Adjuvant radiotherapy was indicated in our clinic for sufferers with parametrial tumor infiltration, tumor-positive resection margins, lymph node metastasis, or two out of 3 of the subsequent negative prognostic aspects: constructive LVSI, tumor dimensions ! forty mm, or tumor infiltration depth ! 
fifteen mm.SCC, squamous mobile carcinoma AC, adenocarcinoma ASC, adenosquamous carcinoma FIGO, global federation of gynecology and obstetrics LVSI, lymph vascular room invasion (hr)HPV, (higher threat) human papillomavirus IQR, inter quartile assortment n (%), variety (share) of clients. Daring values are substantial (P<0.05). Clinical data are missing for FIGO stage (n = 2), tumor diameter (n = 33), tumor infiltration depth (n = 13), parametrial infiltration (n = 3), LVSI (n = 22), lymph node metastasis (n = 2), and resection margins (n = 4). HPV was considered negative if no HPV DNA was detected or only low-risk type HPV (n = 1). In three tumors both HPV 16 and HPV 18 were detected.Mutation spectra of the histological subtypes are visualized in Fig 1, and mutation frequencies are summarized in Table 2. In 103 tumors (34%), 123 somatic mutations were detected. In 4% of the tumors more than one mutation was detected. No significant difference in somatic mutation prevalence was found between the histological subtypes (36% in SCC, 38% in AC, and 28% in ASC). However, a different mutation distribution was observed. 1000413-72-8 PIK3CA mutations were detected more frequently in SCC than AC (P = 0.025). KRAS mutations were detected more frequently in AC than SCC (P<0.001) or ASC (P<0.001). PTEN mutations were detected in 4% of all tumors and most frequently in AC (9%). CTNNB1 mutations were detected in 3% of all tumors and most frequently in SCC (4%).Binary logistic regression analysis assessed whether the overall somatic mutation status and gene-specific mutation status correlated with clinicopathological parameters for the total patient cohort or within the SCC, AC, and ASC subgroups. Overall, patients with a positive somatic mutation status were significantly older at disease onset (mean age 49 vs. 45 years P = 0.004). This feature was explained by the strong association between older age and PIK3CA Fig 1. Mutation Spectrum. Mutation spectrum of 301 cervical cancers (top panel) and separate spectra for squamous cell carcinoma (SCC), adenocarcinoma (AC), and adenosquamous carcinoma (ASC). N, number of mutated samples %, percentage mutated samples within the cohort. The mutation spectrum is visualized from left to right in percentages: blue bars, samples with ! 2 mutations green bars, samples with a single mutation. Only significant P-values are shown25225882 between cohorts (all other values: see Table 2)mutation in SCC patients (mean age 53 vs. 45 years P = 0.003). In addition, having a PIK3CA mutation was associated with FIGO stage II in the SCC subtype (42% vs. 15% P = 0.001).