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  1. Article ; Online: Raxibacumab.

    Mazumdar, Sohini

    mAbs

    2009  Volume 1, Issue 6, Page(s) 531–538

    Abstract: Raxibacumab (ABthrax) is a human IgG1 monoclonal antibody against Bacillus anthracis protective antigen. HGS is currently providing stockpiles of the agent to the US government for use in the prevention and treatment of inhalation anthrax. As of May 2009, ...

    Abstract Raxibacumab (ABthrax) is a human IgG1 monoclonal antibody against Bacillus anthracis protective antigen. HGS is currently providing stockpiles of the agent to the US government for use in the prevention and treatment of inhalation anthrax. As of May 2009, the candidate was undergoing review by the US Food and Drug Administration. The availability of bioterrorism countermeasures has become more important since the September 2001 anthrax attacks, and development of raxibacumab is a significant advance in this area.
    MeSH term(s) Animals ; Anthrax/immunology ; Anthrax/therapy ; Antibodies, Monoclonal/therapeutic use ; Antibodies, Monoclonal, Humanized ; Antigens, Bacterial/immunology ; Bacillus anthracis/immunology ; Bacillus anthracis/pathogenicity ; Bacterial Toxins/antagonists & inhibitors ; Bioterrorism/prevention & control ; Device Approval ; Humans ; United States
    Chemical Substances Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Antigens, Bacterial ; Bacterial Toxins ; raxibacumab (794PGL549S)
    Language English
    Publishing date 2009-11-29
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2537838-7
    ISSN 1942-0870 ; 1942-0870
    ISSN (online) 1942-0870
    ISSN 1942-0870
    DOI 10.4161/mabs.1.6.10195
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Golimumab.

    Mazumdar, Sohini / Greenwald, David

    mAbs

    2009  Volume 1, Issue 5, Page(s) 422–431

    Abstract: Golimumab, a human anti-TNFalpha IgG1kappa monoclonal antibody, was approved in the US and Canada in April 2009 as a treatment for rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis, and is undergoing regulatory review in the EU for ... ...

    Abstract Golimumab, a human anti-TNFalpha IgG1kappa monoclonal antibody, was approved in the US and Canada in April 2009 as a treatment for rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis, and is undergoing regulatory review in the EU for these indications. The product was developed by Centocor and Janssen Pharmaceutical KK (Johnson & Johnson subsidiaries), in collaboration with Schering-Plough and Mitsubishi Tanabe Pharma. Golimumab faces numerous protein therapeutic competitors on the market, but, as the first patient-administered, once-monthly dosed anti-TNFalpha drug, it will likely be an attractive option for patients.
    MeSH term(s) Animals ; Antibodies, Monoclonal/administration & dosage ; Antibodies, Monoclonal/adverse effects ; Antibodies, Monoclonal/immunology ; Antibodies, Monoclonal/therapeutic use ; Arthritis, Psoriatic/drug therapy ; Arthritis, Psoriatic/immunology ; Arthritis, Rheumatoid/drug therapy ; Arthritis, Rheumatoid/immunology ; Clinical Trials as Topic ; Dose-Response Relationship, Drug ; Drug Therapy, Combination ; Female ; Humans ; Infant, Newborn ; Male ; Methotrexate/administration & dosage ; Methotrexate/therapeutic use ; Pregnancy ; Spondylitis, Ankylosing/drug therapy ; Spondylitis, Ankylosing/immunology ; Treatment Outcome ; Tumor Necrosis Factor-alpha/immunology
    Chemical Substances Antibodies, Monoclonal ; Tumor Necrosis Factor-alpha ; golimumab (91X1KLU43E) ; Methotrexate (YL5FZ2Y5U1)
    Language English
    Publishing date 2009-09-15
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2537838-7
    ISSN 1942-0870 ; 1942-0870
    ISSN (online) 1942-0870
    ISSN 1942-0870
    DOI 10.4161/mabs.1.5.9286
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: CoREST1 promotes tumor formation and tumor stroma interactions in a mouse model of breast cancer.

    Mazumdar, Sohini / Arendt, Lisa M / Phillips, Sarah / Sedic, Maja / Kuperwasser, Charlotte / Gill, Grace

    PloS one

    2015  Volume 10, Issue 3, Page(s) e0121281

    Abstract: Regulators of chromatin structure and gene expression contribute to tumor formation and progression. The co-repressor CoREST1 regulates the localization and activity of associated histone modifying enzymes including lysine specific demethylase 1 (LSD1) ... ...

    Abstract Regulators of chromatin structure and gene expression contribute to tumor formation and progression. The co-repressor CoREST1 regulates the localization and activity of associated histone modifying enzymes including lysine specific demethylase 1 (LSD1) and histone deacetylase 1 (HDAC1). Although several CoREST1 associated proteins have been reported to enhance breast cancer progression, the role of CoREST1 in breast cancer is currently unclear. Here we report that knockdown of CoREST1 in the basal-type breast cancer cell line, MDA-MB-231, led to significantly reduced incidence and diminished size of tumors compared to controls in mouse xenograft studies. Notably, CoREST1-depleted cells gave rise to tumors with a marked decrease in angiogenesis. CoREST1 knockdown led to a decrease in secreted angiogenic and inflammatory factors, and mRNA analysis suggests that CoREST1 promotes expression of genes related to angiogenesis and inflammation including VEGF-A and CCL2. CoREST1 knockdown decreased the ability of MDA-MB-231 conditioned media to promote endothelial cell tube formation and migration. Further, tumors derived from CoREST1-depleted cells had reduced macrophage infiltration and the secretome of CoREST1 knockdown cells was deficient in promoting macrophage migration and macrophage-mediated angiogenesis. Taken together, these findings reveal that the epigenetic regulator CoREST1 promotes tumorigenesis in a breast cancer model at least in part through regulation of gene expression patterns in tumor cells that have profound non-cell autonomous effects on endothelial and inflammatory cells in the tumor microenvironment.
    MeSH term(s) Animals ; Carcinogenesis/metabolism ; Carcinogenesis/pathology ; Cell Communication ; Cell Line, Tumor ; Cell Movement ; Disease Models, Animal ; Female ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Human Umbilical Vein Endothelial Cells/metabolism ; Humans ; Macrophage Activation ; Macrophages/metabolism ; Mammary Neoplasms, Animal/blood supply ; Mammary Neoplasms, Animal/genetics ; Mammary Neoplasms, Animal/metabolism ; Mammary Neoplasms, Animal/pathology ; Mice ; Neovascularization, Pathologic/metabolism ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Stromal Cells/metabolism ; Stromal Cells/pathology ; Xenograft Model Antitumor Assays
    Chemical Substances Nerve Tissue Proteins ; Rcor2 protein, mouse ; Repressor Proteins
    Language English
    Publishing date 2015
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0121281
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: CoREST1 promotes tumor formation and tumor stroma interactions in a mouse model of breast cancer.

    Sohini Mazumdar / Lisa M Arendt / Sarah Phillips / Maja Sedic / Charlotte Kuperwasser / Grace Gill

    PLoS ONE, Vol 10, Iss 3, p e

    2015  Volume 0121281

    Abstract: Regulators of chromatin structure and gene expression contribute to tumor formation and progression. The co-repressor CoREST1 regulates the localization and activity of associated histone modifying enzymes including lysine specific demethylase 1 (LSD1) ... ...

    Abstract Regulators of chromatin structure and gene expression contribute to tumor formation and progression. The co-repressor CoREST1 regulates the localization and activity of associated histone modifying enzymes including lysine specific demethylase 1 (LSD1) and histone deacetylase 1 (HDAC1). Although several CoREST1 associated proteins have been reported to enhance breast cancer progression, the role of CoREST1 in breast cancer is currently unclear. Here we report that knockdown of CoREST1 in the basal-type breast cancer cell line, MDA-MB-231, led to significantly reduced incidence and diminished size of tumors compared to controls in mouse xenograft studies. Notably, CoREST1-depleted cells gave rise to tumors with a marked decrease in angiogenesis. CoREST1 knockdown led to a decrease in secreted angiogenic and inflammatory factors, and mRNA analysis suggests that CoREST1 promotes expression of genes related to angiogenesis and inflammation including VEGF-A and CCL2. CoREST1 knockdown decreased the ability of MDA-MB-231 conditioned media to promote endothelial cell tube formation and migration. Further, tumors derived from CoREST1-depleted cells had reduced macrophage infiltration and the secretome of CoREST1 knockdown cells was deficient in promoting macrophage migration and macrophage-mediated angiogenesis. Taken together, these findings reveal that the epigenetic regulator CoREST1 promotes tumorigenesis in a breast cancer model at least in part through regulation of gene expression patterns in tumor cells that have profound non-cell autonomous effects on endothelial and inflammatory cells in the tumor microenvironment.
    Keywords Medicine ; R ; Science ; Q
    Subject code 616
    Language English
    Publishing date 2015-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article: Cell-state transitions regulated by SLUG are critical for tissue regeneration and tumor initiation.

    Phillips, Sarah / Prat, Aleix / Sedic, Maja / Proia, Theresa / Wronski, Ania / Mazumdar, Sohini / Skibinski, Adam / Shirley, Stephanie H / Perou, Charles M / Gill, Grace / Gupta, Piyush B / Kuperwasser, Charlotte

    Stem cell reports

    2014  Volume 2, Issue 5, Page(s) 633–647

    Abstract: Perturbations in stem cell activity and differentiation can lead to developmental defects and cancer. We use an approach involving a quantitative model of cell-state transitions in vitro to gain insights into how SLUG/SNAI2, a key developmental ... ...

    Abstract Perturbations in stem cell activity and differentiation can lead to developmental defects and cancer. We use an approach involving a quantitative model of cell-state transitions in vitro to gain insights into how SLUG/SNAI2, a key developmental transcription factor, modulates mammary epithelial stem cell activity and differentiation in vivo. In the absence of SLUG, stem cells fail to transition into basal progenitor cells, while existing basal progenitor cells undergo luminal differentiation; together, these changes result in abnormal mammary architecture and defects in tissue function. Furthermore, we show that in the absence of SLUG, mammary stem cell activity necessary for tissue regeneration and cancer initiation is lost. Mechanistically, SLUG regulates differentiation and cellular plasticity by recruiting the chromatin modifier lysine-specific demethylase 1 (LSD1) to promoters of lineage-specific genes to repress transcription. Together, these results demonstrate that SLUG plays a dual role in repressing luminal epithelial differentiation while unlocking stem cell transitions necessary for tumorigenesis.
    MeSH term(s) Animals ; Cell Differentiation ; Cell Line ; Cell Lineage ; Cell Transformation, Neoplastic ; Disease-Free Survival ; Gene Expression Regulation ; Histones/metabolism ; Humans ; Mammary Glands, Human/cytology ; Mice ; Mice, Inbred NOD ; Mice, Knockout ; Mice, SCID ; Neoplasms/metabolism ; Neoplasms/mortality ; Neoplasms/pathology ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; RNA, Messenger/metabolism ; Regeneration ; Snail Family Transcription Factors ; Stem Cell Transplantation ; Stem Cells/cytology ; Stem Cells/metabolism ; Transcription Factors/antagonists & inhibitors ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transplantation, Heterologous
    Chemical Substances Histones ; Proto-Oncogene Proteins c-myc ; RNA, Messenger ; SNAI1 protein, human ; SNAI2 protein, human ; Snai2 protein, mouse ; Snail Family Transcription Factors ; Transcription Factors
    Language English
    Publishing date 2014-04-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2720528-9
    ISSN 2213-6711
    ISSN 2213-6711
    DOI 10.1016/j.stemcr.2014.03.008
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Cell-State Transitions Regulated by SLUG Are Critical for Tissue Regeneration and Tumor Initiation

    Sarah Phillips / Aleix Prat / Maja Sedic / Theresa Proia / Ania Wronski / Sohini Mazumdar / Adam Skibinski / Stephanie H. Shirley / Charles M. Perou / Grace Gill / Piyush B. Gupta / Charlotte Kuperwasser

    Stem Cell Reports, Vol 2, Iss 5, Pp 633-

    2014  Volume 647

    Abstract: Perturbations in stem cell activity and differentiation can lead to developmental defects and cancer. We use an approach involving a quantitative model of cell-state transitions in vitro to gain insights into how SLUG/SNAI2, a key developmental ... ...

    Abstract Perturbations in stem cell activity and differentiation can lead to developmental defects and cancer. We use an approach involving a quantitative model of cell-state transitions in vitro to gain insights into how SLUG/SNAI2, a key developmental transcription factor, modulates mammary epithelial stem cell activity and differentiation in vivo. In the absence of SLUG, stem cells fail to transition into basal progenitor cells, while existing basal progenitor cells undergo luminal differentiation; together, these changes result in abnormal mammary architecture and defects in tissue function. Furthermore, we show that in the absence of SLUG, mammary stem cell activity necessary for tissue regeneration and cancer initiation is lost. Mechanistically, SLUG regulates differentiation and cellular plasticity by recruiting the chromatin modifier lysine-specific demethylase 1 (LSD1) to promoters of lineage-specific genes to repress transcription. Together, these results demonstrate that SLUG plays a dual role in repressing luminal epithelial differentiation while unlocking stem cell transitions necessary for tumorigenesis.
    Keywords Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
    Subject code 571
    Language English
    Publishing date 2014-05-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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