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Article ; Online: Gonadal and gonadosomatic mosaicism in NF1: report of two families.

Seidl-Philipp, Magdalena / Veyt, Nathalie / Schnaiter, Simon / Krogsdam, Anne / Schwendinger, Simon / Maertens, Ophélia / Fauth, Christine / Schmuth, Matthias / Legius, Eric / Wimmer, Katharina / Brems, Hilde

Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG

2024 Volume 22, Issue 3, Page(s) 426–428

MeSH term(s)	Humans ; Mosaicism ; Neurofibromatosis 1
Language	English
Publishing date	2024-01-07
Publishing country	Germany
Document type	Letter
ZDB-ID	2093479-8
ISSN	1610-0387 ; 1610-0379
ISSN (online)	1610-0387
ISSN	1610-0379
DOI	10.1111/ddg.15302
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Article ; Online: Gonadales und gonadosomatisches Neurofibromatose-Typ-1-Mosaik: ein Bericht über zwei Familien: Gonadal and gonadosomatic mosaicism in NF1: report of two families.

Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG

2024 Volume 22, Issue 3, Page(s) 426–429

MeSH term(s)	Humans ; Mosaicism ; Neurofibromatoses
Language	English
Publishing date	2024-03-06
Publishing country	Germany
Document type	Letter
ZDB-ID	2093479-8
ISSN	1610-0387 ; 1610-0379
ISSN (online)	1610-0387
ISSN	1610-0379
DOI	10.1111/ddg.15302_g
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Article ; Online: Paths of resistance to EGFR inhibitors: is NF enough?

Maertens, Ophélia / Cichowski, Karen

Cancer discovery

2014 Volume 4, Issue 5, Page(s) 519–521

Abstract: Although the majority of patients with EGFR-mutant lung cancer respond well to EGF receptor (EGFR) tyrosine kinase inhibitors (TKI), all patients eventually develop resistance. The mechanism of acquired resistance is still unknown for a considerable ... ...

Abstract	Although the majority of patients with EGFR-mutant lung cancer respond well to EGF receptor (EGFR) tyrosine kinase inhibitors (TKI), all patients eventually develop resistance. The mechanism of acquired resistance is still unknown for a considerable subset of cases. This study reveals the NF1 tumor suppressor gene as a new mediator of resistance to EGFR TKIs and provides a mechanistic rationale for developing combination therapies.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Drug Resistance, Neoplasm ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Mutation ; Neurofibromin 1/genetics ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Receptor, Epidermal Growth Factor/antagonists & inhibitors ; Receptor, Epidermal Growth Factor/genetics
Chemical Substances	Antineoplastic Agents ; Neurofibromin 1 ; Protein Kinase Inhibitors ; Receptor, Epidermal Growth Factor (EC 2.7.10.1)
Language	English
Publishing date	2014-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-14-0286
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Zs.A 6916: Show issues

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Article ; Online: An expanding role for RAS GTPase activating proteins (RAS GAPs) in cancer.

Maertens, Ophélia / Cichowski, Karen

Advances in biological regulation

2014 Volume 55, Page(s) 1–14

Abstract: The RAS pathway is one of the most commonly deregulated pathways in human cancer. Mutations in RAS genes occur in nearly 30% of all human tumors. However in some tumor types RAS mutations are conspicuously absent or rare, despite the fact that RAS and ... ...

Abstract	The RAS pathway is one of the most commonly deregulated pathways in human cancer. Mutations in RAS genes occur in nearly 30% of all human tumors. However in some tumor types RAS mutations are conspicuously absent or rare, despite the fact that RAS and downstream effector pathways are hyperactivated. Recently, RAS GTPase Activating Proteins (RAS GAPs) have emerged as an expanding class of tumor suppressors that, when inactivated, provide an alternative mechanism of activating RAS. RAS GAPs normally turn off RAS by catalyzing the hydrolysis of RAS-GTP. As such, the loss of a RAS GAP would be expected to promote excessive RAS activation. Indeed, this is the case for the NF1 gene, which plays an established role in a familial tumor predisposition syndrome and a variety of sporadic cancers. However, there are 13 additional RAS GAP family members in the human genome. We are only now beginning to understand why there are so many RAS GAPs, how they differentially function, and what their potential role(s) in human cancer are. This review will focus on our current understanding of RAS GAPs in human disease and will highlight important outstanding questions.
MeSH term(s)	Carrier Proteins/physiology ; Drug Resistance, Neoplasm ; GTPase-Activating Proteins/physiology ; Genes, Neurofibromatosis 1/physiology ; Guanine Nucleotide Exchange Factors/physiology ; Humans ; Neoplasms/genetics ; Neoplasms/metabolism ; Neurofibromin 1/physiology ; Tumor Suppressor Proteins/physiology ; ras GTPase-Activating Proteins/genetics ; ras GTPase-Activating Proteins/physiology
Chemical Substances	Carrier Proteins ; DAB2IP protein, human ; GTPase-Activating Proteins ; Guanine Nucleotide Exchange Factors ; IQ motif containing GTPase activating protein 1 ; IQGAP2 protein, human ; Neurofibromin 1 ; RASAL2 protein, human ; Tumor Suppressor Proteins ; ras GTPase-Activating Proteins
Language	English
Publishing date	2014-05
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2667413-0
ISSN	2212-4934 ; 2212-4926
ISSN (online)	2212-4934
ISSN	2212-4926
DOI	10.1016/j.jbior.2014.04.002
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Uc I Zs.364: Show issues

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Article ; Online: Genetic modifiers of the BRD4-NUT dependency of NUT midline carcinoma uncovers a synergism between BETis and CDK4/6is.

Liao, Sida / Maertens, Ophélia / Cichowski, Karen / Elledge, Stephen J

Genes & development

2018 Volume 32, Issue 17-18, Page(s) 1188–1200

Abstract: Bromodomain and extraterminal (BET) domain inhibitors (BETis) show efficacy on NUT midline carcinoma (NMC). However, not all NMC patients respond, and responders eventually develop resistance and relapse. Using CRISPR and ORF expression screens, we ... ...

Abstract	Bromodomain and extraterminal (BET) domain inhibitors (BETis) show efficacy on NUT midline carcinoma (NMC). However, not all NMC patients respond, and responders eventually develop resistance and relapse. Using CRISPR and ORF expression screens, we systematically examined the ability of cancer drivers to mediate resistance of NMC to BETis and uncovered six general classes/pathways mediating resistance. Among these, we showed that RRAS2 attenuated the effect of JQ1 in part by sustaining ERK pathway function during BRD4 inhibition. Furthermore, overexpression of Kruppel-like factor 4 (KLF4), mediated BETi resistance in NMC cells through restoration of the E2F and MYC gene expression program. Finally, we found that expression of cyclin D1 or an oncogenic cyclin D3 mutant or RB1 loss protected NMC cells from BETi-induced cell cycle arrest. Consistent with these findings, cyclin-dependent kinase 4/6 (CDK4/6) inhibitors showed synergistic effects with BETis on NMC in vitro as well as in vivo, thereby establishing a potential two-drug therapy for NMC.
MeSH term(s)	Animals ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Azepines/pharmacology ; Azepines/therapeutic use ; Carcinoma, Squamous Cell/drug therapy ; Carcinoma, Squamous Cell/enzymology ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/metabolism ; Cell Cycle Proteins ; Cell Line, Tumor ; Cyclin-Dependent Kinase 4/antagonists & inhibitors ; Cyclin-Dependent Kinase 6/antagonists & inhibitors ; Cyclins/metabolism ; Drug Resistance, Neoplasm ; E2F Transcription Factors/genetics ; E2F Transcription Factors/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Gene Expression ; Humans ; Kruppel-Like Transcription Factors/metabolism ; Membrane Proteins/genetics ; Mice ; Mice, Nude ; Monomeric GTP-Binding Proteins/genetics ; Mutation ; Nuclear Proteins/antagonists & inhibitors ; Oncogene Proteins/antagonists & inhibitors ; Piperazines/pharmacology ; Piperazines/therapeutic use ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; Pyridines/pharmacology ; Pyridines/therapeutic use ; Transcription Factors/antagonists & inhibitors ; Triazoles/pharmacology ; Triazoles/therapeutic use
Chemical Substances	(+)-JQ1 compound ; Azepines ; BRD4 protein, human ; Cell Cycle Proteins ; Cyclins ; E2F Transcription Factors ; GKLF protein ; Kruppel-Like Transcription Factors ; Membrane Proteins ; NUTM1 protein, human ; Nuclear Proteins ; Oncogene Proteins ; Piperazines ; Protein Kinase Inhibitors ; Proto-Oncogene Proteins c-myc ; Pyridines ; Transcription Factors ; Triazoles ; Cyclin-Dependent Kinase 4 (EC 2.7.11.22) ; Cyclin-Dependent Kinase 6 (EC 2.7.11.22) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; RRAS2 protein, human (EC 3.6.1) ; Monomeric GTP-Binding Proteins (EC 3.6.5.2) ; palbociclib (G9ZF61LE7G)
Language	English
Publishing date	2018-08-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.315648.118
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Zs.A 2292: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Imaging Mass Spectrometry Reveals Tumor Metabolic Heterogeneity.

Zhang, Yang / Guillermier, Christelle / De Raedt, Thomas / Cox, Andrew G / Maertens, Ophelia / Yimlamai, Dean / Lun, Mingyue / Whitney, Adam / Maas, Richard L / Goessling, Wolfram / Cichowski, Karen / Steinhauser, Matthew L

iScience

2020 Volume 23, Issue 8, Page(s) 101355

Abstract: Malignant tumors exhibit high degrees of genomic heterogeneity at the cellular level, leading to the view that subpopulations of tumor cells drive growth and treatment resistance. To examine the degree to which tumors also exhibit metabolic heterogeneity ...

Abstract	Malignant tumors exhibit high degrees of genomic heterogeneity at the cellular level, leading to the view that subpopulations of tumor cells drive growth and treatment resistance. To examine the degree to which tumors also exhibit metabolic heterogeneity at the level of individual cells, we employed multi-isotope imaging mass spectrometry (MIMS) to quantify utilization of stable isotopes of glucose and glutamine along with a label for cell division. Mouse models of melanoma and malignant peripheral nerve sheath tumors (MPNSTs) exhibited striking heterogeneity of substrate utilization, evident in both proliferating and non-proliferating cells. We identified a correlation between metabolic heterogeneity, proliferation, and therapeutic resistance. Heterogeneity in metabolic substrate usage as revealed by incorporation of glucose and glutamine tracers is thus a marker for tumor proliferation. Collectively, our data demonstrate that MIMS provides a powerful tool with which to dissect metabolic functions of individual cells within the native tumor environment.
Language	English
Publishing date	2020-07-10
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2020.101355
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Article ; Online: Defining key signaling nodes and therapeutic biomarkers in NF1-mutant cancers.

Malone, Clare F / Fromm, Jody A / Maertens, Ophélia / DeRaedt, Thomas / Ingraham, Rachel / Cichowski, Karen

Cancer discovery

2014 Volume 4, Issue 9, Page(s) 1062–1073

Abstract: Unlabelled: NF1 encodes a RAS GTPase-activating protein. Accordingly, aberrant RAS activation underlies the pathogenesis of NF1-mutant cancers. Nevertheless, it is unclear which RAS pathway components represent optimal therapeutic targets. Here, we ... ...

Abstract	Unlabelled: NF1 encodes a RAS GTPase-activating protein. Accordingly, aberrant RAS activation underlies the pathogenesis of NF1-mutant cancers. Nevertheless, it is unclear which RAS pathway components represent optimal therapeutic targets. Here, we identify mTORC1 as the key PI3K effector in NF1-mutant nervous system malignancies and conversely show that mTORC2 and AKT are dispensable. However, we find that tumor regression requires sustained inhibition of both mTORC1 and MEK. Transcriptional profiling studies were therefore used to establish a signature of effective mTORC1-MEK inhibition in vivo. We unexpectedly found that the glucose transporter GLUT1 was potently suppressed, but only when both pathways were inhibited. Moreover, unlike VHL- and LKB1-mutant cancers, reduction of (18)F-FDG uptake required the suppression of both mTORC1 and MEK. Together, these studies identify optimal and suboptimal therapeutic targets in NF1-mutant malignancies and define a noninvasive means of measuring combined mTORC1-MEK inhibition in vivo, which can be readily incorporated into clinical trials. Significance: This work demonstrates that mTORC1 and MEK are key therapeutic targets in NF1-mutant cancers and establishes a noninvasive biomarker of effective, combined target inhibition that can be evaluated in clinical trials.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Biomarkers/metabolism ; Class Ia Phosphatidylinositol 3-Kinase/metabolism ; Fluorodeoxyglucose F18/metabolism ; Glucose Transporter Type 1/metabolism ; Humans ; Mechanistic Target of Rapamycin Complex 1 ; Molecular Targeted Therapy ; Multiprotein Complexes/metabolism ; Neoplasms/diagnosis ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms, Nerve Tissue/diagnosis ; Neoplasms, Nerve Tissue/drug therapy ; Neoplasms, Nerve Tissue/genetics ; Neoplasms, Nerve Tissue/metabolism ; Nerve Sheath Neoplasms/diagnosis ; Nerve Sheath Neoplasms/drug therapy ; Nerve Sheath Neoplasms/genetics ; Nerve Sheath Neoplasms/metabolism ; Neurofibromin 1/genetics ; Neurofibromin 1/metabolism ; Positron-Emission Tomography ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Signal Transduction/drug effects ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Antineoplastic Agents ; Biomarkers ; Glucose Transporter Type 1 ; Multiprotein Complexes ; Neurofibromin 1 ; Protein Kinase Inhibitors ; Fluorodeoxyglucose F18 (0Z5B2CJX4D) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Class Ia Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2014-06-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-14-0159
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Article: Targeting Refractory Sarcomas and Malignant Peripheral Nerve Sheath Tumors in a Phase I/II Study of Sirolimus in Combination with Ganetespib (SARC023).

Kim, AeRang / Lu, Yao / Okuno, Scott H / Reinke, Denise / Maertens, Ophélia / Perentesis, John / Basu, Mitali / Wolters, Pamela L / De Raedt, Thomas / Chawla, Sant / Chugh, Rashmi / Van Tine, Brian A / O'Sullivan, Geraldine / Chen, Alice / Cichowski, Karen / Widemann, Brigitte C

Sarcoma

2020 Volume 2020, Page(s) 5784876

Abstract: Purpose: Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive soft tissue sarcomas. Combining Hsp90 inhibitors to enhance endoplasmic reticulum stress with mTOR inhibition results in dramatic MPNST shrinkage in a genetically engineered MPNST ...

Abstract	Purpose: Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive soft tissue sarcomas. Combining Hsp90 inhibitors to enhance endoplasmic reticulum stress with mTOR inhibition results in dramatic MPNST shrinkage in a genetically engineered MPNST mouse model. Ganetespib is an injectable potent small molecule inhibitor of Hsp90. Sirolimus is an oral mTOR inhibitor. We sought to determine the safety, tolerability, and recommended dose of ganetespib and sirolimus in patients with refractory sarcomas and assess clinical benefits in patients with unresectable/refractory MPNSTs. Results: Twenty patients were enrolled (10 per phase). Toxicities were manageable; most frequent non-DLTs were diarrhea, elevated liver transaminases, and fatigue. The recommended dose of ganetespib was 200 mg/m Conclusion: Despite promising preclinical rationale and tolerability of the combination therapy, no responses were observed, and the study did not meet parameters for further evaluation in MPNSTs. This trial was registered with (NCT02008877).
Language	English
Publishing date	2020-01-30
Publishing country	Egypt
Document type	Journal Article
ZDB-ID	1338527-6
ISSN	1357-714X
ISSN	1357-714X
DOI	10.1155/2020/5784876
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Zs.A 5073: Show issues

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Article ; Online: A Deregulated HOX Gene Axis Confers an Epigenetic Vulnerability in KRAS-Mutant Lung Cancers.

Guerra, Stephanie L / Maertens, Ophélia / Kuzmickas, Ryan / De Raedt, Thomas / Adeyemi, Richard O / Guild, Caroline J / Guillemette, Shawna / Redig, Amanda J / Chambers, Emily S / Xu, Man / Tiv, Hong / Santagata, Sandro / Jänne, Pasi A / Elledge, Stephen J / Cichowski, Karen

Cancer cell

2020 Volume 37, Issue 5, Page(s) 705–719.e6

Abstract: While KRAS mutations are common in non-small cell lung cancer (NSCLC), effective treatments are lacking. Here, we report that half of KRAS-mutant NSCLCs aberrantly express the homeobox protein HOXC10, largely due to unappreciated defects in PRC2, which ... ...

Abstract	While KRAS mutations are common in non-small cell lung cancer (NSCLC), effective treatments are lacking. Here, we report that half of KRAS-mutant NSCLCs aberrantly express the homeobox protein HOXC10, largely due to unappreciated defects in PRC2, which confers sensitivity to combined BET/MEK inhibitors in xenograft and PDX models. Efficacy of the combination is dependent on suppression of HOXC10 by BET inhibitors. We further show that HOXC10 regulates the expression of pre-replication complex (pre-RC) proteins in sensitive tumors. Accordingly, BET/MEK inhibitors suppress pre-RC proteins in cycling cells, triggering stalled replication, DNA damage, and death. These studies reveal a promising therapeutic strategy for KRAS-mutant NSCLCs, identify a predictive biomarker of response, and define a subset of NSCLCs with a targetable epigenetic vulnerability.
MeSH term(s)	Acrylonitrile/analogs & derivatives ; Acrylonitrile/pharmacology ; Aniline Compounds/pharmacology ; Animals ; Apoptosis ; Biomarkers, Tumor/genetics ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/pathology ; Cell Proliferation ; Epigenesis, Genetic ; Female ; Gene Expression Regulation, Neoplastic ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; MAP Kinase Kinase 1/antagonists & inhibitors ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Mutation ; Protein Kinase Inhibitors/pharmacology ; Proteins/antagonists & inhibitors ; Proto-Oncogene Proteins p21(ras)/genetics ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Chemical Substances	Aniline Compounds ; Biomarkers, Tumor ; HOXC10 protein, human ; Homeodomain Proteins ; KRAS protein, human ; MEK inhibitor I ; Protein Kinase Inhibitors ; Proteins ; bromodomain and extra-terminal domain protein, human ; MAP Kinase Kinase 1 (EC 2.7.12.2) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; Acrylonitrile (MP1U0D42PE)
Language	English
Publishing date	2020-04-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2020.03.004
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Zs.A 5650: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: MAPK Pathway Suppression Unmasks Latent DNA Repair Defects and Confers a Chemical Synthetic Vulnerability in

Maertens, Ophélia / Kuzmickas, Ryan / Manchester, Haley E / Emerson, Chloe E / Gavin, Alessandra G / Guild, Caroline J / Wong, Terence C / De Raedt, Thomas / Bowman-Colin, Christian / Hatchi, Elodie / Garraway, Levi A / Flaherty, Keith T / Pathania, Shailja / Elledge, Stephen J / Cichowski, Karen

Cancer discovery

2019 Volume 9, Issue 4, Page(s) 526–545

Abstract: Although the majority ... ...

Abstract	Although the majority of
MeSH term(s)	DNA Repair/genetics ; Genes, ras/genetics ; Humans ; MAP Kinase Kinase Kinases/genetics ; Melanoma/genetics ; Proto-Oncogene Proteins B-raf
Chemical Substances	Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; MAP Kinase Kinase Kinases (EC 2.7.11.25)
Language	English
Publishing date	2019-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-18-0879
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