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Review
. 2017 Nov 16;9(7):7739-7748.
doi: 10.18632/oncotarget.22471. eCollection 2018 Jan 26.

Review on comparative efficacy of bevacizumab, panitumumab and cetuximab antibody therapy with combination of FOLFOX-4 in KRAS-mutated colorectal cancer patients

Surajit Pathak  1 , Sushmitha S  1 , Antara Banerjee  1 , Francesco Marotta  2 , Madhumala Gopinath  1 , Ramachandran Murugesan  1 , Hong Zhang  3 , Bhavani B  1 , Agnishwar Girigoswami  1 , Jose Sollano  4 , Xiao-Feng Sun  5
Affiliations
Review

Review on comparative efficacy of bevacizumab, panitumumab and cetuximab antibody therapy with combination of FOLFOX-4 in KRAS-mutated colorectal cancer patients

Surajit Pathak et al. Oncotarget. .

Abstract

Colorectal cancer, fourth leading form of cancer worldwide and is increasing in alarming rate in the developing countries. Treating colorectal cancer has become a big challenge worldwide and several antibody therapies such as bevacizumab, panitumumab and cetuximab are being used with limited success. Moreover, mutation in KRAS gene which is linked with the colorectal cancer initiation and progression further interferes with the antibody therapies. Considering median progression free survival and overall survival in account, this review focuses to identify the most efficient antibody therapy in combination with chemotherapy (FOLFOX-4) in KRAS mutated colorectal cancer patients. The bevacizumab plus FOLFOX-4 therapy shows about 9.3 months and 8.7 months of progression free survival for KRAS wild and mutant type, respectively. The overall survival is about 34.8 months for wild type whereas for the mutant it is inconclusive for the same therapy. In comparison, panitumumab results in better progression-free survival which is about (9.6 months) and overall survival is about (23.9 months) for the wild type KRAS and the overall survival is about 15.5 months for the mutant KRAS. Cetuximab plus FOLFOX-4 therapy shows about 7.7 months and 5.5 months of progression-free survival for wild type KRAS and mutant type, respectively. Thus, panitumumab shows significant improvement in overall survival rate for wild type KRAS, validating as a cost effective therapeutic for colorectal cancer therapy. This review depicts that panitumumab along with FOLFOX-4 has a higher response in colorectal cancer patients than the either of the two monoclonal antibodies plus FOLFOX-4.

Keywords: KRAS; bevacizumab; cetuximab; colorectal cancer; panitumumab.

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Conflict of interest statement

CONFLICTS OF INTEREST No potential conflicts of interest were disclosed.

Figures

Figure 1
Figure 1. PRISMA flowchart for article screening (example)
Figure 2
Figure 2
(A) Meta-analysis for wild type progression free survival of panitumumab, bevacizumab and cetuximab antibody therapies alone or in combination with FOLFOX-4 (for panitumumab and cetuximab). (B) Meta-analysis for mutant type progression free survival of panitumumab, bevacizumab and cetuximab antibody therapies alone or in combination with FOLFOX-4 (for panitumumab and cetuximab).
Figure 3
Figure 3
(A) Meta-analysis for wild type overall survival of panitumumab, bevacizumab and cetuximab antibody therapies alone or in combination with FOLFOX-4 (for panitumumab and cetuximab). (B) Meta-analysis for mutant type overall survival of panitumumab, bevacizumab and cetuximab antibody therapies alone or in combination with FOLFOX-4 (for panitumumab and cetuximab).
See this image and copyright information in PMC

References

    1. Smith G, Carey FA, Beattie J, Wilkie MJ, Lightfoot TJ, Coxhead J, Garner RC, Steele RJ, Wolf CR. Mutations in APC, Kirsten-ras, and p53—alternative genetic pathways to colorectal cancer. Proc Natl Acad Sci USA. 2002;99:9433–38. - PMC - PubMed
    1. Schuebel KE, Chen W, Cope L, Glöckner SC, Suzuki H, Yi JM, Chan TA, Van Neste L, Van Criekinge W, van den Bosch S, van Engeland M, Ting AH, Jair K, et al. Comparing the DNA hypermethylome with gene mutations in human colorectal cancer. PLoS Genet. 2007;3:1709–23. - PMC - PubMed
    1. Pathak S, Meng WJ, Zhang H, Gnosa S, Nandy SK, Adell G, Holmlund B, Sun XF. Tafazzin protein expression is associated with tumorigenesis and radiation response in rectal cancer: a study of Swedish clinical trial on preoperative radiotherapy. PLoS One. 2014;9:e98317. - PMC - PubMed
    1. Brink M, de Goeij AF, Weijenberg MP, Roemen GM, Lentjes MH, Pachen MM, Smits KM, de Bruïne AP, Goldbohm RA, van den Brandt PA. K-ras oncogene mutations in sporadic colorectal cancer in The Netherlands Cohort Study. Carcinogenesis. 2003;24:703–10. - PubMed
    1. Lièvre A, Bachet JB, Boige V, Cayre A, Le Corre D, Buc E, Ychou M, Bouché O, Landi B, Louvet C, André T, Bibeau F, Diebold MD, et al. KRAS mutations as an independent prognostic factor in patients with advanced colorectal cancer treated with cetuximab. J Clin Oncol. 2008;26:374–79. - PubMed