also present a means by which drugs of this kind could help more cancer patients.

Every cell contains thousands of tiny receptors that help it communicate with other cells. These receptors are involved in countless physiological processes, such as taste and smell perception and heart rate. A couple of dozen of these receptors form their own family the kinase receptors (RTKs), which are implicated in cancer. The so-called IGF-1 receptor is particularly important for cancer cell survival, and as soon as this receptor encounters the right hormone (type 1 insulin-like growth factor, or IGF-1) into the cancer cell open a number of communication channels, helping it to grow, rapidly divide and protect itself against treatment.

Blocking this receptor with an antibody that binds to it and makes it inaccessible to IGF-1 has long been regarded as the key to a potential cancer therapy, the idea being that it will eventually lead to the death of the tumour cell. Several drugs companies have therefore been developing such antibodies in order to treat the most aggressive forms of cancer, and after some promising laboratory tests, have tested a number of these preparations on patients. However, the drugs have generally given disappointing results and helped only a small minority of patients (including children with Ewing's sarcoma), leading some companies to discontinue clinical trials focusing on the IGF-1 receptor.

The Karolinska Institutet team has now systematically analysed the different IGF-1-related triggered communication channels within a cancer ce
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Karolinska Institutet
Source:Eurekalert

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