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Related Concept Videos

Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

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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.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
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Metastasis02:30

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Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
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Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
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Targeted Cancer Therapies02:57

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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Cancer-Critical Genes II: Tumor Suppressor Genes01:05

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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Related Experiment Video

Updated: Dec 14, 2025

The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues
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Immune escape: A critical hallmark in solid tumors.

Keywan Mortezaee1

  • 1Cancer and Immunology Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran; Department of Anatomy, School of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran.

Life Sciences
|July 23, 2020
PubMed
Summary

Solid tumors impair the immune system, leading to an imbalance that affects cancer treatment. Strategies are needed to overcome challenges with immune checkpoint inhibitor (ICI) therapy for better patient outcomes.

Keywords:
CTL-associated antigen-4 (CTLA-4)Cytotoxic T lymphocytes (CTLs)Immune checkpoint inhibitor (ICI)ImmunosuppressionImmunotherapyProgrammed death ligand 1 (PD-L1)Programmed death-1 receptor (PD-1)Tumor microenvironment (TME)

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Area of Science:

  • Oncology
  • Immunology
  • Cancer Biology

Background:

  • Solid tumors are characterized by an incapacitated immune system, with an imbalance in cellular dispersion and functionality within the tumor microenvironment (TME).
  • Factors such as altered metabolism, chronic hypoxia, and inflammation in the TME contribute to immune malfunctioning.
  • Tumor cells hijack checkpoint receptors like programmed death-1 (PD-1) and CTLA-4, further impairing innate immune sensing.

Purpose of the Study:

  • To explore the complexities of the tumor immune ecosystem and identify strategies to rebalance the immune system.
  • To address the limitations of current immune checkpoint inhibitor (ICI) therapies, including their ineffectiveness in 'cold' tumors, potential adverse effects, and acquired resistance.

Main Methods:

  • Review and synthesis of current knowledge on tumor immunology and the TME.
  • Analysis of the mechanisms underlying immune suppression in solid tumors.
  • Evaluation of the efficacy and challenges associated with immune checkpoint inhibitor (ICI) therapy.

Main Results:

  • Immune checkpoint inhibitor (ICI) therapy shows promise but is not universally effective, particularly for 'cold' tumors.
  • Patients may experience severe adverse effects and develop resistance to ICI therapy.
  • Significant challenges remain in optimizing ICI therapy for diverse tumor types.

Conclusions:

  • Further research is crucial to update our understanding of the tumor immune ecosystem.
  • Developing tumor type-dependent dosing strategies and utilizing appropriate adjuvants are essential for improving responses to ICI therapy.
  • Overcoming resistance and enhancing the efficacy of ICI therapy require a comprehensive approach to immune modulation.