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Area of Science:

  • Oncology
  • Hematology
  • Molecular Biology

Background:

  • Oncogenic events significantly alter cancer cell interactions with their microenvironment, particularly affecting angiogenesis, inflammation, and hemostasis.
  • Mutant oncogenes and tumor suppressor gene losses modulate the expression of angiogenic, inflammatory, and procoagulant factors, including tissue factor (TF).
  • Coagulation system dysregulation is implicated in various cancer stages, from initiation and angiogenesis to invasion and metastasis.

Purpose of the Study:

  • To elucidate the intricate relationship between oncogenic events and the coagulation system in cancer progression.
  • To highlight how altered expression of coagulation factors and receptors by cancer cells influences tumor behavior.
  • To explore the potential of targeting the coagulation system for cancer diagnostics and therapeutics.

Main Methods:

  • Review of oncogenes (EGFR, HER2, RAS, MET, PML-RARα) and tumor suppressor genes (PTEN, p53) roles.
  • Analysis of microRNAs (miR-19b, miR-520) involvement in cancer-coagulation crosstalk.
  • Investigation of ectopic coagulation factor production and procoagulant microparticle release by cancer cells.
  • Examination of protease-activated receptors (PAR1/2) deregulation and their signaling.
  • Consideration of microenvironmental factors (hypoxia) and cellular processes (EMT, TIC) in this interplay.

Main Results:

  • Oncogenes and tumor suppressors reprogram the cancer cell coagulome, affecting TF, PAI-1, and COX2 levels.
  • Cancer cells can ectopically produce coagulation factors (e.g., FVII) and release procoagulant microparticles.
  • Deregulation of PAR1/2 alters cancer cell responses to coagulation factor signaling.
  • The coagulation system, particularly TF, acts as a molecular switch in cancer dormancy and progression.
  • Tumor-initiating cells (TICs) express TF and PARs, suggesting their role in coagulation-mediated effects.

Conclusions:

  • The coagulation system is a critical regulator of cancer progression, influencing all stages from initiation to metastasis.
  • TF's role as a molecular switch highlights its potential as a prognostic and therapeutic target.
  • Understanding cancer subtype-specific interactions with the coagulation system may yield novel diagnostic and therapeutic strategies.
  • Targeting the crosstalk between cancer cells and the coagulation cascade presents promising opportunities for oncology.