Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Chimeric mouse tumor models reveal differences in pathway activation between ERBB family- and KRAS-dependent lung adenocarcinomas.

Nature biotechnology - 1 Jan 2010

Zhou Yinghui, Rideout William M, Zi Tong, Bressel Angela, Reddypalli Shailaja, Rancourt Rebecca, Woo Jin-Kyeung, Horner James W, Chin Lynda, Chiu M Isabel, Bosenberg Marcus, Jacks Tyler, Clark Steven C, Depinho Ronald A, Robinson Murray O, Heyer Joerg

Abstract excerpt

To recapitulate the stochastic nature of human cancer development, we have devised a strategy for generating mouse tumor models that involves stepwise genetic manipulation of embryonic stem (ES) cells and chimera generation. Tumors in the chimeric animals develop from engineered cells in the context of normal tissue. Adenocarcinomas arising in an allelic series of lung cancer models containing HER2 (also known as...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Adenocarcinoma
Share to Chimera

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Embryonic Stem Cells

Share to ErbB Receptors

Share to Piperazines

Share to Proto-Oncogene Proteins p21(ras)

Share to Quinazolines

Share to Respiratory Insufficiency

Source

Identifiers

PMID: 20023657
DOI: 10.1038/nbt.1595

Genes

KRAS
EGFR
ERBB2

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Chimeric mouse tumor models reveal differences in pathway activation between ERBB family- and KRAS-dependent lung adenocarcinomas.PMID 20023657Read ↗

Combinatorial Inactivation of Tumor Suppressors Efficiently Initiates Lung Adenocarcinoma with Therapeutic Vulnerabilities.Semantic proximity Read ↗

Combinatorial tumor suppressor inactivation efficiently initiates lung adenocarcinoma with therapeutic vulnerabilitiesSemantic proximity Read ↗

Mouse Models of CancerSemantic proximity Read ↗

Modeling K-Ras-driven lung adenocarcinoma in mice: preclinical validation of therapeutic targets.Semantic proximity Read ↗

Mouse models of human non-small-cell lung cancer: raising the bar.Semantic proximity Read ↗

A Mouse Model System to Genetically Dissect the Molecular Mechanisms Regulating TumorigenesisSemantic proximity Read ↗

RAS signaling and anti-RAS therapy: lessons learned from genetically engineered mouse models, human cancer cells, and patient-related studies.Semantic proximity Read ↗

Kras mutant genetically engineered mouse models of human cancers are genomically heterogeneous.Semantic proximity Read ↗

Transcriptomic classification of genetically engineered mouse models of breast cancer identifies human subtype counterpartsSemantic proximity Read ↗

ERBB signalling contributes to immune evasion in KRAS-driven lung adenocarcinomaSemantic proximity Read ↗

Genetically Engineered Mouse Models: Closing the Gap between Preclinical Data and Trial OutcomesSemantic proximity Read ↗

Global expression profiling and pathway analysis of mouse mammary tumor reveals strain and stage specific dysregulated pathways in breast cancer progression.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.