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Digestive system deep infiltrating endometriosis: What do we know.

Wenze Yin1, Xiaoqing Li2, Peng Liu3

  • 1Department of Hepatic Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China.

Journal of Cellular and Molecular Medicine
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Digestive system infiltrating endometriosis (DSIE) is a rare condition mimicking cancer. Understanding its unique mechanisms, like nerve recruitment and fibrosis, is crucial for developing new treatments beyond surgery.

Keywords:
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Area of Science:

  • Gastroenterology
  • Gynecology
  • Oncology

Background:

  • Digestive system infiltrating endometriosis (DSIE) is an uncommon manifestation of endometriosis.
  • It commonly affects the intestines, liver, gallbladder, and pancreas.
  • DSIE shares symptoms with general endometriosis but includes unique gastrointestinal issues like obstruction and bleeding.

Purpose of the Study:

  • To elucidate the unique biological behavior and pathophysiological mechanisms of DSIE.
  • To highlight DSIE's distinct characteristics compared to general endometriosis.
  • To underscore the need for novel therapeutic strategies.

Main Methods:

  • Review of DSIE pathophysiology, including deep invasive characteristics.
  • Analysis of angiogenesis patterns (angiogenesis, vasculogenesis, inosculation) and their regulation.
  • Examination of neurofibril recruitment, fibrosis, and repeated tissue injury and repair (ReTIAR) mechanisms.
  • Investigation of cell migration pathways (E-cadherin, N-cadherin) contributing to aggressiveness.
  • Comparison of DSIE's clinical presentation and behavior to malignant tumors.

Main Results:

  • DSIE exhibits deep invasive properties with lymph node metastasis, angiogenesis, nerve recruitment, and fibrosis.
  • Angiogenesis in DSIE follows three patterns regulated by hypoxia-hormone cytokines.
  • Nerve growth factors drive neurofibril recruitment, causing severe pain and contributing to fibrosis and aggressiveness.
  • ReTIAR mechanisms, inflammation, and oxidative stress accelerate fibrosis and potential cancer-related mutations.
  • DSIE's collective cell migration via E-cadherin and N-cadherin contributes to aggressiveness, leading to misdiagnosis as malignancy.

Conclusions:

  • DSIE possesses unique pathophysiological mechanisms distinct from general endometriosis.
  • Its aggressive behavior, nerve involvement, and potential for misdiagnosis necessitate further research.
  • Novel treatments are urgently needed to effectively manage DSIE, given its complexity and resemblance to cancer.