<abstract xmlns="http://www.w3.org/1999/xhtml">

<p> The review describes the role of cells of extracellular matrix (ECM) as a source of neoplastic outgrowths additional to the original tumour. The cells undergo a spontaneous transformation or stimulation by the original tumour through intercellular signals, e.g. through Shh protein (sonic hedgehog). Additionally, cells of an inflammatory infiltrate, which frequently accompany malignant tumours and particularly carcinomas, may regulate tumour cell behaviour. This is either by restricting tumour proliferation or, inversely, by induction and stimulation of the proliferation of another tumour cell type, e.g. mesenchymal cells. The latter type of tumour may involve formation of histologically differentiated stromal tumours (GIST), which probably originate from interstitial cells of Cajal in the alimentary tract. Occasionally, e.g. in gastric carcinoma, proliferation involves lymphoid follicles and lymphocytes of GALT (gut-associated lymphoid tissue), which gives rise to lymphoma. The process is preceded by the earlier stage of intestinal metaplasia, or is induced by gastritis alone. This is an example of primary involvement of inflammatory infiltrate cells in neoplastic progression. Despite the numerous histogenetic classifications of tumours (zygotoma benignum et zygotoma malignum, or mesenchymomata maligna et mesenchymomata benigna), currently in oncological diagnosis the view prevails that the direction of tumour differentiation and its degree of histologic malignancy (grading) are more important factors than the histogenesis of the tumour.</p>
</abstract>

The review describes the role of cells of extracellular matrix (ECM) as a source of neoplastic outgrowths additional to the original tumour. The cells undergo a spontaneous transformation or stimulation by the original tumour through intercellular signals, e.g. through Shh protein (sonic hedgehog). Additionally, cells of an inflammatory infiltrate, which frequently accompany malignant tumours and particularly carcinomas, may regulate tumour cell behaviour. This is either by restricting tumour proliferation or, inversely, by induction and stimulation of the proliferation of another tumour cell type, e.g. mesenchymal cells. The latter type of tumour may involve formation of histologically differentiated stromal tumours (GIST), which probably originate from interstitial cells of Cajal in the alimentary tract. Occasionally, e.g. in gastric carcinoma, proliferation involves lymphoid follicles and lymphocytes of GALT (gut-associated lymphoid tissue), which gives rise to lymphoma. The process is preceded by the earlier stage of intestinal metaplasia, or is induced by gastritis alone. This is an example of primary involvement of inflammatory infiltrate cells in neoplastic progression. Despite the numerous histogenetic classifications of tumours (zygotoma benignum et zygotoma malignum, or mesenchymomata maligna et mesenchymomata benigna), currently in oncological diagnosis the view prevails that the direction of tumour differentiation and its degree of histologic malignancy (grading) are more important factors than the histogenesis of the tumour.

Extracellular matrix in tumours as a source of additional neoplastic lesions - a review

Department of Pathomorphology and Forensic Veterinary Sciences, Department of Pathology

Wroclaw University of Environmental and Life Sciences

Journal of Veterinary Research

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

The review describes the role of cells of extracellular matrix (ECM) as a source of neoplastic outgrowths additional to the original tumour. The cells undergo...

Extracellular matrix in tumours as a source of additional neoplastic lesions - a review

Data publikacji: 25 mar 2014

Zakres stron: 1 - 9

DOI: https://doi.org/10.2478/bvip-2014-0001

Słowa kluczowe
neoplasia, extracellular matrix (ECM), tumour cell-tumour cell communication, tumour cell-EM communication.

© 2014 National Veterinary Research Institute in Pulawy

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Extracellular matrix in tumours as a source of additional neoplastic lesions - a review

Data publikacji: 25 mar 2014

Zakres stron: 1 - 9

DOI: https://doi.org/10.2478/bvip-2014-0001

Słowa kluczoweneoplasia, extracellular matrix (ECM), tumour cell-tumour cell communication, tumour cell-EM communication.

© 2014 National Veterinary Research Institute in Pulawy

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Słowa kluczowe
neoplasia, extracellular matrix (ECM), tumour cell-tumour cell communication, tumour cell-EM communication.