Childhood body fatness and the risk of epithelial ovarian cancer: A population-based case-control study in Montreal, Canada.

OBJECTIVE: To assess the association between childhood body fatness and epithelial ovarian cancer (EOC), and whether this association differs by type of EOC. METHODS: Using data from a population-based case-control study (497 cases and 902 controls) in Montreal, Canada conducted 2011-2016, we examined the association between childhood body fatness and EOC, overall and separately for invasive vs. borderline EOCs. A figure rating scale was used to measure body fatness at ages 5 and 10. Multivariable logistic regression was used to estimate adjusted odds ratios (aORs) and 95% confidence intervals (95% CI). Quantitative bias analyses were conducted to assess the impact of exposure misclassification and non-participation. RESULTS: The aOR (95% CI) of overall EOC for high vs. low body fatness was 1.07 (0.85-1.34) at age 5 and 1.28 (0.98-1.68) at age 10. The associations were stronger for invasive EOC, specifically the endometrioid histological type. For borderline cancers, the aORs were below the null value with wide confidence intervals. Bias analyses did not reveal a strong influence of non-participation. Non-differential exposure misclassification may have biased aORs towards the null for invasive cancers but did not appear to have an appreciable influence on the aORs for borderline cancers. CONCLUSIONS: Childhood body fatness may be a risk factor for invasive EOC in later adult life. Our study highlights the potential importance of examining early life factors for a comprehensive understanding of EOC development.

Underwater Endoscopic Mucosal Resection Versus Conventional Endoscopic Mucosal Resection for Superficial Non-ampullary Duodenal Epithelial Tumors ≤20 mm: A Systematic Review With Meta-analysis.

BACKGROUND: Underwater endoscopic mucosal resection (UEMR) is increasingly applied in the treatment of superficial non-ampullary duodenal epithelial tumors (SNADETs). This meta-analysis aimed to assess the efficacy and safety of UEMR for SNADETs ≤20 mm in comparison with conventional endoscopic mucosal resection (CEMR). METHODS: The following electronic databases were searched from 2012 until November 20, 2021: PubMed, Embase, Scopus, Web of Science databases, and Cochrane Library. The primary outcomes were the rates of en bloc resection and complete (R0) resection, and the secondary outcomes were procedure time, adverse events (delayed bleeding and delayed perforation), and recurrence rate. RESULTS: A total of 6 studies with 679 lesions (331 underwent UEMR and 348 CEMR) were included in this study. The pooled analysis showed that UMER achieves a similar en bloc resection rate (87.6 vs. 89.9%; odds ratio [OR], 1.29; 95% confidence interval [CI], 0.45 to 3.73; P =0.64; I2 =74%), a similar R0 resection rate (67.3 vs. 73.6%; OR, 1.11; 95% CI, 0.55 to 2.23; P =0.78; I2 =59%), a shorter procedure time (min) (mean difference [MD], -4.05, 95% CI: -6.40 to -1.71; P =0.0007; I2 =70%) compared with CEMR. There were no significant differences in the rates of delayed bleeding, delayed perforation, and recurrence (2.4 vs. 1.7%, 0 vs. 0.6%, 2.2 vs. 4.4%, respectively). CONCLUSION: This meta-analysis demonstrated that UEMR appears to be an effective and safe alternative to CEMR for SNADETs ≤20 mm.

Underwater Versus Conventional Endoscopic Mucosal Resection for Superficial Non-ampullary Duodenal Epithelial Tumors: A Systematic Review and Meta-Analysis.

BACKGROUND/AIMS: Duodenal underwater endoscopic mucosal resection (UEMR) has been suggested as a feasible treatment option for superficial non-ampullary duodenal epithelial tumors (SNADETs). However, its efficacy and safety have not been fully established yet. Thus, the objective of this systematic review and meta-analysis was to determine the efficacy and safety of UEMR as compared with conventional endoscopic mucosal resection (CEMR) in the treatment of SNADETs. METHODS: We conducted a comprehensive literature search in PubMed, EMBASE, the Cochrane Library. Studies comparing CEMR and UEMR for the resection of SNADET were included. Outcomes included en-bloc and complete resection rates, adverse events, and procedure time. RESULTS: A total of six studies with 2454 lesions were included in the quantitative synthesis. En-bloc and complete resection rates were not significantly different between UEMR and CEMR (OR for en-bloc resection: 0.997 [95% CI 0.439-2.266]; OR for complete resection: 0.960 [95% CI 0.628-1.468]). There was no significant risk difference for perforation (risk difference: - 0.002; 95% CI - 0.009 to 0.005) or delayed bleeding (risk difference: - 0.001; 95% CI - 0.014 to 0.011). Procedure time was significantly shorter in the UEMR (standardized mean difference: - 1.294; 95% CI - 2.461 to - 0.127). The risk of recurrence was not significantly different between UEMR and CEMR (risk difference: 0.001; 95% CI - 0.041 to 0.044). CONCLUSION: Although our results did not show any superiority of UEMR over CEMR in the treatment of SNADETs, UEMR showed equivalent efficacy and safety as compared with CEMR and was associated with a shorter procedure time.

Alcohol consumption, cigarette smoking and cancer of unknown primary risk: Results from the Netherlands Cohort Study.

Cancer of unknown primary (CUP) is a metastasised malignancy with no identifiable primary tumour origin. Despite the frequent occurrence and bleak prognosis of CUP, research into its aetiology is scarce. Our study investigates alcohol consumption, tobacco smoking and CUP risk. We used data from the Netherlands Cohort Study, a cohort that includes 120 852 participants aged 55 to 69 years, who completed a self-administered questionnaire on cancer risk factors at baseline. Cancer follow-up was established through record linkage to the Netherlands Cancer Registry and Dutch Pathology Registry. After 20.3 years of follow-up, 963 CUP cases and 4288 subcohort members were available for case-cohort analyses. Multivariable-adjusted hazard ratios (HRs) were calculated using proportional hazard models. In general, CUP risk increased with higher levels of alcohol intake (Ptrend = .02). The association was more pronounced in participants who drank ≥30 g of ethanol per day (HR: 1.57, 95% confidence interval [CI]: 1.20-2.05) compared to abstainers. Current smokers were at an increased CUP risk (HR: 1.59, 95% CI: 1.29-1.97) compared to never smokers. We observed that the more the cigarettes or the longer a participant smoked, the higher the CUP risk was (Ptrend = .003 and Ptrend = .02, respectively). Interaction on additive scale was found for participants with the highest exposure categories of alcohol consumption and cigarette smoking frequency and CUP risk. Our findings demonstrate that alcohol consumption and cigarette smoking are associated with increased CUP risk. Lifestyle recommendations for cancer prevention regarding not drinking alcohol and avoiding exposure to smoking are therefore also valid for CUP.

Occurrence of seromucinous borderline tumours in the peritoneal lesions after bilateral salpingo-oophorectomy.

A 65-year-old woman with a previous history of bilateral salpingo-oophorectomy had peritoneal cysts, increasing in size over 15 years and an increasing cancer antigen 19-9 (CA 19-9) level. The size of the cysts eventually reached 86 mm and 70 mm. As malignant transformation of endometriosis was suspected, we performed peritoneal cystectomy and hysterectomy. Histopathology revealed seromucinous borderline tumours (SMBTs) derived from endometriosis. One month after surgery, her CA 19-9 level had decreased. It is rare for SMBT to occur after bilateral salpingo-oophorectomy; surgical management is the best treatment at present.

Hyperinsulinemia Drives Epithelial Tumorigenesis by Abrogating Cell Competition.

Metabolic diseases such as type 2 diabetes are associated with increased cancer incidence. Here, we show that hyperinsulinemia promotes epithelial tumorigenesis by abrogating cell competition. In Drosophila eye imaginal epithelium, oncogenic scribble (scrib) mutant cells are eliminated by cell competition when surrounded by wild-type cells. Through a genetic screen, we find that flies heterozygous for the insulin receptor substrate chico allow scrib cells to evade cell competition and develop into tumors. Intriguingly, chico is required in the brain's insulin-producing cells (IPCs) to execute cell competition remotely. Mechanistically, chico downregulation in IPCs causes hyperinsulinemia by upregulating a Drosophila insulin Dilp2, which activates insulin-mTOR signaling and thus boosts protein synthesis in scrib cells. A diet-induced increase in insulin levels also triggers scrib tumorigenesis, and pharmacological repression of protein synthesis prevents hyperinsulinemia-induced scrib overgrowth. Our findings provide an in vivo mechanistic link between metabolic disease and cancer risk via systemic regulation of cell competition.

Respiratory epithelial adenomatoid hamartoma: a diagnostic challenge in sinonasal lesions.

Respiratory epithelial adenomatoid hamartoma (REAH) is a rare lesion in nasal cavity first reported by Wenig and Heffner in 1995. Most commonly seen in men in third to ninth decade of life. Majority of cases presents as a polypoidal mass in one or both nasal cavities. We experienced such a case of REAH originating from the nasal septum, in posterior aspect, treated by endoscopic approach. It is important to differentiate REAH from other sinonasal pathologies like inverted papilloma and low grade sinonasal adenocarcinoma. Complete surgical resection is the treatment of choice.

Leptin Receptor Antagonists' Action on HDAC Expression Eliminating the Negative Effects of Leptin in Ovarian Cancer.

BACKGROUND/AIM: A common finding in cancer cells is the overexpression of histone deacetylases (HDACs), leading to altered expression and activity of numerous proteins involved in carcinogenesis. Considering that leptin can modulate the levels of HDACs, we hypothesised that leptin receptor antagonists can alter HDAC expression. MATERIALS AND METHODS: HDAC expression in cells exposed to leptin and leptin receptor antagonists (SHLA and Lan2) were evaluated in ovarian epithelial (OVCAR-3, CaOV3) and folliculoma (COV434, KGN) cells. RESULTS: Higher HDAC expression was found in epithelial compared to folliculoma cells. Leptin increased class I and II HDACs only in OVCAR-3 cells, and SHLA was more potent then Lan-2. In folliculoma cells, leptin only increased class II HDAC expression, Lan-2 was more potent than SHLA in the COV434 and neither antagonist affected the KGN cells. CONCLUSION: SHLA and Lan2 eliminate the negative effects of leptin on HDAC expression in a cell-type-dependent manner. This is the first report testing leptin receptor blockers as HDAC inhibitors in ovarian cancer cells.

Charged-Iron-Particles Found in Galactic Cosmic Rays are Potent Inducers of Epithelial Ovarian Tumors.

Astronauts traveling in deep space are exposed to high-charge and energy (HZE) particles from galactic cosmic rays. We have previously determined that irradiation of adult female mice with iron HZE particles induces DNA double-strand breaks, oxidative damage and apoptosis in ovarian follicles, causing premature ovarian failure. These effects occur at lower doses than with conventional photon irradiation. Ovarian failure with resultant loss of negative feedback and elevated levels of gonadotropin hormones is thought to play a role in the pathophysiology of ovarian cancer. Therefore, we hypothesized that charged-iron-particle irradiation induces ovarian tumorigenesis in mice. In this study, three-month-old female mice were exposed to 0 cGy (sham) or 50 cGy iron ions and aged to 18 months. The 50 cGy irradiated mice had increased weight gain with age and lack of estrous cycling, consistent with ovarian failure. A total of 47% and 7% of mice irradiated with 50 cGy had unilateral and bilateral ovarian tumors, respectively, whereas 14% of mice in the 0 cGy group had unilateral tumors. The tumors contained multiple tubular structures, which were lined with cells positive for the epithelial marker cytokeratin, and had few proliferating cells. In some tumors, packets of cells between the tubular structures were immunopositive for the granulosa cell marker FOXL2. Based on these findings, tumors were diagnosed as tubular adenomas or mixed tubular adenoma/granulosa cell tumors. In conclusion, charged-iron-particle-radiation induces ovarian tumors in mice, raising concerns about ovarian tumors as late sequelae of deep space travel in female astronauts.

Pre-operative core muscle index in combination with hypoalbuminemia is associated with poor prognosis in advanced ovarian cancer.

BACKGROUND AND OBJECTIVES: Age and frailty have been correlated with poor clinical outcomes in cancer. Core muscle index (CMI) and nutritional status are integral in assessing frailty. We explored the effect of pre-operative serum albumin and body composition on clinical outcomes in patients with epithelial ovarian cancer (EOC). METHODS: We identified stage III-IV EOC patients undergoing primary cytoreductive surgery from 2007 to 2015. Data were abstracted from medical records. Body composition measurements were obtained from pre-operative imaging. Psoas muscle cross-sectional area was normalized to height2 to determine CMI. Sarcopenia was defined as CMI below the population mean. The influence of sarcopenia on short-term morbidity was evaluated. Relationships among body composition measurements and albumin were assessed with Spearman correlations. Patient characteristics and body composition measurements between patients with and without sarcopenia were compared with parametric and non-parametric statistical methods. Kaplan-Meier survival curves were compared using log-rank. RESULTS: 102 women met inclusion criteria. Sarcopenia correlated with albumin (P = 0.0002). Sarcopenia was not associated with short-term morbidity or time to recurrence. Sarcopenia was associated with nearly a fourfold increased risk of death when hypoalbuminemia was present (P = 0.02). CONCLUSIONS: Pre-operative sarcopenia in combination with hypoalbuminemia was associated with significantly worse survival.

The origin of endometriosis-associated ovarian cancer from uterine neoplastic lesions.

Endometriosis is a risk factor for type I epithelial ovarian cancer but an issue to be clarified is the site of origin of endometriosis associated ovarian cancer. Here we proposed that the uterus may be the organ of origin of ovarian endometrioid cancer associated with endometriosis. Thus, the first neoplastic transformation would characterize the uterine cells migrating in the pelvis via retrograde menstruation and they would implant secondarily on the ovary. Supporting this hypothesis, an higher incidence of synchronous precancerous and cancerous endometrial pathology in patients affected by ovarian endometrioid cancer associated with endometriosis was showed. Moreover, uterine endometrial type I carcinoma resembles endometriosis associated endometrioid ovarian cancer in behavior and prognosis. This hypothesis is also supported by epidemiologic evidence showing a protective effect for tubal ligation and oral contraceptive use for endometriosis associated endometrioid ovarian cancer. Endometriosis and endometrioid ovarian carcinoma might represent two distinct biological entities characterized by the same organ of origin (the uterus), the same pathogenetic mechanism (transtubal reflux) and the same target organ (the ovary). By shifting the early events of ovarian carcinogenesis to the endometrium, prevention approaches as salpingectomy/tubal ligation and intervention at uterine corpus level may play an important role.

Mediation analysis of alcohol consumption, DNA methylation, and epithelial ovarian cancer.

Epigenetic factors and consumption of alcohol, which suppresses DNA methylation, may influence the development and progression of epithelial ovarian cancer (EOC). However, there is a lack of understanding whether these factors interact to affect the EOC risk. In this study, we aimed to gain insight into this relationship by identifying leukocyte-derived DNA methylation markers acting as potential mediators of alcohol-associated EOC. We implemented a causal inference test (CIT) and the VanderWeele and Vansteelandt multiple mediator model to examine CpG sites that mediate the association between alcohol consumption and EOC risk. We modified one step of the CIT by adopting a high-dimensional inference procedure. The data were based on 196 cases and 202 age-matched controls from the Mayo Clinic Ovarian Cancer Case-Control Study. Implementation of the CIT test revealed two CpG sites (cg09358725, cg11016563), which represent potential mediators of the relationship between alcohol consumption and EOC case-control status. Implementation of the VanderWeele and Vansteelandt multiple mediator model further revealed that these two CpGs were the key mediators. Decreased methylation at both CpGs was more common in cases who drank alcohol at the time of enrollment vs. those who did not. cg11016563 resides in TRPC6 which has been previously shown to be overexpressed in EOC. These findings suggest two CpGs may serve as novel biomarkers for EOC susceptibility.

The role of MicroRNA molecules and MicroRNA-regulating machinery in the pathogenesis and progression of epithelial ovarian cancer.

MicroRNA molecules are small, single-stranded RNA molecules that function to regulate networks of genes. They play important roles in normal female reproductive tract biology, as well as in the pathogenesis and progression of epithelial ovarian cancer. DROSHA, DICER, and Argonaute proteins are components of the microRNA-regulatory machinery and mediate microRNA production and function. This review discusses aberrant expression of microRNA molecules and microRNA-regulating machinery associated with clinical features of epithelial ovarian cancer. Understanding the regulation of microRNA molecule production and function may facilitate the development of novel diagnostic and therapeutic strategies to improve the prognosis of women with epithelial ovarian cancer. Additionally, understanding microRNA molecules and microRNA-regulatory machinery associations with clinical features may influence prevention and early detection efforts.

Do some epithelial ovarian cancers originate from a fallopian tube ciliate cell lineage?

There is a general agreement that a large subpopulation of serous ovarian cancers arise from the fallopian tube mucosal epithelium. However, there is still some debate as to whether the cancers originate from a secretory or ciliate cell lineage. One well established method for determining the origin of a cell line is to document the expression of genes and proteins that are cell type specific. Lineage or tissue specific patterns of gene expression are evidence of direct decent from a given cell type within a tissue. It has recently been established that the Tumor Protein TAp73 gene (TP73) is expressed in basal epithelial cells that develop into multiciliate cells. TP73 expression is therefore a marker for basal stem cells that are predestined to differentiate into cells with motile cilia and its expression is maintained in fully differentiated multiciliate cells. Interestingly TP73 expression has also been observed in a high percentage of epithelial ovarian cancers. With this in mind, it is hypothesized that a high percentage of epithelial ovarian cancers which express TP73 originate from a ciliate cell lineage.

Time Trends in the Incidence and Mortality of Ovarian Cancer in Ireland, Northern Ireland, and Israel, 1994-2013.

OBJECTIVES: The aims of this study were to compare time trends in ovarian cancer incidence and mortality in populations with (1) similar genetics but different health care systems (Ireland and Northern Ireland [NI]) and (2)different genetics but similar health care system (Israeli Jews and Arabs) and to interpret the results. METHODS: Age-standardized rates of ovarian cancer incidence and mortality for 1994-2013 in the 3 countries were obtained from national cancer registries and national statistics. Time trends in incidence, mortality, and incidence-to-mortality ratio were assessed by linear regression models applied to each country and between populations (Ireland-NI, Ireland-Israeli Jews, Israeli Jews-Arabs). Joinpoint analysis was used to calculate the annual percentage change (APC). RESULTS: Ovarian cancer incidence and mortality rates in 1994 were similar in the countries studied. Thereafter a reduction in incidence and mortality was observed in Ireland (incidence APC1994-2013 = -0.75%, P < 0.05; mortality APC1994-2013 = -0.67%, P < 0.05), NI (incidence APC1998-2013 = -1.5%, P < 0.05; mortality APC2005-2013 = -3.8%, P < 0.05), and Israeli Jews (incidence APC1994-2013 = -2.2%, P < 0.05; mortality APC1994-2013 = -1.2%, P < 0.05). Trends in Israeli Arabs remained stable. Significant incidence trend differences between Ireland and Israeli Jews (P = 0.009) and between Israeli Jews and Arabs (P = 0.004) were observed. The only significant trend difference for mortality was between Israeli Jews and Arabs (P = 0.038). Incidence-to-mortality ratios showed stable trends in all groups except for Israeli Jews (APC1994-2013 = -1.0%, P < 0.05). CONCLUSIONS: Time trends in ovarian cancer incidence (decreasing) and mortality (decreasing) were similar in Ireland, NI, and Israeli Jews, following global trends, with a more prominent incidence decline in Israeli Jews. Decreasing mortality trends are driven by falling incidence in the countries studied rather than improved survival.

Polymorphic expression of glutathione transferases A1, M1, P1 and T1 in epithelial ovarian cancer: a Serbian case-control study.

PURPOSE: Since several studies have proposed that epithelial ovarian cancer should not be considered as a single disease entity and that it results from an accumulation of genetic changes, we aimed to assess the polymorphic expression of major cytosolic glutathione S-transferases (GSTM1, T1, A1 and P1) with respect to ovarian cancer susceptibility and aggressiveness. METHODS: This case-control study was conducted on 93 newly diagnosed epithelial ovarian cancer patients and 178 healthy matched controls. The multiplex polymerase chain reaction (PCR) was used to detect homozygous deletions of GSTM1 and GSTT1 genes. Analysis of the single nucleotide polymorphism (SNP) GSTA1 C69T was performed using PCR-restriction fragment length polymorphism (RFLP), while for SNP GSTP1 Ile105Val real-time PCR was used. RESULTS: No significant association to ovarian cancer risk was found for individual GSTM1, GSTA1 and GSTP1 genotypes (p>0.05). However, the carriers of GSTT1-active genotype were at 2-fold higher risk of ovarian cancer development (95%CI: 1.00-4.01, p=0.049), which was even more elevated in the subgroup of patients with positive family history of cancer. Moreover, the frequency of all three GST genotypes that might be associated to ovarian cancer risk (GSTT1-active, GSTA1-active and GSTP1-referent) was significantly higher in patients than in the control group (p=0.042). Even more, patients who were carriers of combination of these three genotypes represented over 64% of the total number of patients within any of the International Federation of Gynecology and Obstetrics (FIGO) stages of ovarian cancer. CONCLUSIONS: This study provides supportive evidence that GSTs might affect both susceptibility and progression of ovarian cancer.

Unexpected epithelial ovarian cancers arising from presumed endometrioma: A 10-year retrospective analysis.

OBJECTIVE: To evaluate the incidence and prognosis of unexpected epithelial ovarian cancers (EOCs) occurring in presumed benign endometrioma. MATERIALS AND METHODS: Patients who underwent primary surgery at Chang Gung Memorial Hospital between November 2003 and October 2013 were searched with the Systematized Nomenclature of Medicine code followed by chart review. RESULTS: The incidence of unexpected EOCs in presumed ovarian endometrioma was 0.14%, as 11 patients were revealed after reviewing 497 patients of pathology-proven EOCs in the current series. All patients were aged ≥ 40 years; seven (63.6%) had inward mass within ovarian cyst in preoperative images, six had cancer antigen-125 (CA-125) > 200 U/mL, and two with CA-125 > 1500 U/mL. Ten patients underwent laparoscopy initially, including five with ovarian preservation at the beginning. Ten patients subsequently completed concurrent or secondary staging surgery, including four totally with laparoscopy. The histologic subtypes had clear-cell (8/11), endometrioid (1/11), mixed clear-cell and endometrioid (1/11), and low-grade serous adenocarcinoma (1/11). Seven patients had endometriosis-associated ovarian carcinoma (EAOC), while the other four were non-EAOC with no endometriosis component. The only mortality was a patient of non-EAOC in Stage IIIc, whereas the other 10 in Stage I were alive. The overall survival rate was 90.9% (10/11) with follow-up ranging from 23 months to 130 months. CONCLUSION: Unexpected EOCs occurring in presumed ovarian endometrioma was rare and, if present, the prognosis was good in Stage I disease with laparoscopic management. Combining parameters of patient's age, CA-125 level, and inward solid mass at imaging could help to raise the precautions.

Lifetime number of ovulatory cycles and epithelial ovarian cancer risk in African American women.

PURPOSE: Incessant ovulation has been consistently linked to epithelial ovarian cancer (EOC). Although reproductive characteristics differ substantially by race, the association between incessant ovulation and EOC has been evaluated only in populations of predominantly white women. In the present study, we examined the association between lifetime number of ovulatory cycles (LOCs) and EOC risk among African American (AA) women. METHODS: We used data from 534 cases and 722 controls enrolled in the African American Cancer Epidemiology Study. LOCs were determined using the standard method, with modifications to include episodes of irregular or missed periods. Multivariable logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association between LOCs and EOC risk overall and by age, while adjusting for appropriate confounders. RESULTS: The mean number of LOCs was 378.2 ± 105.8 for cases and 346.4 ± 117.3 for controls. Women in the highest tertile of LOCs had 59% higher odds of EOC compared to women in the lowest tertile (OR = 1.59; 95% CI = 1.15-2.20). When examining this relationship by age, the positive association with EOC was stronger among women <50 years of age (OR for highest vs. lowest tertile = 2.61; 95% CI = 1.15-5.94), followed by women aged 50-60 years (OR = 2.27; 95% CI = 1.30-3.94). Yet, no association was present among women aged >60 years (OR = 0.79; 95% CI = 0.45-1.40). CONCLUSIONS: In a population of AA women, we observed a positive association between LOCs and EOC risk, providing further support for the hypothesis that incessant ovulation contributes to the etiology of EOC.

18F-FDG PET/CT as predictor of tumour biology and prognosis in epithelial ovarian carcinoma. / PET/TC con 18F-FDG como predictor de la biología tumoral y del pronóstico en el cáncer epitelial ovárico.

OBJECTIVE: To investigate the relationship between maximum standardised uptake value (SUVmax) of ovarian lesions and histopathology subtypes, and their involvement in the response and prognosis of patients with epithelial ovarian carcinoma (EOC). MATERIAL AND METHODS: A retrospective analysis of 31 patients with EOC and 18F-FDG-PET/CT before treatment, including an assessment of the SUVmax of ovarian lesion. Histopathological diagnosis and follow-up was performed. A study was made on the relationship between the SUVmax and histological type (type I and II) and tumour stage, as well as the role of various parameters (SUVmax, histology, stage) on the patient outcomes (complete response [CR], overall survival [OS], disease-free survival [DFS], and disease-free [DF] status, at 12 and 24 months). RESULTS: The medium SUVmax in type I lesions was lower than in type II (6.3 and 9.3, respectively; P=.03). A 7.1 cut-off was set for SUVmax in order to identify type II EOC (sensitivity: 77.8%, specificity: 69.2%; AUC=0.748; P=.02). No significant relationship was found between tumour stage and SUVmax. CR was more common in early stages; relative risk (RR) of 1.64; P=.003, as well as in type I tumours and a lower SUVmax. Tumour stage was decisive in DFS (P=.04), LE24m (0.07) and OS (P=.08). Longer DFS and a higher percentage of DF 24m were observed in type I tumours (RR: 1.32; P=.26). CONCLUSIONS: SUVmax was related to EOC histology, so could predict the response and prognosis of these patients. No association was found between glycolytic activity of the primary tumor with the response and prognosis.

Pelvic Inflammatory Disease and the Risk of Ovarian Cancer and Borderline Ovarian Tumors: A Pooled Analysis of 13 Case-Control Studies.

Inflammation has been implicated in ovarian carcinogenesis. However, studies investigating the association between pelvic inflammatory disease (PID) and ovarian cancer risk are few and inconsistent. We investigated the association between PID and the risk of epithelial ovarian cancer according to tumor behavior and histotype. We pooled data from 13 case-control studies, conducted between 1989 and 2009, from the Ovarian Cancer Association Consortium (OCAC), including 9,162 women with ovarian cancers, 2,354 women with borderline tumors, and 14,736 control participants. Study-specific odds ratios were estimated and subsequently combined into a pooled odds ratio using a random-effects model. A history of PID was associated with an increased risk of borderline tumors (pooled odds ratio (pOR) = 1.32, 95% confidence interval (CI): 1.10, 1.58). Women with at least 2 episodes of PID had a 2-fold increased risk of borderline tumors (pOR = 2.14, 95% CI: 1.08, 4.24). No association was observed between PID and ovarian cancer risk overall (pOR = 0.99, 95% CI: 0.83, 1.19); however, a statistically nonsignificantly increased risk of low-grade serous tumors (pOR = 1.48, 95% CI: 0.92, 2.38) was noted. In conclusion, PID was associated with an increased risk of borderline ovarian tumors, particularly among women who had had multiple episodes of PID. Although our results indicated a histotype-specific association with PID, the association of PID with ovarian cancer risk is still somewhat uncertain and requires further investigation.