The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Prognostic Impact of Deficient DNA Mismatch Repair in Patients With Stage III Colon Cancer From a Randomized Trial of FOLFOX-Based Adjuvant Chemotherapy
Open accessAbstract
Purpose: The association of deficient DNA mismatch repair (dMMR) with prognosis in patients with colon cancer treated with adjuvant fluorouracil, leucovorin, and oxaliplatin (FOLFOX) chemotherapy remains unknown. Patients and Methods: Resected, stage III colon carcinomas from patients (N = 2,686) randomly assigned to FOLFOX ± cetuximab (North Central Cancer Treatment Group N0147 trial) were analyzed for mismatch repair (MMR) protein expression and mutations in BRAF V600E(exon 15) and KRAS (codons 12 and 13). Association of biomarkers with disease-free survival (DFS) was determined using Cox models. A validation cohort (Cancer and Leukemia Group B 88903 trial) was used. Results: dMMR was detected in 314 (12%) of 2,580 tumors, of which 49.3% and 10.6% had BRAF V600E or KRAS mutations, respectively. MMR status was not prognostic overall (adjusted hazard ratio [HR], 0.82; 95% CI, 0.64 to 1.07; P = .14), yet significant interactions were found between MMR and primary tumor site (P interaction= .009) and lymph node category (N1 v N2; P interaction= .014). Favorable DFS was observed for dMMR versus proficient MMR proximal tumors (HR, 0.71; 95% CI, 0.53 to 0.94; P = .018) but not dMMR distal tumors (HR, 1.71; 95% CI, 0.99 to 2.95; P = .056), adjusting for mutations and covariates. Any survival benefit of dMMR was lost in N2 tumors. Mutations in BRAF V600E(HR, 1.37; 95% CI, 1.08 to 1.70; P = .009) or KRAS (HR, 1.44; 95% CI, 1.21 to 1.70; P < .001) were independently associated with worse DFS. The observed MMR by tumor site interaction was validated in an independent cohort of stage III colon cancers (P interaction= .037). Conclusion: The prognostic impact of MMR depended on tumor site, and this interaction was validated in an independent cohort. Among dMMR cancers, proximal tumors had favorable outcome, whereas distal or N2 tumors had poor outcome. BRAF or KRAS mutations were independently associated with adverse outcome.
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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
Ribic, C. M., Sargent, D. J., Moore, M. J., Thibodeau, S. N., French, A. J., Goldberg, R. M., Hamilton, S. R., Laurent-Puig, P., Gryfe, R., Shepherd, L. E., et al. (2003) · New England Journal of Medicine · doi:10.1056/nejmoa022289 · Cited by 2,160
Self-citationWild-Type BRAF Is Required for Response to Panitumumab or Cetuximab in Metastatic Colorectal Cancer
Di Nicolantonio, F., Martini, M., Molinari, F., Sartore-Bianchi, A., Arena, S., Saletti, P., De Dosso, S., Mazzucchelli, L., Frattini, M., Siena, S., et al. (2008) · Journal of Clinical Oncology · doi:10.1200/jco.2008.18.0786 · Cited by 1,591
RAF/RAS oncogenes and mismatch-repair status
Rajagopalan, H., Bardelli, A., Lengauer, C., Kinzler, K. W., Vogelstein, B., & Velculescu, V. E. (2002) · Nature · doi:10.1038/418934a · Cited by 1,224 · cited 1×
“The BRAF oncogene encodes a serine/ threonine kinase and is a downstream effector of the Ras/Raf/MAPK signaling pathway.(8,9) BRAF or KRAS mutations predict nonresponse to anti–epidermal growth factor receptor antibody therapy in metastatic CRCs, although only KRAS has been validated.”
BackgroundAllegra, C. J., Jessup, J. M., Somerfield, M. R., Hamilton, S. R., Hammond, E. H., Hayes, D. F., McAllister, P. K., Morton, R. F., & Schilsky, R. L. (2009) · Journal of Clinical Oncology · doi:10.1200/jco.2009.21.9170 · Cited by 1,156
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Richman, S. D., Seymour, M. T., Chambers, P., Elliott, F., Daly, C. L., Meade, A. M., Taylor, G., Barrett, J. H., & Quirke, P. (2009) · Journal of Clinical Oncology · doi:10.1200/jco.2009.22.4295 · Cited by 560
Cited by
Chalabi, M., Fanchi, L. F., Dijkstra, K. K., Van den Berg, J. G., Aalbers, A. G., Sikorska, K., Lopez-Yurda, M., Grootscholten, C., Beets, G. L., Snaebjornsson, P., et al. (2020) · Nature Medicine · doi:10.1038/s41591-020-0805-8 · Cited by 1,417
Petrelli, F., Tomasello, G., Borgonovo, K., Ghidini, M., Turati, L., Dallera, P., Passalacqua, R., Sgroi, G., & Barni, S. (2017) · JAMA Oncology · doi:10.1001/jamaoncol.2016.4227 · Cited by 729
André, T., de Gramont, A., Vernerey, D., Chibaudel, B., Bonnetain, F., Tijeras-Raballand, A., Scriva, A., Hickish, T., Tabernero, J., Van Laethem, J. L., et al. (2015) · Journal of Clinical Oncology · doi:10.1200/jco.2015.63.4238 · Cited by 683
Pathways of Colorectal Carcinogenesis
Nguyen, L. H., Goel, A., & Chung, D. C. (2020) · Gastroenterology · doi:10.1053/j.gastro.2019.08.059 · Cited by 606
Biomarker-guided therapy for colorectal cancer: strength in complexity
Sveen, A., Kopetz, S., & Lothe, R. A. (2020) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-019-0241-1 · Cited by 320
Metadata
- Authors
- Sinicrope, F. A., Mahoney, M. R., Smyrk, T. C., Thibodeau, S. N., Warren, R. S., Bertagnolli, M. M., Nelson, G. D., Goldberg, R. M., Sargent, D. J., & Alberts, S. R.
- Venue
- Journal of Clinical Oncology
- Published
- 2013-10-10
- Volume
- 31
- Issue
- 29
- Pages
- 3664-3672
- ISSN
- 0732-183X (ISSN-L)
- 1527-7755
- OpenAlex
- W2163145856
- Cited by
- 279
- References
- 7
- FWCI
- 14.23
- Type
- journal article
- Language
- en
- Open access
- green
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- Sinicrope, F. A., Mahoney, M. R., Smyrk, T. C., Thibodeau, S. N., Warren, R. S., Bertagnolli, M. M., Nelson, G. D., Goldberg, R. M., Sargent, D. J., & Alberts, S. R. (2013). Prognostic Impact of Deficient DNA Mismatch Repair in Patients With Stage III Colon Cancer From a Randomized Trial of FOLFOX-Based Adjuvant Chemotherapy. Journal of Clinical Oncology. https://doi.org/10.1200/jco.2013.48.9591
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