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  1. Article ; Online: Iron, Copper, and Selenium: Cancer's Thing for Redox Bling.

    Terzi, Erdem M / Possemato, Richard

    Cold Spring Harbor perspectives in medicine

    2024  Volume 14, Issue 4

    Abstract: Cells require micronutrients for numerous basic functions. Among these, iron, copper, and selenium are particularly critical for redox metabolism, and their importance is heightened during oncogene-driven perturbations in cancer. In this review, which ... ...

    Abstract Cells require micronutrients for numerous basic functions. Among these, iron, copper, and selenium are particularly critical for redox metabolism, and their importance is heightened during oncogene-driven perturbations in cancer. In this review, which particularly focuses on iron, we describe how these micronutrients are carefully chaperoned about the body and made available to tissues, a process that is designed to limit the toxicity of free iron and copper or by-products of selenium metabolism. We delineate perturbations in iron metabolism and iron-dependent proteins that are observed in cancer, and describe the current approaches being used to target iron metabolism and iron-dependent processes.
    MeSH term(s) Humans ; Iron/metabolism ; Selenium/metabolism ; Copper/metabolism ; Micronutrients ; Oxidation-Reduction ; Neoplasms/drug therapy
    Chemical Substances Iron (E1UOL152H7) ; Selenium (H6241UJ22B) ; Copper (789U1901C5) ; Micronutrients
    Language English
    Publishing date 2024-04-01
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2157-1422
    ISSN (online) 2157-1422
    DOI 10.1101/cshperspect.a041545
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  2. Article ; Online: Minding the Ls and Qs.

    Possemato, Richard

    Nature metabolism

    2019  Volume 1, Issue 3, Page(s) 308–309

    Language English
    Publishing date 2019-03-04
    Publishing country Germany
    Document type Journal Article
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-019-0046-7
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  3. Article ; Online: Retraction: Cancer-Associated PP2A Aα Subunits Induce Functional Haploinsufficiency and Tumorigenicity.

    Chen, Wen / Arroyo, Jason D / Timmons, Jamie C / Possemato, Richard / Hahn, William C

    Cancer research

    2024  Volume 84, Issue 6, Page(s) 935

    Language English
    Publishing date 2024-03-14
    Publishing country United States
    Document type Retraction of Publication
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-24-0434
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  4. Article ; Online: Leveraging the iron-starvation response to promote ferroptosis.

    Alvarez, Samantha W / Possemato, Richard

    Oncotarget

    2018  Volume 9, Issue 13, Page(s) 10830–10831

    Language English
    Publishing date 2018-02-03
    Publishing country United States
    Document type Editorial
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.24395
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  5. Article ; Online: Allosteric regulation of CAD modulates de novo pyrimidine synthesis during the cell cycle.

    Shin, Jong / Mir, Hannan / Khurram, Maaz A / Fujihara, Kenji M / Dynlacht, Brian D / Cardozo, Timothy J / Possemato, Richard

    Nature metabolism

    2023  Volume 5, Issue 2, Page(s) 277–293

    Abstract: Metabolism is a fundamental cellular process that is coordinated with cell cycle progression. Despite this association, a mechanistic understanding of cell cycle phase-dependent metabolic pathway regulation remains elusive. Here we report the mechanism ... ...

    Abstract Metabolism is a fundamental cellular process that is coordinated with cell cycle progression. Despite this association, a mechanistic understanding of cell cycle phase-dependent metabolic pathway regulation remains elusive. Here we report the mechanism by which human de novo pyrimidine biosynthesis is allosterically regulated during the cell cycle. Combining traditional synchronization methods and metabolomics, we characterize metabolites by their accumulation pattern during cell cycle phases and identify cell cycle phase-dependent regulation of carbamoyl-phosphate synthetase 2, aspartate transcarbamylase and dihydroorotase (CAD), the first, rate-limiting enzyme in de novo pyrimidine biosynthesis. Through systematic mutational scanning and structural modelling, we find allostery as a major regulatory mechanism that controls the activity change of CAD during the cell cycle. Specifically, we report evidence of two Animalia-specific loops in the CAD allosteric domain that involve sensing and binding of uridine 5'-triphosphate, a CAD allosteric inhibitor. Based on homology with a mitochondrial carbamoyl-phosphate synthetase homologue, we identify a critical role for a signal transmission loop in regulating the formation of a substrate channel, thereby controlling CAD activity.
    MeSH term(s) Humans ; Allosteric Regulation ; Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing)/chemistry ; Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing)/metabolism ; Cell Cycle ; Pyrimidines/pharmacology ; Phosphates
    Chemical Substances Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing) (EC 6.3.5.5) ; Pyrimidines ; Phosphates
    Language English
    Publishing date 2023-02-06
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-023-00735-9
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  6. Article ; Online: Mitigation of Osteoclast-Mediated Arthritic Bone Remodeling By Short Chain Fatty Acids.

    Yang, Katharine Lu / Mullins, Briana J / Lejeune, Alannah / Ivanova, Ellie / Shin, Jong / Bajwa, Sofia / Possemato, Richard / Cadwell, Ken / Scher, Jose U / Koralov, Sergei B

    Arthritis & rheumatology (Hoboken, N.J.)

    2024  Volume 76, Issue 4, Page(s) 647–659

    Abstract: Objective: The objective for this study was to evaluate the effects of short chain fatty acids (SCFAs) on arthritic bone remodeling.: Methods: We treated a recently described preclinical murine model of psoriatic arthritis (PsA), R26STAT3C: Results! ...

    Abstract Objective: The objective for this study was to evaluate the effects of short chain fatty acids (SCFAs) on arthritic bone remodeling.
    Methods: We treated a recently described preclinical murine model of psoriatic arthritis (PsA), R26STAT3C
    Results: The osteoporosis condition in R26STAT3C
    Conclusion: We demonstrated how gut microbiota-derived SCFAs can regulate distal pathology (ie, osteoporosis) and identified a potential therapeutic option for restoring bone density in rheumatic disease, further highlighting the critical role of the gut-bone axis in these disorders.
    MeSH term(s) Mice ; Animals ; Osteoclasts/metabolism ; Arthritis, Psoriatic/metabolism ; Bone Remodeling ; Cell Differentiation ; Osteoporosis/metabolism ; Fatty Acids, Volatile/metabolism ; Fatty Acids, Volatile/pharmacology
    Chemical Substances Fatty Acids, Volatile
    Language English
    Publishing date 2024-02-18
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.42765
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 24: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  7. Article ; Online: Iron-sulfur cluster deficiency can be sensed by IRP2 and regulates iron homeostasis and sensitivity to ferroptosis independent of IRP1 and FBXL5.

    Terzi, Erdem M / Sviderskiy, Vladislav O / Alvarez, Samantha W / Whiten, Gabrielle C / Possemato, Richard

    Science advances

    2021  Volume 7, Issue 22

    Abstract: Intracellular iron levels are strictly regulated to support homeostasis and avoid iron-mediated ROS production. Loss of iron-sulfur cluster (ISC) synthesis can increase iron loading and promote cell death by ferroptosis. Iron-responsive element-binding ... ...

    Abstract Intracellular iron levels are strictly regulated to support homeostasis and avoid iron-mediated ROS production. Loss of iron-sulfur cluster (ISC) synthesis can increase iron loading and promote cell death by ferroptosis. Iron-responsive element-binding proteins IRP1 and IRP2 posttranscriptionally regulate iron homeostasis. IRP1 binding to target mRNAs is competitively regulated by ISC occupancy. However, IRP2 is principally thought to be regulated at the protein level via E3 ubiquitin ligase FBXL5-mediated degradation. Here, we show that ISC synthesis suppression can activate IRP2 and promote ferroptosis sensitivity via a previously unidentified mechanism. At tissue-level O
    Language English
    Publishing date 2021-05-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.abg4302
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  8. Article ; Online: Amino acid management in cancer.

    Tsun, Zhi-Yang / Possemato, Richard

    Seminars in cell & developmental biology

    2015  Volume 43, Page(s) 22–32

    Abstract: Amino acids have a dual role in cellular metabolism, as they are both the building blocks for protein synthesis and intermediate metabolites which fuel other biosynthetic reactions. Recent work has demonstrated that deregulation of both arms of amino ... ...

    Abstract Amino acids have a dual role in cellular metabolism, as they are both the building blocks for protein synthesis and intermediate metabolites which fuel other biosynthetic reactions. Recent work has demonstrated that deregulation of both arms of amino acid management are common alterations seen in cancer. Among the most highly consumed nutrients by cancer cells are the amino acids glutamine and serine, and the biosynthetic pathways that metabolize them are required in various cancer subtypes and the object of current efforts to target cancer metabolism. Also altered in cancer are components of the machinery which sense amino acid sufficiency, nucleated by the mechanistic target of rapamycin (mTOR), a key regulator of cell growth via modulation of key processes including protein synthesis and autophagy. The precise ways in which altered amino acid management supports cellular transformation remain mostly elusive, and a fuller mechanistic understanding of these processes will be important for efforts to exploit such alterations for cancer therapy.
    MeSH term(s) Citric Acid Cycle/physiology ; Glutamine/metabolism ; Humans ; Neoplasms/pathology ; Protein Biosynthesis/physiology ; Serine/metabolism ; Signal Transduction/physiology ; TOR Serine-Threonine Kinases/metabolism
    Chemical Substances Glutamine (0RH81L854J) ; Serine (452VLY9402) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2015-08-12
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1312473-0
    ISSN 1096-3634 ; 1084-9521
    ISSN (online) 1096-3634
    ISSN 1084-9521
    DOI 10.1016/j.semcdb.2015.08.002
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    Zs.A 2918: Show issues Location:
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  9. Article ; Online: PhosphoDisco: A Toolkit for Co-regulated Phosphorylation Module Discovery in Phosphoproteomic Data.

    Schraink, Tobias / Blumenberg, Lili / Hussey, Grant / George, Sabrina / Miller, Brecca / Mathew, Nithu / González-Robles, Tania J / Sviderskiy, Vladislav / Papagiannakopoulos, Thales / Possemato, Richard / Fenyö, David / Ruggles, Kelly V

    Molecular & cellular proteomics : MCP

    2023  Volume 22, Issue 8, Page(s) 100596

    Abstract: Kinases are key players in cancer-relevant pathways and are the targets of many successful precision cancer therapies. Phosphoproteomics is a powerful approach to study kinase activity and has been used increasingly for the characterization of tumor ... ...

    Abstract Kinases are key players in cancer-relevant pathways and are the targets of many successful precision cancer therapies. Phosphoproteomics is a powerful approach to study kinase activity and has been used increasingly for the characterization of tumor samples leading to the identification of novel chemotherapeutic targets and biomarkers. Finding co-regulated phosphorylation sites which represent potential kinase-substrate sets or members of the same signaling pathway allows us to harness these data to identify clinically relevant and targetable alterations in signaling cascades. Unfortunately, studies have found that databases of co-regulated phosphorylation sites are only experimentally supported in a small number of substrate sets. To address the inherent challenge of defining co-regulated phosphorylation modules relevant to a given dataset, we developed PhosphoDisco, a toolkit for determining co-regulated phosphorylation modules. We applied this approach to tandem mass spectrometry based phosphoproteomic data for breast and non-small cell lung cancer and identified canonical as well as putative new phosphorylation site modules. Our analysis identified several interesting modules in each cohort. Among these was a new cell cycle checkpoint module enriched in basal breast cancer samples and a module of PRKC isozymes putatively co-regulated by CDK12 in lung cancer. We demonstrate that modules defined by PhosphoDisco can be used to further personalized cancer treatment strategies by establishing active signaling pathways in a given patient tumor or set of tumors, and in providing new ways to classify tumors based on signaling activity.
    MeSH term(s) Humans ; Phosphorylation ; Carcinoma, Non-Small-Cell Lung ; Lung Neoplasms ; Signal Transduction ; Tandem Mass Spectrometry
    Language English
    Publishing date 2023-06-30
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2075924-1
    ISSN 1535-9484 ; 1535-9476
    ISSN (online) 1535-9484
    ISSN 1535-9476
    DOI 10.1016/j.mcpro.2023.100596
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    Zs.A 5599: Show issues Location:
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  10. Article ; Online: Association of hyperglycemia and molecular subclass on survival in IDH-wildtype glioblastoma.

    Liu, Elisa K / Vasudevaraja, Varshini / Sviderskiy, Vladislav O / Feng, Yang / Tran, Ivy / Serrano, Jonathan / Cordova, Christine / Kurz, Sylvia C / Golfinos, John G / Sulman, Erik P / Orringer, Daniel A / Placantonakis, Dimitris / Possemato, Richard / Snuderl, Matija

    Neuro-oncology advances

    2022  Volume 4, Issue 1, Page(s) vdac163

    Abstract: Background: Hyperglycemia has been associated with worse survival in glioblastoma. Attempts to lower glucose yielded mixed responses which could be due to molecularly distinct GBM subclasses.: Methods: Clinical, laboratory, and molecular data on 89 ... ...

    Abstract Background: Hyperglycemia has been associated with worse survival in glioblastoma. Attempts to lower glucose yielded mixed responses which could be due to molecularly distinct GBM subclasses.
    Methods: Clinical, laboratory, and molecular data on 89 IDH-wt GBMs profiled by clinical next-generation sequencing and treated with Stupp protocol were reviewed. IDH-wt GBMs were sub-classified into RTK I (Proneural), RTK II (Classical) and Mesenchymal subtypes using whole-genome DNA methylation. Average glucose was calculated by time-weighting glucose measurements between diagnosis and last follow-up.
    Results: Patients were stratified into three groups using average glucose: tertile one (<100 mg/dL), tertile two (100-115 mg/dL), and tertile three (>115 mg/dL). Comparison across glucose tertiles revealed no differences in performance status (KPS), dexamethasone dose, MGMT methylation, or methylation subclass. Overall survival (OS) was not affected by methylation subclass (
    Conclusion: Higher average glucose values were associated with poorer OS in RTKI and Mesenchymal IDH-wt GBM, but not RTKII. There were no discernible epigenetic or metabolomic differences between tumors in different glucose environments, suggesting a potential survival benefit to lowering systemic glucose in selected molecular subtypes.
    Language English
    Publishing date 2022-10-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 3009682-0
    ISSN 2632-2498 ; 2632-2498
    ISSN (online) 2632-2498
    ISSN 2632-2498
    DOI 10.1093/noajnl/vdac163
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