CMT 170 Cell Line

The tumourigenic and metastatic CMT 170 murine cell line is sub-line of CMT 64 and an in vivo mouse tumourigenesis system to study the growth characteristics and metastasis of mouse tumour lines.

Contributors

Inventor Institute
Leonard Franks Cancer Research UK, London Research Institute: Lincoln's Inn Fields
Cat. #: 153332
Unit size: 1×10^6 cells / vial
Cancer types: Lung cancer
Research Fields: Cancer
Organism: Mouse
Tissue: Lung
Gender: Female
Model: Cancer cell line
Growth properties: Adherent
Cancer Types In Detail: Lung carcinoma;Metastatic
Product description: CMT 170 is a highly metastatic murine alveogenic lung carcinoma cell line, derived from the parental CMT 64 line. Developed in 1984 at the Cancer Research UK London Research Institute (Lincoln's Inn Fields), CMT 170 was established through subcloning and in vivo selection for enhanced metastatic potential from pooled lung metastases of CMT 64. Compared to CMT 64, CMT 170 displays increased metastasis and is a useful tool to investigate the mechanisms and origins of metastatic progression in lung cancer.
Gender: Female
Production details: To generate CMT 170, adult female C57B/T mice (aged 4–6 months) were subcutaneously injected with CMT 167 culture passage number 4 cells (generated from the parental CMT 64 line). Following tumour development, cells were harvested from resulting lung metastases. Epithelial outgrowths from these metastatic sites were cultured and selectively expanded based on their high metastatic potential. Through this process of subcloning and in vivo screening, the CMT 170 cell line was established as a more aggressively metastatic variant of CMT 64.
Cellosaurus ID: CVCL_B492
Disease: Cancer
Format: Frozen
Shipping conditions: Dry ice
Growth medium: DMEM with 2mM Glutamine and 10% FCS.
Subculture routine: Split sub-confluent cultures (70-80%) 1:4 to 1:10 seeding at approximately 3 x 104 cells/cm² using 0.05% trypsin or trypsin/EDTA; 5% CO₂; 37°C. Please also see detailed protocol within the Product Datasheet in the Documentation section below.
References:

Franks et al. 1984. Br J Cancer. 49(4):423-9. PMID: 6324837

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