In the field of cancer research, Lewis lung carcinoma (LLC) has become the preferred model for many scientists to study lung cancer due to its unique characteristics. Since its discovery by Dr. Margaret Lewis in 1951, the use of this autotransplantation mouse model has gradually attracted attention. Especially in research on understanding tumor metastasis, biological therapy and the effectiveness of chemotherapy, the LLC model has demonstrated its special value.
LLC is a highly mutagenic Kras/Nras mutant cancer that harbors mutations in many inherited genes. These characteristics allow this model to simulate the development of human lung adenocarcinoma.
Lewis lung cancer is unique in that it is the only reproducible autologous transplant model of lung cancer. This means that in transplantation experiments using immunocompatible mice, LLC tumor responses are durable and stable. This is particularly critical for preclinical trials using mouse models, as they are better able to predict the potential effects of treatments.
Although autologous transplantation models offer many advantages, they often face certain challenges, especially when translating therapies from different species into human treatments. For example, some mice that show promising anticancer results fail in human clinical trials, possibly because differences in the gene products of mice and humans prevent the therapeutic effects from being translated. Therefore, it is critical to select the most appropriate animal model for research.
The real challenge lies in how to accurately simulate the tumor microenvironment in mouse models to more truly reflect the human tumor formation process.
The Lewis lung cancer model serves as an orthotopic model, meaning the researchers achieved an accurate simulation of the tumor microenvironment by injecting the tumor directly into the mouse's lungs. The advantage of this method is that it can better simulate the growth and metastasis of tumors in the human body. However, this technology is also often more difficult and technically demanding than other methods.
Through studies of LLC, we found that it is highly metastatic in immunocompatible mice. When tumors are injected subcutaneously into mice, LLC can quickly metastasize to the lungs, providing us with a model to examine the mechanism of tumor metastasis. Studies have shown that this tumor is characterized by high vascularization and varying degrees of tumor shrinkage and tissue degeneration.
The Lewis lung cancer model is of great research value, especially for the properties of tumor metastasis and angiogenesis.
In terms of chemotherapy research, the Lewis lung cancer model also provides an important experimental platform. For example, drugs such as Navelbine and Carboplatin have been tested and shown to significantly inhibit tumor growth and improve survival in mice. Through this guided research, we can delve deeper into the potential of new anti-cancer drugs.
In addition to traditional chemotherapy drugs, scientists have also explored other special treatments, such as melittin, a bee toxin. Research has found that this peptide can effectively inhibit tumor growth and affect tumor-associated macrophages, thereby reducing the further spread of cancer cells. This new treatment pathway demonstrates the potential of LLC models in anti-tumor therapeutic research.
The diversity of the Lewis lung cancer model also extends to studies of the effects of cannabinoids on tumors, which have shown that cannabinoids not only inhibit tumor cell growth but also improve survival in mice, further opening up new directions in cancer treatment.
When we deeply study the mechanism of Lewis lung cancer and its value as a mouse model, we can't help but think about future research: In the exploration of cancer treatment, are there other animal models with more potential that can provide more accurate information? Clinical prediction?