Role of gene amplification in drug resistance

Schoenlein, Patricia V.

doi:10.1007/978-1-4615-2632-2_9

Cited by 8 publications

(5 citation statements)

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“…The latter has been studied extensively where it plays a major role in the development of drug resistance in both tumorigenic cells and cultured cell lines [2]. This occurs by the drug selecting for cells that carry units of amplified DNA (amplicons) containing genes that confer resistance by increasing the production of either the drug's target protein or a protein that detoxifies it.…”

Section: Introductionmentioning

confidence: 99%

“…This occurs by the drug selecting for cells that carry units of amplified DNA (amplicons) containing genes that confer resistance by increasing the production of either the drug's target protein or a protein that detoxifies it. Besides the beneficial gene, the amplicon may also contain other genes in usually at least 50 kb of flanking DNA [2]. Indeed, newly amplified genes may be contained in very large regions of DNA, tens of megabases long, which subsequently become more condensed [3].…”

Section: Introductionmentioning

confidence: 99%

“…contain numerous DNA rearrangements) or homogeneous (i.e. with very few or no detectable rearrangements) [2], and can be organized as head-to-tail direct repeats or contain inverted sequences [1]. Evidence for the former has come from studies of the breakpoints between amplicons containing multidrug reAbbreviations used : IPCR, inverse PCR ; RACE, rapid amplification of cDNA ends.…”

Section: Introductionmentioning

confidence: 99%

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Structure and organization of amplicons containing the E4 esterase genes responsible for insecticide resistance in the aphid Myzus persicae (Sulzer)

Field

Devonshire

1997

Biochemical Journal

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Insecticide resistance in the aphid Myzus persicae results primarily from the amplification of genes encoding the insecticidedetoxifying esterase, E4. Here we report the analysis of flanking DNA co-amplified with the E4 gene. The 5h end of this gene has an untranslated leader sequence interspersed by two introns, and the promoter region lacks TATA and CAAT boxes. The DNA breakpoint involved in the generation of the amplification is just upstream (approx. 250 bp) of the putative E4 transcription start site ; thus the E4 gene is very close to the 5h end of the approx.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Structure and organization of amplicons containing the E4 esterase genes responsible for insecticide resistance in the aphid Myzus persicae (Sulzer)

Field

Devonshire

1997

Biochemical Journal

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“…Thus, the occurring problem of drug resistance and metastatic spread makes reduces the effectiveness of standard therapeutic approaches, such as surgery, chemotherapy, and radiotherapy. It has been also noted that patients after chemotherapeutic protocols progressively develop genetic mutations (26)(27)(28). It may be a consequence of either activation of proto-oncogenes or inactivation of tumorsuppressor genes.…”

Section: Discussionmentioning

confidence: 99%

Cisplatin and Vinorelbine -Mediated Electrochemotherapeutic Approach Against Multidrug Resistant Small Cell Lung Cancer (H69AR) In Vitro

et al. 2019

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Background/Aim: Small cell lung cancer (SCLC) originates from neuroendocrine branchial cells (15-20%). It is regarded as distinct from other lung cancers due to its biological and clinical features. In most cases of SCLC, surgery or radiotherapy alone is not an effective cure. The aim of our study was to examine the cytotoxic effects of chemotherapy supported by electroporation (EP) on a resistant SCLC model, in vitro. Material and Methods: The multidrug resistant small lung cell line H69AR was used to evaluate the cytotoxic effects of cisplatin (CPPD) and vinorelbine (Navirel ® ; NAV) at lower doses when used with EP. Cells were treated with different concentrations of CPPD and NAV, alone or in combination with the following EP parameters: 400-1200 V/cm, 8 pulses of 100 μs duration, at 1Hz. The cell viability was estimated by MTT assay after 24 and 48 h. Apoptotic cells were detected by neutral comet assay and immunofluorescence assay with PARP-6. Results: CPPD and NAV alone showed a dose-dependent effect on cell viability. Cytostatic drugs combined with EP revealed increased anticancer activity. Lower doses of CPPD or NAV delivered by EP were as effective as higher doses of these drugs without EP. The electrochemotherapeutic protocols increased the number of apoptotic cells and increased immunoreactivity of PARP-6. Our results indicated higher sensitivity of H69AR cells to NAV supported by EP. Conclusion: In SCLC cells, an increased anticancer activity was potentiated by exposure of cells to high intensity electricpulses and low drug doses. It is suggested that this method could be effectively applied in the treatment of lung cancer.

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“…In fact, based on an analysis of several hundred different human cancers, it can be estimated that approximately 50% of human cancers will express the MDR1 gene at some time during therapy. 15 (Details about the cloning and genetic analysis of MDR genes can be found in reviews by Schoenlein 16,17 and Gottesman et al 4…”

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confidence: 99%

Molecular genetic analysis and biochemical characterization of mammalian P-glycoproteins involved in multidrug resistance

Hrycyna

2001

Seminars in Cell & Developmental Biology

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Role of gene amplification in drug resistance

Cited by 8 publications

References 143 publications

Structure and organization of amplicons containing the E4 esterase genes responsible for insecticide resistance in the aphid Myzus persicae (Sulzer)

Structure and organization of amplicons containing the E4 esterase genes responsible for insecticide resistance in the aphid Myzus persicae (Sulzer)

Cisplatin and Vinorelbine -Mediated Electrochemotherapeutic Approach Against Multidrug Resistant Small Cell Lung Cancer (H69AR) In Vitro

Molecular genetic analysis and biochemical characterization of mammalian P-glycoproteins involved in multidrug resistance

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