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Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

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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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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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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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Updated: Jun 5, 2025

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
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Senescence Reprogramming by MTHFD2 Deficiency Facilitates Tumor Progression.

Ping Wang1,2, Zhou Fang3, Wei Pei2

  • 1Medical College, Anhui University of Science and Technology, Huainan, AnHui, China.

Journal of Cancer
|December 13, 2024
PubMed
Summary

Aging significantly impacts cancer by increasing genomic instability and altering immune responses. MTHFD2 is identified as a key regulator of cancer cell senescence, influencing tumor growth and the senescence-associated secretory phenotype (SASP).

Keywords:
MTHFD2cell cyclesenescencetumor

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A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth
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Area of Science:

  • Oncology
  • Gerontology
  • Molecular Biology

Background:

  • Cancer incidence and mortality rise with age, yet molecular changes in aging tumors are poorly understood.
  • Age over sixty is a critical factor in cancer prognosis, necessitating research into age-related molecular alterations.
  • Understanding aging's molecular impact on cancer is crucial for developing effective, age-tailored treatments.

Purpose of the Study:

  • To investigate demographic differences in cancer patients concerning age.
  • To develop a gene-based prognostic model for aging-associated cancers, assessing the impact of cellular senescence.
  • To identify key molecular regulators of senescence in cancer.

Main Methods:

  • Demographic analysis of young versus elderly cancer patients.
  • Development of an aging-related gene prognostic model using gene expression and coefficients.
  • Computation of risk scores to stratify patients into high-risk and low-risk cohorts.
  • Single-cell RNA sequencing to analyze cellular composition in different risk groups.

Main Results:

  • Older cancer patients exhibit increased genomic instability and somatic mutations.
  • Alterations in immune response, inflammatory pathways, and cell cycle regulation are observed in aging tumors.
  • High-risk cohorts show increased exhausted T cells, myeloid cells, and B cells; MTHFD2 deletion promotes tumor growth via senescence and SASP.

Conclusions:

  • MTHFD2 acts as a critical molecular regulator of senescence in cancer.
  • MTHFD2 deletion induces tumor cell senescence and stimulates the senescence-associated secretory phenotype (SASP).
  • Tailored methodologies are essential for effective cancer management in aging populations.