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.

Basic information

Original name

Differences in Transcript Levels of ABC Transporters Between Pancreatic Adenocarcinoma and Nonneoplastic Tissues

Authors

MOHELNIKOVA-DUCHONOVA, Beatrice (203 Czech Republic), Veronika BRYNYCHOVA (203 Czech Republic), Martin OLIVERIUS (203 Czech Republic), Eva HONSOVA (203 Czech Republic), Zdeněk KALA (203 Czech Republic, guarantor, belonging to the institution), Katarína MÚČKOVÁ (703 Slovakia, belonging to the institution) and Pavel SOUCEK (203 Czech Republic)

Edition

Pancreas, USA, Lippincott Williams Wilkins, 2013, 0885-3177

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

30200 3.2 Clinical medicine

Country of publisher

United States of America

Confidentiality degree

není předmětem státního či obchodního tajemství

Impact factor

Impact factor: 3.008

RIV identification code

RIV/00216224:14110/13:00072145

Organization unit

Faculty of Medicine

DOI

UT WoS

000317655200022

Keywords in English

pancreas; carcinoma; ABC transporters; expression; KRAS

Tags

International impact, Reviewed
Změněno: 14/2/2014 18:44, Ing. Mgr. Věra Pospíšilíková

Abstract

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.