2013
Differences in Transcript Levels of ABC Transporters Between Pancreatic Adenocarcinoma and Nonneoplastic Tissues
MOHELNIKOVA-DUCHONOVA, Beatrice; Veronika BRYNYCHOVA; Martin OLIVERIUS; Eva HONSOVA; Zdeněk KALA et al.Základní údaje
Originální název
Differences in Transcript Levels of ABC Transporters Between Pancreatic Adenocarcinoma and Nonneoplastic Tissues
Autoři
MOHELNIKOVA-DUCHONOVA, Beatrice; Veronika BRYNYCHOVA; Martin OLIVERIUS; Eva HONSOVA; Zdeněk KALA; Katarína MÚČKOVÁ a Pavel SOUCEK
Vydání
Pancreas, USA, Lippincott Williams Wilkins, 2013, 0885-3177
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
30200 3.2 Clinical medicine
Stát vydavatele
Spojené státy
Utajení
není předmětem státního či obchodního tajemství
Impakt faktor
Impact factor: 3.008
Označené pro přenos do RIV
Ano
Kód RIV
RIV/00216224:14110/13:00072145
Organizační jednotka
Lékařská fakulta
UT WoS
Klíčová slova anglicky
pancreas; carcinoma; ABC transporters; expression; KRAS
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 14. 2. 2014 18:44, Ing. Mgr. Věra Pospíšilíková
Anotace
V originále
Objectives: The aim of this study was to evaluate transcript levels of all 49 human ATP-binding cassette transporters (ABCs) in one of the most drug-resistant cancers, namely, the pancreatic ductal adenocarcinoma (PDAC). Association of ABCs levels with clinical-pathologic characteristics and KRAS mutation status was followed as well. Methods: Tumors and adjacent nonneoplastic tissues were obtained from 32 histologically verified PDAC patients. The transcript profile of ABCs was assessed using quantitative real-time polymerase chain reaction with a relative standard curve. KRAS mutations in exon 2 were assessed by high-resolution melting analysis and sequencing. Results: Most ABCs were deregulated in PDAC and 10 ABCs were associated with clinical-pathologic characteristics. KRAS mutations did not change the global expression profile of ABCs. Conclusions: The expression of ABC transporters was significantly deregulated in PDAC tumors when compared to nonmalignant tissues. The observed up-regulation of ABCB4, ABCB11, ABCC1, ABCC3, ABCC5, ABCC10, and ABCG2 in tumors may contribute to the generally poor treatment response of PDAC. The up-regulation of ABCA1, ABCA7, and ABCG1 implicates a serious impairment of cellular cholesterol homeostasis in PDAC. On the other hand, the observed down-regulation of ABCA3, ABCC6, ABCC7, and ABCC8 suggests a possible role of stem cells in the development and progression of PDAC.