Abstract
The hypothesis of this work is that, in order to escape the natural immune surveillance mechanisms, cancer cells and the surrounding microenvironment might express ectopically genes that are physiologically present in the placenta to mediate fetal immune-tolerance. These natural “placental immune-editing switch” mechanisms (PIES) may represent the result of millions of years of mammalian evolution developed to allow materno-fetal tolerance. Here, we introduce genes of the immune regulatory pathways that are either similarly over- or under-expressed in tumor vs normal tissue. Our analysis was carried out in primary breast cancer with metastatic homolateral axillary lymph nodes as well as placenta tissue (both uterine decidual tissue and term placenta tissue) from a pregnant woman. Gene expression profiling of paired non-self and self tissues (i.e. placenta/uterus; breast cancer/normal breast tissue; metastatic lymphnode/normal lymphnode tissue) was performed using the PanCancer Immune gene panel, a 770 Nanostring gene expression panel. Our findings reveal overlapping in specific immune gene expression in placenta and cancer tissue, suggesting that these genes might play an important role in maintaining immune tolerance both physiologically (in the placenta) and pathologically (in the cancer setting).
Highlights
Cancer microenvironment has been recognized to be a crucial determinant of cancer cells behavior through both positive and negative effects on tumor growth
The breast carcinoma was classified as lobular breast carcinoma (LBC), with some areas of in situ component, stage pT2 pN2a Mo (5/15 axillary lymph nodes with metastatic disease), and with immunohistochemistry characteristics of Luminal A subtype (ER60%+, PR50%+, HER-2 negative and Ki67 5% positivity)
The gene expression profiling analysis was designed to assess whether there were common patterns of immune gene expression shared between placenta and cancer tissue
Summary
Cancer microenvironment has been recognized to be a crucial determinant of cancer cells behavior through both positive and negative effects on tumor growth. A typical immune response in a health individual originates with dendritic cells (DC), which are responsible for initiating all antigen-specific immune responses. As such, they can be considered the master regulators of the immune response. They can be considered the master regulators of the immune response These cells activate T cells by a complex molecular mechanism by which the peptides are presented by the MHC molecules and are recognized by T-cell receptors, and these T cells can differentiate into various effectors including cytotoxic and helper T cells
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