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  1. Article ; Online: DDS Profile: Juanita L. Merchant, MD, PhD.

    Merchant, Juanita L

    Digestive diseases and sciences

    2022  Volume 68, Issue 1, Page(s) 16–20

    MeSH term(s) Humans ; Education, Medical, Graduate ; Biomedical Research
    Language English
    Publishing date 2022-10-27
    Publishing country United States
    Document type Editorial
    ZDB-ID 304250-9
    ISSN 1573-2568 ; 0163-2116
    ISSN (online) 1573-2568
    ISSN 0163-2116
    DOI 10.1007/s10620-022-07725-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: DDS Perspective: The Joy of Discovery and the Art of Mentoring.

    Merchant, Juanita L

    Digestive diseases and sciences

    2022  Volume 68, Issue 1, Page(s) 21–23

    MeSH term(s) Humans ; Mentoring ; Mentors
    Language English
    Publishing date 2022-10-27
    Publishing country United States
    Document type Journal Article
    ZDB-ID 304250-9
    ISSN 1573-2568 ; 0163-2116
    ISSN (online) 1573-2568
    ISSN 0163-2116
    DOI 10.1007/s10620-022-07726-y
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  3. Article ; Online: Moving Up a NOTCH: Defining the Stem Cell Niche in the Gastric Antrum.

    Merchant, Juanita L

    Cellular and molecular gastroenterology and hepatology

    2021  Volume 13, Issue 1, Page(s) 339–340

    MeSH term(s) Pyloric Antrum ; Receptors, Notch ; Stem Cell Niche ; Stem Cells
    Chemical Substances Receptors, Notch
    Language English
    Publishing date 2021-10-30
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 2819778-1
    ISSN 2352-345X ; 2352-345X
    ISSN (online) 2352-345X
    ISSN 2352-345X
    DOI 10.1016/j.jcmgh.2021.10.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Book ; Online ; E-Book: Physiology of the gastrointestinal tract

    Said, Hamid M. / Ghishan, Fayez K. / Kaunitz, Jonathan D. / Merchant, Juanita L. / Wood, Jackie D.

    2018  

    Author's details editor-in-chief Hamid M. Said ; associate editors Fayez K. Ghishan, Jonathan D. Kaunitz, Juanita L. Merchant, Jackie D. Wood
    Keywords Humans ; Gastrointestinal Tract / physiology ; Gastrointestinal Tract / physiology / Electronic Books ; Gastrointestinal system ; MEDICAL / Physiology ; SCIENCE / Life Sciences / Human Anatomy & Physiology ; Gastrointestinal system / Physiology ; Gastrointestinaltrakt ; Physiologie ; Verdauungskanal
    Subject Humanphysiologie ; Mensch ; Körperfunktion ; Canalis alimentorius ; Verdauungstrakt ; Verdauungsorgan ; Verdauungsapparat ; Apparatus digestorius ; Verdauungssystem ; Magen-Darm-Kanal ; Magen-Darm-Trakt ; Magen-Darmtrakt
    Subject code 612.32
    Language English
    Size 1 Online-Ressource (xxxvii, 1687, I24), Illustrationen, Diagramme
    Edition Sixth edition
    Publisher Elsevier Academic Press
    Publishing place London
    Publishing country Great Britain
    Document type Book ; Online ; E-Book
    Note Enthält Vol. 1 und Vol. 2
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    HBZ-ID HT030057824
    ISBN 978-0-12-812426-0 ; 9780128099544 ; 0-12-812426-1 ; 0128099542
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  5. Article: Parietal Cell Death by Cytokines.

    Merchant, Juanita L

    Cellular and molecular gastroenterology and hepatology

    2018  Volume 5, Issue 4, Page(s) 636–637

    Language English
    Publishing date 2018-02-15
    Publishing country United States
    Document type Editorial
    ZDB-ID 2819778-1
    ISSN 2352-345X
    ISSN 2352-345X
    DOI 10.1016/j.jcmgh.2018.01.019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: The immune microenvironment in gastric adenocarcinoma.

    Zavros, Yana / Merchant, Juanita L

    Nature reviews. Gastroenterology & hepatology

    2022  Volume 19, Issue 7, Page(s) 451–467

    Abstract: Like most solid tumours, the microenvironment of epithelial-derived gastric adenocarcinoma (GAC) consists of a variety of stromal cell types, including fibroblasts, and neuronal, endothelial and immune cells. In this article, we review the role of the ... ...

    Abstract Like most solid tumours, the microenvironment of epithelial-derived gastric adenocarcinoma (GAC) consists of a variety of stromal cell types, including fibroblasts, and neuronal, endothelial and immune cells. In this article, we review the role of the immune microenvironment in the progression of chronic inflammation to GAC, primarily the immune microenvironment driven by the gram-negative bacterial species Helicobacter pylori. The infection-driven nature of most GACs has renewed awareness of the immune microenvironment and its effect on tumour development and progression. About 75-90% of GACs are associated with prior H. pylori infection and 5-10% with Epstein-Barr virus infection. Although 50% of the world's population is infected with H. pylori, only 1-3% will progress to GAC, with progression the result of a combination of the H. pylori strain, host susceptibility and composition of the chronic inflammatory response. Other environmental risk factors include exposure to a high-salt diet and nitrates. Genetically, chromosome instability occurs in ~50% of GACs and 21% of GACs are microsatellite instability-high tumours. Here, we review the timeline and pathogenesis of the events triggered by H. pylori that can create an immunosuppressive microenvironment by modulating the host's innate and adaptive immune responses, and subsequently favour GAC development.
    MeSH term(s) Adenocarcinoma/complications ; Epstein-Barr Virus Infections/complications ; Epstein-Barr Virus Infections/metabolism ; Gastric Mucosa/metabolism ; Helicobacter Infections/complications ; Helicobacter Infections/microbiology ; Helicobacter pylori ; Herpesvirus 4, Human ; Humans ; Inflammation/complications ; Stomach Neoplasms/etiology ; Stomach Neoplasms/metabolism ; Tumor Microenvironment
    Language English
    Publishing date 2022-03-14
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 2493722-8
    ISSN 1759-5053 ; 1759-5045
    ISSN (online) 1759-5053
    ISSN 1759-5045
    DOI 10.1038/s41575-022-00591-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: MENIN-mediated regulation of gastrin gene expression and its role in gastrinoma development.

    Elvis-Offiah, Uloma B / Duan, Suzann / Merchant, Juanita L

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2023  Volume 37, Issue 5, Page(s) e22913

    Abstract: The Multiple Endocrine Neoplasia I (MEN1) locus encodes the protein MENIN, which functions as a tumor suppressor protein in neuroendocrine tissues. Gastrinomas are neuroendocrine neoplasms that overproduce the hormone gastrin and can arise sporadically ... ...

    Abstract The Multiple Endocrine Neoplasia I (MEN1) locus encodes the protein MENIN, which functions as a tumor suppressor protein in neuroendocrine tissues. Gastrinomas are neuroendocrine neoplasms that overproduce the hormone gastrin and can arise sporadically or as part of the MEN1 syndrome, in which mutations in the MEN1 gene lead to loss or inactivation of MENIN protein. Gastrin is a peptide hormone that is primarily synthesized in the gastric antrum and stimulates the secretion of histamine from enterochromaffin-like (ECL) cells and subsequently acid from parietal cells in the gastric corpus. In addition, gastrin exerts a mitogenic function primarily on ECL cells and progenitor cells in the gastric isthmus. Current studies seek to understand how MEN1 mutations generate a mutant MENIN protein that abrogates its tumor suppressor function. Mutations in the MEN1 gene are broadly distributed throughout its nine protein-coding exons, making it difficult to correlate protein structure with its function. Although disruption of the Men1 locus in mice causes functional neuroendocrine tumors in the pituitary and pancreas, gastrinomas do not develop in these transgenic animal models. Prior studies of human gastrinomas suggest that tissue-specific microenvironmental cues in the submucosal foregut may contribute to tumorigenesis by reprogramming of epithelial cells toward the neuroendocrine phenotype. Accordingly, recent studies suggest that neural crest-derived cells are also sensitive to reprogramming when MEN1 is deleted or mutated. Thus, the goal of this report is to review our current understanding of how MENIN modulates gastrin gene expression while highlighting its role in the prevention/suppression of neuroendocrine cell transformation.
    MeSH term(s) Humans ; Animals ; Mice ; Gastrinoma/genetics ; Gastrinoma/pathology ; Gastrins/genetics ; Gastrins/metabolism ; Multiple Endocrine Neoplasia Type 1/genetics ; Multiple Endocrine Neoplasia Type 1/metabolism ; Transcription Factors/genetics ; Pancreatic Neoplasms/pathology ; Gene Expression ; Proto-Oncogene Proteins/genetics
    Chemical Substances Gastrins ; Transcription Factors ; Men1 protein, mouse ; Proto-Oncogene Proteins
    Language English
    Publishing date 2023-04-19
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.202201809RR
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MO 296: Show issues

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  8. Article ; Online: Myeloid-Derived Suppressor Cells: Therapeutic Target for Gastrointestinal Cancers.

    Arshad, Junaid / Rao, Amith / Repp, Matthew L / Rao, Rohit / Wu, Clinton / Merchant, Juanita L

    International journal of molecular sciences

    2024  Volume 25, Issue 5

    Abstract: Gastrointestinal cancers represent one of the more challenging cancers to treat. Current strategies to cure and control gastrointestinal (GI) cancers like surgery, radiation, chemotherapy, and immunotherapy have met with limited success, and research has ...

    Abstract Gastrointestinal cancers represent one of the more challenging cancers to treat. Current strategies to cure and control gastrointestinal (GI) cancers like surgery, radiation, chemotherapy, and immunotherapy have met with limited success, and research has turned towards further characterizing the tumor microenvironment to develop novel therapeutics. Myeloid-derived suppressor cells (MDSCs) have emerged as crucial drivers of pathogenesis and progression within the tumor microenvironment in GI malignancies. Many MDSCs clinical targets have been defined in preclinical models, that potentially play an integral role in blocking recruitment and expansion, promoting MDSC differentiation into mature myeloid cells, depleting existing MDSCs, altering MDSC metabolic pathways, and directly inhibiting MDSC function. This review article analyzes the role of MDSCs in GI cancers as viable therapeutic targets for gastrointestinal malignancies and reviews the existing clinical trial landscape of recently completed and ongoing clinical studies testing novel therapeutics in GI cancers.
    MeSH term(s) Humans ; Myeloid-Derived Suppressor Cells/metabolism ; Gastrointestinal Neoplasms/metabolism ; Myeloid Cells ; Immunotherapy ; Tumor Microenvironment
    Language English
    Publishing date 2024-03-04
    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/ijms25052985
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  9. Article ; Online: Schlafen4

    Ding, Lin / Sheriff, Sulaiman / Sontz, Ricky A / Merchant, Juanita L

    Frontiers in immunology

    2023  Volume 14, Page(s) 1139391

    Abstract: Introduction: MDSCs express SCHLAFEN 4 (SLFN4) in : Methods: Single-cell RNA sequencing was performed on immune cells sorted from PBMCs and stomachs prepared from uninfected and 6-month : Results: Slfn4: Conclusion: Taken together, SLFN4 ... ...

    Abstract Introduction: MDSCs express SCHLAFEN 4 (SLFN4) in
    Methods: Single-cell RNA sequencing was performed on immune cells sorted from PBMCs and stomachs prepared from uninfected and 6-month
    Results: Slfn4
    Conclusion: Taken together, SLFN4 regulates the activity of the GTPase pathway in MDSCs and precludes these cells from succumbing to the massive ROS generation when they acquire MDSC function.
    MeSH term(s) Mice ; Animals ; Helicobacter ; Myeloid-Derived Suppressor Cells/metabolism ; GTP Phosphohydrolases/metabolism ; Sildenafil Citrate ; Reactive Oxygen Species/metabolism ; Helicobacter felis ; Metaplasia ; Felis ; Guanosine Triphosphate/metabolism
    Chemical Substances GTP Phosphohydrolases (EC 3.6.1.-) ; Sildenafil Citrate (BW9B0ZE037) ; Reactive Oxygen Species ; Guanosine Triphosphate (86-01-1)
    Language English
    Publishing date 2023-06-02
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1139391
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: The bHLH transcription factor ASCL1 promotes differentiation of endocrine cells in the stomach and is regulated by Notch signaling.

    Hibdon, Elise S / Keeley, Theresa M / Merchant, Juanita L / Samuelson, Linda C

    American journal of physiology. Gastrointestinal and liver physiology

    2023  Volume 325, Issue 5, Page(s) G458–G470

    Abstract: Notch signaling regulates gastrointestinal stem cell proliferation and differentiation yet Notch-regulated transcriptional effectors of gastric epithelial cell differentiation are poorly understood. Here we tested the role of the bHLH transcription ... ...

    Abstract Notch signaling regulates gastrointestinal stem cell proliferation and differentiation yet Notch-regulated transcriptional effectors of gastric epithelial cell differentiation are poorly understood. Here we tested the role of the bHLH transcription factor Achaete-Scute homolog 1 (ASCL1) in gastric epithelial cell differentiation, and its regulation by Notch. Newborn
    MeSH term(s) Animals ; Mice ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Cell Differentiation/physiology ; Enteroendocrine Cells/metabolism ; Gastrins ; Mice, Knockout ; Stomach
    Chemical Substances Basic Helix-Loop-Helix Transcription Factors ; Gastrins ; Ascl1 protein, mouse
    Language English
    Publishing date 2023-09-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 603840-2
    ISSN 1522-1547 ; 0193-1857
    ISSN (online) 1522-1547
    ISSN 0193-1857
    DOI 10.1152/ajpgi.00043.2023
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