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Acta Medica Medianae
Vol. 49, No 3, September, 2010

UDK 61
ISSN 0365-4478(Printed version)
ISSN 1821-2794(Online)


Correspondence to:

Vuka Katić

Bulevar Nemanjića 74/13

18000 Niš, Srbija

E-mail: vuka.katic@gmail.com






Professional article
UDC:  616.33-006-091.8





Vuka Katić1, Boris Đinđić2, Vesna Živković3, Danica Marković4, Bojana Marković- Živković4, Ivan Ilić3 and Dušan Mihajlović4



                       Retired Professor of Pathology1

                       Institute of Pathologic Physiology, Faculty of Medicine University of Niš2

                       Institute of Pathology, Faculty of Medicine University of Niš3

                       Faculty of Medicine University of Niš4



Gastrointestinal stromal tumors (GIST) are the most frequent mesenchymal tumors of gastrointestinal system and they are characterised by extreme variability in clinical, hystopathological and genetic features. It is considered that all GISToms have a malignant potential. Ethiological factors which cause GISToms have not been clarified yet, and genetic basis is not easy to be determined since GISToms are mostly sporadic. However, certain genetic and cytogenetic aberations which have been determined can be considered to have an impact on the onset of GISToms. Macroscopic picture is polymorphic, but they can most frequently be seen as large, mushroom-like, intraluminal, clearly limited pseudo-incapsulated submucosal masses. Hystomorphology of these tumors shows a high spectar of structural and cellular variations. They are most frequently built out of spindle cells (60-70% of cases), rarely of epitheloid (about 30% of cases) and very rarely of mixed and transitional type (intermedial). Stroma is predominantly loose or poorly colagenized with neoangiogenesis, which is markedly in GISToms with a higher malignant potential. Most of GISToms (95%) express transmembrane receptors KIT (CD 117), CD 34, vimentine, specific neurogenic and smooth muscle cells markers. The most successful therapies are: surgical ressection, imatinib and sunitinib (in case of imatinib resistence) therapy (tyrosine kinase receptor blockers). Research are being conducted all over the world with the aim of finding new and more efficient drug therapies that would not manifest resistency. Acta Medica Medianae 2010;49(3):58-64.


Key words: gastrointestinal stromal tumors, GIST, c-kit protein, imatinib, morphology