Abstract
Colorectal cancer (CRC) is a genetically, anatomically, and transcriptionally heterogeneous disease. The prognosis for a CRC patient depends on the stage of the tumor at diagnosis and widely differs accordingly. The tumor microenvironment (TME) in CRC is an important factor affecting targeted cancer therapy. The TME has a dynamic composition including various cell types, such as cancer-associated fibroblasts, tumor-associated macrophages, regulatory T cells, and myeloid-derived suppressor cells, as well as extracellular factors that surround cancer cells and have functional and structural roles under physiological and pathological conditions. Moreover, the TME can limit the efficacy of therapeutic agents through high interstitial pressure, fibrosis, and the degradation of the therapeutic agents by enzymatic activity. For this reason, the TME is a fertile ground for the discovery of new drugs. The aim of this narrative review is to present current knowledge and future perspectives regarding the TME composition based on strategies for patients with CRC.
Highlights
Colorectal cancer (CRC) is among the three leading causes of cancer-related deaths, with an estimated one million new cases and 600,000 deaths per year globally [1]
Bevacizumab, a monoclonal antibody against vascular endothelial growth factor (VEGF), was the first angiogenesis inhibitor approved for the treatment of renal cancer [24] and, subsequently, was used as a first-line option for metastatic CRC following the publication of data obtained by a combined analysis by Kabbinavar and colleagues [25]
myeloid-derived suppressor cells (MDSCs) represent a population of granulocytes and monocytes which, together with tumor-associated neutrophils (TANs), tumor-associated macrophages (TAMs), and regulatory dendritic cells, constitute the population of myeloid regulatory cells (MRC)
Summary
Colorectal cancer (CRC) is among the three leading causes of cancer-related deaths, with an estimated one million new cases and 600,000 deaths per year globally [1]. Fibrosis, and the degradation of the therapeutic agent by enzymatic activity It is it is a fertile ground for the discovery of new drugs (Figures 2 and 3) [8]. The “angiogenic switch” is induced by esis as a hallmark of cancer. The “angiogenic switch” is induced by hypoxic hypoxic tumor that stimulate the overproduction of pro-angiogenic such as tumor cells that cells stimulate the overproduction of pro-angiogenic factors suchfactors as the vascular the vascular endothelial growth factor (VEGF). TME is is essential essential for for the the improvement improvement and and design design of of novel therapeutic strategies for colorectal cancer [13,14].
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