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Poster display session: Basic science, Endocrine tumours, Gastrointestinal tumours - colorectal & non-colorectal, Head and neck cancer (excluding thyroid), Melanoma and other skin tumours, Neuroendocrine tumours, Thyroid cancer, Tumour biology & pathology

4287 - Retrospective RAS Analysis of the EPIC Trial: Cetuximab Plus Irinotecan vs Irinotecan in Patients (pts) With Second-Line Metastatic Colorectal Cancer (mCRC)

Date

21 Oct 2018

Session

Poster display session: Basic science, Endocrine tumours, Gastrointestinal tumours - colorectal & non-colorectal, Head and neck cancer (excluding thyroid), Melanoma and other skin tumours, Neuroendocrine tumours, Thyroid cancer, Tumour biology & pathology

Topics

Immunotherapy;  Translational Research

Tumour Site

Colon and Rectal Cancer

Presenters

Alberto Sobrero

Citation

Annals of Oncology (2018) 29 (suppl_8): viii150-viii204. 10.1093/annonc/mdy281

Authors

A. Sobrero1, H.J. Lenz2, C. Eng3, W. Scheithauer4, G. Middleton5, W. Chen6, R. Esser7, J. Nippgen8, H. Burris9

Author affiliations

  • 1 Medical Oncology, Policlinico San Martino IRCCS, 16132 - Genova/IT
  • 2 Medical Oncology, University of Southern California, Los Angeles/US
  • 3 Department Of Gastrointestinal Medical Oncology, M. D. Anderson Cancer Center, Houston/US
  • 4 Clinical Department Of Oncology, Medical University of Vienna, Vienna/AT
  • 5 Institute Of Immunology And Immunotherapy, University of Birmingham, Birmingham/GB
  • 6 R&d Global Biostatistics & Epidemiology, EMD Serono, Beijing/CN
  • 7 Global Medical Affairs Oncology, Merck KGaA, Darmstadt/DE
  • 8 Medical Oncology, Merck KGaA, Darmstadt/DE
  • 9 Drug Development, Tennessee Oncology, Nashville/US

Resources

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Abstract 4287

Background

The multicenter, open-label, randomized, phase 3 EPIC study (EMR 062202-025) investigated the addition of cetuximab to irinotecan vs irinotecan in pts with EGFR-expressing mCRC who had previously progressed on first-line fluoropyrimidine- and oxaliplatin-based chemotherapy. The primary endpoint was overall survival (OS). We present the extended RAS analysis (KRAS/NRAS exons 2, 3, and 4) for the EPIC study population.

Methods

1298 RAS-unselected pts were enrolled from May 2003 to February 2006. Existing DNA samples were reanalyzed using BEAMing (beads, emulsion, amplification, magnetics) technology. RAS wild-type (wt) status was defined as having all alleles be analyzable and a sum of RAS mutations of ≤ 5%. Baseline characteristics, efficacy, safety, and post-study therapy were assessed. 10.3% had no RAS data available.

Results

Among the 452 (231 in the cetuximab + irinotecan arm and 221 in the irinotecan arm) pts with RAS wt mCRC, baseline characteristics were comparable to those of the unselected population. 67.5% had 1 prior line of therapy. In the cetuximab + irinotecan vs irinotecan arms, median progression-free survival (PFS) was 5.4 vs 2.6 months (HR, 0.57 [95% CI, 0.46-0.69]; P < .0001), median OS was 12.3 vs 12.0 months (HR, 0.91 [95% CI, 0.71-1.17; P = .4645]), and overall response rate (ORR) was 29.4% vs 5.0% (OR, 8.12 [95% CI, 4.04-17.40]; P < .0001), respectively. 76.4% and 61.8% of pts in the cetuximab + irinotecan vs irinotecan arms, respectively, experienced a grade ≥ 3 adverse event. 47.1% of pts in the irinotecan arm received cetuximab in a subsequent line of therapy vs 11.3% in the cetuximab + irinotecan arm.

Conclusions

This retrospective analysis confirms that cetuximab-based therapy is suitable as a standard, second-line treatment for pts with RAS wt mCRC. Specifically, the addition of cetuximab to irinotecan significantly improved PFS and ORR in this population. A large proportion of pts in the irinotecan arm crossed over to receive post-study cetuximab, potentially masking any OS benefit of the addition of cetuximab to irinotecan in this study. Benefits appear clinically relevantly higher than for pts with RAS-unselected or KRAS wt mCRC.

Clinical trial identification

EMR 062202-025.

Legal entity responsible for the study

Merck KGaA.

Funding

Merck KGaA.

Editorial Acknowledgement

Medical writing support was provided by ClinicalThinking, and was funded by Merck KGaA, Darmstadt, Germany.

Disclosure

R. Esser: Employee, stock ownership: Merck KGaA. J. Nippgen: Employee: Merck KGaA. H. Burris: Consultancy (Includes expert testimony): Mersana, AstraZeneca, Forma, Janssen, Novartis, Roche/Genentech, TG Therapeutics, Medimmune, Bristol-Myers Squibb; Research funding: Roche/Genentech, Bristol-Myers Squibb, Incyte, Tarveda Therapeutics, Mersana, AstraZeneca, Medimmune, Macrogenics, Novartis, Boehringer Ingelheim, Lilly, Seattle Genetics, Abbvie, Bayer, Celldex, Merck, Celgene, Agios, Jounce Therapeutics, Moderna Therapeutics, CytomX Therapeutics, GlaxoSmithKline, Verastem, Tesaro, Immunocore, Takeda, millennium, BioMed Valley Discoveries, Pfizer, PTC Therapeutics, TG Therapeutics, Loxo, Vertex, eFFECTOR Therapeutics, Janssen, Gilead Sciences, Valent Technologies. All other authors have declared no conflicts of interest.

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