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  1. Article ; Online: Targeting Angiogenesis via Resolution of Inflammation.

    Kelly, Abigail G / Panigrahy, Dipak

    Cold Spring Harbor perspectives in medicine

    2023  Volume 13, Issue 3

    Abstract: Angiogenesis, the growth of new blood vessels, plays a critical role in tissue repair and regeneration, as well as in cancer. A paradigm shift is emerging in our understanding of the resolution of inflammation as an active biochemical process with the ... ...

    Abstract Angiogenesis, the growth of new blood vessels, plays a critical role in tissue repair and regeneration, as well as in cancer. A paradigm shift is emerging in our understanding of the resolution of inflammation as an active biochemical process with the discovery of novel endogenous specialized pro-resolving mediators (SPMs), including resolvins. Angiogenesis and the resolution of inflammation are critical interdependent processes. Disrupted inflammation resolution can accelerate tumor growth, which is angiogenesis-dependent. SPMs, including resolvins and lipoxins, inhibit physiologic and pathological angiogenesis at nanogram concentrations. The failure of resolution of inflammation is an emerging hallmark of angiogenesis-dependent diseases including arthritis, psoriasis, diabetic retinopathy, age-related macular degeneration, inflammatory bowel disease, atherosclerosis, endometriosis, Alzheimer's disease, and cancer. Whereas therapeutic angiogenesis repairs tissue damage (e.g., limb ischemia), inhibition of pathological angiogenesis suppresses tumor growth and other non-neoplastic diseases such as retinopathies. Stimulation of resolution of inflammation via pro-resolving lipid mediators promotes the repair of tissue damage and wound healing, accelerates tissue regeneration, and inhibits cancer. Here we provide an overview of the mechanisms of cross talk between angiogenesis and inflammation resolution in chronic inflammation-driven diseases. Stimulating the resolution of inflammation via pro-resolving lipid mediators has emerged as a promising new field to treat angiogenic diseases.
    MeSH term(s) Humans ; Inflammation/pathology ; Atherosclerosis/drug therapy ; Atherosclerosis/pathology ; Ischemia ; Lipids ; Neovascularization, Pathologic ; Inflammation Mediators/therapeutic use
    Chemical Substances Lipids ; Inflammation Mediators
    Language English
    Publishing date 2023-03-01
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ISSN 2157-1422
    ISSN (online) 2157-1422
    DOI 10.1101/cshperspect.a041172
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Preface.

    Panigrahy, Dipak / Gilligan, Molly

    Cancer metastasis reviews

    2020  Volume 39, Issue 1, Page(s) 1–2

    MeSH term(s) Central Nervous System Neoplasms/therapy ; Child ; Hematologic Neoplasms/therapy ; Humans ; Neoplasms/therapy ; Neuroblastoma/therapy ; Pediatrics/methods
    Language English
    Publishing date 2020-01-29
    Publishing country Netherlands
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 604857-2
    ISSN 1573-7233 ; 0167-7659
    ISSN (online) 1573-7233
    ISSN 0167-7659
    DOI 10.1007/s10555-020-09862-1
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  3. Article ; Online: Preface.

    Panigrahy, Dipak / Gilligan, Molly

    Cancer metastasis reviews

    2019  Volume 38, Issue 4, Page(s) 551–552

    MeSH term(s) Animals ; Child ; Humans ; Neoplasms/diagnosis ; Neoplasms/therapy ; Pediatrics/methods
    Language English
    Publishing date 2019-12-20
    Publishing country Netherlands
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 604857-2
    ISSN 1573-7233 ; 0167-7659
    ISSN (online) 1573-7233
    ISSN 0167-7659
    DOI 10.1007/s10555-019-09838-w
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  4. Article ; Online: Notch signaling in malignant gliomas: supporting tumor growth and the vascular environment.

    Kipper, Franciele C / Kieran, Mark W / Thomas, Ajith / Panigrahy, Dipak

    Cancer metastasis reviews

    2022  Volume 41, Issue 3, Page(s) 737–747

    Abstract: Glioblastoma is the most malignant form of glioma, which is the most commonly occurring tumor of the central nervous system. Notch signaling in glioblastoma is considered to be a marker of an undifferentiated tumor cell state, associated with tumor stem ... ...

    Abstract Glioblastoma is the most malignant form of glioma, which is the most commonly occurring tumor of the central nervous system. Notch signaling in glioblastoma is considered to be a marker of an undifferentiated tumor cell state, associated with tumor stem cells. Notch is also known for facilitating tumor dormancy escape, recurrence and progression after treatment. Studies in vitro suggest that reducing, removing or blocking the expression of this gene triggers tumor cell differentiation, which shifts the phenotype away from stemness status and consequently facilitates treatment. In contrast, in the vasculature, Notch appears to also function as an important receptor that defines mature non-leaking vessels, and increasing its expression promotes tumor normalization in models of cancer in vivo. Failures in clinical trials with Notch inhibitors are potentially related to their opposing effects on the tumor versus the tumor vasculature, which points to the need for a greater understanding of this signaling pathway.
    MeSH term(s) Brain Neoplasms/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Glioblastoma/genetics ; Glioma/pathology ; Humans ; Neoplastic Stem Cells/pathology ; Signal Transduction
    Language English
    Publishing date 2022-05-27
    Publishing country Netherlands
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 604857-2
    ISSN 1573-7233 ; 0167-7659
    ISSN (online) 1573-7233
    ISSN 0167-7659
    DOI 10.1007/s10555-022-10041-7
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  5. Article ; Online: Debris-stimulated tumor growth: a Pandora's box?

    Haak, Victoria M / Huang, Sui / Panigrahy, Dipak

    Cancer metastasis reviews

    2021  Volume 40, Issue 3, Page(s) 791–801

    Abstract: Current cancer therapies aim at eradicating cancer cells from the body. However, killing cells generates cell "debris" which can promote tumor progression. Thus, therapy can be a double-edged sword. Specifically, injury and debris generated by cancer ... ...

    Abstract Current cancer therapies aim at eradicating cancer cells from the body. However, killing cells generates cell "debris" which can promote tumor progression. Thus, therapy can be a double-edged sword. Specifically, injury and debris generated by cancer therapies, including chemotherapy, radiation, and surgery, may offset their benefit by promoting the secretion of pro-tumorigenic factors (e.g., eicosanoid-driven cytokines) that stimulate regrowth and metastasis of surviving cells. The debris produced by cytotoxic cancer therapy can also contribute to a tumor microenvironment that promotes tumor progression and recurrence. Although not well understood, several molecular mechanisms have been implicated in debris-stimulated tumor growth that we review here, such as the involvement of extracellular vesicles, exosomal miR-194-5p, Bax, Bak, Smac, HMGB1, cytokines, and caspase-3. We discuss the cases of pancreatic and other cancer types where debris promotes postoperative tumor recurrence and metastasis, thus offering a new opportunity to prevent cancer progression intrinsically linked to treatment by stimulating resolution of tumor-promoting debris.
    MeSH term(s) Antineoplastic Agents ; Cell Line, Tumor ; Cytokines ; Eicosanoids ; Humans ; MicroRNAs ; Neoplasms/therapy ; Tumor Microenvironment
    Chemical Substances Antineoplastic Agents ; Cytokines ; Eicosanoids ; MicroRNAs
    Language English
    Publishing date 2021-10-19
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 604857-2
    ISSN 1573-7233 ; 0167-7659
    ISSN (online) 1573-7233
    ISSN 0167-7659
    DOI 10.1007/s10555-021-09998-8
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  6. Article ; Online: Preface.

    Gartung, Allison / Panigrahy, Dipak

    Cancer metastasis reviews

    2018  Volume 37, Issue 2-3, Page(s) 201–202

    MeSH term(s) Animals ; Disease Susceptibility ; Humans ; Lipid Metabolism ; Neoplasms/etiology ; Neoplasms/metabolism ; Neoplasms/pathology ; Signal Transduction
    Language English
    Publishing date 2018-08-16
    Publishing country Netherlands
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 604857-2
    ISSN 1573-7233 ; 0167-7659
    ISSN (online) 1573-7233
    ISSN 0167-7659
    DOI 10.1007/s10555-018-9758-5
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  7. Article ; Online: Different modalities of host cell death and their impact on

    Nisa, Annuurun / Kipper, Franciele C / Panigrahy, Dipak / Tiwari, Sangeeta / Kupz, Andreas / Subbian, Selvakumar

    American journal of physiology. Cell physiology

    2022  Volume 323, Issue 5, Page(s) C1444–C1474

    Abstract: Mycobacterium ... ...

    Abstract Mycobacterium tuberculosis
    MeSH term(s) Humans ; Tuberculosis/microbiology ; Tuberculosis/prevention & control ; Mycobacterium tuberculosis/metabolism ; Cell Death ; Macrophages/metabolism ; Granuloma/metabolism ; Granuloma/microbiology ; Granuloma/pathology ; Host-Pathogen Interactions
    Language English
    Publishing date 2022-10-03
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00246.2022
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  8. Article ; Online: Resolution of inflammation: An organizing principle in biology and medicine.

    Panigrahy, Dipak / Gilligan, Molly M / Serhan, Charles N / Kashfi, Khosrow

    Pharmacology & therapeutics

    2021  Volume 227, Page(s) 107879

    Abstract: The resolution of inflammation has emerged as a critical endogenous process that protects host tissues from prolonged or excessive inflammation that can become chronic. Failure of the resolution of inflammation is a key pathological mechanism that drives ...

    Abstract The resolution of inflammation has emerged as a critical endogenous process that protects host tissues from prolonged or excessive inflammation that can become chronic. Failure of the resolution of inflammation is a key pathological mechanism that drives the progression of numerous inflammation-driven diseases. Essential polyunsaturated fatty acid (PUFA)-derived autacoid mediators termed 'specialized pro-resolving mediators' (SPMs) regulate endogenous resolution programs by limiting further neutrophil tissue infiltration and stimulating local immune cell (e.g., macrophage)-mediated clearance of apoptotic polymorphonuclear neutrophils, cellular debris, and microbes, as well as counter-regulating eicosanoid/cytokine production. The SPM superfamily encompasses lipoxins, resolvins, protectins, and maresins. Our understanding of the resolution phase of acute inflammation has grown exponentially in the past three decades with the discovery of novel pro-resolving lipid mediators, their pro-efferocytosis mechanisms, and their receptors. Technological advancement has further facilitated lipid mediator metabolipidomic based profiling of healthy and diseased human tissues, highlighting the extraordinary therapeutic potential of SPMs across a broad array of inflammatory diseases including cancer. As current front-line cancer therapies such as surgery, chemotherapy, and radiation may induce various unwanted side effects such as robust pro-inflammatory and pro-tumorigenic host responses, characterizing SPMs and their receptors as novel therapeutic targets may have important implications as a new direction for host-targeted cancer therapy. Here, we discuss the origins of inflammation resolution, key discoveries and the failure of resolution mechanisms in diseases with an emphasis on cancer, and future directions focused on novel therapeutic applications for this exciting and rapidly expanding field.
    MeSH term(s) Biology ; Humans ; Inflammation/drug therapy ; Inflammation/pathology ; Medicine
    Language English
    Publishing date 2021-04-27
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 194735-7
    ISSN 1879-016X ; 0163-7258
    ISSN (online) 1879-016X
    ISSN 0163-7258
    DOI 10.1016/j.pharmthera.2021.107879
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  9. Article ; Online: COVID-19 and cancer: start the resolution!

    Barksdale, Chantal / Kipper, Franciele C / Tripathy, Shreya / Subbian, Selvakumar / Serhan, Charles N / Panigrahy, Dipak

    Cancer metastasis reviews

    2022  Volume 41, Issue 1, Page(s) 1–15

    Abstract: Coronavirus disease 2019 (COVID-19) due to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been an ongoing pandemic causing significant morbidity and mortality worldwide. The "cytokine storm" is a critical driving force in ...

    Abstract Coronavirus disease 2019 (COVID-19) due to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been an ongoing pandemic causing significant morbidity and mortality worldwide. The "cytokine storm" is a critical driving force in severe COVID-19 cases, leading to hyperinflammation, multi-system organ failure, and death. A paradigm shift is emerging in our understanding of the resolution of inflammation from a passive course to an active biochemical process driven by endogenous specialized pro-resolving mediators (SPMs), such as resolvins, protectins, lipoxins, and maresins. SPMs stimulate macrophage-mediated debris clearance and counter pro-inflammatory cytokine production, a process collectively termed as the "resolution of inflammation." Hyperinflammation is not unique to COVID-19 and also occurs in neoplastic conditions, putting individuals with underlying health conditions such as cancer at elevated risk of severe SARS-CoV-2 infection. Despite approaches to block systemic inflammation, there are no current therapies designed to stimulate the resolution of inflammation in patients with COVID-19 or cancer. A non-immunosuppressive therapeutic approach that reduces the cytokine storm in patients with COVID-19 and cancer is urgently needed. SPMs are potent immunoresolvent and organ-protective lipid autacoids that stimulate the resolution of inflammation, facilitate clearance of infections, reduce thrombus burden, and promote a return to tissue homeostasis. Targeting endogenous lipid mediators, such as SPMs, offers an entirely novel approach to control SARS-CoV-2 infection and cancer by increasing the body's natural reserve of pro-resolving mediators without overt toxicity or immunosuppression.
    MeSH term(s) COVID-19 ; Cytokine Release Syndrome/etiology ; Humans ; Inflammation ; Neoplasms ; Pandemics ; SARS-CoV-2
    Language English
    Publishing date 2022-02-21
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 604857-2
    ISSN 1573-7233 ; 0167-7659
    ISSN (online) 1573-7233
    ISSN 0167-7659
    DOI 10.1007/s10555-021-10017-z
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  10. Article ; Online: Regulation of inflammation in cancer by dietary eicosanoids.

    Yang, Haixia / Rothenberger, Eva / Zhao, Tong / Fan, Wendong / Kelly, Abigail / Attaya, Ahmed / Fan, Daidi / Panigrahy, Dipak / Deng, Jianjun

    Pharmacology & therapeutics

    2023  Volume 248, Page(s) 108455

    Abstract: Background: Cancer is a major burden of disease worldwide and increasing evidence shows that inflammation contributes to cancer development and progression. Eicosanoids are derived from dietary polyunsaturated fatty acids, such as arachidonic acid (AA), ...

    Abstract Background: Cancer is a major burden of disease worldwide and increasing evidence shows that inflammation contributes to cancer development and progression. Eicosanoids are derived from dietary polyunsaturated fatty acids, such as arachidonic acid (AA), and are mainly produced by a series of enzymatic pathways that include cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P-450 epoxygenase (CYP). Eicosanoids consist of at least several hundred individual molecules and play important roles in the inflammatory response and inflammation-related cancers.
    Scope and approach: Dietary sources of AA and biosynthesis of eicosanoids from AA through different metabolic pathways are summarized. The bioactivities of eicosanoids and their potential molecular mechanisms on inflammation and cancer are revealed. Additionally, current challenges and limitations in eicosanoid research on inflammation-related cancer are discussed.
    Key findings and conclusions: Dietary AA generates a large variety of eicosanoids, including prostaglandins, thromboxane A2, leukotrienes, cysteinyl leukotrienes, lipoxins, hydroxyeicosatetraenoic acids (HETEs), and epoxyeicosatrienoic acids (EETs). Eicosanoids exert different bioactivities and mechanisms involved in the inflammation and related cancer developments. A deeper understanding of eicosanoid biology may be advantageous in cancer treatment and help to define cellular targets for further therapeutic development.
    MeSH term(s) Humans ; Eicosanoids/metabolism ; Arachidonic Acid/metabolism ; Neoplasms/metabolism ; Leukotrienes ; Inflammation/metabolism ; Cyclooxygenase 2
    Chemical Substances Eicosanoids ; Arachidonic Acid (27YG812J1I) ; Leukotrienes ; Cyclooxygenase 2 (EC 1.14.99.1)
    Language English
    Publishing date 2023-05-29
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 194735-7
    ISSN 1879-016X ; 0163-7258
    ISSN (online) 1879-016X
    ISSN 0163-7258
    DOI 10.1016/j.pharmthera.2023.108455
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