|
1
|
Cerea G, Ricotta R, Schiavetto I, et al:
Cetuximab for treatment of metastatic colorectal cancer. Ann Oncol.
17(Suppl 7): vii66–vii67. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
2
|
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.
Lancet Oncol. 11:753–762. 2010.PubMed/NCBI
|
|
3
|
Sartore-Bianchi A, Bencardino K,
Cassingena A, et al: Therapeutic implications of resistance to
molecular therapies in metastatic colorectal cancer. Cancer Treat
Rev. 36(Suppl 3): S1–S5. 2010. View Article : Google Scholar
|
|
4
|
Sartore-Bianchi A, Bencardino K, Di
Nicolantonio F, et al: Integrated molecular dissection of the
epidermal growth factor receptor (EFGR) oncogenic pathway to
predict response to EGFR-targeted monoclonal antibodies in
metastatic colorectal cancer. Target Oncol. 5:19–28. 2010.
View Article : Google Scholar
|
|
5
|
De Roock W, De Vriendt V, Normanno N, et
al: KRAS, BRAF, PIK3CA, and PTEN mutations: implications for
targeted therapies in metastatic colorectal cancer. Lancet Oncol.
12:594–603. 2011.PubMed/NCBI
|
|
6
|
Benvenuti S, Sartore-Bianchi A, Di
Nicolantonio F, et al: Oncogenic activation of the RAS/RAF
signaling pathway impairs the response of metastatic colorectal
cancers to anti-epidermal growth factor receptor antibody
therapies. Cancer Res. 67:2643–2648. 2007. View Article : Google Scholar
|
|
7
|
Loupakis F, Ruzzo A, Cremolini C, et al:
KRAS codon 61, 146 and BRAF mutations predict resistance to
cetuximab plus irinotecan in KRAS codon 12 and 13 wild-type
metastatic colorectal cancer. Br J Cancer. 101:715–721. 2009.
View Article : Google Scholar
|
|
8
|
Di Nicolantonio F, Martini M, Molinari F,
et al: Wild-type BRAF is required for response to panitumumab or
cetuximab in metastatic colorectal cancer. J Clin Oncol.
26:5705–5712. 2008.
|
|
9
|
Dufort S, Richard MJ and de Fraipont F:
Pyrosequencing method to detect KRAS mutation in formalin-fixed and
paraffin-embedded tumor tissues. Anal Biochem. 391:166–168. 2009.
View Article : Google Scholar : PubMed/NCBI
|
|
10
|
Whitehall V, Tran K, Umapathy A, et al: A
multicenter blinded study to evaluate KRAS mutation testing
methodologies in the clinical setting. J Mol Diagn. 11:543–552.
2009. View Article : Google Scholar
|
|
11
|
Kobunai T, Watanabe T, Yamamoto Y and
Eshima K: The frequency of KRAS mutation detection in human colon
carcinoma is influenced by the sensitivity of assay methodology: a
comparison between direct sequencing and real-time PCR. Biochem
Biophys Res Commun. 395:158–162. 2010. View Article : Google Scholar
|
|
12
|
Weichert W, Schewe C, Lehmann A, et al:
KRAS genotyping of paraffin-embedded colorectal cancer tissue in
routine diagnostics: comparison of methods and impact of histology.
J Mol Diagn. 12:35–42. 2010. View Article : Google Scholar
|
|
13
|
Heideman DA, Lurkin I, Doeleman M, et al:
KRAS and BRAF mutation analysis in routine molecular diagnostics:
comparison of three testing methods on formalin-fixed,
paraffin-embedded tumor-derived DNA. J Mol Diagn. 14:247–255. 2012.
View Article : Google Scholar
|
|
14
|
Lee S, Brophy VH, Cao J, et al: Analytical
performance of a PCR assay for the detection of KRAS mutations
(codons 12/13 and 61) in formalin-fixed paraffin-embedded tissue
samples of colorectal carcinoma. Virchows Arch. 460:141–149. 2012.
View Article : Google Scholar
|
|
15
|
Wang HZ, Huang XF, Wang Y, et al: Clinical
features, diagnosis, treatment and prognosis of multiple primary
colorectal carcinoma. World J Gastroenterol. 10:2136–2139.
2004.PubMed/NCBI
|
|
16
|
Yoon JW, Lee SH, Ahn BK, et al: Clinical
characteristics of multiple primary colorectal cancers. Cancer Res
Treat. 40:71–74. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
17
|
Mulder SA, Kranse R, Damhuis RA, et al:
Prevalence and prognosis of synchronous colorectal cancer: a Dutch
population-based study. Cancer Epidemiol. 35:442–447. 2011.
View Article : Google Scholar : PubMed/NCBI
|
|
18
|
Nosho K, Kure S, Irahara N, et al: A
prospective cohort study shows unique epigenetic, genetic, and
prognostic features of synchronous colorectal cancers.
Gastroenterology. 137:1609–1620. e1–e3. 2009. View Article : Google Scholar
|
|
19
|
Tsao JL, Tavaré S, Salovaara R, et al:
Colorectal adenoma and cancer divergence. Evidence of multilineage
progression. Am J Pathol. 154:1815–1824. 1999. View Article : Google Scholar : PubMed/NCBI
|
|
20
|
Balschun K, Haag J, Wenke AK, et al: KRAS,
NRAS, PIK3CA exon 20, and BRAF genotypes in synchronous and
metachronous primary colorectal cancers diagnostic and therapeutic
implications. J Mol Diagn. 13:436–445. 2011. View Article : Google Scholar
|
|
21
|
Sobin LH, Gospodarowicz MK and Wittekind
C: TNM Classification of Malignant Tumours. 7th Edition.
Wiley-Blackwell; Chichester: 2009
|
|
22
|
Tol J, Nagtegaal ID and Punt CJ: BRAF
mutation in metastatic colorectal cancer. N Engl J Med. 361:98–99.
2009. View Article : Google Scholar : PubMed/NCBI
|
|
23
|
Baldus SE, Schaefer KL, Engers R, et al:
Prevalence and heterogeneity of KRAS, BRAF, and PIK3CA mutations in
primary colorectal adenocarcinomas and their corresponding
metastases. Clin Cancer Res. 16:790–799. 2010. View Article : Google Scholar
|
|
24
|
Voutsina A, Tzardi M, Kalikaki A, et al:
Combined analysis of KRAS and PIK3CA mutations, MET and PTEN
expression in primary tumors and corresponding metastases in
colorectal cancer. Mod Pathol. 26:302–313. 2013. View Article : Google Scholar : PubMed/NCBI
|
