Although p53 mutations were associated with tobacco smoking and alcohol drinking, this association disappeared in virus-unrelated HNSCC.
Seven mutations were associated with impaired peptide loading in vivo, as detected by SDS stability assays.
These mutations were associated with ciprofloxacin resistance in strains isolated in Italy in 2000.
None of the specific baseline drug resistance mutations were associated with a higher rate of virologic failure after 12 or 24 weeks of HAART.
Moreover, many neuroligin gene mutations were associated with autism, but the pathophysiological relevance of these mutations is often unknown, and their mechanisms of action uninvestigated.
In the context of the clinical cohort, the presence of either KRAS or NRAS mutations or the concomitant presence of KRAS/NRAS mutations were associated with shorter TFS (p = 0.07, p = 0.05, and p = 0.02, respectively) (Table 1, Fig. 1c).
Different driver mutations were associated with distinct patterns of specific metabolites, such as lower levels of several lipid-glycerophosphocholines in tumors with mutated TP53.
Exon 4 mutations were associated with large, solitary metastases occurring at long disease-free intervals compared with exon 3 mutations, which presented with small, numerous lesions.
Watanabe and colleagues made the interesting observation that in colorectal carcinoma, MLL3 mutations were associated with increased MSI, though no mechanism has been proposed (Watanabe et al., 2011).
In multivariable models, TET2 mutations were associated with shorter EFS (P =.004), lower CR rate (P =.03), and shorter DFS (P =.05) only among favorable-risk CN-AML patients.
TP53 and CHEK2 mutations were associated with lack of response to epirubicin monotherapy.
