Aggressive Breast Cancer during Pregnancy with a Rare Form of Metastasis in the Maternal Placenta.
Ontology highlight
ABSTRACT:
SUBMITTER: Vetter G
PROVIDER: S-EPMC4069211 | biostudies-literature | 2014 Jun
REPOSITORIES: biostudies-literature
Publications
Aggressive Breast Cancer during Pregnancy with a Rare Form of Metastasis in the Maternal Placenta.
Vetter G G Zimmermann F F Bruder E E Schulzke S S Hösli I I Vetter M M
Geburtshilfe und Frauenheilkunde 20140601 6
Breast cancer is the second most common cancer diagnosed during pregnancy. Here we describe a 29-year-old patient with a recurrence of breast cancer with simultaneous brain, pulmonary and placenta metastasis. An overview of the literature on placenta metastases is provided together with a report on the interdisciplinary medical management. ...[more]
Similar Datasets
Project description:Although recent studies have demonstrated that microRNAs (miRNAs or miRs) regulate fundamental natural killer (NK) cellular processes, including cytotoxicity and cytokine production, little is known about the miRNA-gene regulatory relationships in maternal peripheral blood NK (pNK) cells during pregnancy. In the present study, to determine the roles of miRNAs within gene regulatory networks of maternal pNK cells, we performed comprehensive miRNA and gene expression profiling of maternal pNK cells using a combination of reverse transcription quantitative PCR (RT-qPCR)-based miRNA array and DNA microarray analyses and analyzed the differential expression levels between first- and third-trimester pNK cells. Furthermore, we constructed regulatory networks for miRNA-mediated gene expression in pNK cells during pregnancy by Ingenuity Pathway Analysis (IPA). PCR-based array analysis revealed that the placenta-derived miRNAs [chromosome 19 miRNA cluster (C19MC) miRNAs] were detected in pNK cells during pregnancy. Twenty-five miRNAs, including six C19MC miRNAs, were significantly upregulated in the third- compared to first-trimester pNK cells. The rapid clearance of C19MC miRNAs also occurred in the pNK cells following delivery. Nine miRNAs, including eight C19MC miRNAs, were significantly downregulated in the post-delivery pNK cells compared to those of the third-trimester. DNA microarray analysis identified 69 NK cell function-related genes that were differentially expressed between the first- and third-trimester pNK cells. On pathway and network analysis, the observed gene expression changes of pNK cells likely contribute to the increase in the cytotoxicity, as well as the cell cycle progression of third- compared to first-trimester pNK cells. Thirteen of the 69 NK cell function-related genes were significantly downregulated between the first- and third-trimester pNK cells. Nine of the 13 downregulated NK-function-associated genes were in silico target candidates of 12 upregulated miRNAs, including C19MC miRNA miR-512-3p. The results of this study suggest that the transfer of placental C19MC miRNAs into maternal pNK cells occurs during pregnancy. The present study provides new insight into maternal NK cell functions.
| S-EPMC4432927 | biostudies-literature
Project description:Exosomes are a subset of extracellular vesicles with an average diameter of ~100nm. Exosomes are released by all cells through an endosome-dependent pathway and carry nucleic acids, proteins, lipids, cytokines and metabolites, mirroring the state of the originating cells. The function of exosomes has been implicated in various reproduction processes, such as embryo development, implantation, decidualization and placentation. Placenta-derived exosomes (pEXO) can be detected in the maternal blood as early as 6 weeks after conception and their levels increase with gestational age. Importantly, alternations in the molecular signatures of pEXO are observed in pregnancy-related complications. Thus, these differentially expressed molecules could be the potential biomarkers for diagnosis of the pregnancy-associated diseases. Recent studies have demonstrated that pEXO play a key role in the establishment of maternal immune tolerance, which is critical for a successful pregnancy. To gain a better understanding of the underlying mechanism, we highlighted the advanced studies of pEXO on immune cells in pregnancy.
| S-EPMC8144714 | biostudies-literature
Project description:Abnormal blood pressure during pregnancy is associated with impaired fetal growth, predisposing the offspring to cardiometabolic abnormalities over the life-course. Placental DNA methylation may be the regulatory pathway through which maternal blood pressure influences fetal and adult health outcomes. Epigenome-wide association study of 301 participants with placenta sample examined associations between DNA methylation and millimetre of mercury increases in systolic and diastolic blood pressure in each trimester. Findings were further examined using gene expression, gene pathway, and functional annotation analyses. Cytosine-(phosphate)-guanine (CpGs) known to be associated with cardiometabolic traits were evaluated. Increased maternal systolic and diastolic blood pressure were associated with methylation of 3 CpGs in the first, 6 CpGs in the second, and 15 CpGs in the third trimester at 5% false discovery rate (P values ranging from 6.6×10-15 to 2.3×10-7). Several CpGs were enriched in pathways including cardiovascular-metabolic development (P=1.0×10-45). Increased systolic and diastolic blood pressure were associated with increased CpG methylation and gene expression at COL12A1, a collagen family gene known for regulatory functions in the heart. Out of 304 previously reported CpGs known to be associated with cardiometabolic traits, 36 placental CpGs were associated with systolic and diastolic blood pressure in our data. The present study provides the first evidence for associations between placental DNA methylation and increased maternal blood pressure during pregnancy at genes implicated in cardiometabolic diseases. Identification of blood pressure-associated methylated sites in the placenta may provide clues to early origins of cardiometabolic dysfunction and inform guidelines for early prevention. Registration- URL: http://www.clinicaltrials.gov. Unique identifier: NCT00912132.
| S-EPMC7122078 | biostudies-literature
Project description:Triple-negative breast cancer (TNBC) is a highly heterogeneous disease defined by the absence of estrogen receptor (ER) and progesterone receptor (PR) expression, and human epidermal growth factor receptor 2 (HER2) overexpression that lacks targeted treatments, leading to dismal clinical outcomes. Thus, better stratification systems that reflect intrinsic and clinically useful differences between TNBC tumors will sharpen the treatment approaches and improve clinical outcomes. The lack of a rational classification system for TNBC also impacts current and emerging therapeutic alternatives. In the past years, several new methodologies to stratify TNBC have arisen thanks to the implementation of microarray technology, high-throughput sequencing, and bioinformatic methods, exponentially increasing the amount of genomic, epigenomic, transcriptomic, and proteomic information available. Thus, new TNBC subtypes are being characterized with the promise to advance the treatment of this challenging disease. However, the diverse nature of the molecular data, the poor integration between the various methods, and the lack of cost-effective methods for systematic classification have hampered the widespread implementation of these promising developments. However, the advent of artificial intelligence applied to translational oncology promises to bring light into definitive TNBC subtypes. This review provides a comprehensive summary of the available classification strategies. It includes evaluating the overlap between the molecular, immunohistochemical, and clinical characteristics between these approaches and a perspective about the increasing applications of artificial intelligence to identify definitive and clinically relevant TNBC subtypes.
| S-EPMC8242253 | biostudies-literature
Project description:BACKGROUND:To study in a large-scale cohort with prospective data the associations between psychosocial stress during pregnancy and placenta weight at birth. Animal data suggest that the placenta is involved in stress-related fetal programming. METHODOLOGY/PRINCIPAL FINDINGS:We defined a priori two types of psychosocial stress during pregnancy, life stress (perceived burdens in major areas of life) and emotional symptoms (e.g. anxiety). We estimated the associations of maternal stress during pregnancy with placenta weight at birth, controlled for length of gestation, by predicting gestational age- and sex-specific z-scores of placenta weight through multiple regression analysis, adjusted for potential confounders (N?=?78,017 singleton pregnancies). Life stress (per increase in stress score by 1, range: 0-18) during pregnancy was associated with increased placenta weight at birth (z-score, reported in 10(-3); B, 14.33; CI, 10.12-18.54). In contrast, emotional symptoms during pregnancy were not associated with placenta weight at birth. CONCLUSIONS/SIGNIFICANCE:Maternal life stress but not emotional symptoms during pregnancy was associated with increased placenta weight at birth; yet, the association-estimate was rather small. Our results may contribute to a better understanding of the role of the placenta in the regulation of intrauterine processes in response to maternal stress.
| S-EPMC3013108 | biostudies-literature
Project description:Maternal pregnancy adaptation is crucial for fetal development and long-term health. Complex interactions occur between maternal digestive and excretory systems as they interface with the developing fetus through the placenta, and transcriptomic regulation in these organs throughout pregnancy is poorly understood. Our objective is to characterize transcriptomic changes across gestation in maternal organs and placenta. Gene expression was quantified in the kidney, liver, and small intestine harvested from nonpregnant and pregnant FVB mice at four time points and placenta at three time points (N = 5/time point) using Affymetrix Mouse Gene 1.0 ST arrays. In maternal organs, we identified 476 genes in the liver, 207 genes in the kidney, and 27 genes in the small intestine that were differentially expressed across gestation (False Discovery Rate [FDR] adjusted q < 0.05). The placenta had a total of 1576 differentially expressed genes between the placenta at either/gd15 or gd19 compared to gd10. We identified a number of pathways enriched for genes differentially expressed across gestation, including 5 pathways in the placenta, 9 pathways in the kidney, and 28 pathways in the liver, including the citrate cycle, retinol metabolism, bile acid synthesis, and steroid bile synthesis, which play functional roles in fetal development and pregnancy maintenance. Characterization of normal longitudinal changes that occur in pregnancy provides context to understand how perturbations in these biochemical pathways and perturbations in nutrient signaling may impact pregnancy.
| S-EPMC6692859 | biostudies-literature
Project description:RNAseq analysis of placental gene expression in samples obtained from 59 smokers (enrolled in the VCSIP RCT: NCT03203603) and 20 never-smokers for reference.
2024-03-07 | GSE253158 | GEO
Project description:The idea that susceptibility to breast cancer is determined not only through inherited germline mutations but also by epigenetic changes induced by alterations in hormonal environment during fetal development is gaining increasing support. Using findings obtained in human and animal studies, this review addresses the mechanisms that may explain why daughters of mothers who took synthetic estrogen diethylstilbestrol (DES) during pregnancy have two times higher breast cancer risk than women who were not exposed to it. The mechanisms likely involve epigenetic alterations, such as increased DNA methylation and modifications in histones and microRNA expression.Further, these alterations may target genes that regulate stem cells and prevent differentiation of their daughter cells. Recent findings in a preclinical model suggest that not only are women exposed to DES in utero at an increased risk of developing breast cancer, but this risk may extend to their daughters and granddaughters as well. It is critical, therefore, to determine if the increased risk is driven by epigenetic alterations in genes that increase susceptibility to breast cancer and if these alterations are reversible.
| S-EPMC4053091 | biostudies-literature
Project description:Although recent studies have revealed that microRNAs (miRNAs) regulate fundamental Natural Killer (NK) cell processes including cytotoxicity and cytokine production, little is known about the miRNA-gene regulatory relationships in maternal peripheral blood NK (pNK) cells during pregnancy. To predict the role of miRNAs within gene regulatory networks of maternal pNK cells during pregnancy, we performed comprehensive miRNA and gene expression profiling of maternal pNK cells using a combination of real-time PCR-based array and DNA microarray analyses and analyzed these differential expression levels between first- and third-trimester pNK cells. Furthermore, we constructed regulatory networks for miRNA-mediated gene expression in pNK cells during pregnancy by Ingenuity Pathway Analysis. By PCR-based array analysis of miRNAs, 12 miRNAs including 6 placenta-derived miRNAs [chromosome 19 microRNA cluster (C19MC) miRNAs] were significantly upregulated in third-trimester pNK cells compared to first-trimester pNK cells. pNK cells incorporated C19MC miRNAs, whose interaction would be mediated via exosomes. Rapid clearance of C19MC miRNAs also occurred in NK cells after delivery. By DNA microarray analysis, 13 NK cell function-related genes were significantly downregulated between first- and third-trimester pNK cells. By pathway and network analysis, 9 downregulated NK-function-associated genes were in silico target candidates of 12 upregulated miRNAs including C19MC miRNA miR-512-3p. The results suggest that transfer of placental C19MC-miRNAs into maternal pNK cells occurs during pregnancy. The present study provides clues to understand maternal NK cell functions Gene expressions in human maternal peripheral blood NK cells were measured at 1st-trimester, 3rd-trimester. Five independent experiments were performed at each term (1st-trimester or 3rd-trimester) using different donors for each experiment.
2015-01-13 | E-GEOD-64884 | biostudies-arrayexpress
Project description:Although recent studies have revealed that microRNAs (miRNAs) regulate fundamental Natural Killer (NK) cell processes including cytotoxicity and cytokine production, little is known about the miRNA-gene regulatory relationships in maternal peripheral blood NK (pNK) cells during pregnancy. To predict the role of miRNAs within gene regulatory networks of maternal pNK cells during pregnancy, we performed comprehensive miRNA and gene expression profiling of maternal pNK cells using a combination of real-time PCR-based array and DNA microarray analyses and analyzed these differential expression levels between first- and third-trimester pNK cells. Furthermore, we constructed regulatory networks for miRNA-mediated gene expression in pNK cells during pregnancy by Ingenuity Pathway Analysis. By PCR-based array analysis of miRNAs, 12 miRNAs including 6 placenta-derived miRNAs [chromosome 19 microRNA cluster (C19MC) miRNAs] were significantly upregulated in third-trimester pNK cells compared to first-trimester pNK cells. pNK cells incorporated C19MC miRNAs, whose interaction would be mediated via exosomes. Rapid clearance of C19MC miRNAs also occurred in NK cells after delivery. By DNA microarray analysis, 13 NK cell function-related genes were significantly downregulated between first- and third-trimester pNK cells. By pathway and network analysis, 9 downregulated NK-function-associated genes were in silico target candidates of 12 upregulated miRNAs including C19MC miRNA miR-512-3p. The results suggest that transfer of placental C19MC-miRNAs into maternal pNK cells occurs during pregnancy. The present study provides clues to understand maternal NK cell functions
2015-01-13 | GSE64884 | GEO