In the AC subtype, PIK3CA mutation correlated with tumor diameter (indicate diameter in PIK3CA-mutated samples 40 mm vs. 26 mm in non-PIK3CA mutated samples P = .011). 
In SCC, squamous cell carcinoma AC, adenocarcinoma ASC, adenosquamous carcinoma. N.A. statistical take a look at not applicable. Frequencies are offered as number (n) of samples with the mutation–one SCC sample is made up of two PPP2R1A mutations (p.P179R and p.R183W) and one particular SCC sample consists of two PIK3CA mutations (p.E542K and p.E545K). P-values have been identified by chi-square examination or Fisher’s precise take a look at bold P-values are regarded as significant (< 0.05). the ASC subtype, having any mutation also correlated with older age (mean age 49 vs. 45 years P = 0.048), parametrial infiltration (23% vs. 10% P = 0.024), and inversely correlated with LVSI (36% vs. 69% P = 0.002). For the whole cohort and within histological subgroups, a positive mutation status was not significantly correlated with hrHPV positivity/negativity or type. Gene specifically hrHPV negativity correlated with a PTEN mutation (5/23 PTEN mutations in hrHPV negative tumors vs. 7/278 PTEN mutations in hrHPV positive tumors, P<0.001). This association between PTEN mutation and hrHPV negativity was also detected in SCC patients separately (3/12 vs. 1/154, P<0.001), but not found in AC and ASC patients. Within the SCC cohort also CDKN2A (1/12 vs. 1/154, P = 0.019), FBXW7 (1/12 vs. 1/154, P = 0.019), FGFR3 (1/12 vs. 0/154, P<0.001) mutations significantly correlated with hrHPV negativity. In 5/12 hrHPV negative SCC patients 11 somatic hot-spot mutations were detected. In one tumor a single PIK3CA E545K mutation was detected, in one tumor a single PTEN R234W mutation was detected, and in three of these tumors three different mutations were detected. One with a combination of PIK3CA p.R88Q, PTEN p.Q214, and CTNNB1 p.S45F, one with a combination of PIK3CA p. E545K, CDKN2A p.R58, and FGFR3 p.S249C, and one with the combination of KRAS p. G12V, PTEN p.R130G, and FBXW7 p.R465H. Within the AC and ASC patient cohorts no correlations were detected between mutation status and hrHPV. Also, no correlations were detected per hot-spot mutation or hrHPV type specifically probably due to small numbers. In Table 3 all hrHPV types detected in this series per hot-spot mutation are shown (Table 3).Within 5 years of primary surgery, 81 (27%) patients suffered from recurrent disease (mean DFS 48 months) and 53 (18%) patients died from cervical cancer (mean DSS 53 months). Univariate survival analyses were performed to determine the correlations between mutational status, histology, and other clinicopathological characteristics and DSS or DFS (Table 4). No difference in DSS was found for patients with tumors with any somatic mutation compared to patients without any somatic mutation
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