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Nem-szteroid gyulladasgatlok alkalmazasa az 5-fluorouracil hatekonysaganak novelesere kíserletes rendszerekben


, : Nem-szteroid gyulladasgatlok alkalmazasa az 5-fluorouracil hatekonysaganak novelesere kíserletes rendszerekben.

A fokozott COX-2-expresszi sz mos ton befoly solja a tumorok kialakul s t s progresszi j t. A COX-2-overexpresszi a sporadikus colorectalis carcinom k 8%- ban igazolhat . A COX-2 enzim a nem-szteroid gyullad sg tl k legismertebb molekul ris c lpontja. A colorectalis r k gy gyszeres kezel s nek alappill r t t bb mint 4 ve az 5-fluorouracil jelenti. Az 5-FU ter pi s hat s nak fokoz s ra sz mos t rekv s ir nyul m s gy gyszerekkel, illetve biomodul torokkal. Az 5-FU a szervezetbe ker lve az aktiv l s mellett igen gyors katabolizmuson megy kereszt l. A leboml s els?, sebess gmeghat roz enzime a dihidropirimidin-dehidrogen z (DPD). Az intratumor lis DPD hamar a klinikai rdekl?d s k z ppontj ba ker lt, mivel az emelkedett DPD-aktivit s az 5-FU citotoxikus hat s nak cs kken s t okozhatja. K s rleteink legf?bb c lja a COX-2 g tl k s az 5-FU kombin lt kezel sek hat s nak vizsg lata k s rleti rendszereken. Ehhez HCA-7 s HT-29 hum n colon adenocarcinoma sejtvonalakat s HT-29 sejtekb?l kialak tott xenograftokat haszn ltunk. K s rleteink sor n vizsg ltuk, hogy a magas COX-2-expresszi , valamint a COX-2-expresszi g tl sa nem-szelekt v COX-2-g tl indomethacinnal s szelekt v COX-2-g tl NS-398-cal befoly solja-e az 5-FU citotoxikus, illetve tumorg tl hat s t. Tov bb , hogy az 5-FU hat konys g nak NSAID-ok tj n t rt n? fokoz s ban milyen mechanizmusok j tszanak szerepet. Eredm nyeink alapj n elmondhat , hogy a COX-2-expresszi befoly solja az 5-FU-kezel ssel szemben mutatott rz kenys get HCA-7 s kollag n-induk lt HT-29 sejtekben, valamint HT-29 xenograftokban, amelynek val sz n?s thet? oka els?sorban a COX-2 s a DPD enzimek koexpresszi ja. Az indomethacin s NS-398 szignifik nsan s szinergista m don fokozta az 5-FU- rz kenys get s a citotoxikus hat st magas COX-2-expresszi t mutat sejtvonalakon s xenograft modellen az ltal, hogy a COX-2-aktivit s cs kkent se mellett p rhuzamosan g tolta a DPD enzim mRNS-expresszi j t s aktivit s t. Mindez a tov bbiakban felveti olyan tfog , nagy betegsz m prospekt v klinikai vizsg lat sz ks g t, amelyben az 5-FU-alap kemoter pi k eset n a tumorok COX-2-st tusza mellett figyelembe venn k a daganatos f jdalmak vagy egy b okok miatt alkalmazott nem-szteroid gyullad sg tl k alkalmaz s t. Magyar Onkol gia 54: 377 381, 21.

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