The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
The Prognostic Value of BRAF Mutation in Colorectal Cancer and Melanoma: A Systematic Review and Meta-Analysis
Open accessAbstract
BACKGROUND: Mutation of BRAF is a predominant event in cancers with poor prognosis such as melanoma and colorectal cancer. BRAF mutation leads to a constitutive activation of mitogen activated protein kinase pathway which is essential for cell proliferation and tumor progression. Despite tremendous efforts made to target BRAF for cancer treatment, the correlation between BRAF mutation and patient survival is still a matter of controversy. METHODS/PRINCIPAL FINDINGS: Clinical studies on the correlation between BRAF mutation and patient survival were retrieved from MEDLINE and EMBASE databases between June 2002 and December 2011. One hundred twenty relevant full text studies were categorized based on study design and cancer type. Publication bias was evaluated for each category and pooled hazard ratio (HR) with 95% confidence interval (CI) was calculated using random or fixed effect meta-analysis based on the percentage of heterogeneity. Twenty six studies on colorectal cancer (11,773 patients) and four studies on melanoma (674 patients) were included in our final meta-analysis. The average prevalence of BRAF mutation was 9.6% in colorectal cancer, and 47.8% in melanoma reports. We found that BRAF mutation increases the risk of mortality in colorectal cancer patients for more than two times; HR = 2.25 (95% CI, 1.82-2.83). In addition, we revealed that BRAF mutation also increases the risk of mortality in melanoma patients by 1.7 times (95% CI, 1.37-2.12). CONCLUSIONS: We revealed that BRAF mutation is an absolute risk factor for patient survival in colorectal cancer and melanoma.
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Cites
Mutations of the BRAF gene in human cancer
Davies, H., Bignell, G. R., Cox, C., Stephens, P., Edkins, S., Clegg, S., Teague, J., Woffendin, H., Garnett, M. J., Bottomley, W., et al. (2002) · Nature · doi:10.1038/nature00766 · Cited by 10,674
Improved survival with vemurafenib in melanoma with BRAF V600E mutation
Chapman, P. B., Hauschild, A., Robert, C., Haanen, J. B., Ascierto, P., Larkin, J., Dummer, R., Garbe, C., Testori, A., Maio, M., et al. (2011) · New England Journal of Medicine · doi:10.1056/nejmoa1103782 · Cited by 7,720
De Roock, W., Claes, B., Bernasconi, D., De Schutter, J., Biesmans, B., Fountzilas, G., Kalogeras, K. T., Kotoula, V., Papamichael, D., Laurent-Puig, P., et al. (2010) · The Lancet Oncology · doi:10.1016/s1470-2045(10)70130-3 · Cited by 2,144
Unresponsiveness of colon cancer to BRAF(V600E) inhibition through feedback activation of EGFR
Prahallad, A., Sun, C., Huang, S., Di Nicolantonio, F., Salazar, R., Zecchin, D., Beijersbergen, R. L., Bardelli, A., & Bernards, R. (2012) · Nature · doi:10.1038/nature10868 · Cited by 2,051
RAS oncogenes: the first 30 years
Malumbres, M., & Barbacid, M. (2003) · Nature Reviews Cancer · doi:10.1038/nrc1097 · Cited by 1,902 · cited 1×
“Constitutive activation of the MAPK pathway in cancers has been frequently observed in various malignancies which is usually due to activating mutations in upstream factors such as RAS and RAF [2].”
BackgroundVan Cutsem, E., Köhne, C.-H., Láng, I., Folprecht, G., Nowacki, M. P., Cascinu, S., Shchepotin, I., Maurel, J., Cunningham, D., Tejpar, S., et al. (2011) · Journal of Clinical Oncology · doi:10.1200/jco.2010.33.5091 · Cited by 1,882
COT drives resistance to RAF inhibition through MAP kinase pathway reactivation
Johannessen, C. M., Boehm, J. S., Kim, S. Y., Thomas, S. R., Wardwell, L., Johnson, L. A., Emery, C. M., Stransky, N., Cogdill, A. P., Barretina, J., et al. (2010) · Nature · doi:10.1038/nature09627 · Cited by 1,460
RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E)
Poulikakos, P. I., Persaud, Y., Janakiraman, M., Kong, X., Ng, C., Moriceau, G., Shi, H., Atefi, M., Titz, B., Gabay, M. T., et al. (2011) · Nature · doi:10.1038/nature10662 · Cited by 1,454
Laurent-Puig, P., Cayre, A., Manceau, G., Buc, E., Bachet, J.-B., Lecomte, T., Rougier, P., Lievre, A., Landi, B., Boige, V., et al. (2009) · Journal of Clinical Oncology · doi:10.1200/jco.2008.21.6796 · Cited by 673
Recovery of phospho-ERK activity allows melanoma cells to escape from BRAF inhibitor therapy
Paraiso, K. H. T., Fedorenko, I. V., Cantini, L. P., Munko, A. C., Hall, M., Sondak, V. K., Messina, J. L., Flaherty, K. T., & Smalley, K. S. M. (2010) · British Journal of Cancer · doi:10.1038/sj.bjc.6605714 · Cited by 314
Cited by
Combined BRAF, EGFR, and MEK Inhibition in Patients with BRAF V600E-Mutant Colorectal Cancer
Corcoran, R. B., André, T., Atreya, C. E., Schellens, J. H. M., Yoshino, T., Bendell, J. C., Hollebecque, A., McRee, A. J., Siena, S., Middleton, G., et al. (2018) · Cancer Discovery · doi:10.1158/2159-8290.cd-17-1226 · Cited by 592
Current targeted therapies in the treatment of advanced colorectal cancer: a review
Moriarity, A., O’Sullivan, J., Kennedy, J., Mehigan, B., & McCormick, P. (2016) · Therapeutic Advances in Medical Oncology · doi:10.1177/1758834016646734 · Cited by 87
Metadata
- Authors
- Safaee Ardekani, G., Jafarnejad, S. M., Tan, L., Saeedi, A., & Li, G.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-10-09
- Volume
- 7
- Issue
- 10
- Pages
- e47054
- ISSN
- 1932-6203 (ISSN-L)
- OpenAlex
- W2135454464
- Cited by
- 224
- References
- 11
- FWCI
- 2.71
- Type
- journal article
- Language
- en
- Open access
- gold
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- Safaee Ardekani, G., Jafarnejad, S. M., Tan, L., Saeedi, A., & Li, G. (2012). The Prognostic Value of BRAF Mutation in Colorectal Cancer and Melanoma: A Systematic Review and Meta-Analysis. PLoS ONE. https://doi.org/10.1371/journal.pone.0047054
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