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Preferential sensitivity to HDAC inhibitors in tumors with CREBBP mutation

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Preferential sensitivity to HDAC inhibitors in tumors with CREBBP mutation. / Hellwig, Malte; Merk, Daniel J; Lutz, Beat; Schüller, Ulrich.

In: CANCER GENE THER, Vol. 27, No. 5, 05.2020, p. 294-300.

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

Harvard

Hellwig, M, Merk, DJ, Lutz, B & Schüller, U 2020, 'Preferential sensitivity to HDAC inhibitors in tumors with CREBBP mutation', CANCER GENE THER, vol. 27, no. 5, pp. 294-300. https://doi.org/10.1038/s41417-019-0099-5

APA

Hellwig, M., Merk, D. J., Lutz, B., & Schüller, U. (2020). Preferential sensitivity to HDAC inhibitors in tumors with CREBBP mutation. CANCER GENE THER, 27(5), 294-300. https://doi.org/10.1038/s41417-019-0099-5

Vancouver

Hellwig M, Merk DJ, Lutz B, Schüller U. Preferential sensitivity to HDAC inhibitors in tumors with CREBBP mutation. CANCER GENE THER. 2020 May;27(5):294-300. https://doi.org/10.1038/s41417-019-0099-5

Bibtex

@article{62323fd71b1a477ca00dff8fd5a582e1,
title = "Preferential sensitivity to HDAC inhibitors in tumors with CREBBP mutation",
abstract = "Mutations in the gene encoding for the histone acetyltransferase (HAT) CREBBP are common driver events in multiple types of human cancer, such as small cell lung cancer (SCLC) or Sonic Hedgehog medulloblastoma (SHH MB). Therefore, therapeutic options targeting such alterations are highly desired. We used human cell lines from SCLC as well as primary mouse tumor cells and genetically engineered mouse models for SHH MB to test treatment options with histone deacetylase inhibitors (HDACi) in CREBBP wild-type and mutated tumors. In contrast to CREBBP wild-type SCLC cells, CREBBP-mutated SCLC cells showed significantly lower IC50 values after treatment with HDACi. In addition, both in vitro and in vivo, HDACi had significant effects on cell proliferation of SHH-driven tumor MB cells harboring a CREBBP-mutation as compared to CREBBP wild-type controls. These data suggest that HDACi may serve as an additional therapeutic option for patients suffering from tumors driven by CREBBP mutations.",
author = "Malte Hellwig and Merk, {Daniel J} and Beat Lutz and Ulrich Sch{\"u}ller",
year = "2020",
month = may,
doi = "10.1038/s41417-019-0099-5",
language = "English",
volume = "27",
pages = "294--300",
journal = "CANCER GENE THER",
issn = "0929-1903",
publisher = "NATURE PUBLISHING GROUP",
number = "5",

}

RIS

TY - JOUR

T1 - Preferential sensitivity to HDAC inhibitors in tumors with CREBBP mutation

AU - Hellwig, Malte

AU - Merk, Daniel J

AU - Lutz, Beat

AU - Schüller, Ulrich

PY - 2020/5

Y1 - 2020/5

N2 - Mutations in the gene encoding for the histone acetyltransferase (HAT) CREBBP are common driver events in multiple types of human cancer, such as small cell lung cancer (SCLC) or Sonic Hedgehog medulloblastoma (SHH MB). Therefore, therapeutic options targeting such alterations are highly desired. We used human cell lines from SCLC as well as primary mouse tumor cells and genetically engineered mouse models for SHH MB to test treatment options with histone deacetylase inhibitors (HDACi) in CREBBP wild-type and mutated tumors. In contrast to CREBBP wild-type SCLC cells, CREBBP-mutated SCLC cells showed significantly lower IC50 values after treatment with HDACi. In addition, both in vitro and in vivo, HDACi had significant effects on cell proliferation of SHH-driven tumor MB cells harboring a CREBBP-mutation as compared to CREBBP wild-type controls. These data suggest that HDACi may serve as an additional therapeutic option for patients suffering from tumors driven by CREBBP mutations.

AB - Mutations in the gene encoding for the histone acetyltransferase (HAT) CREBBP are common driver events in multiple types of human cancer, such as small cell lung cancer (SCLC) or Sonic Hedgehog medulloblastoma (SHH MB). Therefore, therapeutic options targeting such alterations are highly desired. We used human cell lines from SCLC as well as primary mouse tumor cells and genetically engineered mouse models for SHH MB to test treatment options with histone deacetylase inhibitors (HDACi) in CREBBP wild-type and mutated tumors. In contrast to CREBBP wild-type SCLC cells, CREBBP-mutated SCLC cells showed significantly lower IC50 values after treatment with HDACi. In addition, both in vitro and in vivo, HDACi had significant effects on cell proliferation of SHH-driven tumor MB cells harboring a CREBBP-mutation as compared to CREBBP wild-type controls. These data suggest that HDACi may serve as an additional therapeutic option for patients suffering from tumors driven by CREBBP mutations.

U2 - 10.1038/s41417-019-0099-5

DO - 10.1038/s41417-019-0099-5

M3 - SCORING: Journal article

C2 - 31068675

VL - 27

SP - 294

EP - 300

JO - CANCER GENE THER

JF - CANCER GENE THER

SN - 0929-1903

IS - 5

ER -