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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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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
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Reprogramming alters the gene expression in somatic cells, transforming them into induced pluripotent stem (iPS) cells over several generations. Scientists can reprogram cells by introducing genes for four transcription factors—Oct4, Sox2, Klf4, and c-Myc (OSKM) by viral or non-viral methods. These factors are also known as Yamanaka factors after Shinya Yamanaka, who first generated iPS cells using mouse skin cells. Yamanaka was awarded the Nobel Prize in Physiology or Medicine in 2012...
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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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A stem cell is an unspecialized cell that can divide without limit as needed and can, under specific conditions, differentiate into specialized cells.
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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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Senescence-associated reprogramming promotes cancer stemness.

Maja Milanovic1, Dorothy N Y Fan1,2,3,4, Dimitri Belenki1

  • 1Charité - Universitätsmedizin Berlin, Medical Department of Hematology, Oncology and Tumor Immunology, and Molekulares Krebsforschungszentrum - MKFZ, Virchow Campus, 13353 Berlin, Germany.

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Chemotherapy-induced cellular senescence can unexpectedly enhance cancer stemness, leading to more aggressive tumors and relapse. Escaping senescence boosts cancer cell growth and tumor initiation potential.

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Area of Science:

  • Oncology
  • Cell Biology
  • Cancer Stem Cell Biology

Background:

  • Cellular senescence is a protective cell-cycle arrest. Key senescence regulators also control stem cell functions (stemness).
  • Increased stemness in cancer cells can drive tumor aggressiveness and poor clinical outcomes.

Purpose of the Study:

  • To investigate if chemotherapy-induced senescence alters stem-cell-related properties in malignant cells.
  • To understand the implications of senescence-associated stemness on cancer aggressiveness and therapeutic outcomes.

Main Methods:

  • Gene expression and functional analyses in senescent and non-senescent B-cell lymphomas from Eμ-Myc transgenic mice.
  • Utilized genetically switchable models targeting H3K9me3 or p53 to study senescence escape.
  • Investigated senescence enforcement in p53-regulatable models of acute lymphoblastic and myeloid leukemia.

Main Results:

  • Senescent lymphomas showed upregulated adult stem cell signatures, activated Wnt signaling, and distinct stem cell markers.
  • Cells escaping senescence exhibited enhanced, Wnt-dependent clonogenic growth and higher in vivo tumor initiation potential.
  • Temporary senescence induction reprogrammed non-stem leukemia cells into self-renewing, leukemia-initiating stem cells.

Conclusions:

  • Senescence-associated stemness is an intrinsic feature that enhances cancer cell aggressiveness upon release from cell-cycle arrest.
  • This phenomenon has significant implications for cancer therapy, particularly in relapse settings.
  • Findings reveal cancer cell plasticity and offer new mechanistic insights into tumor recurrence.