TY  - GEN
AB  - The HER2+ subtype of breast cancer typically results from amplification of the proto-oncogene ERBB2, that causes overexpression of the mitogenic cell surface receptor kinase HER2. Absent targeted therapies, this subtype is one of the most aggressive and invasive of all the breast cancer subtypes. However, because overexpressed HER2 is often the key oncogenic driver in this subtype, it has been a successful target for clinical agents that inhibit it specifically. Trastuzumab, pertuzumab, T-DM1, and lapatinib, are all FDA approved drugs that have significantly improved progression-free survival in HER2+ patients. Despite this, long term survival benefits have been hampered by de novo or emergent resistance to these targeted agents. While cell-intrinsic secondary mutations that result in drug tolerance have been well studied, the less well understood and remarkably complex cell-extrinsic tumor microenvironment has shown a substantial capacity to cause drug resistance in otherwise drug sensitive tumor cells.
AU  - Watson, Spencer S.
DA  - 2017
DO  - 10.6083/m43n22wj
DO  - DOI
ID  - 7609
KW  - Tumor Microenvironment
KW  - Drug Resistance
KW  - breast cancer
L1  - https://digitalcollections.ohsu.edu/record/7609/files/Watson.Spencer.2017.pdf
L2  - https://digitalcollections.ohsu.edu/record/7609/files/Watson.Spencer.2017.pdf
L4  - https://digitalcollections.ohsu.edu/record/7609/files/Watson.Spencer.2017.pdf
LK  - https://digitalcollections.ohsu.edu/record/7609/files/Watson.Spencer.2017.pdf
N2  - The HER2+ subtype of breast cancer typically results from amplification of the proto-oncogene ERBB2, that causes overexpression of the mitogenic cell surface receptor kinase HER2. Absent targeted therapies, this subtype is one of the most aggressive and invasive of all the breast cancer subtypes. However, because overexpressed HER2 is often the key oncogenic driver in this subtype, it has been a successful target for clinical agents that inhibit it specifically. Trastuzumab, pertuzumab, T-DM1, and lapatinib, are all FDA approved drugs that have significantly improved progression-free survival in HER2+ patients. Despite this, long term survival benefits have been hampered by de novo or emergent resistance to these targeted agents. While cell-intrinsic secondary mutations that result in drug tolerance have been well studied, the less well understood and remarkably complex cell-extrinsic tumor microenvironment has shown a substantial capacity to cause drug resistance in otherwise drug sensitive tumor cells.
PB  - Oregon Health and Science University
PY  - 2017
T1  - Microenvironment mediated resistance to her2 targeted therapeutics in her2+ breast cancer
TI  - Microenvironment mediated resistance to her2 targeted therapeutics in her2+ breast cancer
UR  - https://digitalcollections.ohsu.edu/record/7609/files/Watson.Spencer.2017.pdf
Y1  - 2017
ER  -