High early growth response 1 (EGR1) expression correlates with resistance to anti-EGFR treatment in vitro and with poorer outcome in metastatic colorectal cancer patients treated with cetuximab

Clinical and Translational Oncology

Volumn 19, Issue 6, 2017, Pages 718-726

  Kumar, S S ^a,b   Tomita, Y ^a,b   Wrin, J ^a,b   Bruhn, M ^a   Swalling, A ^a   Mohammed, M ^a   Price, T J ^a,b   Hardingham, J E ^a,b  

^a QUEEN ELIZABETH HOSPITAL   (Australia)

^b UNIVERSITY OF ADELAIDE   (Australia)

Author keywords

Anti EGFR therapy; Colorectal cancer; EGR1; Predictive biomarker; Resistance

Indexed keywords

BIOLOGICAL MARKER; CETUXIMAB; EARLY GROWTH RESPONSE FACTOR 1; PROTEIN KINASE B; ANTINEOPLASTIC AGENT; EGFR PROTEIN, HUMAN; EGR1 PROTEIN, HUMAN; EPIDERMAL GROWTH FACTOR RECEPTOR; TUMOR MARKER;

ARTICLE; CELL PROLIFERATION; CELL PROLIFERATION ASSAY; GENE OVEREXPRESSION; GENE SILENCING; HUMAN; HUMAN CELL; HUMAN TISSUE; IMMUNOHISTOCHEMISTRY; METASTATIC COLORECTAL CANCER; PROTEIN EXPRESSION; REAL TIME POLYMERASE CHAIN REACTION; RNA INTERFERENCE; ANTAGONISTS AND INHIBITORS; BIOSYNTHESIS; COHORT ANALYSIS; COLORECTAL TUMOR; DRUG RESISTANCE; GENETICS; KAPLAN MEIER METHOD; MORTALITY; PILOT STUDY;

ANTINEOPLASTIC AGENTS; BIOMARKERS, TUMOR; CETUXIMAB; COHORT STUDIES; COLORECTAL NEOPLASMS; DRUG RESISTANCE, NEOPLASM; EARLY GROWTH RESPONSE PROTEIN 1; HUMANS; KAPLAN-MEIER ESTIMATE; PILOT PROJECTS; RECEPTOR, EPIDERMAL GROWTH FACTOR;

EID: 85006997794     PISSN: 1699048X     EISSN: 16993055     Source Type: Journal    
DOI: 10.1007/s12094-016-1596-8     Document Type: Article

References (25)

1. Roda D, Cervantes A. Biomarkers in colorectal cancer: the future is getting closer. Clin Transl Oncol. 2010;12(4):241–2. doi:10.1007/s12094-010-0498-4.
2. Karapetis CS, Khambata-Ford S, Jonker DJ, O’Callaghan CJ, Tu D, Tebbutt NC, et al. K-ras mutations and benefit from cetuximab in advanced colorectal cancer. N Engl J Med. 2008;359(17):1757–65.
3. Douillard J-Y, Oliner KS, Siena S, Tabernero J, Burkes R, Barugel M, et al. Panitumumab–FOLFOX4 treatment and RAS mutations in colorectal cancer. N Engl J Med. 2013;369(11):1023–34. doi:10.1056/NEJMoa1305275.
4. Clarke SJ, Karapetis CS, Gibbs P, Pavlakis N, Desai J, Michael M, et al. Overview of biomarkers in metastatic colorectal cancer: tumour, blood and patient-related factors. Crit Rev Oncol/Hematol. 2013;85(2):121–35.
5. Peeters M, Oliner KS, Parker A, Siena S, Van Cutsem E, Huang J, et al. Massively parallel tumor multigene sequencing to evaluate response to panitumumab in a randomized phase III study of metastatic colorectal cancer. Clin Cancer Res. 2013;19(7):1902–12. doi:10.1158/1078-0432.ccr-12-1913.
6. Misale S, Di Nicolantonio F, Sartore-Bianchi A, Siena S, Bardelli A. Resistance to anti-EGFR therapy in colorectal cancer: from heterogeneity to convergent evolution. Cancer Discov. 2014;4(11):1269–80. doi:10.1158/2159-8290.CD-14-04622159-8290.CD-14-0462.
7. Zhou M, Yu P, Hou K, Fu L, Chen Y, Qu J, et al. Effect of RAS status on anti-EGFR monoclonal antibodies +5-FU infusion-based chemotherapy in first-line treatment of metastatic colorectal cancer: a meta-analysis. Meta Gene. 2016;9:110–9. doi:10.1016/j.mgene.2016.05.001.
8. Pietrantonio F, Petrelli F, Coinu A, Di Bartolomeo M, Borgonovo K, Maggi C, et al. Predictive role of BRAF mutations in patients with advanced colorectal cancer receiving cetuximab and panitumumab: a meta-analysis. Eur J Cancer. 2015;51(5):587–94.
9. Bronte G, Silvestris N, Castiglia M, Galvano A, Passiglia F, Sortino G, et al. New findings on primary and acquired resistance to anti-EGFR therapy in metastatic colorectal cancer: do all roads lead to RAS? Oncotarget. 2015;6(28):24780–96.
10. Van Cutsem E, Cervantes A, Adam R, Sobrero A, Van Krieken JH, Aderka D, et al. ESMO consensus guidelines for the management of patients with metastatic colorectal cancer. Ann Oncol. 2016;. doi:10.1093/annonc/mdw235.
11. Karapetis CS, Jonker D, Daneshmand M, Hanson JE, O’Callaghan CJ, Marginean C, et al. PIK3CA, BRAF, and PTEN status and benefit from cetuximab in the treatment of advanced colorectal cancer—results from NCIC CTG/AGITG CO.17. Clin Cancer Res. 2014;20(3):744–53. doi:10.1158/1078-0432.ccr-13-0606.
12. Sree Kumar S, Price TJ, Townsend A, Hocking C, Hardingham JE. Predictive biomarkers of response to anti-EGF receptor monoclonal antibody therapies. Colorectal Cancer. 2014;3:223–32.
13. Siu L, Shapiro J, Jonker D, Karapetis C, Zalcberg J, Simes J et al. Phase III randomized trial of cetuximab (CET) plus either brivanib alaninate (BRIV) or placebo in patients (pts) with metastatic (MET) chemotherapy refractory K-RAS wild-type (WT) colorectal carcinoma (CRC): The NCIC Clinical Trials Group and AGITG CO.20 trial. J Clin Oncol. 2012;30(4 (suppl)):386.
14. Jhawer M, Goel S, Wilson AJ, Montagna C, Ling YH, Byun DS, et al. PIK3CA mutation/PTEN expression status predicts response of colon cancer cells to the epidermal growth factor receptor inhibitor cetuximab. Cancer Res. 2008;68(6):1953–61.
15. Miyata K, Yotsumoto F, Nam S, Kuroki M, Miyamoto S. Regulatory mechanisms of the HB-EGF autocrine loop in inflammation, homeostasis, development and cancer. Anticancer Res. 2012;32(6):2347–52.
16. Topham C, Tighe A, Ly P, Bennett A, Sloss O, Nelson L, et al. MYC is a major determinant of mitotic cell fate. Cancer Cell. 2015;28(1):129–40. doi:10.1016/j.ccell.2015.06.001.
17. Agarwal E, Brattain MG, Chowdhury S. Cell survival and metastasis regulation by Akt signalling in colorectal cancer. Cell Signal. 2013;25(8):1711–9. doi:10.1016/j.cellsig.2013.03.025.
18. Mahalingam D, Natoni A, Keane M, Samali A, Szegezdi E. Early growth response-1 is a regulator of DR5-induced apoptosis in colon cancer cells. Br J Cancer. 2010;102(4):754–64. doi:http://www.nature.com/bjc/journal/v102/n4/suppinfo/6605545s1.html.
19. Hong Y, Ho KS, Eu KW, Cheah PY. A susceptibility gene set for early onset colorectal cancer that integrates diverse signaling pathways: implication for tumorigenesis. Clin Cancer Res. 2007;13(4):1107–14. doi:10.1158/1078-0432.CCR-06-1633.
20. Song LJ, Liu RJ, Zeng Z, Alper SL, Cui HJ, Lu Y et al. Gastrin inhibits a novel, pathological colon cancer signaling pathway involving EGR1, AE2, and P-ERK. J Mol Med (Berlin, Germany). 2012;90(6):707–18. doi:10.1007/s00109-011-0851-2.
21. Scaltriti M, Baselga J. The epidermal growth factor receptor pathway: a model for targeted therapy. Clin Cancer Res. 2006;12(18):5268–72. doi:10.1158/1078-0432.ccr-05-1554.
22. Kavuri SM, Jain N, Galimi F, Cottino F, Leto SM, Migliardi G, et al. HER2 activating mutations are targets for colorectal cancer treatment. Cancer Discov. 2015;5(8):832–41. doi:10.1158/2159-8290.cd-14-1211.
23. Cushman SM, Jiang C, Hatch AJ, Shterev I, Sibley AB, Niedzwiecki D, et al. Gene expression markers of efficacy and resistance to cetuximab treatment in metastatic colorectal cancer: results from CALGB 80203 (alliance). Clin Cancer Res. 2015;21(5):1078–86. doi:10.1158/1078-0432.CCR-14-2313.
24. Bigatto V, De Bacco F, Casanova E, Reato G, Lanzetti L, Isella C, et al. TNF-α promotes invasive growth through the MET signaling pathway. Mol Oncol. 2015;9(2):377–88. doi:10.1016/j.molonc.2014.09.002.
25. Zwang Y, Oren M, Yarden Y. Consistency test of the cell cycle: roles for p53 and EGR1. Cancer Res. 2012;72(5):1051–4. doi:10.1158/0008-5472.can-11-3382.