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HER2 Receptor and Bcr-Abl

by Kevin Ahern, PhD
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    The next receptor I want to talk about is a special form of the human epidermal growth factor receptor called the HER2 receptor. Now, this receptor has mutation effects that affect its gene expression, not the actual protein itself. I need to tell you first a little bit about the receptor. Now HER2 is an unusual form of the epidermal growth factor receptor; there are many different epidermal growth factor receptors. Normally HER2 does not require EGF binding for dimerization and activation, meaning that two different monomer HER2 receptors, if they find each other can activate each other without EGF and cause the process of cell division to occur. Since HER2 is made at a very low level inside of cells, this normally isn’t a problem because it’s rare that the two individual monomers find each other to activate the process of cell division. So, however, there are mutations that happen to the control region for the expression of HER2, that if they happen will cause HER2 to be made in large quantities. Well when this happens, HER2 finds itself all the time. And since when it finds itself, and doesn’t require EGF, every time it finds a partner, it’s going to stimulate the process of cell division. That means that mutations that increase the quantity of HER2 are problematic. Now, mutations that increase the levels of HER2 are found in several types of cancer. It’s found actually in 15-30% of breast cancers. It’s found commonly in ovarian cancer, stomach cancer and also in uterine cancer. Now, fortunately this type of cancer is actually fairly easy to treat. It’s treated with a monoclonal antibody known as herceptin. And this treatment has revolutionized the treatment of cancers that affect HER2, because it has very few side effects and the way that...

    About the Lecture

    The lecture HER2 Receptor and Bcr-Abl by Kevin Ahern, PhD is from the course Hormones and Signal Transduction. It contains the following chapters:

    • HER2 Receptor
    • Other Mutations – Bcr-Abl

    Included Quiz Questions

    1. It is inhibited by Trastuzumab/Herceptin.
    2. It requires EGF to bind to it.
    3. It stimulates cells to divide when it is a monomer.
    4. All of the answers are true.
    5. None of the answers are true.
    1. It creates a tyrosine kinase that binds Gleevec differently from other tyrosine kinases.
    2. It is a tyrosine kinase that is more active than the Abl protein unmutated.
    3. It is treated with Gleevec, a GTPase inhibitor.
    4. All of the answers are true.
    5. None of the answers are true.

    Author of lecture HER2 Receptor and Bcr-Abl

     Kevin Ahern, PhD

    Kevin Ahern, PhD


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