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Wpływ wybranych cytokin prozapalnych oraz stresu oksydacyjnego na kancerogenezę i progresję gruczolakoraków jelita i prostaty
1
Oddział Urologii, Szpital „GeoMedical”, Katowice
2
Katedra i Zakład Biochemii, Wydział Lekarski z Oddziałem Lekarsko-Dentystycznym w Zabrzu, Śląski Uniwersytet Medyczny w Katowicach
3
Centrum Medyczne „Antrum”, Laboratorium „Demeter”, Bytom
4
Niepubliczny Zakład Opieki Zdrowotnej, Szpital „Jakubiec”, Myszków
5
Katedra Pielęgniarstwa, Wyższa Szkoła Zarządzania w Częstochowie
Autor do korespondencji
Ann. Acad. Med. Siles. 2019;73:182-193
SŁOWA KLUCZOWE
DZIEDZINY
STRESZCZENIE
Nowotwory jelita grubego i prostaty są jednymi z najczęściej występujących nowotworów w Polsce, a zapadalność na nie stale rośnie. Przewlekły stan zapalny i stres oksydacyjny są znanymi czynnikami promującymi rozwój nowotworów. Cytokiny prozapalne, takie jak IL-1β, IL-6, IL-8 oraz TNF-α, są wytwarzane w prawidłowych komórkach i odpowiadają za kontrolę kluczowych procesów. Związana z występowaniem przewlekłego stanu zapalnego nadprodukcja może jednak indukować transformację nowotworową, a następnie wspomagać rozwój nowotworu przez ekspresję cytokin przez komórki mikrośrodowiska guza. Stężenie cytokin prozapalnych w surowicy krwi oraz ekspresja w tkance guza mogą być czynnikami diagnostycznymi i prognostycznymi u pacjentów chorych na raka jelita grubego lub prostaty, a terapia antycytokinowa może wydłużyć czas ich przeżycia.
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