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  1. Article ; Online: The MAPK Pathway in Pulmonary Langerhans Cell Histiocytosis.

    Jouenne, Fanélie / Tazi, Abdellatif

    Archivos de bronconeumologia

    2022  Volume 59, Issue 6, Page(s) 347–349

    MeSH term(s) Humans ; Histiocytosis, Langerhans-Cell/complications ; MAP Kinase Signaling System
    Language Spanish
    Publishing date 2022-04-27
    Publishing country Spain
    Document type Editorial
    ZDB-ID 733126-5
    ISSN 1579-2129 ; 0300-2896
    ISSN (online) 1579-2129
    ISSN 0300-2896
    DOI 10.1016/j.arbres.2022.02.015
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Pulmonary Langerhans cell histiocytosis - an update on pathogenesis and treatment.

    Jouenne, Fanélie / Benattia, Amira / Tazi, Abdellatif

    Current opinion in pulmonary medicine

    2023  Volume 29, Issue 5, Page(s) 451–458

    Abstract: Purpose of review: Pulmonary Langerhans cell histiocytosis (PLCH) is a rare diffuse cystic lung disease that affects young to middle-aged smoking adults of both genders. The identification of molecular alterations in the canonical mitogen-activated ... ...

    Abstract Purpose of review: Pulmonary Langerhans cell histiocytosis (PLCH) is a rare diffuse cystic lung disease that affects young to middle-aged smoking adults of both genders. The identification of molecular alterations in the canonical mitogen-activated protein kinase (MAPK) signalling pathway in most specific lesions has demonstrated the clonal/neoplastic nature of PLCH. We will summarize the progress made in the understanding of the pathogenesis of adult PLCH, and briefly highlight the recent findings useful for the management of the patients.
    Recent findings: The MAPK pathway is constantly activated in PLCH lesions. Apart from the BRAFV600E mutation, other driver somatic genomic alterations in this pathway (mainly MAP2K1  mutations/deletions and BRAF deletions) have been identified in the lesions, paving the way for targeted treatment. Smoking appears to promote the recruitment of MAPK-activated circulating myeloid precursors to the lung. The long-term survival of PLCH is more favourable with a 10-year survival >90%. Lung cancer and chronic respiratory failure are the main causes of death. Few patients develop severe pulmonary complications within the 5 years after diagnosis, justifying a close longitudinal follow-up of the patients.
    Summary: PLCH is a MAPK driven neoplasia with inflammatory properties. The place of targeted therapies in severe forms of PLCH warrants further evaluation.
    MeSH term(s) Adult ; Middle Aged ; Humans ; Male ; Female ; Lung/pathology ; Lung Diseases/therapy ; Histiocytosis, Langerhans-Cell/genetics ; Histiocytosis, Langerhans-Cell/therapy ; Smoking/adverse effects ; Lung Neoplasms/pathology ; Mitogen-Activated Protein Kinases
    Chemical Substances Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2023-07-06
    Publishing country United States
    Document type Review ; Journal Article
    ZDB-ID 1285505-4
    ISSN 1531-6971 ; 1070-5287 ; 1078-1641
    ISSN (online) 1531-6971
    ISSN 1070-5287 ; 1078-1641
    DOI 10.1097/MCP.0000000000000988
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Mitogen-activating protein kinase pathway alterations in Langerhans cell histiocytosis.

    Jouenne, Fanélie / Benattia, Amira / Tazi, Abdellatif

    Current opinion in oncology

    2020  Volume 33, Issue 2, Page(s) 101–109

    Abstract: Purpose of review: Langerhans cell histiocytosis (LCH) is a rare disorder characterized by the infiltration of involved tissues by specialized dendritic cells. The demonstration of the constant activation of the mitogen-activated protein kinase (MAPK) ... ...

    Abstract Purpose of review: Langerhans cell histiocytosis (LCH) is a rare disorder characterized by the infiltration of involved tissues by specialized dendritic cells. The demonstration of the constant activation of the mitogen-activated protein kinase (MAPK) pathway in LCH lesions has been a breakthrough in the understanding of the pathogenesis of this rare disease. We will summarize the current knowledge on MAPK alterations in LCH and the new therapeutic options indicated by these findings.
    Recent findings: Since the description of the B-Raf proto-oncogene, serine/threonine kinase (BRAF)V600E mutation in LCH lesions, several other molecular alterations affecting the MAPK pathway have been identified in most cases. Based on these driver alterations, LCH cells were shown to be derived from hematopoietic precursors, which yielded the current concept of LCH as a myeloid inflammatory neoplasia. MAPK pathway inhibitors have emerged as an innovative therapy in severe forms of LCH, resulting in virtually no acquired resistance. However, although they are highly effective, their effect is only temporary, as the disease relapses upon discontinuation of the treatment.
    Summary: LCH is an inflammatory myeloid neoplastic disorder, driven by mutations activating the MAPK pathway. MAPK-targeted treatments represent an important stepforward in the management of patients with severe progressive LCH.
    MeSH term(s) Animals ; Histiocytosis, Langerhans-Cell/drug therapy ; Histiocytosis, Langerhans-Cell/enzymology ; Histiocytosis, Langerhans-Cell/genetics ; Histiocytosis, Langerhans-Cell/pathology ; Humans ; MAP Kinase Signaling System ; Molecular Targeted Therapy
    Language English
    Publishing date 2020-12-14
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1049384-0
    ISSN 1531-703X ; 1040-8746
    ISSN (online) 1531-703X
    ISSN 1040-8746
    DOI 10.1097/CCO.0000000000000707
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Dramatic Response After Switching MEK Inhibitors in a Patient With Refractory Mixed Histiocytosis.

    Roeser, Anais / Jouenne, Fanelie / Vercellino, Laetitia / Calvani, Julien / Goldwirt, Lauriane / Lorillon, Gwenael / Tazi, Abdellatif

    Journal of hematology

    2022  Volume 11, Issue 5, Page(s) 185–189

    Abstract: We report the case of a patient with progressive multisystem mixed histiocytosis associating Langerhans cell histiocytosis (LCH) and Erdheim-Chester disease (ECD) involving the bone marrow, whose lesions harbored ... ...

    Abstract We report the case of a patient with progressive multisystem mixed histiocytosis associating Langerhans cell histiocytosis (LCH) and Erdheim-Chester disease (ECD) involving the bone marrow, whose lesions harbored the
    Language English
    Publishing date 2022-10-31
    Publishing country Canada
    Document type Case Reports
    ZDB-ID 2662519-2
    ISSN 1927-1220 ; 1927-1220
    ISSN (online) 1927-1220
    ISSN 1927-1220
    DOI 10.14740/jh1030
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Inactivation of kindlin-3 increases human melanoma aggressiveness through the collagen-activated tyrosine kinase receptor DDR1.

    Reger De Moura, Coralie / Louveau, Baptiste / Jouenne, Fanélie / Vilquin, Paul / Battistella, Maxime / Bellahsen-Harrar, Yaelle / Sadoux, Aurélie / Menashi, Suzanne / Dumaz, Nicolas / Lebbé, Céleste / Mourah, Samia

    Oncogene

    2024  

    Abstract: The role of the focal adhesion protein kindlin-3 as a tumor suppressor and its interaction mechanisms with extracellular matrix constitute a major field of investigation to better decipher tumor progression. Besides the well-described role of kindlin-3 ... ...

    Abstract The role of the focal adhesion protein kindlin-3 as a tumor suppressor and its interaction mechanisms with extracellular matrix constitute a major field of investigation to better decipher tumor progression. Besides the well-described role of kindlin-3 in integrin activation, evidence regarding modulatory functions between melanoma cells and tumor microenvironment are lacking and data are needed to understand mechanisms driven by kindlin-3 inactivation. Here, we show that kindlin-3 inactivation through knockdown or somatic mutations increases BRAF
    Language English
    Publishing date 2024-04-03
    Publishing country England
    Document type Journal Article
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/s41388-024-03014-3
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  6. Article ; Online: The key role of oncopharmacology in therapeutic management, from common to rare cancers: A literature review.

    Louveau, Baptiste / Jouenne, Fanélie / Kaguelidou, Florentia / Landras, Alexandra / Goldwirt, Lauriane / Mourah, Samia

    Therapie

    2020  Volume 75, Issue 2, Page(s) 183–193

    Abstract: The therapeutic management of cancers has undergone considerable changes due to the emergence of genomics tools and tumor molecular deciphering. In this context, a dual pharmacological approach based on pharmacogenomic analyses and therapeutic drug ... ...

    Abstract The therapeutic management of cancers has undergone considerable changes due to the emergence of genomics tools and tumor molecular deciphering. In this context, a dual pharmacological approach based on pharmacogenomic analyses and therapeutic drug monitoring is now part of the routine care in cancer management for personalized therapies. First, molecular and immune profiling of tumors allows the emergence of new pharmacological targets in common as well as in rare cancers. Second, pharmacogenomic analyses coupled to therapeutic drug monitoring guide the prescription by adjusting regimen and managing drug resistance.
    MeSH term(s) Antineoplastic Agents/therapeutic use ; Drug Resistance, Neoplasm ; Humans ; Medical Oncology/trends ; Molecular Targeted Therapy ; Neoplasms/drug therapy ; Pharmacogenetics ; Pharmacology/trends ; Rare Diseases/drug therapy
    Chemical Substances Antineoplastic Agents
    Language English
    Publishing date 2020-02-13
    Publishing country France
    Document type Journal Article ; Review
    ZDB-ID 603474-3
    ISSN 1958-5578 ; 0040-5957
    ISSN (online) 1958-5578
    ISSN 0040-5957
    DOI 10.1016/j.therap.2020.02.010
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  7. Article: TERT Expression Induces Resistance to BRAF and MEK Inhibitors in BRAF-Mutated Melanoma In Vitro.

    Delyon, Julie / Vallet, Anaïs / Bernard-Cacciarella, Mélanie / Kuzniak, Isabelle / Reger de Moura, Coralie / Louveau, Baptiste / Jouenne, Fanélie / Mourah, Samia / Lebbé, Céleste / Dumaz, Nicolas

    Cancers

    2023  Volume 15, Issue 11

    Abstract: Because BRAF-mutated melanomas are addicted to the Mitogen Activated Protein Kinase (MAPK) pathway they show a high response rate to BRAF and MEK inhibitors. However, the clinical responses to these inhibitors are often short-lived with the rapid onset ... ...

    Abstract Because BRAF-mutated melanomas are addicted to the Mitogen Activated Protein Kinase (MAPK) pathway they show a high response rate to BRAF and MEK inhibitors. However, the clinical responses to these inhibitors are often short-lived with the rapid onset of resistance to treatment. Deciphering the molecular mechanisms driving resistance has been the subject of intense research. Recent in vitro and clinical data have suggested a link between expression of telomerase and resistance to targeted therapy in melanoma. TERT promoter mutations are the main mechanism for the continuous upregulation of telomerase in melanoma and co-occur frequently with BRAF alterations. To understand how TERT promoter mutations could be associated with resistance to targeted therapy in melanoma, we conducted translational and in vitro studies. In a cohort of V600E-BRAF-mutated melanoma patients, we showed that the TERT promoter mutation status and TERT expression tended to be associated with response to BRAF and MEK inhibitors. We demonstrated that TERT overexpression in BRAF-mutated melanoma cells reduced sensitivity to BRAF and MEK independently of TERT's telomer maintenance activity. Interestingly, inhibition of TERT reduced growth of BRAF-mutated melanoma including resistant cells. TERT expression in melanoma can therefore be a new biomarker for resistance to MAPK inhibitors as well as a novel therapeutic target.
    Language English
    Publishing date 2023-05-24
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers15112888
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  8. Article ; Online: Melanoma Risk and Melanocyte Biology.

    Bertrand, Julie U / Steingrimsson, Eirikur / Jouenne, Fanélie / Bressac-de Paillerets, Brigitte / Larue, Lionel

    Acta dermato-venereologica

    2020  Volume 100, Issue 11, Page(s) adv00139

    Abstract: Cutaneous melanoma arises from melanocytes following genetic, epigenetic and allogenetic (i.e. other than epi/genetic) modifications. An estimated 10% of cutaneous melanoma cases are due to inherited variants or de novo mutations in approximately 20 ... ...

    Abstract Cutaneous melanoma arises from melanocytes following genetic, epigenetic and allogenetic (i.e. other than epi/genetic) modifications. An estimated 10% of cutaneous melanoma cases are due to inherited variants or de novo mutations in approximately 20 genes, found using linkage, next-generation sequencing and association studies. Based on these studies, 3 classes of predisposing melanoma genes have been defined based on the frequency of the variants in the general population and lifetime risk of developing a melanoma: (i) ultra-rare variants with a high risk, (ii) rare with a moderate risk, and (iii) frequent variants with a low risk. Most of the proteins encoded by these genes have been shown to be involved in melanoma initiation, including proliferation and senescence bypass. This paper reviews the role(s) of these genes in the transformation of melanocytes into melanoma. It also describes their function in the establishment and renewal of melanocytes and the biology of pigment cells, if known.
    MeSH term(s) Animals ; Biomarkers, Tumor/genetics ; Cell Lineage ; Genetic Predisposition to Disease ; Humans ; Melanins/metabolism ; Melanocytes/metabolism ; Melanocytes/pathology ; Melanoma/ethnology ; Melanoma/genetics ; Melanoma/metabolism ; Melanoma/pathology ; Melanosomes/metabolism ; Melanosomes/pathology ; Mutation ; Mutation Rate ; Phenotype ; Risk Assessment ; Risk Factors ; Skin Neoplasms/ethnology ; Skin Neoplasms/genetics ; Skin Neoplasms/metabolism ; Skin Neoplasms/pathology ; Whites/genetics
    Chemical Substances Biomarkers, Tumor ; Melanins
    Language English
    Publishing date 2020-06-03
    Publishing country Sweden
    Document type Journal Article ; Review
    ZDB-ID 80007-7
    ISSN 1651-2057 ; 0001-5555
    ISSN (online) 1651-2057
    ISSN 0001-5555
    DOI 10.2340/00015555-3494
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  9. Article ; Online: Combined PDE4+MEK inhibition shows antiproliferative effects in NRASQ61 mutated melanoma preclinical models.

    Louveau, Baptiste / Reger De Moura, Coralie / Jouenne, Fanélie / Sadoux, Aurélie / Allayous, Clara / Da Meda, Laetitia / Bernard-Cacciarella, Mélanie / Baroudjian, Barouyr / Lebbé, Céleste / Mourah, Samia / Dumaz, Nicolas

    Melanoma research

    2023  Volume 34, Issue 2, Page(s) 186–192

    Abstract: Upregulation of phosphodiesterase type 4 (PDE4) has been associated with worse prognosis in several cancers. In melanomas harboring NRAS mutations, PDE4 upregulation has been shown to trigger a switch in signaling from BRAF to RAF1 which leads to mitogen- ...

    Abstract Upregulation of phosphodiesterase type 4 (PDE4) has been associated with worse prognosis in several cancers. In melanomas harboring NRAS mutations, PDE4 upregulation has been shown to trigger a switch in signaling from BRAF to RAF1 which leads to mitogen-activated protein kinase pathway activation. Previous in vitro evidence showed that PDE4 inhibition induced death in NRASQ61mut melanoma cells and such a strategy may thus be a relevant therapeutic option in those cases with no molecular targeted therapies approved to date. In this study, we generated patient-derived xenografts (PDX) from two NRASQ61mut melanoma lesions. We performed ex vivo histoculture drug response assays and in vivo experiments. A significant ex vivo inhibition of proliferation with the combination of roflumilast+cobimetinib was observed compared to dimethyl sulfoxide control in both models (51 and 67%). This antiproliferative effect was confirmed in vivo for PDX-1 with a 56% inhibition of tumor growth. To decipher molecular mechanisms underlying this effect, we performed transcriptomic analyses and revealed a decrease in MKI67, RAF1 and CCND1 expression under bitherapy. Our findings strengthen the therapeutic interest of PDE4 inhibitors and support further experiments to evaluate this approach in metastatic melanoma.
    MeSH term(s) Animals ; Humans ; Dimethyl Sulfoxide ; Disease Models, Animal ; Melanoma/drug therapy ; Melanoma/genetics ; Mitogen-Activated Protein Kinase Kinases ; Skin Neoplasms ; MAP Kinase Kinase Kinases/metabolism
    Chemical Substances Dimethyl Sulfoxide (YOW8V9698H) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2) ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; PDE4A protein, human (EC 3.1.4.17)
    Language English
    Publishing date 2023-12-22
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1095779-0
    ISSN 1473-5636 ; 0960-8931
    ISSN (online) 1473-5636
    ISSN 0960-8931
    DOI 10.1097/CMR.0000000000000950
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 3378: Show issues Location:
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  10. Article ; Online: Clinicopathologic and molecular characterization of melanomas mutated for CTNNB1 and MAPK.

    Oulès, Bénédicte / Mourah, Samia / Baroudjian, Barouyr / Jouenne, Fanélie / Delyon, Julie / Louveau, Baptiste / Gruber, Aurélia / Lebbé, Céleste / Battistella, Maxime

    Virchows Archiv : an international journal of pathology

    2021  Volume 480, Issue 2, Page(s) 475–480

    Abstract: Wnt/β-catenin signaling plays crucial roles in melanocyte biology and may be implicated in melanoma progression. In this study, we retrospectively examined a real-life cohort of melanomas mutated for β-catenin (CTNNB1), in association or not with a MAPK ... ...

    Abstract Wnt/β-catenin signaling plays crucial roles in melanocyte biology and may be implicated in melanoma progression. In this study, we retrospectively examined a real-life cohort of melanomas mutated for β-catenin (CTNNB1), in association or not with a MAPK mutation (of BRAF or NRAS), and analyzed their clinical, histopathological, and molecular characteristics. Our results indicate that, regardless of the presence of a concurrent MAPK mutation, CTNNB1
    MeSH term(s) Humans ; Melanoma/genetics ; Melanoma/pathology ; Mutation/genetics ; Proto-Oncogene Proteins B-raf/genetics ; Retrospective Studies ; Skin Neoplasms/genetics ; Skin Neoplasms/pathology ; beta Catenin/genetics ; Melanoma, Cutaneous Malignant
    Chemical Substances CTNNB1 protein, human ; beta Catenin ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1)
    Language English
    Publishing date 2021-05-20
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 1184867-4
    ISSN 1432-2307 ; 0945-6317
    ISSN (online) 1432-2307
    ISSN 0945-6317
    DOI 10.1007/s00428-021-03119-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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