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Article ; Online: Spatial sequestration of activated-caspase 3 in aggresomes mediates resistance of neuroblastoma cell to bortezomib treatment.

Berthenet, Kévin / Aïmontché, Eliézer / El Mrini, Sara / Brière, Johan / Pion, Nathalie / Iacono, Isabelle / Brejon, Stéphanie / Monier, Karine / Catez, Frédéric / Ichim, Gabriel / Combaret, Valérie / Mertani, Hichem C / Diaz, Jean-Jacques / Albaret, Marie Alexandra

Scientific reports

2024 Volume 14, Issue 1, Page(s) 3768

Abstract: Neuroblastoma (NB) is the most common pediatric tumor and is currently treated by several types of therapies including chemotherapies, such as bortezomib treatment. However, resistance to bortezomib is frequently observed by mechanisms that remain to be ... ...

Abstract	Neuroblastoma (NB) is the most common pediatric tumor and is currently treated by several types of therapies including chemotherapies, such as bortezomib treatment. However, resistance to bortezomib is frequently observed by mechanisms that remain to be deciphered. Bortezomib treatment leads to caspase activation and aggresome formation. Using models of patients-derived NB cell lines with different levels of sensitivity to bortezomib, we show that the activated form of caspase 3 accumulates within aggresomes of NB resistant cells leading to an impairment of bortezomib-induced apoptosis and increased cell survival. Our findings unveil a new mechanism of resistance to chemotherapy based on an altered subcellular distribution of the executioner caspase 3. This mechanism could explain the resistance developed in NB patients treated with bortezomib, emphasizing the potential of drugs targeting aggresomes.
MeSH term(s)	Child ; Humans ; Bortezomib/pharmacology ; Bortezomib/therapeutic use ; Caspase 3/pharmacology ; Cell Line, Tumor ; Apoptosis ; Neuroblastoma/drug therapy ; Neuroblastoma/pathology ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use
Chemical Substances	Bortezomib (69G8BD63PP) ; Caspase 3 (EC 3.4.22.-) ; Antineoplastic Agents
Language	English
Publishing date	2024-02-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-024-54140-7
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Article ; Online: Management of a Composite Pheochromocytoma (Pheochromocytoma/Neuroblastoma) in Adult Patient Recurring After Several Years: A Complex Case Report.

Magnier, Orlane / Chabre, Olivier / Schiff, Isabelle / Sartelet, Hervé / Combaret, Valérie / Roux, Julie / Sturm, Nathalie / Berthozat, Claudine / Pavillet, Julien / Plantaz, Dominique

Journal of adolescent and young adult oncology

2022 Volume 12, Issue 4, Page(s) 604–610

Abstract: Pheochromocytoma/neuroblastoma composite tumors are rare entities for which little is known. We report an atypical case of a 39-year-old man with secondary bone locations of a composite tumor, 7 years after resection of adrenal neuroblastoma, with ... ...

Abstract	Pheochromocytoma/neuroblastoma composite tumors are rare entities for which little is known. We report an atypical case of a 39-year-old man with secondary bone locations of a composite tumor, 7 years after resection of adrenal neuroblastoma, with constitutional alteration of SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily A, member 4 whose role is unknown. The diagnosis of a peripheral neuroblastic tumor in adulthood is difficult and even more so when it is a composite tumor. In the absence of a standard of care, management is varied and discussions about treatment modalities for these patients are complex.
MeSH term(s)	Male ; Humans ; Adult ; Pheochromocytoma/diagnosis ; Pheochromocytoma/surgery ; Pheochromocytoma/pathology ; Neoplasm Recurrence, Local ; Neuroblastoma/pathology ; Adrenal Gland Neoplasms/diagnosis ; Adrenal Gland Neoplasms/surgery
Language	English
Publishing date	2022-09-28
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	2607978-1
ISSN	2156-535X ; 2156-5333
ISSN (online)	2156-535X
ISSN	2156-5333
DOI	10.1089/jayao.2022.0059
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Article: Cell-Free DNA Extracted from CSF for the Molecular Diagnosis of Pediatric Embryonal Brain Tumors.

Chicard, Mathieu / Iddir, Yasmine / Masliah Planchon, Julien / Combaret, Valérie / Attignon, Valéry / Saint-Charles, Alexandra / Frappaz, Didier / Faure-Conter, Cécile / Beccaria, Kévin / Varlet, Pascale / Geoerger, Birgit / Baulande, Sylvain / Pierron, Gaelle / Bouchoucha, Yassine / Doz, François / Delattre, Olivier / Waterfall, Joshua J / Bourdeaut, Franck / Schleiermacher, Gudrun

Cancers

2023 Volume 15, Issue 13

Abstract: Background: Liquid biopsies are revolutionary tools used to detect tumor-specific genetic alterations in body fluids, including the use of cell-free DNA (cfDNA) for molecular diagnosis in cancer patients. In brain tumors, cerebrospinal fluid (CSF) cfDNA ...

Abstract	Background: Liquid biopsies are revolutionary tools used to detect tumor-specific genetic alterations in body fluids, including the use of cell-free DNA (cfDNA) for molecular diagnosis in cancer patients. In brain tumors, cerebrospinal fluid (CSF) cfDNA might be more informative than plasma cfDNA. Here, we assess the use of CSF cfDNA in pediatric embryonal brain tumors (EBT) for molecular diagnosis. Methods: The CSF cfDNA of pediatric patients with medulloblastoma ( Results: 15/25 CSF cfDNA samples yielded informative results, with informative CNA and SNVs in 11 and 15 cases, respectively. For cases with paired tumor and CSF cfDNA WES ( Conclusion: CSF cfDNA sequencing yielded informative results in 60% (15/25) of all cases, with informative results in 83% (15/18) of all cases analyzed by WES. These results pave the way for the implementation of these novel approaches for molecular diagnosis and minimal residual disease monitoring.
Language	English
Publishing date	2023-07-07
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers15133532
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Article ; Online: Environmental cues from neural crest derivatives act as metastatic triggers in an embryonic neuroblastoma model.

Ben Amar, Dounia / Thoinet, Karine / Villalard, Benjamin / Imbaud, Olivier / Costechareyre, Clélia / Jarrosson, Loraine / Reynaud, Florie / Novion Ducassou, Julia / Couté, Yohann / Brunet, Jean-François / Combaret, Valérie / Corradini, Nadège / Delloye-Bourgeois, Céline / Castellani, Valérie

Nature communications

2022 Volume 13, Issue 1, Page(s) 2549

Abstract: Embryonic malignant transformation is concomitant to organogenesis, often affecting multipotent and migratory progenitors. While lineage relationships between malignant cells and their physiological counterparts are extensively investigated, the ... ...

Abstract	Embryonic malignant transformation is concomitant to organogenesis, often affecting multipotent and migratory progenitors. While lineage relationships between malignant cells and their physiological counterparts are extensively investigated, the contribution of exogenous embryonic signals is not fully known. Neuroblastoma (NB) is a childhood malignancy of the peripheral nervous system arising from the embryonic trunk neural crest (NC) and characterized by heterogeneous and interconvertible tumor cell identities. Here, using experimental models mimicking the embryonic context coupled to proteomic and transcriptomic analyses, we show that signals released by embryonic sympathetic ganglia, including Olfactomedin-1, induce NB cells to shift from a noradrenergic to mesenchymal identity, and to activate a gene program promoting NB metastatic onset and dissemination. From this gene program, we extract a core signature specifically shared by metastatic cancers with NC origin. This reveals non-cell autonomous embryonic contributions regulating the plasticity of NB identities and setting pro-dissemination gene programs common to NC-derived cancers.
MeSH term(s)	Cell Differentiation/genetics ; Child ; Cues ; Humans ; Neural Crest ; Neuroblastoma/genetics ; Neuroblastoma/pathology ; Proteomics
Language	English
Publishing date	2022-05-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-30237-3
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Article: Suprarenal Masses in Very Young Infants: Is It Safe to Watch and Wait? Report of a SIOPEN Observational Study Results.

Papadakis, Vassilios / Segura, Vanessa / Conte, Massimo / Plantaz, Dominique / Di Cataldo, Andrea / Schleiermacher, Gudrun / Wheeler, Kate / Bermúdez, Jose D / Ash, Shifra / Brichard, Bénédicte / Ladenstein, Ruth / Combaret, Valérie / Sarnacki, Sabine / Fagnani, Anna Maria / Granata, Claudio / Cañete, Adela

Cancers

2022 Volume 14, Issue 16

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2022-08-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14164007
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Article ; Online: The RNA helicase DDX17 controls the transcriptional activity of REST and the expression of proneural microRNAs in neuronal differentiation.

Lambert, Marie-Pierre / Terrone, Sophie / Giraud, Guillaume / Benoit-Pilven, Clara / Cluet, David / Combaret, Valérie / Mortreux, Franck / Auboeuf, Didier / Bourgeois, Cyril F

Nucleic acids research

2018 Volume 46, Issue 15, Page(s) 7686–7700

Abstract: The Repressor Element 1-silencing transcription factor (REST) represses a number of neuronal genes in non-neuronal cells or in undifferentiated neural progenitors. Here, we report that the DEAD box RNA helicase DDX17 controls important REST-related ... ...

Abstract	The Repressor Element 1-silencing transcription factor (REST) represses a number of neuronal genes in non-neuronal cells or in undifferentiated neural progenitors. Here, we report that the DEAD box RNA helicase DDX17 controls important REST-related processes that are critical during the early phases of neuronal differentiation. First, DDX17 associates with REST, promotes its binding to the promoter of a subset of REST-targeted genes and co-regulates REST transcriptional repression activity. During neuronal differentiation, we observed a downregulation of DDX17 along with that of the REST complex that contributes to the activation of neuronal genes. Second, DDX17 and its paralog DDX5 regulate the expression of several proneural microRNAs that are known to target the REST complex during neurogenesis, including miR-26a/b that are also direct regulators of DDX17 expression. In this context, we propose a new mechanism by which RNA helicases can control the biogenesis of intronic miRNAs. We show that the processing of the miR-26a2 precursor is dependent on RNA helicases, owing to an intronic regulatory region that negatively impacts on both miRNA processing and splicing of its host intron. Our work places DDX17 in the heart of a pathway involving REST and miRNAs that allows neuronal gene repression.
MeSH term(s)	Cell Line, Tumor ; DEAD-box RNA Helicases/genetics ; DEAD-box RNA Helicases/metabolism ; Gene Expression Profiling ; Humans ; MCF-7 Cells ; MicroRNAs/genetics ; Neural Stem Cells/metabolism ; Neurogenesis/genetics ; Neurons/metabolism ; Repressor Proteins/genetics ; Repressor Proteins/metabolism
Chemical Substances	MicroRNAs ; RE1-silencing transcription factor ; Repressor Proteins ; DDX17 protein, human (EC 3.6.1.-) ; Ddx5 protein, human (EC 3.6.1.-) ; DEAD-box RNA Helicases (EC 3.6.4.13)
Language	English
Publishing date	2018-06-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gky545
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Zs.A 1067: Show issues

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Article: Alterations in Homologous Recombination-Related Genes and Distinct Platinum Response in Metastatic Triple-Negative Breast Cancers: A Subgroup Analysis of the ProfiLER-01 Trial.

Bonnet, Elise / Haddad, Véronique / Quesada, Stanislas / Baffert, Kim-Arthur / Lardy-Cléaud, Audrey / Treilleux, Isabelle / Pissaloux, Daniel / Attignon, Valéry / Wang, Qing / Buisson, Adrien / Heudel, Pierre-Etienne / Bachelot, Thomas / Dufresne, Armelle / Eberst, Lauriane / Toussaint, Philippe / Bonadona, Valérie / Lasset, Christine / Viari, Alain / Sohier, Emilie /

Paindavoine, Sandrine / Combaret, Valérie / Pérol, David / Ray-Coquard, Isabelle / Blay, Jean-Yves / Trédan, Olivier

Journal of personalized medicine

2022 Volume 12, Issue 10

Abstract: Background: a specific subset of metastatic triple-negative breast cancers (mTNBC) is characterized by homologous recombination deficiency (HRD), leading to enhanced sensitivity to platinum-based chemotherapy. Apart from mutations in : Methods: next- ... ...

Abstract	Background: a specific subset of metastatic triple-negative breast cancers (mTNBC) is characterized by homologous recombination deficiency (HRD), leading to enhanced sensitivity to platinum-based chemotherapy. Apart from mutations in Methods: next-generation sequencing and promoter methylation of Results: mutations in
Language	English
Publishing date	2022-09-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662248-8
ISSN	2075-4426
ISSN	2075-4426
DOI	10.3390/jpm12101595
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Article ; Online: 68Ga-DOTATOC and FDG PET Imaging of Preclinical Neuroblastoma Models.

Provost, Claire / Prignon, Aurélie / Cazes, Alex / Combaret, Valérie / Delattre, Olivier / Janoueix-Lerosey, Isabelle / Montravers, Françoise / Talbot, Jean-Noël

Anticancer research

2016 Volume 36, Issue 9, Page(s) 4459–4466

Abstract: Background/aim: Somatostatine receptors subtype 2 (SSTR2) are regarded as a potential target in neuroblastoma (NB) for imaging and promising therapeutic approaches. The purpose of this study was to evaluate and compare the SSTR2 status by (68)Ga-[ ... ...

Abstract	Background/aim: Somatostatine receptors subtype 2 (SSTR2) are regarded as a potential target in neuroblastoma (NB) for imaging and promising therapeutic approaches. The purpose of this study was to evaluate and compare the SSTR2 status by (68)Ga-[tetraxetan-D-Phe1, Tyr3]-octreotide ((68)Ga-DOTATOC) positron-emission tomography (PET) and the tumour metabolic activity by (18)F-fluorodeoxyglucose (FDG) PET in different experimental models of NB. Materials and methods: Three cell lines of human NB with different levels of expression of SSTR2 were grafted into nude mice. Animals were imaged with FDG and (68)Ga-DOTATOC and the maximum standardized uptake value (SUVmax) was determined to quantify tracer uptake. Ex vivo biodistribution of (68)Ga-DOTATOC and immunohistochemical analysis of NB xenografts were performed. Results: Compared with FDG, the SUVmax of (68)Ga-DOTATOC uptake by the tumour was lower but the ratio to background was higher; there was a strong positive correlation between SUVmax values observed with the two tracers (r(2)=0.65). Sorting the cell lines according to uptake of FDG or (68)Ga-DOTATOC, injected activity per gram of tissue, Ki67 index or expression of SSTR2 assessed visually led to the same classification. Conclusion: (68)Ga-DOTATOC allows preclinical imaging of NB according to the intensity of the expression of SSTR2. In contrast with what has been reported for neuroendocrine tumours, in this NB model, the (68)Ga-DOTATOC uptake was positively correlated with FDG uptake and with Ki67 index, usual markers of tumour aggressiveness. If confirmed in humans, this result would favour a theranostic application of (68)Ga-DOTATOC in NB, even in advanced stages.
MeSH term(s)	Animals ; Brain Neoplasms/diagnostic imaging ; Cell Line, Tumor ; Disease Models, Animal ; Fluorodeoxyglucose F18/chemistry ; Gallium Radioisotopes/chemistry ; Humans ; Immunohistochemistry ; Ki-67 Antigen/metabolism ; Mice ; Mice, Nude ; Neoplasm Metastasis ; Neoplasm Transplantation ; Neuroblastoma/diagnostic imaging ; Octreotide/analogs & derivatives ; Octreotide/chemistry ; Organometallic Compounds/chemistry ; Positron-Emission Tomography ; Receptors, Somatostatin/metabolism ; Tissue Distribution
Chemical Substances	Ga(III)-DOTATOC ; Gallium Radioisotopes ; Ki-67 Antigen ; Organometallic Compounds ; Receptors, Somatostatin ; SSTR2 protein, human ; Fluorodeoxyglucose F18 (0Z5B2CJX4D) ; Octreotide (RWM8CCW8GP)
Language	English
Publishing date	2016-09-14
Publishing country	Greece
Document type	Journal Article
ZDB-ID	604549-2
ISSN	1791-7530 ; 0250-7005
ISSN (online)	1791-7530
ISSN	0250-7005
DOI	10.21873/anticanres.10990
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Zs.A 1642: Show issues

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Article ; Online: Targeting netrin-3 in small cell lung cancer and neuroblastoma.

Jiang, Shan / Richaud, Mathieu / Vieugué, Pauline / Rama, Nicolas / Delcros, Jean-Guy / Siouda, Maha / Sanada, Mitsuaki / Redavid, Anna-Rita / Ducarouge, Benjamin / Hervieu, Maëva / Breusa, Silvia / Manceau, Ambroise / Gattolliat, Charles-Henry / Gadot, Nicolas / Combaret, Valérie / Neves, David / Ortiz-Cuaran, Sandra / Saintigny, Pierre / Meurette, Olivier /

Walter, Thomas / Janoueix-Lerosey, Isabelle / Hofman, Paul / Mulligan, Peter / Goldshneider, David / Mehlen, Patrick / Gibert, Benjamin

EMBO molecular medicine

2021 Volume 13, Issue 4, Page(s) e12878

Abstract: The navigation cue netrin-1 is well-documented for its key role in cancer development and represents a promising therapeutic target currently under clinical investigation. Phase 1 and 2 clinical trials are ongoing with NP137, a humanized monoclonal ... ...

Abstract	The navigation cue netrin-1 is well-documented for its key role in cancer development and represents a promising therapeutic target currently under clinical investigation. Phase 1 and 2 clinical trials are ongoing with NP137, a humanized monoclonal antibody against netrin-1. Interestingly, the epitope recognized by NP137 in netrin-1 shares 90% homology with its counterpart in netrin-3, the closest member to netrin-1 in humans, for which little is known in the field of cancer. Here, we unveiled that netrin-3 appears to be expressed specifically in human neuroblastoma (NB) and small cell lung cancer (SCLC), two subtypes of neuroectodermal/neuroendocrine lineages. Netrin-3 and netrin-1 expression are mutually exclusive, and the former is driven by the MYCN oncogene in NB, and the ASCL-1 or NeuroD1 transcription factors in SCLC. Netrin-3 expression is correlated with disease stage, aggressiveness, and overall survival in NB. Mechanistically, we confirmed the high affinity of netrin-3 for netrin-1 receptors and we demonstrated that netrin-3 genetic silencing or interference using NP137, delayed tumor engraftment, and reduced tumor growth in animal models. Altogether, these data support the targeting of netrin-3 in NB and SCLC.
MeSH term(s)	Animals ; Humans ; Lung Neoplasms ; Netrin-1 ; Netrins ; Neuroblastoma ; Small Cell Lung Carcinoma
Chemical Substances	Netrins ; netrin-3 ; Netrin-1 (158651-98-0)
Language	English
Publishing date	2021-03-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2467145-9
ISSN	1757-4684 ; 1757-4676
ISSN (online)	1757-4684
ISSN	1757-4676
DOI	10.15252/emmm.202012878
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Zs.A 6784: Show issues

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Article ; Online: Activated ALK signals through the ERK-ETV5-RET pathway to drive neuroblastoma oncogenesis.

Lopez-Delisle, Lucille / Pierre-Eugène, Cécile / Louis-Brennetot, Caroline / Surdez, Didier / Raynal, Virginie / Baulande, Sylvain / Boeva, Valentina / Grossetête-Lalami, Sandrine / Combaret, Valérie / Peuchmaur, Michel / Delattre, Olivier / Janoueix-Lerosey, Isabelle

Oncogene

2018 Volume 37, Issue 11, Page(s) 1417–1429

Abstract: Activating mutations of the ALK receptor occur in a subset of neuroblastoma tumors. We previously demonstrated that Alk mutations cooperate with MYCN overexpression to induce neuroblastoma in mice and identified Ret as being strongly upregulated in MYCN/ ... ...

Abstract	Activating mutations of the ALK receptor occur in a subset of neuroblastoma tumors. We previously demonstrated that Alk mutations cooperate with MYCN overexpression to induce neuroblastoma in mice and identified Ret as being strongly upregulated in MYCN/Alk
MeSH term(s)	Anaplastic Lymphoma Kinase/genetics ; Anaplastic Lymphoma Kinase/metabolism ; Animals ; Carcinogenesis/genetics ; Carcinogenesis/pathology ; Cells, Cultured ; DNA-Binding Proteins/physiology ; Female ; Gain of Function Mutation/physiology ; HEK293 Cells ; Humans ; MAP Kinase Signaling System/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Nude ; Mice, Transgenic ; Neuroblastoma/genetics ; Neuroblastoma/pathology ; Proto-Oncogene Proteins c-ret/physiology ; Signal Transduction/genetics ; Transcription Factors/physiology ; Xenograft Model Antitumor Assays
Chemical Substances	DNA-Binding Proteins ; ETV5 protein, human ; Transcription Factors ; ALK protein, human (EC 2.7.10.1) ; Anaplastic Lymphoma Kinase (EC 2.7.10.1) ; Proto-Oncogene Proteins c-ret (EC 2.7.10.1) ; RET protein, human (EC 2.7.10.1)
Language	English
Publishing date	2018-01-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-017-0039-5
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