Protein analyses of microdissected primary glioma tissue showed up-regulation and activation of MT1-MMP and LN 5 γ 2 at the invasive edge of the tumors, supporting this observation.
Our own recent work suggests that by inhibiting the interaction between cancer cell and TME - in particular, Fibronectin, which was predominately produced by those cells at the leading invasive edge of the tumor, inhibits their migratory capacity - metastasis can be blocked (summarized in [5]).
Analyses of 57 clinical human glioma biopsies of World Health Organization grade I to IV tumors displaying a distinct invasive edge and 39 glioma specimens that only contain the central region of the tumor showed that Ang2, MMP-2, MT1-MMP, and LN 5 γ 2 were co-overexpressed in invasive areas but not in the central regions of the glioma tissues.
Interestingly, enhanced metastasis in the absence of a carcinoma cell response to TGF-β stimulation has been shown to involve increased chemokine production resulting in recruitment of pro-metastatic myeloid derived suppressor cell (MDSC) populations to the tumor microenvironment at the leading invasive edge.
Its activity is found to be very high and localized at the invasive edge of the tumors [2].
Malignant cells at the invasive edge of the tumour tended to show increased staining that was more pronounced if the invasive edge was penetrating the subserosal tissue.
Transitional tissue contained the invasive edge on the luminal side including both tumour and normal tissue.
These samples contain, next to tumour and adjacent normal tissue, the invasive edge.
The imaging agents effectively labeled microscopic tumor areas, including the invasive edge (Fig. 2e, T/M).
The selected blocks were those in which mucosa, invasive edge and viable tumour were present.
The predominant site of distribution, for example, intratumoral, invasive edge of tumour was noted.
