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In the presence of a brain tumour, endothelial cells may undergo phenotypic and functional changes, which result in promotion of tumour growth (Demeule et al., 2004).

Last but not least, there is also increasing evidence that the resident cells of chronic wounds may undergo phenotypic changes that impair their capacity for proliferation and movement.

Furthermore, these cells also may undergo phenotypic changes, known as epithelial-mesenchymal transition (EMT), which allows them to travel to the site of metastasis formation without getting affected by conventional treatment.

Furthermore, it was shown that tumor cells that are spreading into the circulation may undergo phenotypic changes, known as EMT, which allows them to travel to the site of metastasis formation without being affected by conventional treatment.

Furthermore, Aktas et al. propose that the persistence of CTC might be associated with stem cell like tumor cells and that these cells may undergo phenotypic changes, described as EMT, which enables them to escape conventional CHT [ 29].

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The immunoreactive protein was also expressed by reactive alveolar epithelial cells of "rapid" progressor lungs, supporting the notion that these cells may undergo a phenotypic shift during the pathogenesis of IPF.

Despite the fact that cultured VSMCs may undergo certain phenotypic changes in vitro, this is still a well-established in vitro model of vascular calcification.

CUPs may undergo substantial phenotypic changes in order to avoid immunological surveillance, and the primary tumor may in fact reside in the same organ as the metastases themselves [ 18].

In vivo, medial vascular smooth muscle cells (VSMCs) are normally quiescent and programmed for contraction but under certain conditions these cells undergo phenotypic modulation which may result in increased proliferation and/or migration from the media [1].

Since the chondrocytes in adult human cartilage are normally quiescent and maintain the matrix in a low turnover stated, understanding how they undergo phenotypic modulation and promote matrix destruction and abnormal repair in OA may to lead to identification of critical targets for therapy to block cartilage damage and promote effective cartilage repair.

Similar pathological changes and effects may also affect other cells relevant of the pathogenesis of OA, including synovial fibroblasts and bone cells as all joint tissues undergo phenotypic modifications in this disorder (Loeser et al. 2012), reflecting the high level of complexity and key involvement of cell-matrix interactions in human OA.

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