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Cancer02:18

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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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Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate DMBA-TPA
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Carcinogenesis trajectories.

Rui Wang1, Zhaopeng Yan2

  • 1Department of Critical Care Medicine, Shengjing Hospital of China Medical University, Shenyang, China.

Frontiers in Cell and Developmental Biology
|December 25, 2025
PubMed
Summary
This summary is machine-generated.

Cancer develops through four main pathways: mutator phenotype, chromosomal instability, dysmetabolism, and stemness. Targeting these distinct cancer origin trajectories offers novel therapeutic strategies.

Keywords:
cancer initiationcancer origincarcinogenesismalignant transformationoncogenesistumorigenesistumorigenic pathway

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Cancer origin patterns significantly influence tumor phenotypes and characteristics.
  • Understanding the distinct pathways of malignant transformation is crucial for developing effective cancer treatments.

Purpose of the Study:

  • To review and explore four distinct carcinogenesis trajectories: mutator phenotype, chromosomal instability, dysmetabolism, and stemness.
  • To elucidate the mechanisms by which each trajectory promotes cancer development and confers unique cellular characteristics.
  • To discuss the potential for targeting these trajectories and their self-reinforcing loops as novel therapeutic strategies.

Main Methods:

  • Review of existing literature on cancer origin and development.
  • Analysis of four distinct carcinogenesis trajectories: mutator phenotype, chromosomal instability, dysmetabolism, and stemness.
  • Examination of oncogenic drivers, self-reinforcing loops, and potential crosstalk among trajectories.

Main Results:

  • The mutator phenotype trajectory involves DNA repair deficiencies leading to hypermutation.
  • Chromosomal instability involves aneuploidy and copy number alterations.
  • Dysmetabolism is driven by oncometabolite accumulation due to metabolic gene alterations.
  • Stemness involves the malignant transformation of stem-like cells.
  • Each trajectory independently drives carcinogenesis and confers distinct cancer cell characteristics.
  • Oncogenic drivers within each trajectory can form self-reinforcing loops, amplifying oncogenic signals.
  • Evidence suggests these trajectories are mutually exclusive during cancer origin, despite potential crosstalk.

Conclusions:

  • Understanding these four carcinogenesis trajectories provides a framework for cancer research.
  • Targeting specific trajectories and disrupting oncogenic loops may offer novel therapeutic avenues.
  • This framework aids in comprehending cancer phenotypes and developing personalized treatment approaches.