2010
DOI: 10.1097/01.cmr.0000382785.44182.38
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Classification and molecular pathogenesis of CTCL

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“…There are a few hypotheses, including chronic antigen stimulation, viral or bacterial, leading to a loss of immune-surveillance and, therefore, the proliferation of neoplastic T-cells. Moreover, chromosomal instability and abnormal expression of genes involved in the cell cycle and a complex series of interactions between different cells in skin microenvironment have been suggested [3][4][5][6]. The inflammatory microenvironment of the skin seems to play a crucial role in CTCL pathogenesis, as the predominance of Th2 over Th1 cells in inflammatory microenvironment seems to be responsible for the suppression of antitumor response, proliferation of malignant cells and escape from immunosurveillance [7][8][9].…”
Section: Introductionmentioning
confidence: 99%
“…There are a few hypotheses, including chronic antigen stimulation, viral or bacterial, leading to a loss of immune-surveillance and, therefore, the proliferation of neoplastic T-cells. Moreover, chromosomal instability and abnormal expression of genes involved in the cell cycle and a complex series of interactions between different cells in skin microenvironment have been suggested [3][4][5][6]. The inflammatory microenvironment of the skin seems to play a crucial role in CTCL pathogenesis, as the predominance of Th2 over Th1 cells in inflammatory microenvironment seems to be responsible for the suppression of antitumor response, proliferation of malignant cells and escape from immunosurveillance [7][8][9].…”
Section: Introductionmentioning
confidence: 99%