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Article ; Online: Holistic pediatric oncology: towards a second Copernican revolution.

André, Nicolas / Castets, Marie / Pasquier, Eddy / Mehlen, Patrick

2023 Volume 9, Issue 9, Page(s) 693–696

Abstract: Recently, a holistic approach to oncology that integrates a whole-body understanding of the etiology and dynamics of cancer and the development of new therapies has been proposed. Herein we discuss how this concept is also relevant to pediatric oncology, ...

Abstract	Recently, a holistic approach to oncology that integrates a whole-body understanding of the etiology and dynamics of cancer and the development of new therapies has been proposed. Herein we discuss how this concept is also relevant to pediatric oncology, with the caveat of specificities that must be considered.
MeSH term(s)	Child ; Humans ; Medical Oncology ; Neoplasms/genetics ; Neoplasms/therapy
Language	English
Publishing date	2023-06-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	2852626-0
ISSN	2405-8025 ; 2405-8033 ; 2405-8033
ISSN (online)	2405-8025 ; 2405-8033
ISSN	2405-8033
DOI	10.1016/j.trecan.2023.05.008
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Cancers évitables - Suffit-il de changer nos comportements ?

Billaud, Marc / Castets, Marie / Trautmann, Alain / Sujobert, Pierre

Medecine sciences : M/S

2023 Volume 39, Issue 5, Page(s) 452–457

Abstract: In France, part of 40 % of preventable cancers can be attributed to lifestyle habits. Epidemiological data show that occupational exposures are a major cause of these cancers. However, despite this evidence, the prevention actions promoted by public ... ...

Title translation	Preventable cancers: Is it enough to change our behaviour?
Abstract	In France, part of 40 % of preventable cancers can be attributed to lifestyle habits. Epidemiological data show that occupational exposures are a major cause of these cancers. However, despite this evidence, the prevention actions promoted by public authorities are focused on changing individual behaviors. In this article, we seek to understand the reasons of the erasure of the role of socio-environmental factors in cancer prevention discourse.
MeSH term(s)	Humans ; Neoplasms/etiology ; Occupational Exposure ; Life Style ; France ; Risk Factors
Language	French
Publishing date	2023-05-23
Publishing country	France
Document type	English Abstract ; Journal Article
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/2023059
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Bone Morphogenic Proteins in Pediatric Diffuse Midline Gliomas: How to Make New Out of Old?

Berthelot, Clément / Huchedé, Paul / Bertrand-Chapel, Adrien / Beuriat, Pierre-Aurélien / Leblond, Pierre / Castets, Marie

International journal of molecular sciences

2024 Volume 25, Issue 6

Abstract: The BMP pathway is one of the major signaling pathways in embryonic development, ontogeny and homeostasis, identified many years ago by pioneers in developmental biology. Evidence of the deregulation of its activity has also emerged in many cancers, with ...

Abstract	The BMP pathway is one of the major signaling pathways in embryonic development, ontogeny and homeostasis, identified many years ago by pioneers in developmental biology. Evidence of the deregulation of its activity has also emerged in many cancers, with complex and sometimes opposing effects. Recently, its role has been suspected in Diffuse Midline Gliomas (DMG), among which Diffuse Intrinsic Pontine Gliomas (DIPG) are one of the most complex challenges in pediatric oncology. Genomic sequencing has led to understanding part of their molecular etiology, with the identification of histone H3 mutations in a large proportion of patients. The epigenetic remodeling associated with these genetic alterations has also been precisely described, creating a permissive context for oncogenic transcriptional program activation. This review aims to describe the new findings about the involvement of BMP pathway activation in these tumors, placing their appearance in a developmental context. Targeting the oncogenic synergy resulting from this pathway activation in an H3K27M context could offer new therapeutic perspectives based on targeting treatment-resistant cell states.
MeSH term(s)	Humans ; Child ; Glioma/metabolism ; Histones/metabolism ; Diffuse Intrinsic Pontine Glioma/genetics ; Diffuse Intrinsic Pontine Glioma/metabolism ; Diffuse Intrinsic Pontine Glioma/pathology ; Mutation ; Signal Transduction ; Bone Morphogenetic Proteins/metabolism
Chemical Substances	Histones ; Bone Morphogenetic Proteins
Language	English
Publishing date	2024-03-15
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25063361
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: The Intricate Epigenetic and Transcriptional Alterations in Pediatric High-Grade Gliomas: Targeting the Crosstalk as the Oncogenic Achilles' Heel.

Huchedé, Paul / Leblond, Pierre / Castets, Marie

Biomedicines

2022 Volume 10, Issue 6

Abstract: Pediatric high-grade gliomas (pHGGs) are a deadly and heterogenous subgroup of gliomas for which the development of innovative treatments is urgent. Advances in high-throughput molecular techniques have shed light on key epigenetic components of these ... ...

Abstract	Pediatric high-grade gliomas (pHGGs) are a deadly and heterogenous subgroup of gliomas for which the development of innovative treatments is urgent. Advances in high-throughput molecular techniques have shed light on key epigenetic components of these diseases, such as K27M and G34R/V mutations on histone 3. However, modification of DNA compaction is not sufficient by itself to drive those tumors. Here, we review molecular specificities of pHGGs subcategories in the context of epigenomic rewiring caused by H3 mutations and the subsequent oncogenic interplay with transcriptional signaling pathways co-opted from developmental programs that ultimately leads to gliomagenesis. Understanding how transcriptional and epigenetic alterations synergize in each cellular context in these tumors could allow the identification of new Achilles' heels, thereby highlighting new levers to improve their therapeutic management.
Language	English
Publishing date	2022-06-03
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines10061311
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Article ; Online: Complex Elucidation of Cells-of-Origin in Pediatric Soft Tissue Sarcoma: From Concepts to Real Life, Hide-and-Seek through Epigenetic and Transcriptional Reprogramming.

Savary, Clara / Picard, Cécile / Corradini, Nadège / Castets, Marie

International journal of molecular sciences

2022 Volume 23, Issue 11

Abstract: Soft tissue sarcoma (STS) comprise a large group of mesenchymal malignant tumors with heterogeneous cellular morphology, proliferative index, genetic lesions and, more importantly, clinical features. Full elucidation of this wide diversity remains a ... ...

Abstract	Soft tissue sarcoma (STS) comprise a large group of mesenchymal malignant tumors with heterogeneous cellular morphology, proliferative index, genetic lesions and, more importantly, clinical features. Full elucidation of this wide diversity remains a central question to improve their therapeutic management and the identity of cell(s)-of-origin from which these tumors arise is part of this enigma. Cellular reprogramming allows transitions of a mature cell between phenotypes, or identities, and represents one key driver of tumoral heterogeneity. Here, we discuss how cellular reprogramming mediated by driver genes in STS can profoundly reshape the molecular and morphological features of a transformed cell and lead to erroneous interpretation of its cell-of-origin. This review questions the fact that the epigenetic context in which a genetic alteration arises has to be taken into account as a key determinant of STS tumor initiation and progression. Retracing the cancer-initiating cell and its clonal evolution, notably via epigenetic approach, appears as a key lever for understanding the origin of these tumors and improving their clinical management.
MeSH term(s)	Cellular Reprogramming/genetics ; Epigenesis, Genetic ; Epigenomics ; Humans ; Sarcoma/genetics ; Sarcoma/therapy ; Soft Tissue Neoplasms/therapy
Language	English
Publishing date	2022-06-04
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23116310
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Article ; Online: The Intricate Epigenetic and Transcriptional Alterations in Pediatric High-Grade Gliomas

Paul Huchedé / Pierre Leblond / Marie Castets

Biomedicines, Vol 10, Iss 1311, p

Targeting the Crosstalk as the Oncogenic Achilles’ Heel

2022 Volume 1311

Abstract	Pediatric high-grade gliomas (pHGGs) are a deadly and heterogenous subgroup of gliomas for which the development of innovative treatments is urgent. Advances in high-throughput molecular techniques have shed light on key epigenetic components of these diseases, such as K27M and G34R/V mutations on histone 3. However, modification of DNA compaction is not sufficient by itself to drive those tumors. Here, we review molecular specificities of pHGGs subcategories in the context of epigenomic rewiring caused by H3 mutations and the subsequent oncogenic interplay with transcriptional signaling pathways co-opted from developmental programs that ultimately leads to gliomagenesis. Understanding how transcriptional and epigenetic alterations synergize in each cellular context in these tumors could allow the identification of new Achilles’ heels, thereby highlighting new levers to improve their therapeutic management.
Keywords	pediatric glioma ; HGG ; epigenetics ; H3K27M ; H3G34R ; transcriptional networks ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Complex Elucidation of Cells-of-Origin in Pediatric Soft Tissue Sarcoma

Clara Savary / Cécile Picard / Nadège Corradini / Marie Castets

International Journal of Molecular Sciences, Vol 23, Iss 6310, p

From Concepts to Real Life, Hide-and-Seek through Epigenetic and Transcriptional Reprogramming

2022 Volume 6310

Abstract	Soft tissue sarcoma (STS) comprise a large group of mesenchymal malignant tumors with heterogeneous cellular morphology, proliferative index, genetic lesions and, more importantly, clinical features. Full elucidation of this wide diversity remains a central question to improve their therapeutic management and the identity of cell(s)-of-origin from which these tumors arise is part of this enigma. Cellular reprogramming allows transitions of a mature cell between phenotypes, or identities, and represents one key driver of tumoral heterogeneity. Here, we discuss how cellular reprogramming mediated by driver genes in STS can profoundly reshape the molecular and morphological features of a transformed cell and lead to erroneous interpretation of its cell-of-origin. This review questions the fact that the epigenetic context in which a genetic alteration arises has to be taken into account as a key determinant of STS tumor initiation and progression. Retracing the cancer-initiating cell and its clonal evolution, notably via epigenetic approach, appears as a key lever for understanding the origin of these tumors and improving their clinical management.
Keywords	sarcoma ; soft tissue sarcoma ; transcriptional networks ; cellular reprogramming ; transdifferentiation ; cell-of-origin ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	571
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Implication of Netrin-1 Gain of Expression in Canine Nodal Lymphoma.

Tortereau, Antonin / Milhau, Nadège / Rhumy, Elodie / Castets, Marie / Ponce, Frédérique / Mehlen, Patrick / Marchal, Thierry

Veterinary sciences

2022 Volume 9, Issue 9

Abstract: Netrin-1 is a member of the laminin superfamily, and is known to interact with specific receptors, called dependence receptors. While upon netrin-1 binding these receptors initiate positive signaling, in absence of netrin-1, these receptors trigger ... ...

Abstract	Netrin-1 is a member of the laminin superfamily, and is known to interact with specific receptors, called dependence receptors. While upon netrin-1 binding these receptors initiate positive signaling, in absence of netrin-1, these receptors trigger apoptosis. Tumor cells can avoid apoptosis by inactivating these receptors or by gaining ligand expression. The aim of the present study was to investigate the expression of netrin-1, the ligand of dependence receptors, in canine healthy lymph nodes (LN), and in lymphomas and to evaluate efficiency of a netrin-1 interfering compound in cell cultures from canine lymphoma. Thirty-two control LN and 169 lymphomas were analyzed through immunohistochemistry. Netrin-1 was expressed in the nucleoli of lymphoid and non-lymphoid cells in controls. Acquisition of a cytoplasmic expression was present in B-cell lymphomas (23.1 % in low-grade and 50.6% in high-grade) and T-cell lymphomas (50.0 % in low-grade and 78.8 % in high-grade), with a significant difference between the high- and low-grade in B-cell lymphomas. Through flow cytometry, we showed a significant increase in netrin-1 expression in either high-grade B-cell and T-cell lymphomas (19 and 5, respectively) compared with healthy LN (5), likewise an RT-qPCR analysis demonstrated a significant increase in netrin-1 expression level in 14 samples of lymphomas compared with eight samples of healthy LN. A T-cell aggressive canine lymphoma cell line and four primary canine nodal lymphomas cell cultures were treated with a netrin-1 interfering antibody. Apoptosis by measuring caspase 3 activity was significantly increased in the cell line and viability was decreased in three of the four primary cell cultures. Together, these data suggest that netrin-1 expression is increased in lymphoma, and more specifically in high-grade lymphomas, and that netrin-1 can act as a survival factor for the neoplastic cells, and so be a therapeutic target.
Language	English
Publishing date	2022-09-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2768971-2
ISSN	2306-7381 ; 2306-7381
ISSN (online)	2306-7381
ISSN	2306-7381
DOI	10.3390/vetsci9090494
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Caspase-8 deficiency induces a switch from TLR3 induced apoptosis to lysosomal cell death in neuroblastoma.

Locquet, Marie-Anaïs / Ichim, Gabriel / Bisaccia, Joseph / Dutour, Aurelie / Lebecque, Serge / Castets, Marie / Weber, Kathrin

Scientific reports

2021 Volume 11, Issue 1, Page(s) 10609

Abstract: In cancer cells only, TLR3 acquires death receptor properties by efficiently triggering the extrinsic pathway of apoptosis with Caspase-8 as apical protease. Here, we demonstrate that in the absence of Caspase-8, activation of TLR3 can trigger a form of ... ...

Abstract	In cancer cells only, TLR3 acquires death receptor properties by efficiently triggering the extrinsic pathway of apoptosis with Caspase-8 as apical protease. Here, we demonstrate that in the absence of Caspase-8, activation of TLR3 can trigger a form of programmed cell death, which is distinct from classical apoptosis. When TLR3 was activated in the Caspase-8 negative neuroblastoma cell line SH-SY5Y, cell death was accompanied by lysosomal permeabilization. Despite caspases being activated, lysosomal permeabilization as well as cell death were not affected by blocking caspase-activity, positioning lysosomal membrane permeabilization (LMP) upstream of caspase activation. Taken together, our data suggest that LMP with its deadly consequences represents a "default" death mechanism in cancer cells, when Caspase-8 is absent and apoptosis cannot be induced.
MeSH term(s)	Apoptosis/drug effects ; Caspase 8/metabolism ; Cell Line, Tumor ; Enzyme Activation/drug effects ; Humans ; Interferon Type I/pharmacology ; Intracellular Membranes/drug effects ; Intracellular Membranes/metabolism ; Lysosomes/drug effects ; Lysosomes/metabolism ; Necroptosis/drug effects ; Neuroblastoma/metabolism ; Neuroblastoma/pathology ; Permeability/drug effects ; Poly I-C/pharmacology ; Toll-Like Receptor 3/metabolism
Chemical Substances	Interferon Type I ; Toll-Like Receptor 3 ; Caspase 8 (EC 3.4.22.-) ; Poly I-C (O84C90HH2L)
Language	English
Publishing date	2021-05-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-89793-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Implication of Netrin-1 Gain of Expression in Canine Nodal Lymphoma

Tortereau, Antonin / Milhau, Nadège / Rhumy, Elodie / Castets, Marie / Ponce, Frédérique / Mehlen, Patrick / Marchal, Thierry

Veterinary sciences. 2022 Sept. 10, v. 9, no. 9

2022

Abstract	Netrin-1 is a member of the laminin superfamily, and is known to interact with specific receptors, called dependence receptors. While upon netrin-1 binding these receptors initiate positive signaling, in absence of netrin-1, these receptors trigger apoptosis. Tumor cells can avoid apoptosis by inactivating these receptors or by gaining ligand expression. The aim of the present study was to investigate the expression of netrin-1, the ligand of dependence receptors, in canine healthy lymph nodes (LN), and in lymphomas and to evaluate efficiency of a netrin-1 interfering compound in cell cultures from canine lymphoma. Thirty-two control LN and 169 lymphomas were analyzed through immunohistochemistry. Netrin-1 was expressed in the nucleoli of lymphoid and non-lymphoid cells in controls. Acquisition of a cytoplasmic expression was present in B-cell lymphomas (23.1 % in low-grade and 50.6% in high-grade) and T-cell lymphomas (50.0 % in low-grade and 78.8 % in high-grade), with a significant difference between the high- and low-grade in B-cell lymphomas. Through flow cytometry, we showed a significant increase in netrin-1 expression in either high-grade B-cell and T-cell lymphomas (19 and 5, respectively) compared with healthy LN (5), likewise an RT-qPCR analysis demonstrated a significant increase in netrin-1 expression level in 14 samples of lymphomas compared with eight samples of healthy LN. A T-cell aggressive canine lymphoma cell line and four primary canine nodal lymphomas cell cultures were treated with a netrin-1 interfering antibody. Apoptosis by measuring caspase 3 activity was significantly increased in the cell line and viability was decreased in three of the four primary cell cultures. Together, these data suggest that netrin-1 expression is increased in lymphoma, and more specifically in high-grade lymphomas, and that netrin-1 can act as a survival factor for the neoplastic cells, and so be a therapeutic target.
Keywords	B-cell lymphoma ; B-lymphocytes ; T-cell lymphoma ; T-lymphocytes ; antibodies ; apoptosis ; caspase-3 ; cell lines ; dogs ; flow cytometry ; immunohistochemistry ; laminin ; ligands ; lymph ; neoplasm cells ; therapeutics ; viability
Language	English
Dates of publication	2022-0910
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2768971-2
ISSN	2306-7381
ISSN	2306-7381
DOI	10.3390/vetsci9090494
Database	NAL-Catalogue (AGRICOLA)

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