A retrospective analysis of these data showed that cetuximab and chemotherapy had a statistically significant increase in respons E-rate and a lower risk of progression of the disease with chemotherapy alone NVP-TAE684 TAE684 in patients with tumors KRASWT compared. Prospective was investigated panitumumab either FOLFOX or FOLFIRI chemotherapy in metastatic frontline. The addition of panitumumab and FOLFOX chemotherapy . Overall, the data support in Table 2 in metastatic colorectal cancer to predict KRAS WT and mutation status of potential sensitivity and resistance definitive or antiEGFR two monoclonal Rpern, independently Ngig independent of the treatment Ngig of prior use as monotherapy or in combination. In particular, w While the KRAS pr Diktiv’s response to therapy antiEGFR established monoclonal Rpern, it was rejected as a prognostic marker.
Unlike KRAS mutational status analysis of EGFR expression in CRC cells failed to pr Diktiven value for therapeutic monoclonal antiEGFR antique Proof body. Cunningham et al. noted that the intensity of t the F staining by immunohistochemistry EGFR does not correlate with the rate of reaction to cetuximab. Similar data were also reported with panitumumab. KRAS mutant CRC missing antiEGFR therapy with monoclonal antibodies Rpern is no worse than in patients with KRAS WT disease. Assessment of KRAS mutation status is a mandatory aspect of the treatment of patients at diagnosis of metastatic colorectal cancer. 3.Mechanisms resistance W KRAS mutations during a major mechanism of primary rwiderstand Monoclonal therapies to antiEGFR antique Bodies are, the mechanisms of resistance in patients with KRAS WT are also defined.
Forty to 60 percent of patients with WT KRAS tumors do not respond to treatment with monoclonal antibodies Rpern antiEGFR respond. Therefore, other m Possible molecular determinants response in patients with monoclonal disease resistant EGFR WT KRAS be identified. The importance and H Abundance of mutations in the RNA CRC remains under investigation. Lambrechts et al. found that RNA, KRAS, BRAF mutations all the other exclusively Occurrences with the status WT combination of these genes were with h Heren response rates and progression-free survival time associated. Lambrechts et al. also reported that NRASmutation was associated with a lack of response to cetuximab. Irahara et al. investigated the relationship between RNA mutations and clinical outcome in a series of 225 colorectal cancers from two prospective cohort studies.
RNA mutations were detected in 2.2% of colorectal cancers. There was no discernible correlation between RNA mutations and clinical and pathological features, including the survival of the patient. However, the low H Abundance of mutations in the RNA obscure a significant relationship. Of Roock et al. performed a retrospective analysis of 700 tumor samples from patients treated with cetuximab plus chemotherapy and found a NRAS mutation frequency of 2.6%. In addition, KRAS wild-type grades, RNA mutations had lower response rate of cetuximab significantly than wild forms RNA. There was however, no significant difference in median PFS and median overall survival between wild-type and mutant RNA.