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Combination of hedgehog signaling blockage and chemotherapy leads to tumor reduction in pancreatic adenocarcinomas

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Combination of hedgehog signaling blockage and chemotherapy leads to tumor reduction in pancreatic adenocarcinomas. / Bahra, Marcus; Kamphues, Carsten; Boas-Knoop, Sabine; Lippert, Steffen; Esendik, Ulrike; Schüller, Ulrich; Hartmann, Wolfgang; Waha, Andreas; Neuhaus, Peter; Heppner, Frank L; Pietsch, Torsten; Koch, Arend.

in: PANCREAS, Jahrgang 41, Nr. 2, 03.2012, S. 222-9.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Bahra, M, Kamphues, C, Boas-Knoop, S, Lippert, S, Esendik, U, Schüller, U, Hartmann, W, Waha, A, Neuhaus, P, Heppner, FL, Pietsch, T & Koch, A 2012, 'Combination of hedgehog signaling blockage and chemotherapy leads to tumor reduction in pancreatic adenocarcinomas', PANCREAS, Jg. 41, Nr. 2, S. 222-9. https://doi.org/10.1097/MPA.0b013e31822896dd

APA

Bahra, M., Kamphues, C., Boas-Knoop, S., Lippert, S., Esendik, U., Schüller, U., Hartmann, W., Waha, A., Neuhaus, P., Heppner, F. L., Pietsch, T., & Koch, A. (2012). Combination of hedgehog signaling blockage and chemotherapy leads to tumor reduction in pancreatic adenocarcinomas. PANCREAS, 41(2), 222-9. https://doi.org/10.1097/MPA.0b013e31822896dd

Vancouver

Bahra M, Kamphues C, Boas-Knoop S, Lippert S, Esendik U, Schüller U et al. Combination of hedgehog signaling blockage and chemotherapy leads to tumor reduction in pancreatic adenocarcinomas. PANCREAS. 2012 Mär;41(2):222-9. https://doi.org/10.1097/MPA.0b013e31822896dd

Bibtex

@article{34ab6e97d3794e779979241c1ebc6507,
title = "Combination of hedgehog signaling blockage and chemotherapy leads to tumor reduction in pancreatic adenocarcinomas",
abstract = "OBJECTIVES: Activation of the hedgehog signal transduction pathway, triggered by hedgehog binding to the transmembrane receptor patched 1 (PTCH1) or by mutations in the PTCH1 gene, plays an important role in the development of various tumors.METHODS: To investigate whether the Hedgehog signaling pathway is also active in human pancreatic adenocarcinomas, we determined the expression levels of the known Hedgehog target genes PTCH1 and GLI-1 in pancreatic tumors. To determine whether alterations in the PTCH1 gene are responsible for this pathway activation, we screened pancreatic carcinomas for mutations in PTCH. To investigate the contribution of hedgehog signaling to the tumorigenicity of pancreatic tumor cells, we blocked the Hedgehog pathway in cultured tumor cells and xenografts using the steroidal alkaloid cyclopamine and the small-molecule Hedgehog inhibitor Hh-Antag.RESULTS: We identified single nucleotide polymorphisms (SNPs) within the PTCH1 gene but no somatic PTCH1 mutations. Pathway-blockage resulted in a significant dose-dependent reduction of tumor cell growth in vitro and in vivo. Moreover, combined treatment with cyclopamine and the conventional antimetabolite gemcitabine revealed a synergistic effect on the reduction of tumor growth in pancreatic adenocarcinoma xenografts.CONCLUSIONS: Inhibition of Hedgehog signaling could be a promising approach for the treatment of pancreatic adenocarcinomas.",
keywords = "Adenocarcinoma, Aged, Animals, Antineoplastic Combined Chemotherapy Protocols, Cell Line, Tumor, Cell Proliferation, Deoxycytidine, Dose-Response Relationship, Drug, Genes, Reporter, Hedgehog Proteins, Humans, Mice, Mice, Nude, Middle Aged, Mutation, Pancreatic Neoplasms, Patched Receptors, Patched-1 Receptor, Polymorphism, Single Nucleotide, Receptors, Cell Surface, Signal Transduction, Time Factors, Transcription Factors, Transfection, Tumor Burden, Veratrum Alkaloids, Xenograft Model Antitumor Assays, Zinc Finger Protein GLI1, Journal Article",
author = "Marcus Bahra and Carsten Kamphues and Sabine Boas-Knoop and Steffen Lippert and Ulrike Esendik and Ulrich Sch{\"u}ller and Wolfgang Hartmann and Andreas Waha and Peter Neuhaus and Heppner, {Frank L} and Torsten Pietsch and Arend Koch",
year = "2012",
month = mar,
doi = "10.1097/MPA.0b013e31822896dd",
language = "English",
volume = "41",
pages = "222--9",
journal = "PANCREAS",
issn = "0885-3177",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

RIS

TY - JOUR

T1 - Combination of hedgehog signaling blockage and chemotherapy leads to tumor reduction in pancreatic adenocarcinomas

AU - Bahra, Marcus

AU - Kamphues, Carsten

AU - Boas-Knoop, Sabine

AU - Lippert, Steffen

AU - Esendik, Ulrike

AU - Schüller, Ulrich

AU - Hartmann, Wolfgang

AU - Waha, Andreas

AU - Neuhaus, Peter

AU - Heppner, Frank L

AU - Pietsch, Torsten

AU - Koch, Arend

PY - 2012/3

Y1 - 2012/3

N2 - OBJECTIVES: Activation of the hedgehog signal transduction pathway, triggered by hedgehog binding to the transmembrane receptor patched 1 (PTCH1) or by mutations in the PTCH1 gene, plays an important role in the development of various tumors.METHODS: To investigate whether the Hedgehog signaling pathway is also active in human pancreatic adenocarcinomas, we determined the expression levels of the known Hedgehog target genes PTCH1 and GLI-1 in pancreatic tumors. To determine whether alterations in the PTCH1 gene are responsible for this pathway activation, we screened pancreatic carcinomas for mutations in PTCH. To investigate the contribution of hedgehog signaling to the tumorigenicity of pancreatic tumor cells, we blocked the Hedgehog pathway in cultured tumor cells and xenografts using the steroidal alkaloid cyclopamine and the small-molecule Hedgehog inhibitor Hh-Antag.RESULTS: We identified single nucleotide polymorphisms (SNPs) within the PTCH1 gene but no somatic PTCH1 mutations. Pathway-blockage resulted in a significant dose-dependent reduction of tumor cell growth in vitro and in vivo. Moreover, combined treatment with cyclopamine and the conventional antimetabolite gemcitabine revealed a synergistic effect on the reduction of tumor growth in pancreatic adenocarcinoma xenografts.CONCLUSIONS: Inhibition of Hedgehog signaling could be a promising approach for the treatment of pancreatic adenocarcinomas.

AB - OBJECTIVES: Activation of the hedgehog signal transduction pathway, triggered by hedgehog binding to the transmembrane receptor patched 1 (PTCH1) or by mutations in the PTCH1 gene, plays an important role in the development of various tumors.METHODS: To investigate whether the Hedgehog signaling pathway is also active in human pancreatic adenocarcinomas, we determined the expression levels of the known Hedgehog target genes PTCH1 and GLI-1 in pancreatic tumors. To determine whether alterations in the PTCH1 gene are responsible for this pathway activation, we screened pancreatic carcinomas for mutations in PTCH. To investigate the contribution of hedgehog signaling to the tumorigenicity of pancreatic tumor cells, we blocked the Hedgehog pathway in cultured tumor cells and xenografts using the steroidal alkaloid cyclopamine and the small-molecule Hedgehog inhibitor Hh-Antag.RESULTS: We identified single nucleotide polymorphisms (SNPs) within the PTCH1 gene but no somatic PTCH1 mutations. Pathway-blockage resulted in a significant dose-dependent reduction of tumor cell growth in vitro and in vivo. Moreover, combined treatment with cyclopamine and the conventional antimetabolite gemcitabine revealed a synergistic effect on the reduction of tumor growth in pancreatic adenocarcinoma xenografts.CONCLUSIONS: Inhibition of Hedgehog signaling could be a promising approach for the treatment of pancreatic adenocarcinomas.

KW - Adenocarcinoma

KW - Aged

KW - Animals

KW - Antineoplastic Combined Chemotherapy Protocols

KW - Cell Line, Tumor

KW - Cell Proliferation

KW - Deoxycytidine

KW - Dose-Response Relationship, Drug

KW - Genes, Reporter

KW - Hedgehog Proteins

KW - Humans

KW - Mice

KW - Mice, Nude

KW - Middle Aged

KW - Mutation

KW - Pancreatic Neoplasms

KW - Patched Receptors

KW - Patched-1 Receptor

KW - Polymorphism, Single Nucleotide

KW - Receptors, Cell Surface

KW - Signal Transduction

KW - Time Factors

KW - Transcription Factors

KW - Transfection

KW - Tumor Burden

KW - Veratrum Alkaloids

KW - Xenograft Model Antitumor Assays

KW - Zinc Finger Protein GLI1

KW - Journal Article

U2 - 10.1097/MPA.0b013e31822896dd

DO - 10.1097/MPA.0b013e31822896dd

M3 - SCORING: Journal article

C2 - 22076568

VL - 41

SP - 222

EP - 229

JO - PANCREAS

JF - PANCREAS

SN - 0885-3177

IS - 2

ER -