[1]Lewis lung carcinoma is a hypermutated Kras/Nras–mutant cancer with extensive regional mutation clusters in its genome.
The major mutational processes in LLC include chromosomal instability, exposure to metabolic mutagens, spontaneous 5–methylcytosine deamination, defective DNA mismatch repair, and reactive oxygen species.
For example, cancer therapies that exhibited promising results in mouse models can and have failed in clinical trials due to physiological differences in the activity of the targeted gene product.
Because of this fidelity to mimicking the tumor microenvironment, orthotopic models are considered to be more physiologically relevant in representing human tumorigenesis.
[6] Tumor progression was observed after subcutaneous injection into the dorsal subcutis for 107 wild type, 129/Black Swiss mice.
[4] The tumors were highly vascularized and metastasized to different sites, including the lungs, lymph nodes, liver, pleural cavity, diaphragm, pericardium, cardiac muscle, pancreas, adipose tissue, and esophagus.
In cases of lung metastasis, large tumor masses underwent necrosis, with some of them hemorrhaging and even fewer exhibiting acute inflammation.
Navelbine and carboplatin, two chemotherapeutics currently on the market, were tested in C57BL mice with Lewis lung carcinoma tumors in their hind flank.
[2] Melittin, a polypeptide found in bee venom, on tumor-associated macrophages has been examined in a Lewis lung carcinoma model.
In the in vivo tests, melittin inhibited rapid tumor growth and was correlated with decreased angiogenesis marker levels, VEGF and CD31.