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Selective regain of egfr gene copies in CD44+/CD24-/low breast cancer cellular model MDA-MB-468.

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Selective regain of egfr gene copies in CD44+/CD24-/low breast cancer cellular model MDA-MB-468. / Agelopoulos, Konstantin; Greve, Burkhard; Schmidt, Hartmut; Pospisil, Heike; Kurtz, Stefan; Bartkowiak, Kai; Andreas, Antje; Wieczorek, Marek; Korsching, Eberhard; Buerger, Horst; Brandt, Burkhard.

In: BMC CANCER, Vol. 10, 2010, p. 78.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Agelopoulos, K, Greve, B, Schmidt, H, Pospisil, H, Kurtz, S, Bartkowiak, K, Andreas, A, Wieczorek, M, Korsching, E, Buerger, H & Brandt, B 2010, 'Selective regain of egfr gene copies in CD44+/CD24-/low breast cancer cellular model MDA-MB-468.', BMC CANCER, vol. 10, pp. 78. https://doi.org/10.1186/1471-2407-10-78

APA

Agelopoulos, K., Greve, B., Schmidt, H., Pospisil, H., Kurtz, S., Bartkowiak, K., Andreas, A., Wieczorek, M., Korsching, E., Buerger, H., & Brandt, B. (2010). Selective regain of egfr gene copies in CD44+/CD24-/low breast cancer cellular model MDA-MB-468. BMC CANCER, 10, 78. https://doi.org/10.1186/1471-2407-10-78

Vancouver

Agelopoulos K, Greve B, Schmidt H, Pospisil H, Kurtz S, Bartkowiak K et al. Selective regain of egfr gene copies in CD44+/CD24-/low breast cancer cellular model MDA-MB-468. BMC CANCER. 2010;10:78. https://doi.org/10.1186/1471-2407-10-78

Bibtex

@article{cbc8c4bec51a436abeb6ba078beec399,
title = "Selective regain of egfr gene copies in CD44+/CD24-/low breast cancer cellular model MDA-MB-468.",
abstract = "Increased transcription of oncogenes like the epidermal growth factor receptor (EGFR) is frequently caused by amplification of the whole gene or at least of regulatory sequences. Aim of this study was to pinpoint mechanistic parameters occurring during egfr copy number gains leading to a stable EGFR overexpression and high sensitivity to extracellular signalling. A deeper understanding of those marker events might improve early diagnosis of cancer in suspect lesions, early detection of cancer progression and the prediction of egfr targeted therapies.",
keywords = "Humans, Female, Kinetics, Cell Line, Tumor, Signal Transduction, Polymorphism, Single Nucleotide, Flow Cytometry methods, Gene Dosage, Gene Expression Profiling, Genetic Variation, Breast Neoplasms metabolism, Receptor, Epidermal Growth Factor genetics, Antigens, CD24 biosynthesis, Antigens, CD44 biosynthesis, Cell Cycle, Humans, Female, Kinetics, Cell Line, Tumor, Signal Transduction, Polymorphism, Single Nucleotide, Flow Cytometry methods, Gene Dosage, Gene Expression Profiling, Genetic Variation, Breast Neoplasms metabolism, Receptor, Epidermal Growth Factor genetics, Antigens, CD24 biosynthesis, Antigens, CD44 biosynthesis, Cell Cycle",
author = "Konstantin Agelopoulos and Burkhard Greve and Hartmut Schmidt and Heike Pospisil and Stefan Kurtz and Kai Bartkowiak and Antje Andreas and Marek Wieczorek and Eberhard Korsching and Horst Buerger and Burkhard Brandt",
year = "2010",
doi = "10.1186/1471-2407-10-78",
language = "Deutsch",
volume = "10",
pages = "78",
journal = "BMC CANCER",
issn = "1471-2407",
publisher = "BioMed Central Ltd.",

}

RIS

TY - JOUR

T1 - Selective regain of egfr gene copies in CD44+/CD24-/low breast cancer cellular model MDA-MB-468.

AU - Agelopoulos, Konstantin

AU - Greve, Burkhard

AU - Schmidt, Hartmut

AU - Pospisil, Heike

AU - Kurtz, Stefan

AU - Bartkowiak, Kai

AU - Andreas, Antje

AU - Wieczorek, Marek

AU - Korsching, Eberhard

AU - Buerger, Horst

AU - Brandt, Burkhard

PY - 2010

Y1 - 2010

N2 - Increased transcription of oncogenes like the epidermal growth factor receptor (EGFR) is frequently caused by amplification of the whole gene or at least of regulatory sequences. Aim of this study was to pinpoint mechanistic parameters occurring during egfr copy number gains leading to a stable EGFR overexpression and high sensitivity to extracellular signalling. A deeper understanding of those marker events might improve early diagnosis of cancer in suspect lesions, early detection of cancer progression and the prediction of egfr targeted therapies.

AB - Increased transcription of oncogenes like the epidermal growth factor receptor (EGFR) is frequently caused by amplification of the whole gene or at least of regulatory sequences. Aim of this study was to pinpoint mechanistic parameters occurring during egfr copy number gains leading to a stable EGFR overexpression and high sensitivity to extracellular signalling. A deeper understanding of those marker events might improve early diagnosis of cancer in suspect lesions, early detection of cancer progression and the prediction of egfr targeted therapies.

KW - Humans

KW - Female

KW - Kinetics

KW - Cell Line, Tumor

KW - Signal Transduction

KW - Polymorphism, Single Nucleotide

KW - Flow Cytometry methods

KW - Gene Dosage

KW - Gene Expression Profiling

KW - Genetic Variation

KW - Breast Neoplasms metabolism

KW - Receptor, Epidermal Growth Factor genetics

KW - Antigens, CD24 biosynthesis

KW - Antigens, CD44 biosynthesis

KW - Cell Cycle

KW - Humans

KW - Female

KW - Kinetics

KW - Cell Line, Tumor

KW - Signal Transduction

KW - Polymorphism, Single Nucleotide

KW - Flow Cytometry methods

KW - Gene Dosage

KW - Gene Expression Profiling

KW - Genetic Variation

KW - Breast Neoplasms metabolism

KW - Receptor, Epidermal Growth Factor genetics

KW - Antigens, CD24 biosynthesis

KW - Antigens, CD44 biosynthesis

KW - Cell Cycle

U2 - 10.1186/1471-2407-10-78

DO - 10.1186/1471-2407-10-78

M3 - SCORING: Zeitschriftenaufsatz

VL - 10

SP - 78

JO - BMC CANCER

JF - BMC CANCER

SN - 1471-2407

ER -