J 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

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.