How are mice infected with cancer? - briefly
Mice are induced to develop tumors by transplanting cultured cancer cells or genetically engineered tumor‑forming strains, by exposing them to chemical carcinogens, or by delivering oncogenic viruses. These methods provide controlled models for studying tumor initiation, progression, and therapeutic response.
How are mice infected with cancer? - in detail
Mice are commonly employed as experimental models for tumor development because their genetics, immune system, and physiology can be manipulated to mimic human malignancies. Several techniques introduce oncogenic processes in laboratory rodents:
-
Genetically engineered strains – insertion of oncogenes (e.g., Myc, Kras) or deletion of tumor‑suppressor genes (e.g., p53, Rb) through germline modification creates animals that spontaneously develop specific cancers. Tissue‑specific promoters restrict expression to organs of interest, allowing study of tumor initiation and progression in a controlled genetic background.
-
Chemical carcinogenesis – administration of mutagenic compounds such as dimethylbenz[a]anthracene (DMBA), 7,12‑dimethylbenz[a]anthracene, or N‑nitrosodiethylamine (DEN) induces DNA damage in target tissues. Protocols vary by dosage, route (oral, intraperitoneal, topical), and exposure schedule, producing tumors that reflect environmental mutagen exposure.
-
Radiation exposure – whole‑body or localized ionizing radiation (X‑ray, γ‑ray) generates DNA double‑strand breaks, leading to malignant transformation. Fractionated dosing regimens reduce acute toxicity while maintaining carcinogenic efficacy.
-
Transplantable tumor models – implantation of established cancer cell lines or patient‑derived xenografts into immunocompromised mice (e.g., nude, SCID) creates reproducible tumors. Subcutaneous, orthotopic, or intravenous injection determines tumor location and metastatic potential.
-
Viral oncogenesis – infection with retroviral vectors carrying oncogenes (e.g., Moloney murine leukemia virus) integrates oncogenic sequences into the host genome, driving tumor formation. Lentiviral and adenoviral systems enable tissue‑specific delivery and temporal control.
-
CRISPR‑mediated somatic editing – in vivo delivery of CRISPR‑Cas9 components via electroporation, lipid nanoparticles, or viral vectors creates targeted mutations in adult mice. This approach reproduces sporadic mutation patterns observed in human cancers.
Each method offers distinct advantages: genetic models provide insight into hereditary cancer mechanisms; chemical and radiation protocols simulate environmental risk factors; transplantable and viral systems allow rapid assessment of therapeutic interventions; CRISPR editing bridges the gap between germline and somatic mutation studies. Selection depends on research objectives, desired tumor type, and required fidelity to human disease pathology.