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Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
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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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Targeting tumor resistance mechanisms.

Louise Gerard1, Laurent Duvivier1, Jean-Pierre Gillet1

  • 1Laboratory of Molecular Cancer Biology, Molecular Physiology Research Unit (URPhyM), Namur Research Institute for Life Sciences (NARILIS), Faculty of Medicine, University of Namur, Namur, Belgium.

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Summary

Understanding cancer resistance mechanisms is key to improving treatment success. New preclinical models and drug discovery approaches are needed to enhance clinical trial predictability.

Keywords:
Therapeutic developmentsorganoidstranslatability of preclinical studiesvenoms

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Area of Science:

  • Oncology
  • Cancer Research
  • Drug Discovery

Background:

  • Cancer develops resistance to treatments via multiple mechanisms, often coexisting within a tumor.
  • Intratumor heterogeneity and the tumor microenvironment significantly influence treatment response and cancer cell adaptation.
  • Current oncology clinical trial success rates are low, highlighting a need for improved preclinical models and drug development.

Purpose of the Study:

  • To explore the mechanisms of cancer treatment resistance.
  • To identify needs for improving preclinical models and drug discovery for better clinical translatability.
  • To highlight the potential of novel approaches like venom-derived compounds.

Main Methods:

  • Single-cell analyses to characterize intratumor heterogeneity.
  • Investigation of microenvironmental influences on treatment response.
  • Review of current limitations in medicinal chemistry and drug scaffold selection.

Main Results:

  • Single-cell analyses reveal complex intratumor heterogeneity and resistance mechanisms.
  • The tumor microenvironment plays a crucial role in cancer cell adaptation to therapy.
  • Existing drug discovery methods have limitations, leaving significant chemical space unexplored.

Conclusions:

  • Characterizing tumor heterogeneity advances understanding of cancer resistance mechanisms.
  • Targeting resistance mechanisms requires improved preclinical models and innovative drug design, potentially from sources like venom.
  • Enhancing the translatability of preclinical studies is critical for increasing oncology clinical trial success rates.