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  1. Article ; Online: Selection of Knees With Subsequent Cartilage Thickness Loss Based on Magnetic Resonance Imaging Semiquantitative Grading: Data From the Osteoarthritis Initiative Foundation for the National Institutes of Health Biomarker Cohort.

    Wirth, Wolfgang / Maschek, Susanne / Wisser, Anna / Guermazi, Ali / Hunter, David J / Kwoh, C Kent / Nevitt, Michael C / Eckstein, Felix / Roemer, Frank W

    Arthritis care & research

    2023  Volume 75, Issue 8, Page(s) 1773–1782

    Abstract: Objective: To investigate which magnetic resonance imaging (MRI)-based articular pathologies are predictive of subsequent medial femorotibial compartment quantitative cartilage thickness loss and therefore suitable for enrichment of clinical trials with ...

    Abstract Objective: To investigate which magnetic resonance imaging (MRI)-based articular pathologies are predictive of subsequent medial femorotibial compartment quantitative cartilage thickness loss and therefore suitable for enrichment of clinical trials with participants showing a high likelihood for structural progression.
    Methods: Semiquantitative MRI Osteoarthritis Knee Score (MOAKS) assessments at baseline and quantitative cartilage thickness measurements at baseline and year-2 follow-up were performed in 599 participants (age 62 years; body mass index 31 kg/m
    Results: Presence of MFTC MOAKS cartilage damage (odds ratio [OR] 2.77 [95% confidence interval (95% CI) 1.76, 4.36]), MFTC bone marrow lesions (OR 2.69 [95% CI 1.89, 3.83]), medial meniscus extrusion or damage (OR 2.21 [95% CI 1.37, 3.55]), as well as MOAKS severity subscales for cartilage and meniscus damage were associated with subsequent progression. The SRM was greater in knees with than in knees without the presence of these pathologies and was associated with the severity of those pathologies.
    Conclusion: MRI-based grading of articular pathologies makes it possible to specifically select progressor knees suitable for inclusion in clinical trials but also to identify knees in which treatment is not indicated (e.g., knees without cartilage damage despite presence of radiographic osteoarthritis).
    MeSH term(s) Humans ; Female ; Middle Aged ; Male ; United States ; Osteoarthritis, Knee/diagnostic imaging ; Osteoarthritis, Knee/pathology ; Cartilage, Articular/diagnostic imaging ; Cartilage, Articular/pathology ; Knee Joint/diagnostic imaging ; Knee Joint/pathology ; Magnetic Resonance Imaging/methods ; Biomarkers ; Musculoskeletal Diseases ; National Institutes of Health (U.S.) ; Disease Progression
    Chemical Substances Biomarkers
    Language English
    Publishing date 2023-02-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 645059-3
    ISSN 2151-4658 ; 0893-7524 ; 2151-464X
    ISSN (online) 2151-4658
    ISSN 0893-7524 ; 2151-464X
    DOI 10.1002/acr.25078
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  2. Article: High resource overlap and small dietary differences are widespread in food‐limited warbler (Parulidae) communities

    Kent, Cody M. / Huh, Kyu Min / Hunter, Sarah Chieko / Judson, Kathryn / Powell, Luke L. / Sherry, Thomas W.

    Ibis. 2022 Jan., v. 164, no. 1

    2022  

    Abstract: Although both interspecific competition and coexistence mechanisms are central to ecological and evolutionary theory, past empirical studies have generally focused on simple (two‐species) communities over short time periods. Experimental tests of these ... ...

    Abstract Although both interspecific competition and coexistence mechanisms are central to ecological and evolutionary theory, past empirical studies have generally focused on simple (two‐species) communities over short time periods. Experimental tests of these species interactions are challenging in complex study systems. Moreover, several studies of ‘imperfect generalists’, consistent with Liem's Paradox, raise questions about the ability of evolved species differences to partition niche space effectively when resources vary considerably across the annual cycle. Here we used a recently developed theoretical framework to combine past research on population‐level processes with observational data on resource use to test for ongoing interspecific competition and understand the nature of resource overlap. We compared species diet overlaps and differences in several distinctive communities centred on a focal species, the American Redstart Setophaga ruticilla replicated both spatially and seasonally, in combination with documentation of population regulation to assess the ability of similar species to partition dietary niche space and limit interspecific competition. Our results document high dietary overlap in most of the communities studied, with only subtle differentiation consistent with known species differences in foraging behaviour and morphology. These findings are largely consistent with species foraging as imperfect generalists. However, in contrast to past studies, the high diet overlaps observed here during times of inferred resource scarcity were driven by low‐value prey taxa (e.g. small ants) and did not involve truly ‘private’ resources. All of these factors increase the potential negative impacts of interspecific competition, and limit the ability of these birds to avoid competition if food availability deteriorates further than observed in our study, either seasonally or at longer intervals.
    Keywords Setophaga ruticilla ; diet ; food availability ; interspecific competition ; observational studies
    Language English
    Dates of publication 2022-01
    Size p. 44-59.
    Publishing place John Wiley & Sons, Ltd
    Document type Article
    Note JOURNAL ARTICLE
    ZDB-ID 2071870-6
    ISSN 1474-919X ; 0019-1019
    ISSN (online) 1474-919X
    ISSN 0019-1019
    DOI 10.1111/ibi.13006
    Database NAL-Catalogue (AGRICOLA)

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  3. Article: Loss of NAT10 disrupts enhancer organization via p300 mislocalization and suppresses transcription of genes necessary for metastasis progression.

    Amin, Ruhul / Ha, Ngoc-Han / Qiu, Tinghu / Holewinski, Ronald / Lam, Khiem C / Lopès, Amélie / Liu, Huaitian / Tran, Andy D / Lee, Maxwell P / Gamage, Supuni Thalalla / Andresson, Thorkell / Goldszmid, Romina S / Meier, Jordan L / Hunter, Kent W

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Acetylation of protein and RNA represent a critical event for development and cancer progression. NAT10 is the only known RNA acetylase that catalyzes the N4-actylcytidine (ac4C) modification of RNAs. Here, we show that the loss of NAT10 significantly ... ...

    Abstract Acetylation of protein and RNA represent a critical event for development and cancer progression. NAT10 is the only known RNA acetylase that catalyzes the N4-actylcytidine (ac4C) modification of RNAs. Here, we show that the loss of NAT10 significantly decreases lung metastasis in allograft and genetically engineered mouse models of breast cancer. NAT10 interacts with a mechanosensitive, metastasis susceptibility protein complex at the nuclear pore. In addition to its canonical role in RNA acetylation, we find that NAT10 interacts with p300 at gene enhancers. NAT10 loss is associated with p300 mislocalization into heterochromatin regions. NAT10 depletion disrupts enhancer organization, leading to alteration of gene transcription necessary for metastatic progression, including reduced myeloid cell-recruiting chemokines that results in a less metastasis-prone tumor microenvironment. Our study uncovers a distinct role of NAT10 in enhancer organization of metastatic tumor cells and suggests its involvement in the tumor-immune crosstalk dictating metastatic outcomes.
    Language English
    Publishing date 2024-01-29
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.01.24.577116
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  4. Article ; Online: Mouse models of cancer: does the strain matter?

    Hunter, Kent W

    Nature reviews. Cancer

    2012  Volume 12, Issue 2, Page(s) 144–149

    Abstract: Mouse models are indispensible tools for understanding the molecular basis of cancer. However, despite the invaluable data provided regarding tumour biology, owing to inbreeding, current mouse models fail to accurately model human populations. ... ...

    Abstract Mouse models are indispensible tools for understanding the molecular basis of cancer. However, despite the invaluable data provided regarding tumour biology, owing to inbreeding, current mouse models fail to accurately model human populations. Polymorphism is the essential characteristic that makes each of us unique humans, with different disease susceptibility, presentation and progression. Therefore, as we move closer towards designing clinical treatment that is based on an individual's unique biological makeup, it is imperative that we understand how inherited variability influences cancer phenotypes, how it can confound experiments and how it can be exploited to reveal new truths about cancer biology.
    MeSH term(s) Animals ; Disease Models, Animal ; Mice ; Neoplasms, Experimental/genetics ; Neoplasms, Experimental/pathology ; Polymorphism, Genetic ; Species Specificity
    Language English
    Publishing date 2012-01-19
    Publishing country England
    Document type Research Support, N.I.H., Intramural ; Review
    ZDB-ID 2062767-1
    ISSN 1474-1768 ; 1474-175X
    ISSN (online) 1474-1768
    ISSN 1474-175X
    DOI 10.1038/nrc3206
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  5. Article ; Online: Structural phenotypes of knee osteoarthritis: potential clinical and research relevance.

    Roemer, Frank W / Jarraya, Mohamed / Collins, Jamie E / Kwoh, C Kent / Hayashi, Daichi / Hunter, David J / Guermazi, Ali

    Skeletal radiology

    2022  Volume 52, Issue 11, Page(s) 2021–2030

    Abstract: A joint contains many different tissues that can exhibit pathological changes, providing many potential targets for treatment. Researchers are increasingly suggesting that osteoarthritis (OA) comprises several phenotypes or subpopulations. Consequently, ... ...

    Abstract A joint contains many different tissues that can exhibit pathological changes, providing many potential targets for treatment. Researchers are increasingly suggesting that osteoarthritis (OA) comprises several phenotypes or subpopulations. Consequently, a treatment for OA that targets only one pathophysiologic abnormality is unlikely to be similarly efficacious in preventing or delaying the progression of all the different phenotypes of structural OA. Five structural phenotypes have been proposed, namely the inflammatory, meniscus-cartilage, subchondral bone, and atrophic and hypertrophic phenotypes. The inflammatory phenotype is characterized by marked synovitis and/or joint effusion, while the meniscus-cartilage phenotype exhibits severe meniscal and cartilage damage. Large bone marrow lesions characterize the subchondral bone phenotype. The hypertrophic and atrophic OA phenotype are defined based on the presence large osteophytes or absence of any osteophytes, respectively, in the presence of concomitant cartilage damage. Limitations of the concept of structural phenotyping are that they are not mutually exclusive and that more than one phenotype may be present. It must be acknowledged that a wide range of views exist on how best to operationalize the concept of structural OA phenotypes and that the concept of structural phenotypic characterization is still in its infancy. Structural phenotypic stratification, however, may result in more targeted trial populations with successful outcomes and practitioners need to be aware of the heterogeneity of the disease to personalize their treatment recommendations for an individual patient. Radiologists should be able to define a joint at risk for progression based on the predominant phenotype present at different disease stages.
    MeSH term(s) Humans ; Osteoarthritis, Knee/pathology ; Knee Joint/pathology ; Osteophyte/complications ; Magnetic Resonance Imaging ; Cartilage, Articular/diagnostic imaging ; Cartilage, Articular/pathology ; Hypertrophy/complications ; Hypertrophy/pathology ; Cartilage Diseases/pathology ; Bone Diseases/pathology ; Phenotype
    Language English
    Publishing date 2022-09-26
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 527592-1
    ISSN 1432-2161 ; 0364-2348
    ISSN (online) 1432-2161
    ISSN 0364-2348
    DOI 10.1007/s00256-022-04191-6
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    Zs.A 1304: Show issues Location:
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  6. Article ; Online: Presence of Magnetic Resonance Imaging-Defined Inflammation Particularly in Overweight and Obese Women Increases Risk of Radiographic Knee Osteoarthritis: The POMA Study.

    Roemer, Frank W / Guermazi, Ali / Hannon, Michael J / Fujii, Tomoko / Omoumi, Patrick / Hunter, David J / Eckstein, Felix / Kwoh, C Kent

    Arthritis care & research

    2022  Volume 74, Issue 8, Page(s) 1391–1398

    Abstract: Objective: The present study was undertaken to assess whether the odds for incident radiographic osteoarthritis (OA) differ between men and women in regard to body mass index (BMI) and inflammatory magnetic resonance imaging (MRI) markers 1 and 2 years ... ...

    Abstract Objective: The present study was undertaken to assess whether the odds for incident radiographic osteoarthritis (OA) differ between men and women in regard to body mass index (BMI) and inflammatory magnetic resonance imaging (MRI) markers 1 and 2 years prior, and whether the presence of inflammation on MRI differs between normal-weight and overweight/obese individuals who develop radiographic OA up to 4 years prior.
    Methods: We studied 355 knees from the Osteoarthritis Initiative study that developed incident radiographic OA and 355 matched controls. MRIs were read for effusion-synovitis and Hoffa-synovitis for up to 4 consecutive annual time points. Subjects were classified as normal-weight (BMI <25), overweight (BMI ≥25 and <30), or obese (BMI ≥30). Conditional logistic regression was used to assess odds of incident radiographic OA for effusion-synovitis and Hoffa-synovitis at 1 and 2 years prior to radiographic OA incidence (i.e., "P-1" and "P-2") considering BMI category. Bivariate logistic regression was used to assess odds of inflammation for cases only.
    Results: One hundred seventy-eight (25.1%) participants were normal weight, 283 (39.9%) overweight, and 249 (35.1%) obese. At P-2, being overweight with Hoffa-synovitis, which had an odds ratio [OR] of 3.26 (95% confidence interval [95% CI] 1.39-7.65), or effusion-synovitis (OR 3.56 [95% CI 1.45-8.75]) was associated with greater odds of incident radiographic OA in women. For those with incident radiographic OA, there were no increased odds of synovitis in the overweight/obese subgroup for most time points, but increased odds for effusion-synovitis were observed at P-2 (OR 2.21 [95% CI 1.11-4.43]).
    Conclusion: Presence of inflammatory markers seems to play a role especially in overweight women, while obese women have increased odds for radiographic OA also in the absence of these markers.
    MeSH term(s) Female ; Humans ; Inflammation/complications ; Knee Joint/diagnostic imaging ; Knee Joint/pathology ; Magnetic Resonance Imaging ; Male ; Obesity/complications ; Obesity/diagnostic imaging ; Obesity/epidemiology ; Osteoarthritis, Knee/diagnostic imaging ; Osteoarthritis, Knee/epidemiology ; Osteoarthritis, Knee/etiology ; Overweight/complications ; Overweight/diagnostic imaging ; Overweight/epidemiology ; Polymethacrylic Acids ; Synovitis/complications ; Synovitis/diagnostic imaging ; Synovitis/epidemiology
    Chemical Substances Polymethacrylic Acids ; poly(n-octyl methacrylate)
    Language English
    Publishing date 2022-05-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 645059-3
    ISSN 2151-4658 ; 0893-7524 ; 2151-464X
    ISSN (online) 2151-4658
    ISSN 0893-7524 ; 2151-464X
    DOI 10.1002/acr.24568
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  7. Article: Tumor cell dormancy as an adaptive cell stress response mechanism.

    Vera-Ramirez, Laura / Hunter, Kent W

    F1000Research

    2017  Volume 6, Page(s) 2134

    Abstract: Metastases are responsible for most cancer-related deaths. The kinetics of tumor relapse is highly heterogeneous, ranging from recurrences shortly after diagnosis to years or even decades after the initial treatment. This subclinical period is known as ... ...

    Abstract Metastases are responsible for most cancer-related deaths. The kinetics of tumor relapse is highly heterogeneous, ranging from recurrences shortly after diagnosis to years or even decades after the initial treatment. This subclinical period is known as tumor dormancy, in which residual disease remains in an undetectable state before finally appearing as an overtly proliferative metastasis. Despite recent advances in our understanding of the molecular mechanisms leading to tumor dormancy, it is still a poorly understood phase of cancer progression, which limits opportunities for the design of successful therapeutic interventions. The influence of the tumor microenvironment at the metastatic site and anti-metastatic immune responses have been shown to play a crucial role in the onset and maintenance of metastatic dormancy. However, there is still a significant gap in our understanding of how dormant cells remain viable in a quiescent state for long periods of time. Here, we review the latest experimental evidence shedding light on the biological processes that enable dormant tumor cells to endure the multiple stresses encountered at the metastatic site.
    Language English
    Publishing date 2017
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2699932-8
    ISSN 2046-1402
    ISSN 2046-1402
    DOI 10.12688/f1000research.12174.1
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  8. Article ; Online: Dysregulation of Mitochondrial Translation Caused by CBFB Deficiency Cooperates with Mutant PIK3CA and Is a Vulnerability in Breast Cancer.

    Malik, Navdeep / Kim, Young-Im / Yan, Hualong / Tseng, Yu-Chou / du Bois, Wendy / Ayaz, Gamze / Tran, Andy D / Vera-Ramirez, Laura / Yang, Howard / Michalowski, Aleksandra M / Kruhlak, Michael / Lee, Maxwell / Hunter, Kent W / Huang, Jing

    Cancer research

    2023  Volume 83, Issue 8, Page(s) 1280–1298

    Abstract: Understanding functional interactions between cancer mutations is an attractive strategy for discovering unappreciated cancer pathways and developing new combination therapies to improve personalized treatment. However, distinguishing driver gene pairs ... ...

    Abstract Understanding functional interactions between cancer mutations is an attractive strategy for discovering unappreciated cancer pathways and developing new combination therapies to improve personalized treatment. However, distinguishing driver gene pairs from passenger pairs remains challenging. Here, we designed an integrated omics approach to identify driver gene pairs by leveraging genetic interaction analyses of top mutated breast cancer genes and the proteomics interactome data of their encoded proteins. This approach identified that PIK3CA oncogenic gain-of-function (GOF) and CBFB loss-of-function (LOF) mutations cooperate to promote breast tumor progression in both mice and humans. The transcription factor CBFB localized to mitochondria and moonlighted in translating the mitochondrial genome. Mechanistically, CBFB enhanced the binding of mitochondrial mRNAs to TUFM, a mitochondrial translation elongation factor. Independent of mutant PI3K, mitochondrial translation defects caused by CBFB LOF led to multiple metabolic reprogramming events, including defective oxidative phosphorylation, the Warburg effect, and autophagy/mitophagy addiction. Furthermore, autophagy and PI3K inhibitors synergistically killed breast cancer cells and impaired the growth of breast tumors, including patient-derived xenografts carrying CBFB LOF and PIK3CA GOF mutations. Thus, our study offers mechanistic insights into the functional interaction between mutant PI3K and mitochondrial translation dysregulation in breast cancer progression and provides a strong preclinical rationale for combining autophagy and PI3K inhibitors in precision medicine for breast cancer.
    Significance: CBFB-regulated mitochondrial translation is a regulatory step in breast cancer metabolism and synergizes with mutant PI3K in breast cancer progression.
    MeSH term(s) Animals ; Female ; Humans ; Mice ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Class I Phosphatidylinositol 3-Kinases/genetics ; Class I Phosphatidylinositol 3-Kinases/metabolism ; Core Binding Factor beta Subunit/genetics ; Core Binding Factor beta Subunit/pharmacology ; Mutation ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphoinositide-3 Kinase Inhibitors/pharmacology ; Signal Transduction/genetics
    Chemical Substances CBFB protein, human ; Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; Core Binding Factor beta Subunit ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Phosphoinositide-3 Kinase Inhibitors ; PIK3CA protein, human (EC 2.7.1.137)
    Language English
    Publishing date 2023-02-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-22-2525
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  9. Book: TRACO

    Hunter, Kent W

    2011  

    Title variant Metastasis, angiogenesis ; Translational research in clinical oncology
    Institution National Institutes of Health (U.S.)
    Author's details Kent Hunter, Enrique Zudaire
    MeSH term(s) Neoplasm Metastasis/genetics ; Neovascularization, Pathologic
    Language English
    Size 1 online resource (1 streaming video file (2 hr., 5 min.) :, sd., col.)
    Publisher National Institutes of Health
    Publishing place Bethesda, Md
    Document type Book
    Note Closed-captioned.
    Database Catalogue of the US National Library of Medicine (NLM)

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  10. Article ; Online: Tumor cell dormancy as an adaptive cell stress response mechanism [version 1; referees

    Laura Vera-Ramirez / Kent W. Hunter

    F1000Research, Vol

    4 approved]

    2017  Volume 6

    Abstract: Metastases are responsible for most cancer-related deaths. The kinetics of tumor relapse is highly heterogeneous, ranging from recurrences shortly after diagnosis to years or even decades after the initial treatment. This subclinical period is known as ... ...

    Abstract Metastases are responsible for most cancer-related deaths. The kinetics of tumor relapse is highly heterogeneous, ranging from recurrences shortly after diagnosis to years or even decades after the initial treatment. This subclinical period is known as tumor dormancy, in which residual disease remains in an undetectable state before finally appearing as an overtly proliferative metastasis. Despite recent advances in our understanding of the molecular mechanisms leading to tumor dormancy, it is still a poorly understood phase of cancer progression, which limits opportunities for the design of successful therapeutic interventions. The influence of the tumor microenvironment at the metastatic site and anti-metastatic immune responses have been shown to play a crucial role in the onset and maintenance of metastatic dormancy. However, there is still a significant gap in our understanding of how dormant cells remain viable in a quiescent state for long periods of time. Here, we review the latest experimental evidence shedding light on the biological processes that enable dormant tumor cells to endure the multiple stresses encountered at the metastatic site.
    Keywords Aging ; Breast Diseases: Benign & Malignant ; Cancer Therapeutics ; Cell Adhesion ; Cell Growth & Division ; Cell Signaling ; Cellular Death & Stress Responses ; Drug Discovery & Design ; Epidemiology ; Gynecological Cancers ; Head & Neck Cancers ; Innate Immunity ; Lung Cancer ; Stem Cells & Regeneration ; Medicine ; R ; Science ; Q
    Subject code 610
    Language English
    Publishing date 2017-12-01T00:00:00Z
    Publisher F1000 Research Ltd
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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