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Updated: Aug 7, 2026

Isolation of Mouse Epidermal Keratinocytes and Their In Vitro Clonogenic Culture
06:16

Isolation of Mouse Epidermal Keratinocytes and Their In Vitro Clonogenic Culture

Published on: August 10, 2019

7,12-Dimethylbenz[a]anthracene-induced mouse keratinocyte malignant transformation independent of Harvey ras

B L Schneider1, G T Bowden, C Sutter

  • 1Department of Radiation Oncology, University of Arizona Medical School, Tucson 85724.

The Journal of Investigative Dermatology
|October 1, 1993
PubMed

Insights

Mouse skin cancer models show tumor development independent of the common c-Ha-ras oncogene. This research offers a new model for studying human epithelial cancers and their genetic changes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Carcinogenesis

Background:

  • Murine models are crucial for understanding multistage carcinogenesis.
  • Investigating genetic alterations in cancer development is key.

Purpose of the Study:

  • To investigate the role of the c-Ha-ras oncogene in 7,12-dimethylbenz[a]anthracene (DMBA)-induced murine keratinocyte transformation.
  • To establish a novel mouse model for human epithelial cancers.

Main Methods:

  • Transfection of high-molecular-weight genomic DNA from DMBA-initiated cell lines into NIH3T3 cells.
  • Polymerase chain reaction (PCR), Xba I restriction analysis, and oligonucleotide differential hybridization to detect c-Ha-ras mutations.
  • Southern and Northern blot analyses to assess gene amplification and expression.

Main Results:

  • DMBA-initiated murine keratinocyte cell lines produced tumors similar to human skin and head/neck cancers.
  • Transfection assays yielded foci distinct from those with activated c-Ha-ras.
  • No point mutations, amplification, or overexpression of the c-Ha-ras gene were detected.

Conclusions:

  • DMBA-induced malignant transformation in murine keratinocytes can occur independently of c-Ha-ras activation.
  • This model provides a unique system for studying genetic changes in epithelial cancer initiation and progression.
  • The absence of c-Ha-ras activation differentiates this model from others, offering new insights into carcinogenesis.

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