Posters
Presentation Type
Poster
Discipline Track
Biomedical Science
Abstract Type
Research/Clinical
Abstract
Background: To guide the treatment with monoclonal antibodies (MAbs) against the epidermal growth factor receptor (EGFR) of metastatic colorectal cancer (mCRC), the FDA recommends prior companion molecular diagnosis (CMDx). It initially recommended screening for mutations in exon 2 of the KRAS gene, and most recently to extend to screening to exons 2, 3, and 4 of KRAS and 2, 3, and 4 of NRAS genes; furthermore, to evaluate the BRAF exon 15 mutation status (including V600E). To date, no studies have been done to compare the cost-benefit of these different CMDXs.
Methods: We have compared the cost of treatment without prior CMDx versus the cost of standard KRAS (exon 2) testing followed by appropriate antiEGFR MAbs treatment. We have also compared these two modalities with the costs of the extended RAS and BRAF testing combined with appropriate therapies. Our pharmacoeconomics (PKE) estimations were based on 10 hypothetical cases of mCRC with mutation prevalence as previously reported by our laboratory.
Results: The therapy cost per patient for treating mCRC with MAbs but without CMDx was estimated at USD 107,345.20. Using guided therapy based on standard KRAS testing approximately 65% of the patients would have been treated with the targeted therapy. Of these patients, close to one-fourth could still be harboring clinically relevant mutations in the remainder of the codons of both RAS genes or BRAF exon 15, with potentially ineffective (KRAS mutants) or partially effective (BRAF mutants) treatment outcomes. On the other hand, beneficial treatments based on extended RAS testing would be prescribed to 50% of the patients with wild-type status. Finally, based on PKE considerations and the direct costs of antiEGFR MAbs treatment, the standard CMDx protocol results in a 35% cost saving by avoiding the prescription of ineffective treatments to patients harboring clinically relevant mutations whereas application of the extended CMDx would result in a 45%.
Conclusions: Even with the inclusion of the cost of testing, the treatment of mCRC with MAbs is more beneficial when guided by the extended RAS+BRAF CMDx as opposed to treatments guided by standard KRAS genetic testing. Furthermore, the patients excluded from ineffective therapies will save resources and time that can be used in seeking more suitable therapeutic alternatives.
Recommended Citation
Fernández-Garza, Luis E.; Sánchez-Ibarra, Hector; Treviño-Sáenz, Daniela; and Barrera-Saldaña, Hugo A., "Pharmacoeconomics of Metastatic Colorectal Cancer Treatment with Targeted Therapies Guided by Companion Molecular Diagnostics" (2023). Research Symposium. 78.
https://scholarworks.utrgv.edu/somrs/theme1/posters/78
Included in
Health Services Research Commons, Oncology Commons, Pharmacoeconomics and Pharmaceutical Economics Commons
Pharmacoeconomics of Metastatic Colorectal Cancer Treatment with Targeted Therapies Guided by Companion Molecular Diagnostics
Background: To guide the treatment with monoclonal antibodies (MAbs) against the epidermal growth factor receptor (EGFR) of metastatic colorectal cancer (mCRC), the FDA recommends prior companion molecular diagnosis (CMDx). It initially recommended screening for mutations in exon 2 of the KRAS gene, and most recently to extend to screening to exons 2, 3, and 4 of KRAS and 2, 3, and 4 of NRAS genes; furthermore, to evaluate the BRAF exon 15 mutation status (including V600E). To date, no studies have been done to compare the cost-benefit of these different CMDXs.
Methods: We have compared the cost of treatment without prior CMDx versus the cost of standard KRAS (exon 2) testing followed by appropriate antiEGFR MAbs treatment. We have also compared these two modalities with the costs of the extended RAS and BRAF testing combined with appropriate therapies. Our pharmacoeconomics (PKE) estimations were based on 10 hypothetical cases of mCRC with mutation prevalence as previously reported by our laboratory.
Results: The therapy cost per patient for treating mCRC with MAbs but without CMDx was estimated at USD 107,345.20. Using guided therapy based on standard KRAS testing approximately 65% of the patients would have been treated with the targeted therapy. Of these patients, close to one-fourth could still be harboring clinically relevant mutations in the remainder of the codons of both RAS genes or BRAF exon 15, with potentially ineffective (KRAS mutants) or partially effective (BRAF mutants) treatment outcomes. On the other hand, beneficial treatments based on extended RAS testing would be prescribed to 50% of the patients with wild-type status. Finally, based on PKE considerations and the direct costs of antiEGFR MAbs treatment, the standard CMDx protocol results in a 35% cost saving by avoiding the prescription of ineffective treatments to patients harboring clinically relevant mutations whereas application of the extended CMDx would result in a 45%.
Conclusions: Even with the inclusion of the cost of testing, the treatment of mCRC with MAbs is more beneficial when guided by the extended RAS+BRAF CMDx as opposed to treatments guided by standard KRAS genetic testing. Furthermore, the patients excluded from ineffective therapies will save resources and time that can be used in seeking more suitable therapeutic alternatives.