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Poster display session

3085 - Sequential therapy with bevacizumab and epidermal growth factor receptor-directed agents for metastatic colorectal carcinoma: a retrospective, registry-based analysis

Date

09 Sep 2017

Session

Poster display session

Topics

Cytotoxic Therapy;  Colon and Rectal Cancer

Presenters

Tomas Buchler

Citation

Annals of Oncology (2017) 28 (suppl_5): v158-v208. 10.1093/annonc/mdx393

Authors

T. Buchler1, R. Chloupkova2, A. Poprach3, O. Fiala4, I. Kiss3, K. Kopeckova5, L. Dusek2, L. Slavicek6, M. Kohoutek7, J. Finek8, M. Svoboda3, L. Petruzelka9, B. Melichar10

Author affiliations

  • 1 Department Of Oncology, First Faculty of Medicine, Charles University and Thomayer University Hospital, 14059 - Prague/CZ
  • 2 Institute Of Biostatistics And Analyses, Masaryk University, Brno/CZ
  • 3 Department Of Comprehensive Cancer Care, Masaryk Memorial Cancer Institute and Masaryk University Faculty of Medicine, 65653 - Brno/CZ
  • 4 Department Of Oncology, University Hospital Plzen and Faculty of Medicine in Pilsen, Charles University, 30460 - Plzen/CZ
  • 5 Department Of Oncology, Motol University Hospital and Second Faculty of Medicine, Charles University, 15006 - Prague/CZ
  • 6 Department Of Oncology, Hospital Jihlava, 58633 - Jihlava/CZ
  • 7 Department Of Oncology, T Bata's Regional Hospital, 762 75 - Zlin/CZ
  • 8 Department Of Oncology, University Hospital Plzen and Faculty of Medicine in Pilsen, Charles University, 30133 - Plzen/CZ
  • 9 Department Of Oncology, First Faculty of Medicine, Charles University and General University Hospital, 128 08 - Prague/CZ
  • 10 Department Of Oncology, Palacky University Medical School and Teaching Hospital, Olomouc, Olomouc/CZ
More

Resources

Abstract 3085

Background

Although bevacizumab and monoclonal antibodies directed against epidermal growth factor receptor (EGFR) cetuximab and panitumumab are commonly used in the treatment of metastatic colorectal cancer (mCRC) without activating RAS mutations, the optimal sequencing of these agents is currently unclear.

Methods

A national registry of targeted therapies was used to analyse baseline characteristics and outcomes of patients with mCRC who received bevacizumab followed by antiEGFR agents or a reverse sequence as first- and second-line treatment. The cohort for analysis included all patients with valid data in the registry who met the following inclusion criteria: a) sequential therapy with first-line cetuximab or panitumumab and second-line bevacizumab or first-line bevacizumab and second-line cetuximab or panitumumab; b) progression documented in the database between the first and the second line; c) first-line therapy using FOLFOX or FOLFIRI regimens as chemotherapy backbone; and d) wild-type KRAS status and wild-type or unknown NRAS status.

Results

The cohort included 490 patients; 181 patients received cetuximab or panitumumab as a part of first-line treatment and bevacizumab as a part of second-line treatment, while 309 patients were treated with the reverse sequence. Median overall survival (OS) from the initiation of first-line therapy was similar for patients treated with the different sequences (Table). No statistically significant differences in OS were detected between patients treated with the different sequences for subgroups of patients defined by age, chemotherapy backbone, synchronous/metachronous metastatic disease, anatomic location of the primary tumour, RAS status, and body-mass index. Progression-free survival, calculated as the time from the initiation of first-line therapy to progression on the second-line therapy moderately favoured the bevacizumab → antiEGFR sequence (Table).Table:

518P

antiEGFR →bevacizumab (n = 181)bevacizumab →antiEGFR (n = 309)log-rank p
OS (months)31.8 (95% CI 27.5–36.1)31.4 (95% CI 27.8–35.0)0.940
Progression-free survival (months)19.3 (95% CI 17.3–21.3)21.1 (95% CI 19.3–23.0)0.016

Conclusions

This retrospective analysis of data from a large patient registry does not support the hypothesis that the sequence of antiEGFR agents and bevacizumab has an impact on OS of mCRC patients.

Clinical trial identification

Legal entity responsible for the study

Tomas Buchler

Funding

Supported by grant AZV 15-26535A from the Czech Health Research Council.

Disclosure

T. Buchler: Research funding, lecture honoraria and travel grants from Roche and Amgen. A. Poprach: Research funding, lecture honoraria and travel grants from Roche, and Amgen. O. Fiala: Research funding, lecture honoraria and travel grants from Roche. I. Kiss: Speakers’ honoraria from Roche, Merck, and Amgen. J. Finek: Lecture honoraria and travel grants from Roche, Merck, Pfizer, Novartis, and Amgen. B. Melichar: Research funding, lecture honoraria and travel grants from Roche, Merck and Amgen. All other authors have declared no conflicts of interest.

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