About 30% of breast cancer patients have tumours that show rapid growth and invasion through the body. A common denominator in all of these cases is the presence of a large number of Her2 proteins in tumour cellular membranes. Consequently, these aggressive tumours are referred to as HER2+. Scientists working in the Metastasis Laboratory (MetLab) at IRB Barcelona headed by ICREA researcher Roger Gomis, have described the molecular mechanism that induces HER2+ tumours to ignore the signals that protect cells from excessive growth. The study is published this week in the specialized journal Cancer Research.
Certain external molecules bind to the Her family proteins, thus instructing the cell to divide. However, when cells have multiple copies of the Her2 gene, as is the case of HER2+ patients, they show uncontrolled division and do not respect the signals from their milieu. The prospects for HER2+ patients changed dramatically about ten years ago when the drug Herceptin came onto the market. This agent binds to Her2 to inhibit its proliferative activity, thereby leading to an improved prognosis and greater survival.
LIP disobeys the body's defense system
When cells detect potential harm, they activate a series of protective responses which often lead to cell death or senescence (no growth). All these mechanisms are systems through which the cell can avoid the irreversible errors that lead them to generate tumours. This explains why tumour cells are removed from the body and replaced by healthy ones. In this context, tumour suppression mechanisms are of particular relevance, among these that induced by the hormone TGF-β and the senescence caused by genes that contribute to the development of malignant cells (OIS).
Through experiments using metastatic cells from patients and animal models, the researchers have discovered that Her2 not only accelerates cell division but also evades these cell arrest systems. He
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| Contact: Nuria Noriega nuria.noriega@irbbarcelona.org Institute for Research in Biomedicine (IRB Barcelona) Source:Eurekalert |
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