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The Tumor Microenvironment02:17

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Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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A Proximal Culture Method to Study Paracrine Signaling Between Cells
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Endometrial Tumour Microenvironment.

Carlos Casas-Arozamena1, Miguel Abal2,3

  • 1Translational Medical Oncology Group (Oncomet), Health Research Institute of Santiago de Compostela (IDIS), University Hospital of Santiago de Compostela (SERGAS), Santiago de Compostela, Spain.

Advances in Experimental Medicine and Biology
|June 29, 2021
PubMed
Summary

Endometrial cancer (EC) is rising due to obesity. The tumor microenvironment, involving stromal cells and cytokines, drives EC growth, invasion, and metastasis, offering future therapeutic targets.

Keywords:
Activated stromaCarcinoma-associated fibroblastsEndometrial cancerEndothelial cellsEpithelial-mesenchymal transitionExtracellular matrixHormone-regulated tissueImmune checkpoint inhibitorsMyometrial invasionOestrogen receptorsPericytesTumour microenvironmentTumour-associated macrophagesTumour-derived growth factorsTumour-infiltrating lymphocytes

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Area of Science:

  • Oncology
  • Gynaecology
  • Cancer Biology

Background:

  • Endometrial cancer (EC) is the most common gynaecological malignancy in developed nations.
  • Increasing incidence is linked to obesity and associated hormone dysregulation.
  • The tumor microenvironment (TME) is crucial in EC development and progression.

Purpose of the Study:

  • To elucidate the role of the tumor microenvironment in endometrial cancer.
  • To identify key cellular and molecular players within the EC TME.
  • To explore potential therapeutic strategies targeting the EC TME.

Main Methods:

  • Review of current literature on endometrial cancer and tumor microenvironment.
  • Analysis of cellular interactions and signaling pathways within the EC TME.
  • Discussion of the impact of stromal cells, cytokines, and growth factors.

Main Results:

  • The TME promotes tumor cell proliferation via unopposed estrogen stimulation.
  • Stromal cells, including cancer-associated fibroblasts and tumor-associated macrophages, secrete factors (SDF-1, TGF-b, HGF) that drive epithelial-to-mesenchymal transition (EMT).
  • Endothelial cells contribute to metastasis through VEGF-mediated lymph node and vascular infiltration.

Conclusions:

  • The tumor microenvironment is a key driver of endometrial cancer growth, invasion, and metastasis.
  • Targeting the immunosuppressive TME in advanced EC presents a promising future therapeutic strategy.
  • Understanding TME components is vital for developing novel EC treatments.