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Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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Related Experiment Video

Updated: May 13, 2025

Analyzing the Communication Between Monocytes and Primary Breast Cancer Cells in an Extracellular Matrix Extract ECME-based Three-dimensional System
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Understanding Merkel Cell Carcinoma: Pathogenic Signaling, Extracellular Matrix Dynamics, and Novel Treatment

Maria Konstantaraki1,2, Aikaterini Berdiaki1, Monica Neagu3,4

  • 1Department of Histology-Embryology, Medical School, University of Crete, 71003 Heraklion, Greece.

Cancers
|April 14, 2025
PubMed
Summary

Merkel cell carcinoma (MCC), an aggressive skin cancer, is driven by viruses or UV radiation. Targeting the tumor microenvironment alongside immune checkpoints may overcome treatment resistance.

Keywords:
Merkel cell carcinomaextracellular matriximmunologysignaling pathwaystargeted molecular treatment

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Area of Science:

  • Oncology
  • Immunology
  • Dermatology

Background:

  • Merkel cell carcinoma (MCC) is a rare, aggressive neuroendocrine skin cancer.
  • It is driven by Merkel cell polyomavirus (MCPyV) or UV-induced mutations, activating oncogenic pathways.
  • Key signaling pathways like PI3K/AKT/mTOR and MAPK promote tumor growth and survival.

Purpose of the Study:

  • To elucidate the role of the tumor microenvironment (TME) in MCC progression and immune escape.
  • To explore the mechanisms of resistance to immune checkpoint inhibitors in MCC.
  • To identify potential therapeutic strategies targeting the TME to enhance treatment efficacy.

Main Methods:

  • Histological analysis of MCC small round blue cells, high mitotic rate, and necrosis.
  • Characterization of the TME, including immune cells and extracellular matrix (ECM) components.
  • Analysis of immune checkpoint molecule expression (e.g., PD-L1) and signaling pathways (e.g., PI3K/AKT/mTOR, MAPK).

Main Results:

  • The TME in MCC is characterized by immunosuppressive cells and elevated PD-L1 expression.
  • The ECM, rich in proteoglycans, collagens, and MMPs, facilitates tumor invasion and immune evasion.
  • Integrin-mediated signaling contributes to therapy resistance.

Conclusions:

  • The TME plays a critical role in MCC pathogenesis and immune evasion.
  • Resistance to current therapies like immune checkpoint inhibitors is a significant challenge.
  • Combined therapeutic strategies targeting the TME (ECM, MMPs, integrins) may improve outcomes for MCC patients.