Abstract

Cellular drug resistance is a major obstacle in cancer therapy. Mechanisms of resistance can be associated with altered expression of ATP-binding cassette (ABC) family of transporters on cell membrane transporters, the most common cause of multi-drug resistance (MDR), but can also include alterations of DNA repair pathways, resistance to apoptosis and target modifications. Anti-cancer treatments may be divided into different categories based on their purpose and action: chemotherapeutic agents damage and kill dividing cells; hormonal treatments prevent cancer cells from receiving signals essential for their growth; targeted drugs are a relatively new cancer treatment that targets specific proteins and pathways that are limited primarily to cancer cells or that are much more prevalent in cancer cells; and antibodies function by either depriving the cancer cells of necessary signals or by causing their direct death. In any case, resistance to anticancer therapies leads to poor prognosis of patients. Thus, identification of novel molecular targets is critical in development of new, efficient and specific cancer drugs. The aim of this review is to describe the impact of genomics in studying some of the most critical pathways involved in cancer drug resistance and in improving drug development. We shall also focus on the emerging role of microRNAs, as key gene expression regulators, in drug resistance. Finally, we shall address the specific mechanisms involved in resistance to tyrosine kinase inhibitors in
Original languageUnknown
Pages (from-to)651-673
JournalCurrent Pharmaceutical Biotechnology
Volume13
Issue number5
Publication statusPublished - 1 Jan 2012

Keywords

  • ABC transporters
  • apoptosis
  • chronic myeloid leukemia
  • DNA repair
  • drug resistance
  • gene expression
  • growth receptors
  • MicroRNAs

Cite this

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title = "Genomics and Cancer Drug Resistance",
abstract = "Cellular drug resistance is a major obstacle in cancer therapy. Mechanisms of resistance can be associated with altered expression of ATP-binding cassette (ABC) family of transporters on cell membrane transporters, the most common cause of multi-drug resistance (MDR), but can also include alterations of DNA repair pathways, resistance to apoptosis and target modifications. Anti-cancer treatments may be divided into different categories based on their purpose and action: chemotherapeutic agents damage and kill dividing cells; hormonal treatments prevent cancer cells from receiving signals essential for their growth; targeted drugs are a relatively new cancer treatment that targets specific proteins and pathways that are limited primarily to cancer cells or that are much more prevalent in cancer cells; and antibodies function by either depriving the cancer cells of necessary signals or by causing their direct death. In any case, resistance to anticancer therapies leads to poor prognosis of patients. Thus, identification of novel molecular targets is critical in development of new, efficient and specific cancer drugs. The aim of this review is to describe the impact of genomics in studying some of the most critical pathways involved in cancer drug resistance and in improving drug development. We shall also focus on the emerging role of microRNAs, as key gene expression regulators, in drug resistance. Finally, we shall address the specific mechanisms involved in resistance to tyrosine kinase inhibitors in",
keywords = "growth receptors, APURINIC/APYRIMIDINIC ENDONUCLEASE ACTIVITY, DNA repair, MicroRNAs, DNA-REPAIR PROTEINS, chronic myeloid leukemia, CHRONIC MYELOID-LEUKEMIA, drug resistance, ASPARAGINE SYNTHETASE EXPRESSION, CELL LUNG-CANCER, ADVANCED BREAST-CANCER, HUMAN OVARIAN-CANCER, ABC transporters, ACUTE LYMPHOBLASTIC-LEUKEMIA, apoptosis, gene expression, GROWTH-FACTOR RECEPTORS, MESSENGER-RNA EXPRESSION, ABC transporters, apoptosis, chronic myeloid leukemia, DNA repair, drug resistance, gene expression, growth receptors, MicroRNAs",
author = "Rodrigues, {Ant{\'o}nio S.} and Joana Dinis and Marta Gromicho and C{\'e}lia Martins and Ant{\'o}nio Laires and Jos{\'e} Rueff",
note = "WOS:000302116600004",
year = "2012",
month = "1",
day = "1",
language = "Unknown",
volume = "13",
pages = "651--673",
journal = "Current Pharmaceutical Biotechnology",
issn = "1389-2010",
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Genomics and Cancer Drug Resistance. / Rodrigues, António S.; Dinis, Joana; Gromicho, Marta; Martins, Célia ; Laires, António; Rueff, José.

In: Current Pharmaceutical Biotechnology, Vol. 13, No. 5, 01.01.2012, p. 651-673.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Genomics and Cancer Drug Resistance

AU - Rodrigues, António S.

AU - Dinis, Joana

AU - Gromicho, Marta

AU - Martins, Célia

AU - Laires, António

AU - Rueff, José

N1 - WOS:000302116600004

PY - 2012/1/1

Y1 - 2012/1/1

N2 - Cellular drug resistance is a major obstacle in cancer therapy. Mechanisms of resistance can be associated with altered expression of ATP-binding cassette (ABC) family of transporters on cell membrane transporters, the most common cause of multi-drug resistance (MDR), but can also include alterations of DNA repair pathways, resistance to apoptosis and target modifications. Anti-cancer treatments may be divided into different categories based on their purpose and action: chemotherapeutic agents damage and kill dividing cells; hormonal treatments prevent cancer cells from receiving signals essential for their growth; targeted drugs are a relatively new cancer treatment that targets specific proteins and pathways that are limited primarily to cancer cells or that are much more prevalent in cancer cells; and antibodies function by either depriving the cancer cells of necessary signals or by causing their direct death. In any case, resistance to anticancer therapies leads to poor prognosis of patients. Thus, identification of novel molecular targets is critical in development of new, efficient and specific cancer drugs. The aim of this review is to describe the impact of genomics in studying some of the most critical pathways involved in cancer drug resistance and in improving drug development. We shall also focus on the emerging role of microRNAs, as key gene expression regulators, in drug resistance. Finally, we shall address the specific mechanisms involved in resistance to tyrosine kinase inhibitors in

AB - Cellular drug resistance is a major obstacle in cancer therapy. Mechanisms of resistance can be associated with altered expression of ATP-binding cassette (ABC) family of transporters on cell membrane transporters, the most common cause of multi-drug resistance (MDR), but can also include alterations of DNA repair pathways, resistance to apoptosis and target modifications. Anti-cancer treatments may be divided into different categories based on their purpose and action: chemotherapeutic agents damage and kill dividing cells; hormonal treatments prevent cancer cells from receiving signals essential for their growth; targeted drugs are a relatively new cancer treatment that targets specific proteins and pathways that are limited primarily to cancer cells or that are much more prevalent in cancer cells; and antibodies function by either depriving the cancer cells of necessary signals or by causing their direct death. In any case, resistance to anticancer therapies leads to poor prognosis of patients. Thus, identification of novel molecular targets is critical in development of new, efficient and specific cancer drugs. The aim of this review is to describe the impact of genomics in studying some of the most critical pathways involved in cancer drug resistance and in improving drug development. We shall also focus on the emerging role of microRNAs, as key gene expression regulators, in drug resistance. Finally, we shall address the specific mechanisms involved in resistance to tyrosine kinase inhibitors in

KW - growth receptors

KW - APURINIC/APYRIMIDINIC ENDONUCLEASE ACTIVITY

KW - DNA repair

KW - MicroRNAs

KW - DNA-REPAIR PROTEINS

KW - chronic myeloid leukemia

KW - CHRONIC MYELOID-LEUKEMIA

KW - drug resistance

KW - ASPARAGINE SYNTHETASE EXPRESSION

KW - CELL LUNG-CANCER

KW - ADVANCED BREAST-CANCER

KW - HUMAN OVARIAN-CANCER

KW - ABC transporters

KW - ACUTE LYMPHOBLASTIC-LEUKEMIA

KW - apoptosis

KW - gene expression

KW - GROWTH-FACTOR RECEPTORS

KW - MESSENGER-RNA EXPRESSION

KW - ABC transporters

KW - apoptosis

KW - chronic myeloid leukemia

KW - DNA repair

KW - drug resistance

KW - gene expression

KW - growth receptors

KW - MicroRNAs

M3 - Article

VL - 13

SP - 651

EP - 673

JO - Current Pharmaceutical Biotechnology

JF - Current Pharmaceutical Biotechnology

SN - 1389-2010

IS - 5

ER -