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Bridget Angus

BIOL 1615
Galvez
July 6, 2016
HER2 Phosphorylation Is Maintained by a PKB Negative Feedback Loop in Response to AntiHER2 Herceptin in Breast Cancer
Introduction:
HER2 is a protein in the Human Epidermal Growth Factor family; it is a receptor that is one of
the causes in breast cancer. A treatment called Herceptin was developed to help bind to the HER2
Receptors and stop phosphorylation, this was an effective treatment in most breast cancers.
However scientist wanted to test the ability of Herceptin and the phosphorylation on this certain
receptor. They already knew that it was a good treatment for HER2 Breast Cancer they needed to
find out if it would completely stop the phosphorylation of this receptor. There is not much
information so it is not understood why they decided to do this research one can only speculate
as to why. The testing showed that Herceptin was not the best treatment out there when used in
correlation with HER2 breast cancer patients.
Scientists were testing to see if phosphorylation in the HER2 genes were abolished and if this
same treatment using Herceptin would affect other receptors like HER3 another protein receptor
in the human epidermal growth factor family using ADAM17 inhibitors and PKB a negative
feedback loop.
They were testing to prove that eventually this treatment stopped working on HER2 gene. If we
were to find a better treatment for Breast Cancer it may lead to a Cure for it as well. It may not
mean something to some people, but it would mean change for several women currently fighting

breast cancer. That they may once and for all be cure of this disease and the fear that they may
have passed it on to their daughter or even sons would mean everything.
Scientist had two agendas; the first was the scientists were trying to find out why Herceptin did
not decrease HER2 Phosphorylation, and the secondary study was on the effects of acute
treatment with Herceptin on HER3 and PKB Phosphorylation.
Materials and Methods:
They used Western blot test, this gave some information but did not tell them the individual
phosphorylation. The second test they used was FERT this method allowed them to see the
phosphorylation. They used mouse genes to aid in the evaluation for this testing.
Results:
This study showed that Herceptin alone was not as effective after 8 months of testing in fact it
was resistant to it. In the other the testing it showed to have stopped phosphorylation on the
HER3 Receptors and PKB negative feedback loop. When Herceptin was used combined with
ADAM17 inhibitor it worked really well and phosphorylation did occur. It helped scientist to see
the defect in the current treatment for breast cancer.
Discussion:
Scientists showed that Herceptin alone did not cause phosphorylation it was when it was used in
combined with another Protein HER3 that it caused a negative feedback loop PKB and the
ADAM17 inhibitor enzyme it allowed phosphorylation to happen. The data collected did prove
what they set out to show and also allowed to prove a second point about adding another enzyme
along with the current treatment that this effect happens. They were limited with what the FDA
would allow, but there is no evidence of this.

Work Cited
Kumar, George L., PhD, and Sunil S. Badva, MD. "Milestones in the Discovery of HER2 ProtoOncogene and Trastuzumab (Herceptin)." (2008)
Gijsen, Merel, Peter King, Tim Perera, Peter J. Parker, Adrian L. Harris, Banafsh Larijani, and
Anthony Kong. "HER2 Phosphorylation Is Maintained by a PKB Negative Feedback

Loop in Response to Anti-HER2 Herceptin in Breast Cancer." PLoS Biology. Public


Library of Science, 21 Dec. 2010. Web. 06 July 2016.

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