BACKGROUND AND OBJECTIVES: Preterm birth (PTB) and congenital heart defect (CHD) are 2 major causes of mortality and disability of perinatal origin. There are limited data on the relation between CHD and PTB. Our objective was to use population-based data to estimate the risk of PTB in newborns with CHD and to study specific associations between categories of CHD and PTB. METHODS: We used data from a population-based cohort study of CHD (EPIdémiologique sur le devenir des enfants porteurs de CARDiopathies congénitales study), including 2189 live births with CHD (excluding isolated atrial septal defects) born between 2005 and 2008. We categorized CHD by using an anatomic and clinical classification. Data from the French National Perinatal Survey of 2003 were used to compare PTB in the EPIdémiologique sur le devenir des enfants porteurs de CARDiopathies congénitales study to that of the general population. RESULTS: Of the newborns with CHD, 13.5% were preterm. The odds of PTB were twofold higher than for the general population (odds ratio 2.0, 95% confidence interval 1.6–2.5), essentially due to an increase in spontaneous PTB for newborns with CHD. The risk of PTB associated with CHD persisted after exclusion of chromosomal or other anomalies. There were significant variations in risk of PTB across the categories of CHD after adjustment for known risk factors of PTB and factors related to medical management of pregnancy and delivery. CONCLUSIONS: We found a higher risk of PTB in newborns with CHD, which was essentially due to spontaneous PTB. Risk of PTB varied for categories of CHD. Our finding may be helpful for generating hypotheses about the developmental links between CHD and PTB.

Congenital heart defects (CHD) and preterm birth (PTB) are major causes of infant mortality. However, limited data exist on risk of mortality associated with PTB for newborns with CHD. Our objective was to assess impact of PTB on risk of infant mortality for newborns with CHD, while taking into account the role of associated anomalies and other potentially confounding factors. We used data on 2172 live births from a prospective population-based cohort study of CHD (the EPICARD Study) and compared neonatal, post-neonatal and overall infant mortality for infants born at <32, 32–34 and 35–36 weeks vs. those born at term (37–41 weeks). Preterm newborns had a 3.8-fold higher risk of infant death (17.9%) than term newborns (4.7%), RR 3.8, 95%CI 2.7–5.2; the risk associated with PTB was more than four-fold higher for neonatal (RR 4.3, 95% CI 2.9–6.6) and three-fold higher for post-neonatal deaths (RR 3.0, 95% CI 1.7–5.2). Survival analysis showed that newborns <35 weeks had a higher risk of mortality, which decreased but persisted after exclusion of associated anomalies and adjustment for potential confounders. Preterm birth is associated with an approximately four-fold higher risk of infant mortality for newborns with CHD. This excess risk appears to be mostly limited to newborns <35 weeks of gestation and is disproportionately due to early deaths.

Background: Breast cancer (BC) is the most frequent cancer and the leading cause of cancer-related death in women. The French National Cancer Institute has created a national cancer cohort to promote cancer research and improve our understanding of cancer using the National Health Data System (SNDS) and amalgamating all cancer sites. So far, no detailed separate data are available for early BC. Objectives: To describe the creation of the French Early Breast Cancer Cohort (FRESH). Methods: All French women aged 18 years or over, with early-stage BC newly diagnosed between 1 January 2011 and 31 December 2017, treated by surgery, and registered in the general health insurance coverage plan were included in the cohort. Patients with suspected locoregional or distant metastases at diagnosis were excluded. BC treatments (surgery, chemotherapy, targeted therapy, radiotherapy, and endocrine therapy), and diagnostic procedures (biopsy, cytology, and imaging) were extracted from hospital discharge reports, outpatient care notes, or pharmacy drug delivery data. The BC subtype was inferred from the treatments received. Results: We included 235,368 patients with early BC in the cohort (median age: 60 years). The BC subtype distribution was as follows: luminal (80.2%), triple-negative (TNBC, 9.5%); HER2⁺ (10.3%), or unidentifiable (n = 44,388, 18.9% of the cohort). Most patients underwent radiotherapy (n = 200,685, 85.3%) and endocrine therapy (n = 165,655, 70.4%), and 38.3% (n = 90,252) received chemotherapy. Treatments and care pathways are described. Conclusions: The FRESH Cohort is an unprecedented population-based resource facilitating future large-scale real-life studies aiming to improve care pathways and quality of care for BC patients.

Most endocervical adenocarcinomas are human papillomavirus (HPV)-related cancers associated with p16 immunostaining. Ovarian metastasis from cervical cancer is a rare phenomenon, the mechanism of dissemination remains unclear. The diagnosis of metastasis may be difficult to establish when the ovarian neoplasm presents features consistent with primary tumor. Immunohistochemical expression of p16 in ovarian tumors can guide the diagnosis of metastasis from HPV-related cervical cancer, but p16 positivity is nonspecific. Identical HPV genotype in the paired endocervical and ovarian tumors is a better marker for cervical origin, which may also be confirmed by identical HPV integration site. Two women presented with HPV18 cervical adenocarcinoma. No signs of disease were visible on MRI after treatment. After several years of follow-up, mucinous ovarian tumors were discovered in both patients. Molecular analyses showed that the ovarian lesions were HPV18-positive; indicating a primary cervical origin. A third woman was diagnosed with grade 1 ovarian endometrioid carcinoma with no peritoneal carcinomatosis. Final histological examination and HPV genotyping revealed HPV18-related in situ endometrioid adenocarcinoma in the endocervix and HPV18-related invasive endometrioid adenocarcinoma in the endometrium and both ovaries. Additional molecular analyses performed in two patients identified the same HPV integration sites in both the ovarian and cervical tumors, confirming that the ovarian mass was a metastasis from the cervical adenocarcinoma. We report three new cases of ovarian neoplasia in which the diagnosis of metastasis from cervical cancer was supported by the same HPV genotype and the same integration site in the paired cervical and ovarian tumors. To our knowledge, this is the first report of molecular evidence of the cervical origin of an ovarian metastasis. HPV screening should be performed in ovarian tumors for all patients with history of cervical neoplasia.