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Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
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Mitogens and the Cell Cycle02:38

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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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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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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.
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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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Induced Pluripotent Stem Cells01:06

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Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
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Tailoring In Vivo Cytotoxicity Assays to Study Immunodominance in Tumor-specific CD8+ T Cell Responses
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CD95 promotes tumour growth.

Lina Chen1, Sun-Mi Park, Alexei V Tumanov

  • 1The Ben May Department for Cancer Research, The University of Chicago, 924 E 57th Street, Chicago, Illinois 60637, USA.

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|May 28, 2010
PubMed
Summary
This summary is machine-generated.

CD95 (Fas) receptor signaling, often linked to cell death, surprisingly promotes tumor growth. Inhibiting CD95, not enhancing it, may be a viable cancer therapy strategy.

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Area of Science:

  • Immunology
  • Cancer Biology
  • Molecular Signaling

Background:

  • CD95 (Fas) receptor is crucial for immune system homeostasis via apoptosis.
  • Tumor cells often downregulate CD95 or resist apoptosis, suggesting CD95 loss aids tumor evasion.
  • Paradoxically, many cancers express CD95 and its ligand (CD95L), hinting at non-apoptotic roles.

Purpose of the Study:

  • To investigate the role of CD95 signaling in tumor growth.
  • To determine if CD95 promotes tumorigenesis through non-apoptotic pathways.
  • To evaluate CD95 as a therapeutic target in cancer.

Main Methods:

  • Analysis of CD95 expression and apoptosis sensitivity in cancer cells.
  • Investigating CD95 signaling in mouse models of ovarian and liver cancer.
  • Elucidating the downstream signaling pathway (JNK/Jun) involved in CD95-mediated tumorigenesis.

Main Results:

  • Cancer cells depend on constitutive CD95 activity, stimulated by cancer-produced CD95L, for growth.
  • Loss of CD95 significantly reduced cancer incidence and tumor size in mouse models.
  • CD95-driven tumor promotion involves the JNK and Jun signaling pathway.

Conclusions:

  • CD95 plays a pro-tumorigenic role in cancer development and progression.
  • Targeting CD95 activity, rather than enhancing it, is a promising therapeutic strategy.
  • Understanding CD95's non-apoptotic functions is critical for developing effective cancer treatments.