Sentence examples for mutation and gains from inspiring English sources

Integration of the CNA and mutation status that were specific to EFS24 failures revealed that 77% of patients who fail to achieve EFS24 have a combination of four variants (FOXO1 mutation and gains in 3q27.3, 11q23.3 and 19q13.32; Figure 3b).

Such exons may have originated from old repeated sequences, with splicing sites altered by mutation, and gained functions with time, and eventually became more frequently spliced.

Only four cases in the whole study had both a mutation and gain of copy number of PIK3CA.

To determine the relation between somatic mutation and gain of gene copy number of PIK3CA gene in breast cancer, we integrated our mutation and gene copy number data.

We did not observe a significant association between somatic mutation and gain of PIK3CA gene copy number in 92 cases of breast tumors (Table 2).

In regard to RFS, patients with wild-type HER2 mRNA < 400 (P=0.066), <span class="lh">mutation and gain of PIK3CA (P=0.06), gain of CDH3 (P<0.001), BIRC5 (P=0.007), MYBL2 (P=0.013), or AIB1 (P=0.013) had or tended to have worse RFS rates than those without.

This view is strengthened by the association of cluster B2 with scar-like tumor fibrosis, a desmoplastic reaction which is common in localized peripheral lung adenocarcinoma, and of cluster B3 with the highest rate of EGFR mutation (93%) as well as the highest rate of the co-occurrence of EFGR mutations and gains or amplifications on 7p (86%).

Although this phenotype has been described in Brugada syndrome due to Na+ channel mutations and gain-of-function Kv11.1 mutant channels [39], it has not been previously reported with dominant-negative Kv11.1 mutations associated with LQT2.

Patients with higher HER2 copy numbers, a combination of mutations and gain of PIK3CA, and gain of MYBL2 and AIB1 had or tended to have worse pCR and RFS rates than the respective counterparts (Table 3).

Tumors with a combination of mutations and gain of PIK3CA, or combined aberrations of the PI3K pathway genes, PIK3CA, PTEN and INPP4B tended to have more difficulty entering pCR than tumors without (P=0.08 and P=0.086).

However, we believe that tumors bearing high levels of COUP-TFII will be resistant to growth inhibitory effects caused by TGF-β signaling and will enable the tumor cells to accumulate mutations and gain metastatic potential.