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Related Concept Videos

Tumor Immunotherapy01:27

Tumor Immunotherapy

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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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mTOR Signaling and Cancer Progression03:03

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
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Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
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Tumor Progression02:07

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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
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Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

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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.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
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The Tumor Microenvironment02:17

The Tumor Microenvironment

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Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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Tumor Interferon Signaling Regulates a Multigenic Resistance Program to Immune Checkpoint Blockade.

Joseph L Benci1, Bihui Xu1, Yu Qiu1

  • 1Department of Radiation Oncology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

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Prolonged interferon signaling drives resistance to cancer immunotherapies like PD1 blockade. Inhibiting this signaling can restore anti-tumor immunity and improve responses to checkpoint inhibitors.

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Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Immune checkpoint blockade (ICB) therapies targeting the PD1 pathway show significant anti-tumor efficacy.
  • However, resistance to ICB is a common clinical challenge, limiting treatment success.
  • Understanding resistance mechanisms is crucial for improving cancer immunotherapy outcomes.

Purpose of the Study:

  • To investigate the role of prolonged interferon signaling in mediating resistance to ICB and combination therapies.
  • To identify the molecular pathways involved in interferon-driven resistance.
  • To explore therapeutic strategies to overcome this resistance.

Main Methods:

  • Analysis of tumor samples and T cell populations.
  • Genetic and pharmacological manipulation of interferon signaling pathways.
  • Assessment of T cell function and tumor response to immunotherapy.

Main Results:

  • Prolonged type I and II interferon signaling promotes PDL1-dependent and independent resistance to ICB and combination therapies.
  • Interferon signaling induces STAT1-related epigenomic changes and upregulates inhibitory receptor ligands.
  • Inhibition of interferon signaling restores T cell function and renders resistant tumors sensitive to ICB monotherapy.
  • Biomarkers of interferon-driven resistance correlate with clinical progression after anti-PD1 therapy.

Conclusions:

  • Tumor interferon signaling is a key driver of adaptive resistance to cancer immunotherapy.
  • Targeting interferon response pathways can overcome resistance and enhance anti-tumor immunity.
  • Inhibiting interferon signaling may bypass the need for complex combinatorial immunotherapy regimens.