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  1. Article ; Online: Regulatory Factor X 7 and its Potential Link to Lymphoid Cancers.

    Fischer, Berenice A / Chelbi, Sonia T / Guarda, Greta

    Trends in cancer

    2019  Volume 6, Issue 1, Page(s) 6–9

    Abstract: Alterations in the Regulatory factor X 7 (RFX7) gene have recurrently been reported in lymphoid cancers. Uncharacterized until recently, this transcription factor regulates genes important for ciliogenesis and for limiting cellular metabolic activity. ... ...

    Abstract Alterations in the Regulatory factor X 7 (RFX7) gene have recurrently been reported in lymphoid cancers. Uncharacterized until recently, this transcription factor regulates genes important for ciliogenesis and for limiting cellular metabolic activity. Here we discuss these observations and conjecture on the links between the reported functions of RFX7 and its potential role in lymphoid cancers, encouraging future studies in these directions.
    MeSH term(s) Animals ; DNA Copy Number Variations ; Disease Models, Animal ; Down-Regulation ; Gene Expression Regulation, Neoplastic ; Genome-Wide Association Study ; Humans ; Leukemia, Lymphoid/genetics ; Leukemia, Lymphoid/pathology ; Lymphoma/genetics ; Lymphoma/pathology ; Mice ; Mutation ; Polymorphism, Single Nucleotide ; Regulatory Factor X Transcription Factors/genetics ; Regulatory Factor X Transcription Factors/metabolism
    Chemical Substances RFX7 protein, human ; Regulatory Factor X Transcription Factors ; Rfx7 protein, mouse
    Language English
    Publishing date 2019-12-03
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    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.2019.11.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: NLRC5, a promising new entry in tumor immunology.

    Chelbi, Sonia T / Guarda, Greta

    Journal for immunotherapy of cancer

    2016  Volume 4, Page(s) 39

    Abstract: The recent use of T cell-based cancer immunotherapies, such as adoptive T-cell transfer and checkpoint blockade, yields increasing clinical benefit to patients with different cancer types. However, decrease of MHC class I expression is a common mechanism ...

    Abstract The recent use of T cell-based cancer immunotherapies, such as adoptive T-cell transfer and checkpoint blockade, yields increasing clinical benefit to patients with different cancer types. However, decrease of MHC class I expression is a common mechanism transformed cells take advantage of to evade CD8(+) T cell-mediated antitumor responses, negatively impacting on the outcome of immunotherapies. Hence, there is an urgent need to develop novel approaches to overcome this limitation. NLRC5 has been recently described as a key transcriptional regulator controlling expression of MHC class I molecules. In this commentary, we summarize and put into perspective a study by Rodriguez and colleagues recently published in Oncoimmunology, addressing the role of NLRC5 in melanoma. The authors demonstrate that NLRC5 overexpression in B16 melanoma allows to recover MHC class I expression, rising tumor immunogenicity and counteracting immune evasion. Possible ways of manipulating NLRC5 activity in tumors will be discussed. Highlighting the therapeutic potential of modulating NLRC5 levels, this publication also encourages evaluation of NLRC5, and by extension MHC class I pathway, as clinical biomarker to select personalized immunotherapeutic strategies.
    Language English
    Publishing date 2016-07-19
    Publishing country England
    Document type Journal Article
    ZDB-ID 2719863-7
    ISSN 2051-1426
    ISSN 2051-1426
    DOI 10.1186/s40425-016-0143-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Why preeclampsia still exists?

    Chelbi, Sonia T / Veitia, Reiner A / Vaiman, Daniel

    Medical hypotheses

    2013  Volume 81, Issue 2, Page(s) 259–263

    Abstract: Preeclampsia (PE) is a deadly gestational disease affecting up to 10% of women and specific of the human species. Preeclampsia is clearly multifactorial, but the existence of a genetic basis for this disease is now clearly established by the existence of ...

    Abstract Preeclampsia (PE) is a deadly gestational disease affecting up to 10% of women and specific of the human species. Preeclampsia is clearly multifactorial, but the existence of a genetic basis for this disease is now clearly established by the existence of familial cases, epidemiological studies and known predisposing gene polymorphisms. PE is very common despite the fact that Darwinian pressure should have rapidly eliminated or strongly minimized the frequency of predisposing alleles. Consecutive pregnancies with the same partner decrease the risk and severity of PE. Here, we show that, due to this peculiar feature, preeclampsia predisposing-alleles can be differentially maintained according to the familial structure. Thus, we suggest that an optimal frequency of PE-predisposing alleles in human populations can be achieved as a result of a trade-off between benefits of exogamy, importance for maintaining genetic diversity and increase of the fitness owing to a stable paternal investment.
    MeSH term(s) Alleles ; Female ; Humans ; Pre-Eclampsia/genetics ; Pre-Eclampsia/physiopathology ; Pregnancy
    Language English
    Publishing date 2013-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 193145-3
    ISSN 1532-2777 ; 0306-9877
    ISSN (online) 1532-2777
    ISSN 0306-9877
    DOI 10.1016/j.mehy.2013.04.034
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: NLRC5 promotes transcription of

    Dang, Anh Thu / Strietz, Juliane / Zenobi, Alessandro / Khameneh, Hanif J / Brandl, Simon M / Lozza, Laura / Conradt, Gregor / Kaufmann, Stefan H E / Reith, Walter / Kwee, Ivo / Minguet, Susana / Chelbi, Sonia T / Guarda, Greta

    iScience

    2020  Volume 24, Issue 1, Page(s) 101900

    Abstract: BTN3A molecules-BTN3A1 in particular-emerged as important mediators of Vγ9Vδ2 T cell activation by phosphoantigens. These metabolites can originate from infections, e.g. ... ...

    Abstract BTN3A molecules-BTN3A1 in particular-emerged as important mediators of Vγ9Vδ2 T cell activation by phosphoantigens. These metabolites can originate from infections, e.g. with
    Language English
    Publishing date 2020-12-07
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2020.101900
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: miR-34a expression, epigenetic regulation, and function in human placental diseases.

    Doridot, Ludivine / Houry, Dorothée / Gaillard, Harald / Chelbi, Sonia T / Barbaux, Sandrine / Vaiman, Daniel

    Epigenetics

    2013  Volume 9, Issue 1, Page(s) 142–151

    Abstract: Preeclampsia (PE) is the major pregnancy-induced hypertensive disorder responsible for maternal and fetal morbidity and mortality that can be associated with intrauterine growth restriction (IUGR). PE and IUGR are thought to be due to a placental defect, ...

    Abstract Preeclampsia (PE) is the major pregnancy-induced hypertensive disorder responsible for maternal and fetal morbidity and mortality that can be associated with intrauterine growth restriction (IUGR). PE and IUGR are thought to be due to a placental defect, occurring early during pregnancy. Several placental microRNAs (miRNAs) have been shown to be deregulated in the context of placental diseases and could thus play a role in the pathophysiology of PE. Here, we show that pri-miR-34a is overexpressed in preeclamptic placentas and that its placental expression is much higher during the first trimester of pregnancy than at term, suggesting a possible developmental role. We explored pri-miR-34a regulation and showed that P53, a known activator of miR-34a, is reduced in all pathological placentas and that hypoxia can induce pri-miR-34a expression in JEG-3 cells. We also studied the methylation status of the miR-34a promoter and revealed hypomethylation in all preeclamptic placentas (associated or not with IUGR), whereas hypoxia induced a hypermethylation in JEG-3 cells at 72 h. Despite the overexpression of pri-miR-34a in preeclampsia, there was a striking decrease of the mature miR-34a in this condition, suggesting preeclampsia-driven alteration of pri-miR-34a maturation. SERPINA3, a protease inhibitor involved in placental diseases, is elevated in IUGR and PE. We show here that miR-34a overexpression in JEG-3 downregulates SERPINA3. The low level of mature miR-34a could thus be an important mechanism contributing to SERPINA3 upregulation in placental diseases. Overall, our results support a role for miR-34a in the pathophysiology of preeclampsia, through deregulation of the pri-miRNA expression and its altered maturation.
    MeSH term(s) Cell Line, Tumor ; Choriocarcinoma/genetics ; Choriocarcinoma/metabolism ; DNA Methylation ; Epigenesis, Genetic ; Female ; Humans ; Hypoxia/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Placenta Diseases/genetics ; Placenta Diseases/metabolism ; Pre-Eclampsia/genetics ; Pre-Eclampsia/metabolism ; Pregnancy ; Promoter Regions, Genetic ; Serpins/genetics ; Serpins/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Uterine Neoplasms/genetics ; Uterine Neoplasms/metabolism
    Chemical Substances MIRN34 microRNA, human ; MicroRNAs ; SERPINA3 protein, human ; Serpins ; Tumor Suppressor Protein p53
    Language English
    Publishing date 2013-09-30
    Publishing country United States
    Document type Journal Article
    ISSN 1559-2308
    ISSN (online) 1559-2308
    DOI 10.4161/epi.26196
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Distinct DNA Methylation Profiles in Ovarian Tumors: Opportunities for Novel Biomarkers.

    Losi, Lorena / Fonda, Sergio / Saponaro, Sara / Chelbi, Sonia T / Lancellotti, Cesare / Gozzi, Gaia / Alberti, Loredana / Fabbiani, Luca / Botticelli, Laura / Benhattar, Jean

    International journal of molecular sciences

    2018  Volume 19, Issue 6

    Abstract: Aberrant methylation of multiple promoter CpG islands could be related to the biology of ovarian tumors and its determination could help to improve treatment strategies. DNA methylation profiling was performed using the Methylation Ligation-dependent ... ...

    Abstract Aberrant methylation of multiple promoter CpG islands could be related to the biology of ovarian tumors and its determination could help to improve treatment strategies. DNA methylation profiling was performed using the Methylation Ligation-dependent Macroarray (MLM), an array-based analysis. Promoter regions of 41 genes were analyzed in 102 ovarian tumors and 17 normal ovarian samples. An average of 29% of hypermethylated promoter genes was observed in normal ovarian tissues. This percentage increased slightly in serous, endometrioid, and mucinous carcinomas (32%, 34%, and 45%, respectively), but decreased in germ cell tumors (20%). Ovarian tumors had methylation profiles that were more heterogeneous than other epithelial cancers. Unsupervised hierarchical clustering identified four groups that are very close to the histological subtypes of ovarian tumors. Aberrant methylation of three genes (
    MeSH term(s) Biomarkers, Tumor/metabolism ; Cluster Analysis ; DNA Methylation/genetics ; Female ; Humans ; Kaplan-Meier Estimate ; Ovarian Neoplasms/genetics ; Promoter Regions, Genetic
    Chemical Substances Biomarkers, Tumor
    Language English
    Publishing date 2018-05-24
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms19061559
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  7. Article ; Online: The transcription factor Rfx7 limits metabolism of NK cells and promotes their maintenance and immunity.

    Castro, Wilson / Chelbi, Sonia T / Niogret, Charlène / Ramon-Barros, Cristina / Welten, Suzanne P M / Osterheld, Kevin / Wang, Haiping / Rota, Giorgia / Morgado, Leonor / Vivier, Eric / Raeber, Miro E / Boyman, Onur / Delorenzi, Mauro / Barras, David / Ho, Ping-Chih / Oxenius, Annette / Guarda, Greta

    Nature immunology

    2018  Volume 19, Issue 8, Page(s) 809–820

    Abstract: Regulatory factor X 7 (Rfx7) is an uncharacterized transcription factor belonging to a family involved in ciliogenesis and immunity. Here, we found that deletion of Rfx7 leads to a decrease in natural killer (NK) cell maintenance and immunity in vivo. ... ...

    Abstract Regulatory factor X 7 (Rfx7) is an uncharacterized transcription factor belonging to a family involved in ciliogenesis and immunity. Here, we found that deletion of Rfx7 leads to a decrease in natural killer (NK) cell maintenance and immunity in vivo. Genomic approaches showed that Rfx7 coordinated a transcriptional network controlling cell metabolism. Rfx7
    MeSH term(s) Animals ; Cell Proliferation ; Cell Survival ; Cells, Cultured ; Chimera ; Energy Metabolism ; Gene Regulatory Networks ; Immunity, Cellular/genetics ; Immunity, Innate/genetics ; Interleukin-15/metabolism ; Janus Kinases/metabolism ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Regulatory Factor X1/genetics ; Regulatory Factor X1/metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism
    Chemical Substances Interleukin-15 ; Regulatory Factor X1 ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Janus Kinases (EC 2.7.10.2)
    Language English
    Publishing date 2018-07-02
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-018-0144-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Promoter methylation and downregulated expression of the

    Gozzi, Gaia / Chelbi, Sonia T / Manni, Paola / Alberti, Loredana / Fonda, Sergio / Saponaro, Sara / Fabbiani, Luca / Rivasi, Francesco / Benhattar, Jean / Losi, Lorena

    Oncology letters

    2016  Volume 12, Issue 4, Page(s) 2811–2819

    Abstract: ... ...

    Abstract TBX15
    Language English
    Publishing date 2016-08-16
    Publishing country Greece
    Document type Journal Article
    ZDB-ID 2573196-8
    ISSN 1792-1082 ; 1792-1074
    ISSN (online) 1792-1082
    ISSN 1792-1074
    DOI 10.3892/ol.2016.5019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: DNA methylation profiling of esophageal adenocarcinoma using Methylation Ligation-dependent Macroarray (MLM).

    Guilleret, Isabelle / Losi, Lorena / Chelbi, Sonia T / Fonda, Sergio / Bougel, Stéphanie / Saponaro, Sara / Gozzi, Gaia / Alberti, Loredana / Braunschweig, Richard / Benhattar, Jean

    Biochemical and biophysical research communications

    2016  Volume 479, Issue 2, Page(s) 231–237

    Abstract: Most types of cancer cells are characterized by aberrant methylation of promoter genes. In this study, we described a rapid, reproducible, and relatively inexpensive approach allowing the detection of multiple human methylated promoter genes from many ... ...

    Abstract Most types of cancer cells are characterized by aberrant methylation of promoter genes. In this study, we described a rapid, reproducible, and relatively inexpensive approach allowing the detection of multiple human methylated promoter genes from many tissue samples, without the need of bisulfite conversion. The Methylation Ligation-dependent Macroarray (MLM), an array-based analysis, was designed in order to measure methylation levels of 58 genes previously described as putative biomarkers of cancer. The performance of the design was proven by screening the methylation profile of DNA from esophageal cell lines, as well as microdissected formalin-fixed and paraffin-embedded (FFPE) tissues from esophageal adenocarcinoma (EAC). Using the MLM approach, we identified 32 (55%) hypermethylated promoters in EAC, and not or rarely methylated in normal tissues. Among them, 21promoters were found aberrantly methylated in more than half of tumors. Moreover, seven of them (ADAMTS18, APC, DKK2, FOXL2, GPX3, TIMP3 and WIF1) were found aberrantly methylated in all or almost all the tumor samples, suggesting an important role for these genes in EAC. In addition, dysregulation of the Wnt pathway with hypermethylation of several Wnt antagonist genes was frequently observed. MLM revealed a homogeneous pattern of methylation for a majority of tumors which were associated with an advanced stage at presentation and a poor prognosis. Interestingly, the few tumors presenting less methylation changes had a lower pathological stage. In conclusion, this study demonstrated the feasibility and accuracy of MLM for DNA methylation profiling of FFPE tissue samples.
    MeSH term(s) Adenocarcinoma/genetics ; Adenocarcinoma/pathology ; Biomarkers, Tumor/genetics ; Cell Line, Tumor ; DNA Methylation ; DNA, Neoplasm/chemistry ; DNA, Neoplasm/genetics ; Esophageal Neoplasms/genetics ; Esophageal Neoplasms/pathology ; Feasibility Studies ; Fixatives/chemistry ; Formaldehyde/chemistry ; Humans ; Microarray Analysis/methods ; Paraffin Embedding ; Polymerase Chain Reaction/methods ; Promoter Regions, Genetic/genetics ; Reproducibility of Results ; Sequence Analysis, DNA/methods ; Tissue Fixation ; Wnt Signaling Pathway/genetics
    Chemical Substances Biomarkers, Tumor ; DNA, Neoplasm ; Fixatives ; Formaldehyde (1HG84L3525)
    Language English
    Publishing date 2016-10-14
    Publishing country United States
    Document type Journal Article
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2016.09.049
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Serum profile in preeclampsia and intra-uterine growth restriction revealed by iTRAQ technology.

    Auer, Jana / Camoin, Luc / Guillonneau, François / Rigourd, Virginie / Chelbi, Sonia T / Leduc, Marjorie / Laparre, Jérôme / Mignot, Thérèse-Marie / Vaiman, Daniel

    Journal of proteomics

    2010  Volume 73, Issue 5, Page(s) 1004–1017

    Abstract: In order to identify new protein markers modified in placental diseases, high-throughput analysis of proteins in the plasma of pregnant women was carried out for normal and pathological pregnancies (Preeclampsia and/or Intra-Uterine Growth Restriction) ... ...

    Abstract In order to identify new protein markers modified in placental diseases, high-throughput analysis of proteins in the plasma of pregnant women was carried out for normal and pathological pregnancies (Preeclampsia and/or Intra-Uterine Growth Restriction) using iTRAQ technology. We could identify 166 proteins that were modified (p<0.05) and the technique used allowed the detection of previously undetected factors, such as various members of the SERPINA clade. The modifications of two proteins (C reactive protein and antichymotrypsin, SERPINA3) were validated on individual samples. Complement and coagulation cascades proteins were significantly enriched among modified protein clusters in the case of intra-uterine growth restriction (p<2.6.10(-11)). Several proteins were specifically enriched in isolated preeclampsia and depleted when preeclampsia was complicated by intra-uterine growth restriction. These findings suggest that the growth restricted foeto-placental unit is able to moderate some changes in maternal plasma composition. Overall, the use of iTRAQ technology, for the first time on this subject, enabled us to provide a new list of proteins modified in placental diseases, among which proteins expressed at a low level that were not accessible by other methods.
    MeSH term(s) Biomarkers ; Blood Proteins/analysis ; C-Reactive Protein/analysis ; Case-Control Studies ; Female ; Fetal Growth Retardation/blood ; Fetal Growth Retardation/diagnosis ; Humans ; Pre-Eclampsia/blood ; Pre-Eclampsia/diagnosis ; Pregnancy ; Serpins/blood
    Chemical Substances Biomarkers ; Blood Proteins ; SERPINA3 protein, human ; Serpins ; C-Reactive Protein (9007-41-4)
    Language English
    Publishing date 2010-03-10
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2400835-7
    ISSN 1876-7737 ; 1874-3919
    ISSN (online) 1876-7737
    ISSN 1874-3919
    DOI 10.1016/j.jprot.2009.12.014
    Database MEDical Literature Analysis and Retrieval System OnLINE

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