A case report of BRAF inhibitor combined with anti-EGFR monoclonal antibody and irinotecan in the treatment of metastatic colon cancer with BRAF V600E mutation and literature review

doi:10.3877/cma.j.issn.2095-3224.2020.03.019

Abstract

Abstract:

The BRAF gene is a member of the RAF kinase family, and BRAF mutations occur in approximately 14% of patients with primary CRC and 8% mCRC. BRAF V600E CRC, as the most common type of BRAF mutation mCRC, has poor conventional treatment efficacy, rapid disease progression, short survival, and poor prognosis. In Cancer Hospital, Chinese Academy of Medical Sciences, we received an advanced colon cancer patient with BRAF V600E mutation. Two-line therapy with chemotherapy and targeted therapy showed no significant tumor reduction. The third-line therapy, BRAF inhibitor combined with chemotherapy and targeted therapy, achieved PR (partial response). The report is as follows.

Key words: Colonic neoplasms, Mutation, BRAF mutations, BRAF inhibitor, Neoplasm metastasis

Liming Peng, Jing Wang, Lin Yang. A case report of BRAF inhibitor combined with anti-EGFR monoclonal antibody and irinotecan in the treatment of metastatic colon cancer with BRAF V600E mutation and literature review[J]. Chinese Journal of Colorectal Diseases(Electronic Edition), 2020, 09(03): 305-309.

/ / Recommend

Add to citation manager EndNote|Ris|BibTeX

URL: https://zhjzcjbdzzz.cma-cmc.com.cn/EN/10.3877/cma.j.issn.2095-3224.2020.03.019

https://zhjzcjbdzzz.cma-cmc.com.cn/EN/Y2020/V09/I03/305

Figures/Tables 3

References 28

[1]	Jemal A, Bray F, Center MM, et al. Global cancer statistics [J]. CA: A Cancer Journal for Clinicians, 2011, 61(2): 69-90.
[2]	Siegel RL, Miller KD, Fedewa SA, et al. Colorectal cancer statistics, 2017 [J]. CA: A Cancer Journal for Clinicians, 2017, 67(3): 177-193.
[3]	Sepulveda AR, Hamilton SR, Allegra CJ, et al. Molecular biomarkers for the evaluation of colorectal cancer: guideline summary from the American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology, and American Society of Clinical Oncology [J]. Journal of Oncology Practice, 2017, 13(5): 333-337.
[4]	Loree JM, Pereira AAL, Lam M, et al. Classifying colorectal cancer by tumor location rather than sidedness highlights a continuum in mutation profiles and consensus molecular subtypes [J]. Clin Cancer Res, 2018, 24(5): 1062-1072.
[5]	Clarke CN, Kopetz ES. BRAF mutant colorectal cancer as a distinct subset of colorectal cancer: clinical characteristics, clinical behavior, and response to targeted therapies [J]. Journal of Gastrointestinal Oncology, 2015, 6(6): 660-667.
[6]	Souglakos J, Philips J, Wang R, et al. Prognostic and predictive value of common mutations for treatment response and survival in patients with metastatic colorectal cancer [J]. British Journal of Cancer, 2009, 101(3): 465-472.
[7]	Salem ME, Weinberg BA, Xiu J, et al. Comparative molecular analyses of left-sided colon, right-sided colon, and rectal cancers [J]. Oncotarget, 2017, 8(49): 86356-86368.
[8]	Tie J, Gibbs P, Lipton L, et al. Optimizing targeted therapeutic development: analysis of a colorectal cancer patient population with the BRAF(V600E) mutation [J]. International Journal of Cancer, 2011, 128(9): 2075-2084.
[9]	Wang X, Wei Q, Gao J, et al. Clinicopathologic features and treatment efficacy of Chinese patients with BRAF-mutated metastatic colorectal cancer: a retrospective observational study [J]. Chinese Journal of Cancer, 2017, 36(1): 81.
[10]	Chen D, Huang JF, Liu K, et al. BRAFV600E mutation and its association with clinicopathological features of colorectal cancer: a systematic review and meta-analysis [J]. PloS One, 2014, 9(3): e90607.
[11]	Samowitz WS, Sweeney C, Herrick J, et al. Poor survival associated with the BRAF V600E mutation in microsatellite-stable colon cancers [J]. Cancer Research, 2005, 65(14): 6063-6069.
[12]	Xu Q, Xu AT, Zhu MM, et al. Predictive and prognostic roles of BRAF mutation in patients with metastatic colorectal cancer treated with anti-epidermal growth factor receptor monoclonal antibodies: a meta-analysis [J]. Journal of Digestive Diseases, 2013, 14(8): 409-416.
[13]	Sinicrope FA, Shi Q, Allegra CJ, et al. Association of DNA mismatch repair and mutations in BRAF and KRAS with survival after recurrence in stage III colon cancers : A secondary analysis of 2 randomized clinical trials [J]. JAMA Oncology, 2017, 3(4): 472-480.
[14]	De Roock W, Claes B, Bernasconi D, et al. Effects of KRAS, BRAF, NRAS, and PIK3CA mutations on the efficacy of cetuximab plus chemotherapy in chemotherapy-refractory metastatic colorectal cancer: a retrospective consortium analysis [J]. The Lancet Oncology, 2010, 11(8): 753-762.
[15]	Cremolini C, Loupakis F, Masi G, et al. FOLFOXIRI or FOLFOXIRI plus bevacizumab as first-line treatment of metastatic colorectal cancer: a propensity score-adjusted analysis from two randomized clinical trials [J]. Annals of Oncology : Official Journal of the European Society for Medical Oncology, 2016, 27(5): 843-849.
[16]	Cremolini C, Loupakis F, Antoniotti C, et al. FOLFOXIRI plus bevacizumab versus FOLFIRI plus bevacizumab as first-line treatment of patients with metastatic colorectal cancer: updated overall survival and molecular subgroup analyses of the open-label, phase 3 TRIBE study [J]. The Lancet Oncology, 2015, 16(13): 1306-1315.
[17]	Pietrantonio F, Petrelli F, Coinu A, et al. Predictive role of BRAF mutations in patients with advanced colorectal cancer receiving cetuximab and panitumumab: a meta-analysis [J]. European Journal of Cancer (Oxford, England : 1990), 2015, 51(5): 587-594.
[18]	Rowland A, Dias MM, Wiese MD, et al. Meta-analysis of BRAF mutation as a predictive biomarker of benefit from anti-EGFR monoclonal antibody therapy for RAS wild-type metastatic colorectal cancer [J]. British Journal of Cancer, 2015, 112(12): 1888-1894.
[19]	Kopetz S, Mcdonough SL, Morris VK, et al. Randomized trial of irinotecan and cetuximab with or without vemurafenib in BRAF-mutant metastatic colorectal cancer (SWOG 1406) [J]. J Clin Oncol, 2017, 35(4_suppl): 520.
[20]	Elez E, Argiles G, Tabernero J. First-line treatment of metastatic colorectal cancer: Interpreting FIRE-3, PEAK, and CALGB/SWOG 80405 [J]. Current Treatment Options in Oncology, 2015, 16(11): 52.
[21]	Kopetz S, Desai J, Chan E, et al. Phase II pilot study of vemurafenib in patients with metastatic BRAF-mutated colorectal cancer [J]. J Clin Oncol, 2015, 33(34): 4032-4038.
[22]	Prahallad A, Sun C, Huang S, et al. Unresponsiveness of colon cancer to BRAF(V600E) inhibition through feedback activation of EGFR [J]. Nature, 2012, 483(7387): 100-103.
[23]	Yang H, Higgins B, Kolinsky K, et al. Antitumor activity of BRAF inhibitor vemurafenib in preclinical models of BRAF-mutant colorectal cancer [J]. Cancer Research, 2012, 72(3): 779-789.
[24]	Corcoran RB, Ebi H, Turke AB, et al. EGFR-mediated re-activation of MAPK signaling contributes to insensitivity of BRAF mutant colorectal cancers to RAF inhibition with vemurafenib [J]. Cancer Discovery, 2012, 2(3): 227-235.
[25]	Atreya CE, Van Cutsem E, Bendell JC, et al. Updated efficacy of the MEK inhibitor trametinib (T), BRAF inhibitor dabrafenib (D), and anti-EGFR antibody panitumumab (P) in patients (pts) with BRAF V600E mutated (BRAFm) metastatic colorectal cancer (mCRC). J Clin oncol, 2015, 33(suppl): a103.
[26]	Pan JH, Zhou H, Zhu SB, et al. Development of small-molecule therapeutics and strategies for targeting RAF kinase in BRAF-mutant colorectal cancer [J]. Cancer Management and Research, 2018, 10(2): 289-301.
[27]	Wang Z, Dai WP, Zang YS. Complete response with fluorouracil and irinotecan with a BRAF(V600E) and EGFR inhibitor in BRAF-mutated metastatic colorectal cancer: a case report [J]. OncoTargets and Therapy, 2019, 12: 443-447.
[28]	Van Cutsem E, Huijberts S, Grothey A, et al. Binimetinib, Encorafenib, and Cetuximab Triplet therapy for patients with BRAF V600E-Mutant metastatic colorectal cancer: safety lead-in results from the phase III BEACON colorectal cancer study [J]. J Clin Oncol, 2019, 37(17): 1460-1469.

Please choose a citation manager

Content to export