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DOI 10.1111/j.1365-2605.2011.01168.x

Медицинская библиотека · International journal of andrology · 2011

Peritubular myoid cell-derived factors and its potential role in the progression of testicular germ cell tumours.

Díez-Torre A, Silván U, Moreno P, Gumucio J, Aréchaga J

СтатьяПоддержка исследования: вне правительства СШАОбзорПеревод в очереди

Аннотация

The tumour surrounding stroma, known as reactive stroma, is a crucial factor to understand cancer cell growth and invasion. In the normal adult testis, the stroma contains extracellular matrix components, fibroblasts, infiltrating leucocytes, lymphocytes, macrophages and capillaries, as well as other specific cell populations, like Leydig cells and a thin myoepithelium surrounding the seminiferous tubules constituted by the peritubular cells. All these cells are an important source of proliferation and survival promoting signals, proteolytic enzymes, migratory cues and pro-angiogenic factors. Ascribable to this pro-invasive activity, the tumour reactive stroma cells, especially cancer-associated myofibroblasts, have emerged as a promising target for cancer therapy. This review is focused on the potential role of the peritubular myoid cells in the development of testicular germ cell tumours as the precursors of cancer-associated myofibroblast and on an experimental model for the study of testis germinal cancer stroma and on the differences between normal and tumour-associated stromal cells, including the molecular mechanisms that mediate the important cancer stroma crosstalk. Special attention will be paid to the cancer-associated myofibroblasts as possible therapeutic targets, because they are one of the main components of the reactive stroma and are known to secrete a variety of paracrine factors that stimulate tumour progression.

Для цитирования: Díez-Torre A, Silván U, Moreno P, Gumucio J, Aréchaga J. Peritubular myoid cell-derived factors and its potential role in the progression of testicular germ cell tumours.. International journal of andrology. 2011. DOI: 10.1111/j.1365-2605.2011.01168.x.

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