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Epidermal growth factor receptor as a potential therapeutic target in triple-negative breast cancer. (Record no. 7478)

MARC details
000 -LEADER
fixed length control field 02229 am a2200193 4500
001 - CONTROL NUMBER
control field 2286
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
Terms of availability 0.00
040 ## - CATALOGING SOURCE
Original cataloging agency Annals of Oncology, Volume 20, Issue 5, Pages 862 - 7, 2009.
082 ## - DEWEY DECIMAL CLASSIFICATION NUMBER
Classification number PUBLICATIONS ARCHIVE CROW
100 ## - MAIN ENTRY--PERSONAL NAME
Personal name Crown, John
9 (RLIN) 34721
245 ## - TITLE STATEMENT
Title Epidermal growth factor receptor as a potential therapeutic target in triple-negative breast cancer.
260 ## - PUBLICATION, DISTRIBUTION, ETC.
Date of publication, distribution, etc. 2009.
490 ## - SERIES STATEMENT
Series statement Staff Publications
Volume/sequential designation Staff Publications- Crown, John
500 ## - GENERAL NOTE
General note The print version of this article is held in the Oncology Resource Centre (Box 1).
650 ## - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element BACKGROUND: No proven targeted therapy is currently available for the treatment of triple-negative breast cancer (TNBC). Epidermal growth factor receptor (EGFR) is frequently overexpressed in TNBC. We studied the activity of EGFR antagonists alone, and in combination with chemotherapy, in TNBC cell lines. MATERIALS AND METHODS: EGFR and phosphorylated EGFR were measured by enzyme-linked immunosorbent assay. Sensitivity to EGFR inhibitors alone and in combination with chemotherapy was assessed. Effects of gefitinib on EGFR signalling and cell cycle were also examined. RESULTS: EGFR was overexpressed in the TNBC compared with the human epidermal growth factor receptor 2 (HER-2)-positive cell lines. Phosphorylation of EGFR was detected in the TNBC cells in response to epidermal growth factor stimulation and was blocked by gefitinib treatment. However, the TNBC cell lines were less sensitive to EGFR inhibition than the HER-2-positive cell lines. Response to gefitinib was associated with reduced phosphorylation of both mitogen activated protein kinase (MAPK) and Akt and induction of G(1) arrest. Gefitinib enhanced response to both carboplatin and docetaxel in the TNBC cells, and the triple combination of gefitinib, carboplatin and docetaxel was synergistic. CONCLUSIONS: Although the TNBC cells are less sensitive to EGFR inhibition than the HER-2-positive cell lines, gefitinib enhanced response to chemotherapy. Gefitinib combined with carboplatin and docetaxel warrants further investigation in TNBC.
9 (RLIN) 35119
700 ## - ADDED ENTRY--PERSONAL NAME
Personal name Corkery, Bill
9 (RLIN) 35120
700 ## - ADDED ENTRY--PERSONAL NAME
Personal name Clynes, M.
9 (RLIN) 35121
710 ## - ADDED ENTRY--CORPORATE NAME
Corporate name or jurisdiction name as entry element ST. LUKE'S PUBLICATION ARCHIVE
9 (RLIN) 32511
Holdings
Withdrawn status Lost status Damaged status Not for loan Home library Current library Shelving location Date acquired Cost, normal purchase price Total Checkouts Full call number Barcode Date last seen Price effective from Koha item type
Not Withdrawn Not Lost Not Damaged Available for Loan St. Luke’s Radiation Oncology Network Dublin St. Luke’s Radiation Oncology Network Dublin AR 14/05/2018 0.00   PUBLICATIONS ARCHIVE CROW 39015000019805 14/05/2018 14/05/2018 2 Week Loan