Abstract
Recent advances in cancer therapy encounter a bottleneck. Relapsing/recurrent disease almost always developed eventually with resistance to the initially effective drugs. Tumor microenvironment has been gradually recognized as a key contributor for cancer progression, epithelial-mesenchymal transition of the cancer cells, angiogenesis, cancer metastasis, and development of drug resistance, while dysregulated immune responses and interactions between various components in the microenvironment all play important roles. Future development of anticancer treatment should take tumor microenvironment into consideration. Besides, we also discuss the limitations of current pre-clinical testing models that mainly come from the impossibility in simulating all detailed carcinogenic mechanisms in human, especially failure to create the same tumor microenvironment. With the cumulating knowledge about tumor microenvironment, the design of a novel anticancer therapy may be facilitated and may have better chance for success in cancer eradication.
Highlights
Cancer is a multifactorial disease and is one of the leading causes of death worldwide
Since some important mutated proteins, such as epithelial growth factor receptor (EGFR), p53, and cmyc, have been recognized as important contributors for carcinogenesis, they have been increasingly taken as major targets for drug development in order to eliminate mutated cancer cells [1,2,3]
By transplanting LLC adenocarcinoma cells via tail vein injection to the mice with same genetic background (C57BL/6 mice) to mimic the original lung tumor environment, we found that lung cancer cells could secrete galectin-1 to affect the differentiation of monocyte into tolerogenic dendritic cells with increased production of IL-10 [42]
Summary
Cancer is a multifactorial disease and is one of the leading causes of death worldwide. Since some important mutated proteins, such as epithelial growth factor receptor (EGFR), p53, and cmyc, have been recognized as important contributors for carcinogenesis, they have been increasingly taken as major targets for drug development in order to eliminate mutated cancer cells [1,2,3]. This common strategy can usually achieve significant effect initially, drug resistance usually comes along with relapsing disease sooner or later. This review discusses the current preclinical testing models and highlights their unsatisfying design, suggesting the need for some new strategies in future anticancer drug development
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