Epigenetic changes found in uterine decidual and placental tissues can also be found in the breast cancer microenvironment of the same unique patient: description and potential interpretations

2017 
// Miguel H. Bronchud 1 , Francesc Tresserra 2 and Bernat Serra Zantop 3 1 Institut Bellmunt Oncologia, Hospital Universitari Dexeus, Grupo Quiron Salud, Barcelona, 08028 Spain 2 Servicio de Anatomia Patologica y Citologia, Hospital Universitari Dexeus, Grupo Quiron Salud, Barcelona, 08028 Spain 3 Servicio de Ginecologia, Obstetricia y Reproduccion, Hospital Universitari Dexeus, Grupo Quiron Salud, Barcelona, 08028 Spain Correspondence to: Miguel H. Bronchud, email: mhbronchud@gmail.com Keywords: materno-fetal tolerance; cancer microenvironment; placental microenvironment; immune vigilance; carcinogenesis Received: April 21, 2017      Accepted: December 02, 2017      Published: December 19, 2017 ABSTRACT Microenvironmental properties are thought to be responsible for feto-maternal tolerance. Speculatively, ectopic expression of placental gene programs might also be related to cancer cells’ ability to escape from immune vigilance mechanisms during carcinogenesis and cancer progression. Recently, we published the first human genomic evidence of similar immune related gene expression profiles in both placenta (placenta and decidual tissue) and cancer (both primary and metastatic) in the same patient with lymph-node positive breast carcinoma during pregnancy. Here we report the first epigenomic analysis of these tissue samples and describe their main findings, with respect to immune related genes regulation (over or under expressed) in cancer cells with regards placental tissues. We confirm significant similarities, and hierarchical clustering (both unsupervised and supervised), in CpG island methylation patterns between decidual/placental and cancer microenvironments, which cannot be easily explained by simple models or unique pathways. Several different cell types are probably involved in these complex immune regulation mechanisms. Cancers may somehow “hijack” gene programs evolved over millions of years to allow for feto-maternal tolerance in placental mammals in order to escape from immune vigilance and spread locally or to distant sites.
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