*2.2.2 The lymphatic system*

Tumor cell entry into the lymphatic system is another major mechanism for tumor cell dissemination. Even in the early phases of tumor formation, changes in lymphatic artery architecture have been seen, under the aid of VEGFC lymphangiogensis can be established quickly using these cells [83]. The lymphatic vasculature can be examined and the interaction of tumor cells with lymphatics can be seen in live tissue by injecting dyes or fluorescent tracers [84]. Cancer cells may extend protrusions via holes in lymph vessel walls before entering the vessels, according to electron microscope photos [85, 86]. To learn more about the cytoskeletal architecture of intravasation cells and their interactions with the lymphatic endothelium, time-lapse imaging should be possible. Interstitial pressure within the tumor affects lymphatic outflow [87]. Interstitial flow can produce autocrine gradients that signal through CC chemokine receptor 7 (CCR7) to induce cell migration in the same direction as the interstitial flow, according to in vitro research. In vivo, however, it is uncertain whether lymphatic channel movement is influenced by interstitial pressure. Trapped breast cancer cells can be discovered in the subcapsular region of lymph nodes after entering lymphatic channels [88]. However, clinically, lymph node metastases might stay in this place or spread to other parts of the node. The admission of tumor cells into the central sections of lymph nodes, as well as their interactions with immune cells, has yet to be captured in high resolution, but when it is, it will likely provide fascinating discoveries.
