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Simplistically - the traditional thought was that Herceptin worked by decreasing the amount of HER 2 receptors on the surface of cells by binding with the receptor (and "disabling" it). Since Herceptin was bound and on the surface of the cells, it was further thought that the Herceptin (a foreign antibody) attracted killer T cells (a type of white blood cell) and the T cells would attack the Herceptin (which is attached to a cancer cell) and destroy both.
However - in this article the researchers are suggesting a different mechanism based on PTEN. PTEN up regulation stimulates p53 and other "cell death" regulators that are present in all cells but may be disabled in cancer cells. In a nutshell, this article is suggesting that Herceptin stimulates the cell to kill itself.
I hope this helps - it is more complicated than that because it is explained that one thing causes another thing which causes another thing which causes the cell to self destruct.
If you think about it, no matter which mechanism is right (the first or this new suggestion) the bottom line is cancer cell death.
Warm regards,
Becky
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