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Adaptive Mechanisms in Cancer Cells02:53

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Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
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Pericyte phenotype switching in cancer.

Bo He1, Ruth Ganss1

  • 1Cancer Microenvironment Laboratory, Harry Perkins Institute of Medical Research, QEII Medical Centre and Centre for Medical Research, The University of Western Australia, Perth, Australia.

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|July 8, 2025
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Cancer pericytes, crucial for tumor growth, can be therapeutically reprogrammed. Harnessing pericyte plasticity offers new strategies to combine targeted cancer therapies with immunotherapy.

Keywords:
angiogenesisblood vessel normalizationcancerimmunotherapypericytes

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Area of Science:

  • Oncology
  • Vascular Biology
  • Cancer Immunology

Background:

  • Pericytes are vital for maintaining blood vessel integrity.
  • In cancer, pericytes transform, promoting tumor progression, vascular instability, and immune evasion.
  • Tumor pericytes exhibit plasticity, enabling a switch between states.

Purpose of the Study:

  • To explore the role of pericyte plasticity in cancer.
  • To investigate therapeutic strategies targeting pericyte phenotype switching.
  • To assess the potential of pericyte modulation in combination cancer therapy.

Main Methods:

  • Analysis of transcriptomics and functional data on tumor pericytes.
  • Investigation of signaling pathways (oncogenic, metabolic, microtubule) influencing pericyte phenotype.
  • Evaluation of Rho kinase activity in pericyte modulation.
  • Preclinical models assessing combination therapy efficacy.

Main Results:

  • Cancer pericytes shift from quiescent to proliferative, matrix-secreting phenotypes.
  • This shift destabilizes tumor vasculature and creates immune-excluded zones.
  • Tumor pericytes can be therapeutically induced to revert to a quiescent, contractile state.
  • Targeting specific pathways can trigger this beneficial phenotype switch.

Conclusions:

  • Pericyte plasticity is a key factor in tumor progression and response to therapy.
  • Targeting pericyte phenotype switching offers a novel strategy for tumor vessel normalization.
  • Harnessing pericyte plasticity can enhance the efficacy of targeted anticancer treatments and immunotherapy.