"Stiborov\u00E1, Marie" . . "RIV/00216208:11130/14:10288965!RIV15-MSM-11130___" . . "There are few problems more frustrating and depressing to oncologists and cancer patients alike than anti-cancer treatment resistance. It comes in two varieties: primary and acquired. More and more cancers become responsive to newly developed therapies that are successful in inducing responses in cancers previously considered intrinsically resistant, and the emphasis gradually moves on more and more problematic acquired types of resistance. Acquired resistance may arise through many types of mechanisms. One of them is a constitutive activation of NF-*kappaB, which has been described in a great number of solid tumours and this activation appears to support cancer cell survival and to reduce the sensitivity against chemotherapeutic drugs. Additionally, some anticancer therapies induce this transcription factor themselves and through this mechanism lower their own efficiency. In some cases, a first cycle of an anti-cancer treatment may select resistant population of tumour cells that subsequently leads to recurrence of disease and to the failure of treatment. This may be particularly true for tumours that are composed of a heterogeneous population of cells, which is exactly the case of prostate tumours. Tumour progression needs a positive and reciprocal feedback between cancer associated fibroblasts (CAFs) and cancer cells. Cancer cells induce and maintain the fibroblasts activated phenotype (activated transcription of certain genes), which produce a series of growth factors and cytokines that sustain tumour progression by promoting extracellular matrix (ECM) remodelling, cell proliferation, angiogenesis and epithelialmesenchymal transition (EMT). A thorough understanding of chemoresistance pathways and how they interact would facilitate two important outcomes. Firstly, identifying patients who will not benefit from chemotherapy prior to their exposure will avoid unnecessary toxicity and allow them to move on to alternative treatment options."@en . "2" . "Sztalmachov\u00E1, Mark\u00E9ta" . "Molecular mechanisms of anti-cancer treatment resistance in prostate tumours"@en . "0032-6739" . . "Gumulec, Jarom\u00EDr" . . . "Molekul\u00E1rn\u00ED mechanismy rezistence u n\u00E1dorov\u00E9ho onemocn\u011Bn\u00ED prostaty" . . "Balvan, Jan" . . . "http://www.prolekare.cz/prakticky-lekar-clanek/molekularni-mechanismy-rezistence-u-nadoroveho-onemocneni-prostaty-48361" . "Kizek, Ren\u00E9" . . "Vznik rezistence n\u00E1dorov\u00FDch bun\u011Bk k l\u00E9\u010Db\u011B je velmi frustruj\u00EDc\u00ED probl\u00E9m pro pacienty i onkology. Vyskytuje se ve dvou variant\u00E1ch: rezistence prim\u00E1rn\u00ED a rezistence z\u00EDskan\u00E1 v pr\u016Fb\u011Bhu l\u00E9\u010Dby. Pokroky ve v\u00FDzkumu poskytuj\u00ED nov\u00E9 l\u00E9\u010Debn\u00E9 strategie a mnoho druh\u016F n\u00E1dor\u016F, kter\u00E9 byly d\u0159\u00EDve pova\u017Eov\u00E1ny za prim\u00E1rn\u011B rezistentn\u00ED, nyn\u00ED odpov\u00EDd\u00E1 na nov\u00E9 l\u00E9\u010Debn\u00E9 postupy. Pozornost se tedy postupn\u011B p\u0159esouv\u00E1 k z\u00E1va\u017En\u00E9mu probl\u00E9mu z\u00EDskan\u00E9 rezistence. Rezistence k l\u00E9\u010Db\u011B m\u016F\u017Ee vznikat mnoha r\u016Fzn\u00FDmi mechanismy. Jedn\u00EDm z nich je konstitutivn\u00ED aktivace transkrip\u010Dn\u00EDch faktor\u016F NF-*kappaB, kter\u00E1 byla pozorov\u00E1na u mnoha n\u00E1dor\u016F. Tato aktivace podporuje p\u0159e\u017E\u00EDv\u00E1n\u00ED n\u00E1dorov\u00FDch bun\u011Bk a sni\u017Euje jejich senzitivitu k chemoterapii. N\u011Bkter\u00E1 chemoterapeutika, kter\u00E1 jsou vyu\u017E\u00EDv\u00E1na k l\u00E9\u010Db\u011B n\u00E1dor\u016F, jsou rovn\u011B\u017E schopna aktivovat NF-*kappaB, a zp\u011Btnou vazbou tak sni\u017Euj\u00ED svoji efektivitu. V n\u011Bkter\u00FDch p\u0159\u00EDpadech m\u016F\u017Ee ji\u017E prvn\u00ED cyklus l\u00E9\u010Dby vyselektovat populaci rezistentn\u00EDch n\u00E1dorov\u00FDch bun\u011Bk, kter\u00E9 zp\u016Fsob\u00ED relaps onemocn\u011Bn\u00ED a v d\u016Fsledku sv\u00E9 rezistence i selh\u00E1n\u00ED n\u00E1sledn\u00E9 l\u00E9\u010Dby. Tento mechanismus vzniku rezistence se uplat\u0148uje zejm\u00E9na u n\u00E1dor\u016F skl\u00E1daj\u00EDc\u00ED se z heterogenn\u00ED populace bun\u011Bk, co\u017E je mimo jin\u00E9 pr\u00E1v\u011B p\u0159\u00EDpad n\u00E1dor\u016F prostaty. Progrese n\u00E1doru prostaty tumoru vy\u017Eaduje pozitivn\u00ED zp\u011Btnou vazbu mezi fibroblasty asociovan\u00FDmi s n\u00E1dorem (CAFs) a n\u00E1dorov\u00FDmi bu\u0148kami. N\u00E1dorov\u00E9 bu\u0148ky udr\u017Euj\u00ED fibroblasty v aktivovan\u00E9m stavu (vy\u0161\u0161\u00ED transkrip\u010Dn\u00ED aktivita n\u011Bkter\u00FDch gen\u016F) a ty produkuj\u00ED r\u016Fstov\u00E9 faktory a cytokiny, kter\u00E9 umo\u017E\u0148uj\u00ED progresi n\u00E1doru zprost\u0159edkovanou remodelac\u00ED extracelul\u00E1rn\u00ED matrix (ECM), proliferac\u00ED n\u00E1dorov\u00FDch bun\u011Bk, podporou angiogeneze a p\u0159em\u011Bny epitelov\u00FDch bun\u011Bk na mezenchymov\u00E9 (EMT). D\u016Fkladn\u00E9 porozum\u011Bn\u00ED mechanism\u016Fm rezistence a jejich vz\u00E1jemn\u00FDm interakc\u00EDm by mohlo p\u0159in\u00E9st dva z\u00E1kladn\u00ED v\u00FDsledky. Prvn\u00EDm v\u00FDsledkem bude identifikace pacient\u016F, kte\u0159\u00ED nemohou profitovat z ur\u010Dit\u00E9 terapie a zvolen\u00ED terapie jin\u00E9. Pacienti tak nebudou vystaveni zbyte\u010Dn\u00FDm ne\u017E\u00E1douc\u00EDm \u00FA\u010Dink\u016Fm jinak ne\u00FA\u010Dinn\u00E9 terapie."@cs . . "Eckschlager, Tom\u00E1\u0161" . "Molekul\u00E1rn\u00ED mechanismy rezistence u n\u00E1dorov\u00E9ho onemocn\u011Bn\u00ED prostaty"@cs . "30323" . "1"^^ . . "Raudensk\u00E1, Martina" . "Praktick\u00FD l\u00E9ka\u0159" . "Polansk\u00E1, Hana" . "I" . . "Adam, Vojt\u011Bch" . "cancer associated fibroblasts (CAFs); p53; PTEN; NF-*kappaB; metallothionein; radioresistance; mechanisms of chemoresistance; signal pathways; anti-androgen resistance"@en . . . "10"^^ . . . "Molekul\u00E1rn\u00ED mechanismy rezistence u n\u00E1dorov\u00E9ho onemocn\u011Bn\u00ED prostaty" . "CZ - \u010Cesk\u00E1 republika" . . "94" . . "Vznik rezistence n\u00E1dorov\u00FDch bun\u011Bk k l\u00E9\u010Db\u011B je velmi frustruj\u00EDc\u00ED probl\u00E9m pro pacienty i onkology. Vyskytuje se ve dvou variant\u00E1ch: rezistence prim\u00E1rn\u00ED a rezistence z\u00EDskan\u00E1 v pr\u016Fb\u011Bhu l\u00E9\u010Dby. Pokroky ve v\u00FDzkumu poskytuj\u00ED nov\u00E9 l\u00E9\u010Debn\u00E9 strategie a mnoho druh\u016F n\u00E1dor\u016F, kter\u00E9 byly d\u0159\u00EDve pova\u017Eov\u00E1ny za prim\u00E1rn\u011B rezistentn\u00ED, nyn\u00ED odpov\u00EDd\u00E1 na nov\u00E9 l\u00E9\u010Debn\u00E9 postupy. Pozornost se tedy postupn\u011B p\u0159esouv\u00E1 k z\u00E1va\u017En\u00E9mu probl\u00E9mu z\u00EDskan\u00E9 rezistence. Rezistence k l\u00E9\u010Db\u011B m\u016F\u017Ee vznikat mnoha r\u016Fzn\u00FDmi mechanismy. Jedn\u00EDm z nich je konstitutivn\u00ED aktivace transkrip\u010Dn\u00EDch faktor\u016F NF-*kappaB, kter\u00E1 byla pozorov\u00E1na u mnoha n\u00E1dor\u016F. Tato aktivace podporuje p\u0159e\u017E\u00EDv\u00E1n\u00ED n\u00E1dorov\u00FDch bun\u011Bk a sni\u017Euje jejich senzitivitu k chemoterapii. N\u011Bkter\u00E1 chemoterapeutika, kter\u00E1 jsou vyu\u017E\u00EDv\u00E1na k l\u00E9\u010Db\u011B n\u00E1dor\u016F, jsou rovn\u011B\u017E schopna aktivovat NF-*kappaB, a zp\u011Btnou vazbou tak sni\u017Euj\u00ED svoji efektivitu. V n\u011Bkter\u00FDch p\u0159\u00EDpadech m\u016F\u017Ee ji\u017E prvn\u00ED cyklus l\u00E9\u010Dby vyselektovat populaci rezistentn\u00EDch n\u00E1dorov\u00FDch bun\u011Bk, kter\u00E9 zp\u016Fsob\u00ED relaps onemocn\u011Bn\u00ED a v d\u016Fsledku sv\u00E9 rezistence i selh\u00E1n\u00ED n\u00E1sledn\u00E9 l\u00E9\u010Dby. Tento mechanismus vzniku rezistence se uplat\u0148uje zejm\u00E9na u n\u00E1dor\u016F skl\u00E1daj\u00EDc\u00ED se z heterogenn\u00ED populace bun\u011Bk, co\u017E je mimo jin\u00E9 pr\u00E1v\u011B p\u0159\u00EDpad n\u00E1dor\u016F prostaty. Progrese n\u00E1doru prostaty tumoru vy\u017Eaduje pozitivn\u00ED zp\u011Btnou vazbu mezi fibroblasty asociovan\u00FDmi s n\u00E1dorem (CAFs) a n\u00E1dorov\u00FDmi bu\u0148kami. N\u00E1dorov\u00E9 bu\u0148ky udr\u017Euj\u00ED fibroblasty v aktivovan\u00E9m stavu (vy\u0161\u0161\u00ED transkrip\u010Dn\u00ED aktivita n\u011Bkter\u00FDch gen\u016F) a ty produkuj\u00ED r\u016Fstov\u00E9 faktory a cytokiny, kter\u00E9 umo\u017E\u0148uj\u00ED progresi n\u00E1doru zprost\u0159edkovanou remodelac\u00ED extracelul\u00E1rn\u00ED matrix (ECM), proliferac\u00ED n\u00E1dorov\u00FDch bun\u011Bk, podporou angiogeneze a p\u0159em\u011Bny epitelov\u00FDch bun\u011Bk na mezenchymov\u00E9 (EMT). D\u016Fkladn\u00E9 porozum\u011Bn\u00ED mechanism\u016Fm rezistence a jejich vz\u00E1jemn\u00FDm interakc\u00EDm by mohlo p\u0159in\u00E9st dva z\u00E1kladn\u00ED v\u00FDsledky. Prvn\u00EDm v\u00FDsledkem bude identifikace pacient\u016F, kte\u0159\u00ED nemohou profitovat z ur\u010Dit\u00E9 terapie a zvolen\u00ED terapie jin\u00E9. Pacienti tak nebudou vystaveni zbyte\u010Dn\u00FDm ne\u017E\u00E1douc\u00EDm \u00FA\u010Dink\u016Fm jinak ne\u00FA\u010Dinn\u00E9 terapie." . "6"^^ . . "11130" . "RIV/00216208:11130/14:10288965" . "[5592EF04AF4F]" . . "Masa\u0159\u00EDk, Michal" . "Molekul\u00E1rn\u00ED mechanismy rezistence u n\u00E1dorov\u00E9ho onemocn\u011Bn\u00ED prostaty"@cs . "Molecular mechanisms of anti-cancer treatment resistance in prostate tumours"@en .