HPV types distribution by 5-years age intervals in the whole sample of CC patients.

<p>The figure shows the frequency distribution of HPV16 single infections (blue circles), pooled frequency of HPV18, HPV45, and HPV39 single infections (green circles), and the pooled frequency of other HPV types (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0109406#pone-0109406-g002" target="_blank">Figure 2</a>) plus HPV31 and all double infections (orange circles) over 5-years age intervals in the whole CC patients (n = 462).</p

Frequencies of different HPV types in CC patients according to age and FIGO staging.

<p>The figure shows the relative frequency (%) of HPV types in CC patients grouped by age in ≤40, between 41 and 55 and>55 years old. Panel A included the patients with FIGO I/II, and panel B patients with FIGO III/IV. Bars labeled as HPV16, HPV18, HPV45, HPV31 and HPV39 include only single infections. Other HPVs group include single infection of HPV types 6, 11, 26, 33, 35, 42, 51, 52, 53, 56, 58, 59, 61, 66, 68, 69, 70, 73, 82, 39-like, 51-like, 82-like and all double infections.</p

Age distribution of patients with cervical cancer (CC).

<p>The age distribution of CC patients divided into 5-year intervals according to tumor histological type (A). The frequency of patients by age, divided into three groups: <41 years, 41–55 years, and>55 years, according to FIGO staging (B). IND, undifferentiated; ASCC, adenosquamous cell carcinoma; ACC, adenocarcinoma; SCC, squamous cell carcinoma.</p

Mean age of cervical cancer patients according to HPV type (n = 462).

<p>a. S.D.  =  standard deviation.</p><p>b. Other HPVs included HPV6, HPV26, HPV39Like, HPV42, HPV51Like, HPV53, HPV61, HPV66, HPV68, HPV69, HPV70, HPV73, HPV82, HPV82Like.</p><p>The mean±S.D.(n) in the whole sample was 50.6±13.0 (462)</p><p>Mean age of cervical cancer patients according to HPV type (n = 462).</p

Frequency of single and double HPV infections in cervical cancer patients (n = 462).

a<p>Includes HPV68, HPV51Like, HPV66, HPV26, HPV39Like, HPV42, HPV61, HPV70, HPV73, HPV82, HPV82Like.</p><p>Frequency of single and double HPV infections in cervical cancer patients (n = 462).</p

Association of life-style factors and HPV types with delayed onset of cervical cancer.

a<p>Patient group ≤40 yrs was taken as reference group and odds ratios were calculated using a logistic regression model including all significant variables of <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0109406#pone-0109406-t003" target="_blank">table 3</a>; reference variable (OR = 1), p value and 95% confidence interval are shown.</p>b<p>Other HPVs includes single infections other than HPV16/18/45/39 and double infections.</p>c<p>Information of six patients was missed.</p>d<p>Include nulliparous (3.4% of total cases).</p>e<p>Patients that have been assisted at least once to Pap screening.</p><p>*Lower-risk factor or reference factor for CC.</p><p>Association of life-style factors and HPV types with delayed onset of cervical cancer.</p

Frequencies of different HPV types in CC patients according to age.

<p>The figure shows the relative frequency (%) of HPV types in CC patients grouped by age in ≤40, between 41 and 55 and>55 years old. Panel A included the patients of the whole sample, panel B patients with Squamous Cell Carcinomas, and panel C included patients with Adenocarcinomas. Bars labeled as HPV16, HPV18, HPV45, HPV31 and HPV39 include only single infections. Other HPVs group includes single infection of HPV types 6, 11, 26, 33, 35, 42, 51, 52, 53, 56, 58, 59, 61, 66, 68, 69, 70, 73, 82, 39-like, 51-like, 82-like and all double infections.</p

Patients followed up on average for 63 months for survival evaluation.

a<p>ACC, Adenocarcinoma. SCC, Squamous Cell Carcinoma. ASCC, Adenosquamous Cell Carcinoma.</p><p>bHT, Radical Hysterectomy. Tele, teletherapy. Brachy, brachytherapy. Chemo, chemotherapy with Cisplatin. i. Means incomplete treatment.</p>c<p>Status alive at the last follow up record and death was caused by primary tumor of cervical cancer, except the case labeled with an asterisk. The cause of death was unknown.</p>d<p>CN indicate the samples analyzed for CN (500 K array), CN/EX indicate the samples analyzed for CN (500 K array) and gene expression (HG 1.0 ST array), and EX indicate the samples analyzed for gene expression (HG 1.0 ST).</p

DAVID functional annotation cluster analysis in the 2006 genes differentially expressed in cervical cancer.

<p>*The cluster number was obtained when the analysis was run with the whole gene set, including up- and down-regulated genes.</p><p>FC = Fold change is the ratio of the proportion of genes in the tested list versus the Human Gene Reference database.</p><p>NC =  No clustered in up (+) and down (−) regulated genes analyzed separately.</p><p>The clusters in italics were enriched when the functional annotation cluster analysis was run at the highest stringency, and the number inside the parenthesis indicated the order the cluster occupied in the list.</p

Segregation of tumors and control samples according to gene expression profile.

<p>Unsupervised hierarchical cluster analysis of 55 CCs and 17 healthy cervical epithelium samples using the expression values of the genes deregulated from glycolysis (panel A) and the anaphase-promoting complex/cyclosome (APC/C)-dependent proteasomal protein catabolic process (panel B) obtained with the HG 1.0 ST microarray. Each row represents a gene and each column represents a sample. Samples name beginning with an “R” are CCs and with a “C” are controls; CCs ending in 1, 2 or 3 belong to low-, medium- or high-CN groups, respectively, whereas those ending with no number were not explored for CN. The length and the subdivision of the branches represent the relationships among the samples based on the intensity of gene expression. The cluster is color-coded using red for upregulation, blue for downregulation, and white for unchanged expression. In panel B, the sub-branches enclosed in squares were considered together in a group with a strong upregulation profile and the remaining upregulated samples were placed in another group with a weak upregulation profile.</p