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Wild-Type BRAF Is Required for Response to Panitumumab or Cetuximab in Metastatic Colorectal Cancer
Open accessAbstract
Purpose: Cetuximab or panitumumab are effective in 10% to 20% unselected metastatic colorectal cancer (CRC) patients. KRAS mutations account for approximately 30% to 40% patients who are not responsive. The serine-threonine kinase BRAF is the principal effector of KRAS. We hypothesized that, in KRAS wild-type patients, BRAF mutations could have a predictive/prognostic value. Patients and Methods: We retrospectively analyzed objective tumor responses, time to progression, overall survival (OS), and the mutational status of KRAS and BRAF in 113 tumors from cetuximab- or panitumumab-treated metastatic CRC patients. The effect of the BRAF V600E mutation on cetuximab or panitumumab response was also assessed using cellular models of CRC. Results: KRAS mutations were present in 30% of the patients and were associated with resistance to cetuximab or panitumumab (P = .011). The BRAF V600E mutation was detected in 11 of 79 patients who had wild-type KRAS. None of the BRAF-mutated patients responded to treatment, whereas none of the responders carried BRAF mutations (P = .029). BRAF-mutated patients had significantly shorter progression-free survival (P = .011) and OS (P < .0001) than wild-type patients. In CRC cells, the introduction of BRAF V600E allele impaired the therapeutic effect of cetuximab or panitumumab. Treatment with the BRAF inhibitor sorafenib restored sensitivity to panitumumab or cetuximab of CRC cells carrying the V600E allele. Conclusion: BRAF wild-type is required for response to panitumumab or cetuximab and could be used to select patients who are eligible for the treatment. Double-hit therapies aimed at simultaneous inhibition of epidermal growth factor receptor and BRAF warrant exploration in CRC patients carrying the V600E oncogenic mutation.
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“preclinical studies have provided a proof of principle that the combined inhibition of EGFR and BRAF can be synergistic in BRAF-mutant CRCs”
From Primary and acquired resistance to EGFR-targeted therapies in colorectal cancer: impact on future treatment strategies (2014) · cites this paper as [52]
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“Although therapies targeting EGFR have some efficacy in CRCs without KRAS mutations (1, 5–8)”
From mTOR Inhibition Specifically Sensitizes Colorectal Cancers with KRAS or BRAF Mutations to BCL-2/BCL-XL Inhibition by Suppressing MCL-1 (2014) · cites this paper as [8]
In the citing paper
“However, the predictive impact of BRAF mutations is tempered by their low prevalence and is further biased by the prominent role of mutant BRAF as a negative prognostic biomarker [54]. Overall, the predictive power of this alteration remains immature and requires further prospective endorsement before clinical applicability [20, 33, 52, 55].”
From Primary and acquired resistance to EGFR-targeted therapies in colorectal cancer: impact on future treatment strategies (2014) · cites this paper as [52]
In the citing paper
“Mutations of BRAF, which encodes the cytoplasmic serine/threonine kinase immediately downstream of RAS, are found in 4–13 % of advanced CRCs and are usually mutually exclusive with KRAS mutations [20, 52].”
From Primary and acquired resistance to EGFR-targeted therapies in colorectal cancer: impact on future treatment strategies (2014) · cites this paper as [52]
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“The BRAF V600E mutation has been described as a predictor of tumor aggressiveness in metastatic disease [33, 52, 53]”
From Primary and acquired resistance to EGFR-targeted therapies in colorectal cancer: impact on future treatment strategies (2014) · cites this paper as [52]
In the citing paper
“the best responses of CRC cell xenografts to such combinations were only disease stabilizations or mild tumor regressions [52, 58-60].”
From Primary and acquired resistance to EGFR-targeted therapies in colorectal cancer: impact on future treatment strategies (2014) · cites this paper as [52]
In the citing paper
“and also of low RRs to cetuximab and panitumumab [18, 20, 52, 53].”
From Primary and acquired resistance to EGFR-targeted therapies in colorectal cancer: impact on future treatment strategies (2014) · cites this paper as [52]
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“Several studies have indicated that the presence of mutant KRAS in CRC tumours correlates with poor prognosis [12, 13] and is associated with lack of response to EGFR inhibitors [14– 17].”
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Messick, C. A., Sanchez, J., DeJulius, K. L., Church, J. M., & Kalady, M. F. (2009) · Surgery · doi:10.1016/j.surg.2009.06.003 · Cited by 18
Current situation of zalutumumab
Rivera, F., Salcedo, M., Vega, N., Blanco, Y., & López, C. (2009) · Expert Opinion on Biological Therapy · doi:10.1517/14712590902932871 · Cited by 18
“There are also some data coming from advanced colorectal cancer studies treated with cetuximab or panitumumab suggesting that other biomarkers could be predictive factors of treatment efficacy with anti EGFR monoclonal antibodies: v-raf murine sarcoma viral oncogene homolog B1 (B-RAF) mutations (another EGFR downstrea…”
BackgroundRole of KRAS let-7 LCS6 SNP in metastatic colorectal cancer patients
Ruzzo, A., Canestrari, E., Galluccio, N., Santini, D., Vincenzi, B., Tonini, G., Magnani, M., & Graziano, F. (2010) · Annals of Oncology · doi:10.1093/annonc/mdq472 · Cited by 18
BRAF Mutations in Colorectal Cancer: Clinical Relevance and Role in Targeted Therapy
Yaeger, R., & Saltz, L. (2012) · Journal of the National Comprehensive Cancer Network · doi:10.6004/jnccn.2012.0148 · Cited by 18
Kondo, N., Tsukuda, M., Taguchi, T., Nakazaki, K., Sakakibara, A., Takahashi, H., Toth, G., & Nishimura, G. (2011) · Cancer Science · doi:10.1111/j.1349-7006.2011.01999.x · Cited by 17
Weng, W., Leung, W., Pang, Y.-J., Kuo, L., & Hsu, H.-H. (2018) · Oncology Letters · doi:10.3892/ol.2018.9408 · Cited by 17
“The evidence identities that ~50% of CRCs exhibit no response to anti-EGFR therapy, including cetuximab or panitumumab (1-11).”
BackgroundMachnicki, M. M., Głodkowska‐Mrówka, E., Lewandowski, T., Płoski, R., Wlodarski, P. K., & Stokłosa, T. (2013) · Acta Biochimica Polonica · doi:10.18388/abp.2013_1951 · Cited by 17
“Clinical response of the anti-EGFR treatment in colorectal cancer with anti-EGFR antibodies (e.g. cetuximab, panitumumab) depends on preserved wild-type status of BRAF (as well as KRAS) (Di Nicolantonio et al., 2008).”
BackgroundMethodIbrahim, E. M., & Abouelkhair, K. M. (2011) · Medical Oncology · doi:10.1007/s12032-010-9760-4 · Cited by 17
“Activating mutations of additional signaling proteins downstream of the EGFR [22, 23], downstream of KRAS such as RAF [ 24 ], and loss of function mutations of tumor suppressor genes such as PTEN [22] may be useful to further refine potential responders.”
BackgroundLin, J.-K., Lin, A.-J., Lin, C., Lan, Y., Yang, S., Li, A. F., & Chang, S. (2011) · Journal of Surgical Oncology · doi:10.1002/jso.21993 · Cited by 18
Panitumumab: A Summary of Clinical Development in Colorectal Cancer and Future Directions
Argilés, G., Dienstmann, R., Élez, E., & Tabernero, J. M. (2012) · Future Oncology · doi:10.2217/fon.12.20 · Cited by 17
Fede, G. D., Bronte, G., Rizzo, S., Rolfo, C. D., Cocorullo, G., Gulotta, G., Bazan, V., & Russo, A. D. (2011) · Expert Opinion on Biological Therapy · doi:10.1517/14712598.2011.594436 · Cited by 17
“They include somatic mutations of BRAF and PI3K catalytic, alpha polypeptide (PI3KCA) genes, the amplification of the EGFR gene and the impaired expression of the phosphatase and tensin homolog (PTEN) protein [53-57].”
Blanke, C. D., Goldberg, R. M., Grothey, A. F., Mooney, M., Roach, N., Saltz, L. B., Welch, J. J., Wood, W. A., & Meropol, N. J. (2011) · The Oncologist · doi:10.1634/theoncologist.2011-0011 · Cited by 17
Němeček, R., Berkovcová, J., Radová, L., Kazda, T., Mlčochová, J., Vychytilova‐Faltejskova, P., Slabý, O., & Svoboda, M. (2016) · OncoTargets and Therapy · doi:10.2147/ott.s102891 · Cited by 17
Serum level of octanoic acid predicts the efficacy of chemotherapy for colorectal cancer
Iemoto, T., Nishiumi, S., Kobayashi, T., Fujigaki, S., Hamaguchi, T., Kato, K., Shoji, H., Matsumura, Y., Honda, K., & Yoshida, M. (2018) · Oncology Letters · doi:10.3892/ol.2018.9731 · Cited by 17
Effectiveness of Vigna unguiculata seed extracts in preventing colorectal cancer
Panzeri, D., Guzzetti, L., Sacco, G., Tedeschi, G., Nonnis, S., Airoldi, C., Labra, M., Fusi, P. A., Forcella, M. E., & Regonesi, M. E. (2020) · Food & Function · doi:10.1039/d0fo00913j · Cited by 17
Bovio, F., Epistolio, S., Mozzi, A., Monti, E., Fusi, P. A., Forcella, M. E., & Frattini, M. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21228805 · Cited by 17
Self-citationWhat Is Known about Theragnostic Strategies in Colorectal Cancer
Parisi, A., Porzio, G., Pulcini, F., Cannita, K., Ficorella, C., Mattei, V., & Monache, S. D. (2021) · Biomedicines · doi:10.3390/biomedicines9020140 · Cited by 17
“Moreover, as anti-EGFR therapy with cetuximab and panitumumab is approved for wild-type RAS mCRC and KRAS and BRAF are considered effective predictors of anti-EGFR therapy [35,36], ctDNA detection could represent an alternative tool for the selection of anti-EGFR treatment due to its correlation with RAS mutational st…”
BackgroundChang, Y., HSU, W.-H., Chang, C.-H., LAN, K.-L., Ting, G., & LEE, T.-W. (2014) · Molecular and Clinical Oncology · doi:10.3892/mco.2014.246 · Cited by 17
Dupont, B., Mariotte, D., Clarisse, B., Galais, M., Bouhier‐Leporrier, K., Grellard, J., Mauff, B. L., Reimund, J., & Gervais, R. (2014) · Future Oncology · doi:10.2217/fon.14.153 · Cited by 17
KRAS and BRAF mutational status in colon cancer from Albanian patients
Martinetti, D., Costanzo, R., Kadare, S., Alimehmeti, M., Colarossi, C., Canzonieri, V., Berretta, M., & Memeo, L. (2014) · Diagnostic Pathology · doi:10.1186/s13000-014-0187-7 · Cited by 17
“BRAF should also be tested together with KRAS to select the patients who are most likely to benefit from the antiEGFR therapy [19,32,33].”
BackgroundResultInfluentialHertogh, G. D., & Geboes, K. (2010) · Archives of Pathology & Laboratory Medicine · doi:10.5858/134.6.853 · Cited by 18
Shuford, R. A., Cairns, A., & Moaven, O. (2020) · Cancers · doi:10.3390/cancers12113481 · Cited by 17
WHO-Klassifikation 2010 für den unteren Gastrointestinaltrakt
Aust, D. E. (2011) · Der Pathologe · doi:10.1007/s00292-011-1505-4 · Cited by 17
Prospective Biomarker Study in Advanced RAS Wild-Type Colorectal Cancer: POSIBA Trial (GEMCAD 10-02)
García‐Albéniz, X., Alonso, V., Escudero, P., Méndez, M., Gallego-Plazas, J., Rodríguez, J. R., Salud, A., Fernández-Plana, J., Manzano, H., Zanui, M., et al. (2019) · The Oncologist · doi:10.1634/theoncologist.2018-0728 · Cited by 16
“Di Nicolantonio, 2008 [6] BRAF Retrospective Retrospective cohort positive NA”
BackgroundUrachal carcinoma: The journey so far and the road ahead
Kumar, R., Harilal, S., Abdelgawad, M. A., Ghoneim, M. M., Kumar, A. J., & Mathew, B. (2023) · Pathology - Research and Practice · doi:10.1016/j.prp.2023.154379 · Cited by 20
Dang, H., Sui, M., He, Q., Xie, J., Liu, Y., Hou, P., & Ji, M. (2023) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2023.125867 · Cited by 16
Targeting tyrosine kinases in cancer
Dumur, C. I., Idowu, M. O., & Powers, C. N. (2012) · Cancer Cytopathology · doi:10.1002/cncy.21225 · Cited by 16
“It has been demonstrated that these molecules contribute to anti-EGFR response, and mutations in these genes have been associated with a poor response to such targeted therapies.(85) Thus, neuroblastoma v-ras oncogene homolog (NRAS), BRAF, and PI3K activating mutations(86) may abrogate the effects of antiEGFR–based th…”
BackgroundPentheroudakis, G. E., Kotteas, E. A., Kotoula, V., Papadopoulou, K., Charalambous, E., Cervantes, A. M. R., Ciuleanu, T., Fountzilas, G., & Pavlidis, N. A. (2014) · Clinical & Experimental Metastasis · doi:10.1007/s10585-014-9666-1 · Cited by 16
“BRAF mutations which are found in 5–10 %of colorectal cancers and 40–60 % of melanomas are associated with poor prognosis, failure of anti-EGFR antibodies (in colorectal cancer) and response to BRAF TK inhibitors (in melanoma) [18, 39–41].”
BackgroundWang, Q., Hu, W., Song, Q., & Wei, J. (2014) · Chinese Medical Sciences Journal · doi:10.1016/s1001-9294(14)60070-5 · Cited by 16
Where cancer genomics should go next: a clinician's perspective
Rafii, A., Touboul, C., Thani, H. A., Suhre, K., & Malek, J. A. (2014) · Human Molecular Genetics · doi:10.1093/hmg/ddu234 · Cited by 16
Caraglia, M., Santini, D., Bronte, G., Rizzo, S., Sortino, G., Rini, G. B., Fede, G. D., & Russo, A. D. (2011) · Current Drug Metabolism · doi:10.2174/138920011798062346 · Cited by 16
“0001) than WT BRAF cases [67].”
Larsson, A. H., Lehn, S., Wangefjord, S., Karnevi, E., Kuteeva, E., Sundström, M., Nodin, B., Uhlén, M., Eberhard, J., Birgisson, H., et al. (2016) · Journal of Translational Medicine · doi:10.1186/s12967-016-0882-0 · Cited by 16
“However, only approximately 40 % of CRC patients with tumours wild-type for KRAS, NRAS and BRAF benefit from such therapy [47–50], and patients who initially respond eventually become resistant to these drugs.”
BackgroundLi, Z.-Z., Bai, L., Wang, F., Zhang, Z.-C., Wang, F., Zeng, Z.-L., Zeng, J., Zhang, D.-S., Wang, F., Wang, Z., et al. (2016) · Medical Oncology · doi:10.1007/s12032-016-0787-z · Cited by 16
Mechanistic characterization of a copper containing thiosemicarbazone with potent antitumor activity
Karlsson, H., Fryknäs, M., Strese, S., Gullbo, J., Westman, G., Bremberg, U., Sjöblom, T., Pandzic, T., Larsson, R. L., & Nygren, P. (2017) · Oncotarget · doi:10.18632/oncotarget.16324 · Cited by 16
“Next, we included colon cancer models able to associate the activity to the KRAS- and BRAF mutation status, established to have predictive and/or prognostic importance in this tumor type [27, 28].”
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“…response to RAF kinase inhibitors or anti-EGFR therapies depends upon the presence of BRAF V600E variant in cancer cells (Domingo et al., 2005; Di Nicolantonio et al., 2008; Yokota et al., 2011), a reliable diagnostic test for the V600E mutation appears to be greatly desirable. ll rights…”
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Lymph node metastases of melanoma: challenges for BRAF mutation detection
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“BRAF mutation status provides several clinical standardof-care applications, such as prediction of responsiveness to BRAF inhibitors in melanoma patients and anti-epidermal growth factor receptor therapy in colorectal cancer patients [5-8,25].”
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Metadata
- Authors
- Di Nicolantonio, F., Martini, M., Molinari, F., Sartore-Bianchi, A., Arena, S., Saletti, P., De Dosso, S., Mazzucchelli, L., Frattini, M., Siena, S., & Bardelli, A.
- Affiliations
- From the Laboratory of Molecular Genetics, The Oncogenomics Center, Institute for Cancer Research and Treatment, University of Torino Medical School, Candiolo; The Falck Division of Medical Oncology, Ospedale Niguarda Ca’ Granda; Italian Foundation for Cancer Research–Institute of Molecular Oncology, Milan, Italy; Laboratory of Molecular Diagnostic, Istituto Cantonale di Patologia, Locarno; and Oncology Institute of Southern Switzerland, Ospedale San Giovanni, Bellinzona, Switzerland
- Azienda Socio Sanitaria Territoriale Grande Ospedale Metropolitano Niguarda (IT)
- Venue
- Journal of Clinical Oncology
- Published
- 2008-12-10
- Volume
- 26
- Issue
- 35
- Pages
- 5705-5712
- ISSN
- 0732-183X (ISSN-L)
- 1527-7755
- OpenAlex
- W2131413118
- Cited by
- 1,591
- References
- 38
- Citations by year
- 2026: 9 · 2025: 18 · 2024: 25 · 2023: 32 · 2022: 35 · 2021: 48 · 2020: 71 · 2019: 54 · 2018: 57 · 2017: 67 · 2016: 126 · 2015: 108 · 2014: 147 · 2013: 146 · 2012: 148
- FWCI
- 87.94
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Oncology (publishedVersion)
- PubMed (publishedVersion)
- Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
- Institutional Research Information System University of Turin (University of Turin) (submittedVersion)
- Funders
- Oncosuisse
- Regione Piemonte
- Topics
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Health Sciences › Medicine › Oncology › Colorectal Cancer Surgical Treatments
- Keywords
- BRAF wild-type, BRAF V600E mutation, KRAS mutation, cetuximab, panitumumab, metastatic colorectal cancer, EGFR inhibitors, treatment resistance, sorafenib, predictive biomarkers, progression-free survival, overall survival
- MeSH terms
- Cetuximab, Sorafenib, Panitumumab, Adult, Aged, Aged, 80 and over, Antibodies, Monoclonal, Antineoplastic Agents, Benzenesulfonates, Cell Survival, Dose-Response Relationship, Drug, Female, Humans, Italy, Male, Middle Aged, Mutation, Neoplasm Metastasis, Niacinamide, Phenylurea Compounds, Proto-Oncogene Proteins, Pyridines, Retrospective Studies, Switzerland, Time Factors, Biomarkers, Tumor, Colorectal Neoplasms, Gene Expression Regulation, Neoplastic, Proto-Oncogene Proteins p21(ras), Treatment Outcome, Disease-Free Survival, Patient Selection, ras Proteins, Drug Resistance, Neoplasm, HT29 Cells, Gene Expression Profiling, Protein Kinase Inhibitors, Proto-Oncogene Proteins B-raf, Antibodies, Monoclonal, Humanized, ErbB Receptors
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