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Further, the associations of KRAS codon 13 mutation with metastatic disease and codon 12 mutation with mucinous tumour type have also been demonstrated previously [ 5].
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Further, KRAS codon 13 mutation correlated with metastatic disease (M1) and p27 negativity.
The purpose of this investigation was to evaluate the efficacy of cisplatin chemotherapy in BRCA1 mutation carriers with metastatic breast cancer.
We conducted a retrospective study to determine the prognostic values of EGFR expression and KRAS mutation in patients with metastatic CRC (mCRC) based on synchronous or metachronous status.
In the current cohort, one BRCA1 mutation carrier presented with metastatic disease 3.5 years after PM (no primary BC found), suggesting the presence of an occult primary tumor that was never found, despite a thorough reexamination of the specimen at the presentation of the metastatic disease.
Our results suggest that inhibition of TOPK could be beneficial for at least two groups of CRC patients together representing 30 40% of all cases, namely, those with a KRAS or BRAF mutation and those with metastatic disease supported by several factors.
Mechanistic studies are needed to evaluate the association of these mutations with the metastatic spread.
K-Ras, B-Raf and p53 mutations were detected in 27, 3 and 32% of the cases, with K-Ras mutations significantly associated with metastatic tumour (P=0.019).
The recovery of a cell block suitable for performance of genetic analysis of EGFR mutations in patients with metastatic adenocarcinoma was considered as additional genetic information.
In this hypothesis, PIK3CA mutations may interfere with metastatic progression of breast cancer cells, while simultaneously accelerating the process of primary tumor formation.
Maeng et al. [ 8] found that phosphoinositide-3-kinase and BRAF mutations were associated with metastatic ESCC and Wang et al. [ 9] found that ESCC was related to polymorphisms in ALDH2 and ADH1B in Chinese females.
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