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Cancer Research

Oncology Mouse Models

Since 1998, ingenious targeting laboratory has supported oncology researchers with custom mouse models contributing to peer reviewed publications in Cancer Cell, Cancer Research, Nature Medicine, and leading oncology journals worldwide.

Our oncology mouse models have advanced understanding of tumor biology, cancer genetics, and therapeutic response across solid tumors and hematological malignancies.

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Oncology mouse models enable researchers to investigate the genetic drivers of cancer, study tumor microenvironment interactions, and evaluate therapeutic approaches in immunocompetent systems. From conditional tumor suppressor knockouts that initiate tissue specific tumors to oncogene knockins expressing driver mutations at physiological levels, the right model design is critical for understanding cancer biology and developing effective treatments.

Genetically engineered mouse models (GEMMs) provide advantages over transplantation models by recapitulating tumor initiation, progression, and microenvironment interactions in their native context.

Tumor Suppressor Models

Conditional Tumor Suppressor Knockouts

Conditional deletion of tumor suppressors enables controlled tumor initiation in specific tissues:

Conditional approaches prevent embryonic lethality and enable tissue specific tumor initiation that models human cancer development.

Combinatorial Tumor Models

Cancer often requires multiple genetic hits. Combining tumor suppressor deletions accelerates tumor development and better models human cancer genetics:

Trp53 + Rb1:Small cell lung cancer, osteosarcoma
Trp53 + Pten:Prostate cancer, breast cancer
Apc + Trp53:Aggressive colorectal cancer
Kras + Trp53:Pancreatic, lung cancer
Learn more about conditional knockouts

Common Tumor Suppressor Targets

GeneFunctionTumor TypesCommon Cre Drivers
Trp53Cell cycle, apoptosisMultiple tumor typesTissue dependent
Rb1Cell cycleRetinoblastoma, SCLCTissue dependent
PtenPI3K pathwayProstate, breast, brainProbasin, MMTV, Nestin
ApcWnt pathwayColorectal, intestinalVillin, CDX2
Brca1/2DNA repairBreast, ovarianMMTV, K14
Nf1Ras pathwayNeurofibroma, MPNSTTissue dependent
Nf2Hippo pathwayMesothelioma, schwannomaTissue dependent
Smad4TGFβ pathwayPancreatic, colorectalPdx1, Villin

Oncogene Models

Conditional Oncogene Knockins

Knockin of activated oncogenes at endogenous loci provides physiological expression.

LSL (Lox Stop Lox) System

The LSL system enables conditional oncogene activation:

  • Oncogene preceded by LoxP flanked transcriptional stop cassette
  • Gene silent until Cre removes stop cassette
  • Enables tissue specific and temporal oncogene activation
  • Widely used for Kras, Braf, and other oncogene models
GeneMutationCancer TypesActivation Strategy
KrasG12D, G12V, G12CLung, pancreatic, colorectalLSL Cre dependent
BrafV600EMelanoma, thyroid, colorectalLSL Cre dependent
EgfrL858R, exon 19 delLung adenocarcinomaConditional expression
Pik3caH1047R, E545KBreast, colorectalConditional expression
MycOverexpressionLymphoma, multiple typesTet regulatable
Her2/NeuActivatedBreast cancerMMTV driven

Cancer Type Specific Models

Lung Cancer

Models for NSCLC and SCLC

  • Kras LSL G12D:Lung adenocarcinoma with SPC Cre or Ad Cre
  • Kras G12D + Trp53:Aggressive lung adenocarcinoma
  • EGFR mutant knockin:TKI sensitive and resistant models
  • Trp53 + Rb1:Small cell lung cancer

Breast Cancer

Models for different breast cancer subtypes

  • MMTV PyMT:Luminal breast cancer model
  • Brca1/2 conditional knockout:BRCA mutant breast cancer
  • Her2 overexpression:HER2 positive breast cancer
  • Trp53 + Pten:Triple negative breast cancer model

Pancreatic Cancer

Models for pancreatic ductal adenocarcinoma

  • KPC (Kras G12D + Trp53):Standard PDAC model with Pdx1 Cre
  • Kras G12D alone:PanIN progression model
  • Smad4 conditional knockout:TGFβ pathway in PDAC

Colorectal Cancer

Models for intestinal and colorectal cancer

  • Apc Min:Germline Apc mutation, intestinal adenomas
  • Apc conditional knockout:Controlled adenoma initiation
  • Apc + Kras + Trp53:Invasive colorectal cancer

Hematological Malignancies

Models for leukemia and lymphoma

  • MLL fusion knockins:Mixed lineage leukemia
  • BCR ABL knockin:CML model
  • Myc overexpression:Lymphoma models
  • Conditional knockouts:CD19 Cre, Vav Cre for hematopoietic lineages

Immuno Oncology Applications

Syngeneic Compatibility

GEMMs on defined strain backgrounds enable immunotherapy studies:

  • Tumors arise in immunocompetent hosts
  • Native tumor microenvironment development
  • Checkpoint inhibitor efficacy studies
  • Combination immunotherapy evaluation

Checkpoint Humanization

Humanized checkpoint models enable testing of clinical antibodies:

  • Combine humanized checkpoints with genetic tumor models
  • Test anti PD1, anti PDL1, anti CTLA4 in autochthonous tumors
  • Evaluate combination approaches

Research Applications

Tumor Biology

  • Tumor initiation and progression
  • Metastasis mechanisms
  • Tumor microenvironment interactions
  • Cancer stem cell biology

Target Validation

  • Genetic validation of therapeutic targets
  • Resistance mechanism identification
  • Synthetic lethality studies
  • Biomarker discovery

Therapeutic Development

  • Targeted therapy efficacy
  • Immunotherapy response
  • Combination therapy optimization
  • Drug resistance modeling

Technical Considerations

Cre Driver Selection

Tissue specific Cre drivers determine tumor location:

  • Match Cre driver to desired tumor site
  • Consider timing of Cre expression
  • Evaluate penetrance and specificity
  • Inducible Cre enables controlled tumor initiation

Strain Background

Strain background affects tumor biology and immunotherapy response:

C57BL/6:Th1 biased, compatible with MC38, B16
BALB/c:Th2 biased, compatible with CT26, 4T1
FVB:Common for transgenic tumor models
Mixed backgrounds:May be required for certain combinations

Selected Publications

Oncology models generated by ingenious targeting laboratory:

Chakrabarti S et al. (2024).

Touch sensation requires the mechanically gated ion channel ELKIN1.

Science 383(6686): 992-998

Clausen BE et al. (1999).

Conditional gene targeting in macrophages and granulocytes using LysMcre mice.

Transgenic Research 8(4): 265-277

What Researchers Say

I'd like to thank the ingenious team for making this mouse for us. We are so excited! Everyone at ingenious has been wonderful to work with throughout the entire process. We will definitely be in contact the next time we need a mouse!

Julia Maxson, PhD

Knight Cancer Institute, Oregon Health & Science University

Start Your Oncology Model Project

Our scientific consultants are ready to discuss your oncology research requirements and recommend the optimal model design for your program. Initial consultation is provided at no charge and includes gene analysis, Cre driver recommendations, and timeline estimates.

✦ New for 2026

Breeding Scheme Architect

Plan complex multi-allele breeding strategies, calculate expected genotype ratios, and estimate time to experimental cohorts—all before starting your project.

Visualize multi-generation breeding paths
Calculate Mendelian ratios automatically
Estimate timeline to study-ready cohorts

Free Research Tool

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Allele 1Gene-flox (conditional)
Allele 2Cre-driver (tissue-specific)
TargetHomozygous knockout

→ 3 generations to target genotype

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Frequently Asked Questions

A tumor suppressor knockout eliminates a gene that normally prevents tumor formation (e.g., p53, PTEN). An oncogene knockin introduces an activating mutation that promotes tumor development (e.g., KRAS G12D, BRAF V600E). Both approaches model different aspects of cancer biology and can be combined in the same mouse.

Yes. Conditional alleles are essential for many cancer models because tumor suppressor genes often cause embryonic lethality when deleted globally. Tissue-specific conditional knockout using Cre drivers enables tumor formation in specific organs while avoiding developmental defects.

Common Cre drivers include tissue-specific promoters (e.g., Albumin-Cre for liver, Kras-Cre for pancreas, MMTV-Cre for mammary gland) and inducible Cre systems (e.g., CreERT2 with tamoxifen) for temporal control of tumor initiation. Selection depends on your target tissue and experimental design.

Syngeneic models involve injecting tumor cell lines into immunocompetent mice and are faster for immunotherapy studies. GEMMs develop tumors spontaneously from defined genetic alterations and better recapitulate tumor evolution and microenvironment. GEMMs require longer timelines but provide more physiologically relevant models.

C57BL/6 is most common for immuno-oncology studies and is compatible with MC38 and B16 syngeneic tumors. BALB/c is used for CT26 and 4T1 tumors. Strain selection affects immune response and tumor growth characteristics, so choose based on your experimental requirements.