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Article ; Online: The Cross-talk Between Intestinal Microbiota and MDSCs Fuels Colitis-associated Cancer Development.

Ashkenazi-Preiser, Hadas / Reuven, Or / Uzan-Yulzari, Atara / Komisarov, Sharon / Cirkin, Roy / Turjeman, Sondra / Even, Carmel / Twaik, Nira / Ben-Meir, Kerem / Mikula, Ivan / Cohen-Daniel, Leonor / Meirow, Yaron / Pikarsky, Eli / Louzoun, Yoram / Koren, Omry / Baniyash, Michal

Cancer research communications

2024 Volume 4, Issue 4, Page(s) 1063–1081

Abstract: Intestinal chronic inflammation is associated with microbial dysbiosis and accumulation of various immune cells including myeloid-derived suppressor cells (MDSC), which profoundly impact the immune microenvironment, perturb homeostasis and increase the ... ...

Abstract	Intestinal chronic inflammation is associated with microbial dysbiosis and accumulation of various immune cells including myeloid-derived suppressor cells (MDSC), which profoundly impact the immune microenvironment, perturb homeostasis and increase the risk to develop colitis-associated colorectal cancer (CAC). However, the specific MDSCs-dysbiotic microbiota interactions and their collective impact on CAC development remain poorly understood. In this study, using a murine model of CAC, we demonstrate that CAC-bearing mice exhibit significantly elevated levels of highly immunosuppressive MDSCs, accompanied by microbiota alterations. Both MDSCs and bacteria that infiltrate the colon tissue and developing tumors can be found in close proximity, suggesting intricate MDSC-microbiota cross-talk within the tumor microenvironment. To investigate this phenomenon, we employed antibiotic treatment to disrupt MDSC-microbiota interactions. This intervention yielded a remarkable reduction in intestinal inflammation, decreased MDSC levels, and alleviated immunosuppression, all of which were associated with a significant reduction in tumor burden. Furthermore, we underscore the causative role of dysbiotic microbiota in the predisposition toward tumor development, highlighting their potential as biomarkers for predicting tumor load. We shed light on the intimate MDSCs-microbiota cross-talk, revealing how bacteria enhance MDSC suppressive features and activities, inhibit their differentiation into mature beneficial myeloid cells, and redirect some toward M2 macrophage phenotype. Collectively, this study uncovers the role of MDSC-bacteria cross-talk in impairing immune responses and promoting tumor growth, providing new insights into potential therapeutic strategies for CAC. Significance: MDSCs-dysbiotic bacteria interactions in the intestine play a crucial role in intensifying immunosuppression within the CAC microenvironment, ultimately facilitating tumor growth, highlighting potential therapeutic targets for improving the treatment outcomes of CAC.
MeSH term(s)	Animals ; Mice ; Myeloid-Derived Suppressor Cells ; Colitis-Associated Neoplasms ; Gastrointestinal Microbiome ; Neoplasms ; Inflammation ; Tumor Microenvironment
Language	English
Publishing date	2024-03-20
Publishing country	United States
Document type	Journal Article
ISSN	2767-9764
ISSN (online)	2767-9764
DOI	10.1158/2767-9764.CRC-23-0421
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Article ; Online: Retraction Notice to "Generalized verrucosis and abnormal T cell activation due to homozygous TAOK2 mutation".

Molho-Pessach, Vered / Ramot, Yuval / Mogilevsky, Maxim / Cohen-Daniel, Leonor / Eisenstein, Eli M / Abu-Libdeh, Abdulsalam / Siam, Ihab / Berger, Michael / Karni, Rotem / Zlotogorski, Abraham

Journal of dermatological science

2023 Volume 108, Issue 2, Page(s) 116

Language	English
Publishing date	2023-02-02
Publishing country	Netherlands
Document type	Journal Article ; Retraction of Publication
ZDB-ID	1024446-3
ISSN	1873-569X ; 0923-1811
ISSN (online)	1873-569X
ISSN	0923-1811
DOI	10.1016/j.jdermsci.2022.12.004
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Article ; Online: Loss of T-cell quiescence by targeting Slfn2 prevents the development and progression of T-ALL.

Goldshtein, Aviya / Zerbib, Shani Mistriel / Omar, Ibrahim / Cohen-Daniel, Leonor / Popkin, Daniel / Berger, Michael

Oncotarget

2016 Volume 7, Issue 30, Page(s) 46835–46847

Abstract: T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy of thymocytes. Despite significant improvement in the treatment of T-ALL, approximately 20% of children and most adults undergo relapse. Previous findings demonstrated that loss of T- ...

Abstract	T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy of thymocytes. Despite significant improvement in the treatment of T-ALL, approximately 20% of children and most adults undergo relapse. Previous findings demonstrated that loss of T-cell quiescence due to a mutation in the Slfn2 gene (elektra) leads to acquisition of an aberrant developmental program by which T-cells lose their renewal capabilities and undergo apoptosis. Here we show that the elektra mutation in Slfn2 completely prevents a severe lymphoproliferative disease caused by overexpression of BCL2 in combination with Fas deficiency in mice. Moreover, Slfn2 impaired-function protects mice from experimental disease similar to human T-ALL by severely impairing the proliferation potential and survival of leukemic T-cells, partially by activation of the p53 tumor suppressor protein. Our study suggest that in certain malignancies, such as T-ALL, a novel therapeutic strategy may be applied by imposing aberrant development of leukemic cells. Furthermore, as the elektra mutation in Slfn2 seems to impair only T-cells and monocytes, targeting Slfn2 is expected to be harmless to other cell types, and thereby could be a promising target for treating malignancies. Together our results demonstrate the potential of targeting Slfn2 and its human paralog for T-ALL treatment.
Language	English
Publishing date	2016-07-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.9390
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Article ; Online: Schlafen2 mutation unravels a role for chronic ER stress in the loss of T cell quiescence.

Omar, Ibrahim / Lapenna, Antonio / Cohen-Daniel, Leonor / Tirosh, Boaz / Berger, Michael

Oncotarget

2016 Volume 7, Issue 26, Page(s) 39396–39407

Abstract: Immunologically naïve lymphocytes are kept in a quiescent state until antigen engagement. These quiescent immune cells are characterized by small cell size, lack of spontaneous proliferation and low metabolic rate. Lymphocyte quiescence is actively ... ...

Abstract	Immunologically naïve lymphocytes are kept in a quiescent state until antigen engagement. These quiescent immune cells are characterized by small cell size, lack of spontaneous proliferation and low metabolic rate. Lymphocyte quiescence is actively enforced condition which ensures the preservation of proper differentiation and proliferation capabilities of naïve and memory lymphocytes. Previously we described a chemically induced mutation in Schlafen2 (Slfn2), termed elektra, which breaks quiescence and compromises immunity. However, the mechanism by which Slfn2 maintains quiescence remains unknown. Here we demonstrate that elektra T cells display chronic ER stress under steady state conditions. Modulation of ER stress response by depletion of either UPR mediators XBP1 or CHOP, improved viability and partially corrected the developmental abnormalities and proliferation capabilities of elektra T cells. Altogether, our results demonstrate a functional connection between Slfn2 induced quiescence in T cells and ER homeostasis, clarifying a novel mechanism by which immune cell quiescence is maintained.
Language	English
Publishing date	2016-06-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.9818
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Article ; Online: Post-transcriptional 3´-UTR cleavage of mRNA transcripts generates thousands of stable uncapped autonomous RNA fragments.

Malka, Yuval / Steiman-Shimony, Avital / Rosenthal, Eran / Argaman, Liron / Cohen-Daniel, Leonor / Arbib, Eliran / Margalit, Hanah / Kaplan, Tommy / Berger, Michael

Nature communications

2017 Volume 8, Issue 1, Page(s) 2029

Abstract: The majority of mammalian genes contain one or more alternative polyadenylation sites. Choice of polyadenylation sites was suggested as one of the underlying mechanisms for generating longer/shorter transcript isoforms. Here, we demonstrate that mature ... ...

Abstract	The majority of mammalian genes contain one or more alternative polyadenylation sites. Choice of polyadenylation sites was suggested as one of the underlying mechanisms for generating longer/shorter transcript isoforms. Here, we demonstrate that mature mRNA transcripts can undergo additional cleavage and polyadenylation at a proximal internal site in the 3'-UTR, resulting in two stable, autonomous, RNA fragments: a coding sequence with a shorter 3'-UTR (body) and an uncapped 3'-UTR sequence downstream of the cleavage point (tail). Analyses of the human transcriptome has revealed thousands of such cleavage positions, suggesting a widespread post-transcriptional phenomenon producing thousands of stable 3'-UTR RNA tails that exist alongside their transcripts of origin. By analyzing the impact of microRNAs, we observed a significantly stronger effect for microRNA regulation at the body compared to the tail fragments. Our findings open a variety of future research prospects and call for a new perspective on 3'-UTR-dependent gene regulation.
MeSH term(s)	3' Untranslated Regions/genetics ; Animals ; Cell Line, Tumor ; Gene Expression Profiling ; Gene Expression Regulation ; HEK293 Cells ; Humans ; Mice, Inbred C57BL ; MicroRNAs/genetics ; Open Reading Frames/genetics ; Polyadenylation ; RNA Caps ; RNA Isoforms/genetics ; RNA Processing, Post-Transcriptional ; RNA, Messenger/genetics
Chemical Substances	3' Untranslated Regions ; MicroRNAs ; RNA Caps ; RNA Isoforms ; RNA, Messenger
Language	English
Publishing date	2017-12-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2041-1723
ISSN (online)	2041-1723
DOI	10.1038/s41467-017-02099-7
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Article ; Online: Slfn2 mutation-induced loss of T-cell quiescence leads to elevated de novo sterol synthesis.

Omar, Ibrahim / Rom, Oren / Aviram, Michael / Cohen-Daniel, Leonor / Gebre, Abraham K / Parks, John S / Berger, Michael

Immunology

2017 Volume 152, Issue 3, Page(s) 484–493

Abstract: Acquisition of a 'quiescence programme' by naive T cells is important to provide a stress-free environment and resistance to apoptosis while preserving their responsiveness to activating stimuli. Therefore, the survival and proper function of naive T ... ...

Abstract	Acquisition of a 'quiescence programme' by naive T cells is important to provide a stress-free environment and resistance to apoptosis while preserving their responsiveness to activating stimuli. Therefore, the survival and proper function of naive T cells depends on their ability to maintain quiescence. Recently we demonstrated that by preventing chronic unresolved endoplasmic reticulum (ER) stress, Schlafen2 (Slfn2) maintains a stress-free environment to conserve a pool of naive T cells ready to respond to a microbial invasion. These findings strongly suggest an intimate association between quiescence and stress signalling. However, the connection between ER stress conditions and loss of T-cell quiescence is unknown. Here we demonstrate that homeostasis of cholesterol and lipids, is disrupted in T cells and monocytes from Slfn2-mutant, elektra, mice with higher levels of lipid rafts and lipid droplets found in these cells. Moreover, elektra T cells had elevated levels of free cholesterol and cholesteryl ester due to increased de novo synthesis and higher levels of the enzyme HMG-CoA reductase. As cholesterol plays an important role in the transition of T cells from resting to active state, and ER regulates cholesterol and lipid synthesis, we suggest that regulation of cholesterol levels through the prevention of ER stress is an essential component of the mechanism by which Slfn2 regulates quiescence.
MeSH term(s)	Animals ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Proliferation ; Cellular Senescence ; Cholesterol/biosynthesis ; Cholesterol Esters/biosynthesis ; Endoplasmic Reticulum Stress ; Genotype ; Hydroxymethylglutaryl CoA Reductases/metabolism ; Lipid Droplets/metabolism ; Lymphocyte Activation ; Membrane Microdomains/metabolism ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Monocytes/immunology ; Monocytes/metabolism ; Mutation ; Phenotype ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Up-Regulation
Chemical Substances	Cell Cycle Proteins ; Cholesterol Esters ; schlafen-2 protein, mouse ; Cholesterol (97C5T2UQ7J) ; Hydroxymethylglutaryl CoA Reductases (EC 1.1.1.-)
Language	English
Publishing date	2017-08-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80124-0
ISSN	1365-2567 ; 0019-2805 ; 0953-4954
ISSN (online)	1365-2567
ISSN	0019-2805 ; 0953-4954
DOI	10.1111/imm.12785
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Article ; Online: Microenvironmental Cues Determine Tumor Cell Susceptibility to Neutrophil Cytotoxicity.

Gershkovitz, Maya / Fainsod-Levi, Tanya / Khawaled, Saleh / Shaul, Merav E / Sionov, Ronit V / Cohen-Daniel, Leonor / Aqeilan, Rami I / Shaul, Yoav D / Fridlender, Zvi G / Granot, Zvi

Cancer research

2018 Volume 78, Issue 17, Page(s) 5050–5059

Abstract: We have recently shown that neutrophil antitumor cytotoxicity is ... ...

Abstract	We have recently shown that neutrophil antitumor cytotoxicity is Ca
MeSH term(s)	Animals ; Cell Line, Tumor ; Cell Proliferation/genetics ; Disease Models, Animal ; Epithelial-Mesenchymal Transition/genetics ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Hydrogen Peroxide/metabolism ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Mice ; Neoplasm Metastasis ; Neutrophil Activation/genetics ; Neutrophil Activation/immunology ; Neutrophils/metabolism ; Neutrophils/pathology ; TRPM Cation Channels/genetics ; Tumor Microenvironment/genetics
Chemical Substances	TRPM Cation Channels ; TRPM2 protein, mouse ; Hydrogen Peroxide (BBX060AN9V)
Language	English
Publishing date	2018-07-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-18-0540
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Article ; Online: Germline DNA replication timing shapes mammalian genome composition.

Yehuda, Yishai / Blumenfeld, Britny / Mayorek, Nina / Makedonski, Kirill / Vardi, Oriya / Cohen-Daniel, Leonor / Mansour, Yousef / Baror-Sebban, Shulamit / Masika, Hagit / Farago, Marganit / Berger, Michael / Carmi, Shai / Buganim, Yosef / Koren, Amnon / Simon, Itamar

Nucleic acids research

2018 Volume 46, Issue 16, Page(s) 8299–8310

Abstract: Mammalian DNA replication is a highly organized and regulated process. Large, Mb-sized regions are replicated at defined times along S-phase. Replication Timing (RT) is thought to play a role in shaping the mammalian genome by affecting mutation rates. ... ...

Abstract	Mammalian DNA replication is a highly organized and regulated process. Large, Mb-sized regions are replicated at defined times along S-phase. Replication Timing (RT) is thought to play a role in shaping the mammalian genome by affecting mutation rates. Previous analyses relied on somatic RT profiles. However, only germline mutations are passed on to offspring and affect genomic composition. Therefore, germ cell RT information is necessary to evaluate the influences of RT on the mammalian genome. We adapted the RT mapping technique for limited amounts of cells, and measured RT from two stages in the mouse germline - primordial germ cells (PGCs) and spermatogonial stem cells (SSCs). RT in germline cells exhibited stronger correlations to both mutation rate and recombination hotspots density than those of RT in somatic tissues, emphasizing the importance of using correct tissues-of-origin for RT profiling. Germline RT maps exhibited stronger correlations to additional genetic features including GC-content, transposable elements (SINEs and LINEs), and gene density. GC content stratification and multiple regression analysis revealed independent contributions of RT to SINE, gene, mutation, and recombination hotspot densities. Together, our results establish a central role for RT in shaping multiple levels of mammalian genome composition.
MeSH term(s)	Animals ; Base Composition/genetics ; Cell Line, Tumor ; Cells, Cultured ; DNA Replication/genetics ; DNA Replication Timing/genetics ; DNA Transposable Elements/genetics ; Female ; Genome/genetics ; Germ Cells/cytology ; Germ Cells/metabolism ; Germ-Line Mutation ; Male ; Mammals/genetics ; Mice, 129 Strain ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; Short Interspersed Nucleotide Elements/genetics ; Stem Cells/cytology ; Stem Cells/metabolism
Chemical Substances	DNA Transposable Elements
Language	English
Publishing date	2018-08-09
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/gky610
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Article ; Online: RETRACTED: Generalized verrucosis and abnormal T cell activation due to homozygous TAOK2 mutation.

Molho-Pessach, Vered / Ramot, Yuval / Mogilevsky, Maxim / Cohen-Daniel, Leonor / Eisenstein, Eli M / Abu-Libdeh, Abdulsalam / Siam, Ihab / Berger, Michael / Karni, Rotem / Zlotogorski, Abraham

publication RETRACTED

Journal of dermatological science

2017 Volume 87, Issue 2, Page(s) 123–129

MeSH term(s)	Biopsy ; Cell Proliferation/genetics ; Child ; Child, Preschool ; Chronic Disease ; Consanguinity ; Female ; Genetic Testing ; Homozygote ; Humans ; Immunologic Deficiency Syndromes/genetics ; Immunologic Deficiency Syndromes/immunology ; Leukocytes, Mononuclear/immunology ; Leukocytes, Mononuclear/metabolism ; Lymphocyte Activation/genetics ; Lymphocyte Activation/immunology ; MAP Kinase Signaling System/immunology ; Mutation ; Papillomavirus Infections/genetics ; Papillomavirus Infections/immunology ; Pedigree ; Phenotype ; Primary Immunodeficiency Diseases ; Protein Serine-Threonine Kinases/genetics ; Recurrence ; Skin/immunology ; Skin/pathology ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Warts/genetics ; Warts/immunology ; Exome Sequencing
Chemical Substances	Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2017-03-27
Publishing country	Netherlands
Document type	Journal Article ; Retracted Publication
ZDB-ID	1024446-3
ISSN	1873-569X ; 0923-1811
ISSN (online)	1873-569X
ISSN	0923-1811
DOI	10.1016/j.jdermsci.2017.03.018
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Article ; Online: TRPM2 Mediates Neutrophil Killing of Disseminated Tumor Cells.

Gershkovitz, Maya / Caspi, Yaki / Fainsod-Levi, Tanya / Katz, Ben / Michaeli, Janna / Khawaled, Saleh / Lev, Shaya / Polyansky, Lola / Shaul, Merav E / Sionov, Ronit V / Cohen-Daniel, Leonor / Aqeilan, Rami I / Shaul, Yoav D / Mori, Yasuo / Karni, Rotem / Fridlender, Zvi G / Binshtok, Alexander M / Granot, Zvi

Cancer research

2018 Volume 78, Issue 10, Page(s) 2680–2690

Abstract: Neutrophils play a critical role in cancer, with both protumor and antitumor neutrophil subpopulations reported. The antitumor neutrophil subpopulation has the capacity to kill tumor cells and limit metastatic spread, yet not all tumor cells are equally ... ...

Abstract	Neutrophils play a critical role in cancer, with both protumor and antitumor neutrophil subpopulations reported. The antitumor neutrophil subpopulation has the capacity to kill tumor cells and limit metastatic spread, yet not all tumor cells are equally susceptible to neutrophil cytotoxicity. Because cells that evade neutrophils have greater chances of forming metastases, we explored the mechanism neutrophils use to kill tumor cells. Neutrophil cytotoxicity was previously shown to be mediated by secretion of H
MeSH term(s)	Animals ; Breast Neoplasms/pathology ; CRISPR-Cas Systems/genetics ; Calcium/metabolism ; Calcium Channels/metabolism ; Cell Line, Tumor ; Cell Proliferation/genetics ; Female ; Humans ; Hydrogen Peroxide/metabolism ; Mice ; Mice, Inbred BALB C ; Neoplastic Cells, Circulating/immunology ; Neoplastic Cells, Circulating/pathology ; Neutrophils/immunology ; Neutrophils/metabolism ; TRPM Cation Channels/genetics ; TRPM Cation Channels/metabolism
Chemical Substances	Calcium Channels ; TRPM Cation Channels ; TRPM2 protein, mouse ; Hydrogen Peroxide (BBX060AN9V) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2018-02-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-17-3614
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