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Melanoma-Derived iPCCs Show Differential Tumorigenicity and Therapy Response

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Melanoma-Derived iPCCs Show Differential Tumorigenicity and Therapy Response. / Bernhardt, Mathias; Novak, Daniel; Assenov, Yassen; Orouji, Elias; Knappe, Nathalie; Weina, Kasia; Reith, Maike; Larribere, Lionel; Gebhardt, Christoffer; Plass, Christoph; Umansky, Viktor; Utikal, Jochen.

In: STEM CELL REP, Vol. 8, No. 5, 09.05.2017, p. 1379-1391.

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

Harvard

Bernhardt, M, Novak, D, Assenov, Y, Orouji, E, Knappe, N, Weina, K, Reith, M, Larribere, L, Gebhardt, C, Plass, C, Umansky, V & Utikal, J 2017, 'Melanoma-Derived iPCCs Show Differential Tumorigenicity and Therapy Response', STEM CELL REP, vol. 8, no. 5, pp. 1379-1391. https://doi.org/10.1016/j.stemcr.2017.03.007

APA

Bernhardt, M., Novak, D., Assenov, Y., Orouji, E., Knappe, N., Weina, K., Reith, M., Larribere, L., Gebhardt, C., Plass, C., Umansky, V., & Utikal, J. (2017). Melanoma-Derived iPCCs Show Differential Tumorigenicity and Therapy Response. STEM CELL REP, 8(5), 1379-1391. https://doi.org/10.1016/j.stemcr.2017.03.007

Vancouver

Bernhardt M, Novak D, Assenov Y, Orouji E, Knappe N, Weina K et al. Melanoma-Derived iPCCs Show Differential Tumorigenicity and Therapy Response. STEM CELL REP. 2017 May 9;8(5):1379-1391. https://doi.org/10.1016/j.stemcr.2017.03.007

Bibtex

@article{2c9675c378a04b62be657fcd871e6af9,
title = "Melanoma-Derived iPCCs Show Differential Tumorigenicity and Therapy Response",
abstract = "A point mutation in the BRAF gene, leading to a constitutively active form of the protein, is present in 45%-60% of patients and acts as a key driver in melanoma. Shortly after therapy induction, resistance to MAPK pathway-specific inhibitors develops, indicating that pathway inhibition is circumvented by epigenetic mechanisms. Here, we mimicked epigenetic modifications in melanoma cells by reprogramming them into metastable induced pluripotent cancer cells (iPCCs) with the ability to terminally differentiate into non-tumorigenic lineages. iPCCs and their differentiated progeny were characterized by an increased resistance against targeted therapies, although the cells harbor the same oncogenic mutations and signaling activity as the parental melanoma cells. Furthermore, induction of a pluripotent state allowed the melanoma-derived cells to acquire a non-tumorigenic cell fate, further suggesting that tumorigenicity is influenced by the cell state.",
keywords = "Animals, Antineoplastic Agents, Carcinogenesis, Cell Line, Cell Lineage, Cells, Cultured, Cellular Reprogramming, Epigenesis, Genetic, Fibroblasts, Humans, Induced Pluripotent Stem Cells, Melanoma, Mice, Mice, Inbred NOD, Mice, SCID, Neoplastic Stem Cells, Neurons, Oncogene Proteins, Journal Article",
author = "Mathias Bernhardt and Daniel Novak and Yassen Assenov and Elias Orouji and Nathalie Knappe and Kasia Weina and Maike Reith and Lionel Larribere and Christoffer Gebhardt and Christoph Plass and Viktor Umansky and Jochen Utikal",
note = "Copyright {\textcopyright} 2017 The Author(s). Published by Elsevier Inc. All rights reserved.",
year = "2017",
month = may,
day = "9",
doi = "10.1016/j.stemcr.2017.03.007",
language = "English",
volume = "8",
pages = "1379--1391",
journal = "STEM CELL REP",
issn = "2213-6711",
publisher = "Cell Press",
number = "5",

}

RIS

TY - JOUR

T1 - Melanoma-Derived iPCCs Show Differential Tumorigenicity and Therapy Response

AU - Bernhardt, Mathias

AU - Novak, Daniel

AU - Assenov, Yassen

AU - Orouji, Elias

AU - Knappe, Nathalie

AU - Weina, Kasia

AU - Reith, Maike

AU - Larribere, Lionel

AU - Gebhardt, Christoffer

AU - Plass, Christoph

AU - Umansky, Viktor

AU - Utikal, Jochen

N1 - Copyright © 2017 The Author(s). Published by Elsevier Inc. All rights reserved.

PY - 2017/5/9

Y1 - 2017/5/9

N2 - A point mutation in the BRAF gene, leading to a constitutively active form of the protein, is present in 45%-60% of patients and acts as a key driver in melanoma. Shortly after therapy induction, resistance to MAPK pathway-specific inhibitors develops, indicating that pathway inhibition is circumvented by epigenetic mechanisms. Here, we mimicked epigenetic modifications in melanoma cells by reprogramming them into metastable induced pluripotent cancer cells (iPCCs) with the ability to terminally differentiate into non-tumorigenic lineages. iPCCs and their differentiated progeny were characterized by an increased resistance against targeted therapies, although the cells harbor the same oncogenic mutations and signaling activity as the parental melanoma cells. Furthermore, induction of a pluripotent state allowed the melanoma-derived cells to acquire a non-tumorigenic cell fate, further suggesting that tumorigenicity is influenced by the cell state.

AB - A point mutation in the BRAF gene, leading to a constitutively active form of the protein, is present in 45%-60% of patients and acts as a key driver in melanoma. Shortly after therapy induction, resistance to MAPK pathway-specific inhibitors develops, indicating that pathway inhibition is circumvented by epigenetic mechanisms. Here, we mimicked epigenetic modifications in melanoma cells by reprogramming them into metastable induced pluripotent cancer cells (iPCCs) with the ability to terminally differentiate into non-tumorigenic lineages. iPCCs and their differentiated progeny were characterized by an increased resistance against targeted therapies, although the cells harbor the same oncogenic mutations and signaling activity as the parental melanoma cells. Furthermore, induction of a pluripotent state allowed the melanoma-derived cells to acquire a non-tumorigenic cell fate, further suggesting that tumorigenicity is influenced by the cell state.

KW - Animals

KW - Antineoplastic Agents

KW - Carcinogenesis

KW - Cell Line

KW - Cell Lineage

KW - Cells, Cultured

KW - Cellular Reprogramming

KW - Epigenesis, Genetic

KW - Fibroblasts

KW - Humans

KW - Induced Pluripotent Stem Cells

KW - Melanoma

KW - Mice

KW - Mice, Inbred NOD

KW - Mice, SCID

KW - Neoplastic Stem Cells

KW - Neurons

KW - Oncogene Proteins

KW - Journal Article

U2 - 10.1016/j.stemcr.2017.03.007

DO - 10.1016/j.stemcr.2017.03.007

M3 - SCORING: Journal article

C2 - 28392221

VL - 8

SP - 1379

EP - 1391

JO - STEM CELL REP

JF - STEM CELL REP

SN - 2213-6711

IS - 5

ER -