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Mouse Models of Cancer Study

Mouse Models of Cancer Study

Mice have long served as models for studying human biology and pathology because of their phylogenetic and physiological similarity with humans. They are also easy to maintain and breed in the laboratory, and hence, many inbred strains are now available for research. Studies on mice have contributed immeasurably to our understanding of cancer biology.
The development of transgenic, knockout, and knock-in mice has led to an exponential increase in their use as model organisms in research,...

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Related Experiment Video

Updated: Jun 12, 2026

Pre-Conditioning the Airways of Mice with Bleomycin Increases the Efficiency of Orthotopic Lung Cancer Cell Engraftment

Pre-Conditioning the Airways of Mice with Bleomycin Increases the Efficiency of Orthotopic Lung Cancer Cell Engraftment

Published on: June 28, 2018

Chimeric mouse models for lung adenocarcinomas.

¹Division of Molecular & Genomic Medicine, National Health Research Institutes, 35 Keyan Road, Zhunan, Miaoli County 350, Taiwan. yrchen@nhri.org.tw

Future Oncology (London, England)

|June 10, 2010

Summary

This summary is machine-generated.

Oncogenic mutations in Epidermal Growth Factor Receptor (EGFR) family and KRAS drive distinct lung adenocarcinoma pathways. This study reveals EGFR-induced tumors activate PI3K/Akt, while KRAS-induced tumors activate JNK signaling.

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Last Updated: Jun 12, 2026

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Orthotopic Transplantation of Syngeneic Lung Adenocarcinoma Cells to Study PD-L1 Expression

Orthotopic Transplantation of Syngeneic Lung Adenocarcinoma Cells to Study PD-L1 Expression

Published on: January 19, 2019

Area of Science:

Oncology
Molecular Biology
Genetics

Background:

Epidermal Growth Factor Receptor (EGFR) family and KRAS mutations are common in non-small-cell lung cancer (NSCLC).
Distinct clinical presentations arise from EGFR and KRAS mutations, but underlying mechanisms remain unclear.
Chimeric mouse models offer a platform to study oncogenic pathway activation in lung adenocarcinoma.

Discussion:

This study investigates pathway activation differences between ERBB family- and KRAS-driven lung adenocarcinomas.
Oncogenic ERBB mutants (including EGFR and HER2) and KRAS were analyzed in chimeric mouse models.
The research elucidates distinct downstream signaling cascades activated by these key oncogenic drivers.

Key Insights:

ERBB family-driven lung tumors show preferential activation of the PI3K/Akt pathway.
KRAS-driven lung cancers exhibit strong activation of the c-Jun N-terminal kinase (JNK) pathway.
Despite converging on common pathways, oncogenic KRAS and ERBB mutants utilize distinct cellular signals for cancer induction.

Outlook:

Understanding these divergent pathways can inform targeted therapy development for NSCLC.
Further research into the specific molecular events downstream of KRAS and ERBB is warranted.
Chimeric mouse models provide a valuable tool for dissecting complex oncogenic signaling networks.