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Direct Reprogramming of Mouse Fibroblasts into Melanocytes
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Cellular reprogramming in skin cancer.

Ihn Young Song1, Allan Balmain1

  • 1Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA 94158, USA.

Seminars in Cancer Biology
|April 12, 2014
PubMed
Summary
This summary is machine-generated.

Tumors may originate from primitive stem cells or differentiated cells that regain stem cell properties. Both models are likely correct, with a continuum of cells of origin influencing cancer development.

Keywords:
Cell of originInflammationMalignant potentialReprogrammingSkin cancerStem cell hierarchyp53

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Area of Science:

  • Oncology
  • Stem Cell Biology
  • Carcinogenesis

Background:

  • Early primitive stem cells are traditionally considered the origin of cancer due to self-renewal and longevity.
  • Emerging evidence indicates normal committed cells can reprogram into reserve stem cells following tissue damage and inflammation.
  • This suggests tumors may arise from differentiated cells that re-acquire stem cell properties via genetic or epigenetic reprogramming.

Purpose of the Study:

  • To explore the dual concept of cancer origin from both primitive stem cells and reprogrammed differentiated cells.
  • To present evidence supporting a continuum of potential cells of origin for tumors.
  • To investigate how cell type and genetic mutations influence tumor lineage and malignant potential.

Main Methods:

  • Utilized mouse skin models of carcinogenesis to study tumor initiation.
  • Examined the role of reprogramming stimuli, such as inflammation, in cells at different differentiation stages.
  • Analyzed the interplay between target cell nature and gene mutations in determining tumor characteristics.

Main Results:

  • Evidence supports that both primitive stem cells and reprogrammed differentiated cells can initiate tumors.
  • A continuum of cells of origin exists, influenced by differentiation state and reprogramming requirements.
  • The specific cell of origin and introduced mutations dictate tumor lineage and malignant potential.

Conclusions:

  • Both primitive stem cells and differentiated cells capable of reprogramming are valid cancer cell-of-origin models.
  • Tumor development is a spectrum, dependent on the cell's differentiation stage and the genetic landscape.
  • Mouse skin carcinogenesis models provide valuable insights into these complex mechanisms.