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  1. Article ; Online: The genomic regulation of metastatic dormancy.

    Gelman, Irwin H

    Cancer metastasis reviews

    2023  Volume 42, Issue 1, Page(s) 255–276

    Abstract: The genomics and pathways governing metastatic dormancy are critically important drivers of long-term patient survival given the considerable portion of cancers that recur aggressively months to years after initial treatments. Our understanding of ... ...

    Abstract The genomics and pathways governing metastatic dormancy are critically important drivers of long-term patient survival given the considerable portion of cancers that recur aggressively months to years after initial treatments. Our understanding of dormancy has expanded greatly in the last two decades, with studies elucidating that the dormant state is regulated by multiple genes, microenvironmental (ME) interactions, and immune components. These forces are exerted through mechanisms that are intrinsic to the tumor cell, manifested through cross-talk between tumor and ME cells including those from the immune system, and regulated by angiogenic processes in the nascent micrometastatic niche. The development of new in vivo and 3D ME models, as well as enhancements to decades-old tumor cell pedigree models that span the development of metastatic dormancy to aggressive growth, has helped fuel what arguably is one of the least understood areas of cancer biology that nonetheless contributes immensely to patient mortality. The current review focuses on the genes and molecular pathways that regulate dormancy via tumor-intrinsic and ME cells, and how groups have envisioned harnessing these therapeutically to benefit patient survival.
    MeSH term(s) Humans ; Neoplasms/pathology ; Genomics
    Language English
    Publishing date 2023-01-05
    Publishing country Netherlands
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 604857-2
    ISSN 1573-7233 ; 0167-7659
    ISSN (online) 1573-7233
    ISSN 0167-7659
    DOI 10.1007/s10555-022-10076-w
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  2. Article ; Online: Metastasis suppressor genes in clinical practice: are they druggable?

    Gelman, Irwin H

    Cancer metastasis reviews

    2023  Volume 42, Issue 4, Page(s) 1169–1188

    Abstract: Since the identification of NM23 (now called NME1) as the first metastasis suppressor gene (MSG), a small number of other gene products and non-coding RNAs have been identified that suppress specific parameters of the metastatic cascade, yet which have ... ...

    Abstract Since the identification of NM23 (now called NME1) as the first metastasis suppressor gene (MSG), a small number of other gene products and non-coding RNAs have been identified that suppress specific parameters of the metastatic cascade, yet which have little or no ability to regulate primary tumor initiation or maintenance. MSG can regulate various pathways or cell biological functions such as those controlling mitogen-activated protein kinase pathway mediators, cell-cell and cell-extracellular matrix protein adhesion, cytoskeletal architecture, G-protein-coupled receptors, apoptosis, and transcriptional complexes. One defining facet of this gene class is that their expression is typically downregulated, not mutated, in metastasis, such that any effective therapeutic intervention would involve their re-expression. This review will address the therapeutic targeting of MSG, once thought to be a daunting task only facilitated by ectopically re-expressing MSG in metastatic cells in vivo. Examples will be cited of attempts to identify actionable oncogenic pathways that might suppress the formation or progression of metastases through the re-expression of specific metastasis suppressors.
    MeSH term(s) Humans ; Genes, Tumor Suppressor ; NM23 Nucleoside Diphosphate Kinases/genetics ; NM23 Nucleoside Diphosphate Kinases/metabolism ; Neoplasm Metastasis
    Chemical Substances NM23 Nucleoside Diphosphate Kinases
    Language English
    Publishing date 2023-09-25
    Publishing country Netherlands
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 604857-2
    ISSN 1573-7233 ; 0167-7659
    ISSN (online) 1573-7233
    ISSN 0167-7659
    DOI 10.1007/s10555-023-10135-w
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  3. Article ; Online: Emerging Roles for AKT Isoform Preference in Cancer Progression Pathways.

    Degan, Seamus E / Gelman, Irwin H

    Molecular cancer research : MCR

    2021  Volume 19, Issue 8, Page(s) 1251–1257

    Abstract: The phosphoinositol-3 kinase (PI3K)-AKT pathway is one of the most mutated in human cancers, predominantly associated with the loss of the signaling antagonist, PTEN, and to lesser extents, with gain-of-function mutations in PIK3CA (encoding PI3K-p110α) ... ...

    Abstract The phosphoinositol-3 kinase (PI3K)-AKT pathway is one of the most mutated in human cancers, predominantly associated with the loss of the signaling antagonist, PTEN, and to lesser extents, with gain-of-function mutations in PIK3CA (encoding PI3K-p110α) and AKT1. In addition, most oncogenic driver pathways activate PI3K/AKT signaling. Nonetheless, drugs targeting PI3K or AKT have fared poorly against solid tumors in clinical trials as monotherapies, yet some have shown efficacy when combined with inhibitors of other oncogenic drivers, such as receptor tyrosine kinases or nuclear hormone receptors. There is growing evidence that AKT isoforms, AKT1, AKT2, and AKT3, have different, often distinct roles in either promoting or suppressing specific parameters of oncogenic progression, yet few if any isoform-preferred substrates have been characterized. This review will describe recent data showing that the differential activation of AKT isoforms is mediated by complex interplays between PTEN, PI3K isoforms and upstream tyrosine kinases, and that the efficacy of PI3K/AKT inhibitors will likely depend on the successful targeting of specific AKT isoforms and their preferred pathways.
    MeSH term(s) Animals ; Disease Progression ; Humans ; Neoplasms/genetics ; Neoplasms/pathology ; Oncogenes/genetics ; Phosphatidylinositol 3-Kinases/genetics ; Protein Isoforms/genetics ; Proto-Oncogene Proteins c-akt/genetics ; Signal Transduction/genetics
    Chemical Substances Protein Isoforms ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2021-04-30
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2098788-2
    ISSN 1557-3125 ; 1541-7786
    ISSN (online) 1557-3125
    ISSN 1541-7786
    DOI 10.1158/1541-7786.MCR-20-1066
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  4. Article ; Online: How the TRAMP Model Revolutionized the Study of Prostate Cancer Progression.

    Gelman, Irwin H

    Cancer research

    2016  Volume 76, Issue 21, Page(s) 6137–6139

    MeSH term(s) Animals ; Disease Models, Animal ; Disease Progression ; History, 20th Century ; Humans ; Male ; Mice ; Mice, Transgenic ; Prostatic Neoplasms/history ; Prostatic Neoplasms/pathology
    Language English
    Publishing date 2016--01
    Publishing country United States
    Document type Historical Article ; Journal Article
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-16-2636
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  5. Article: Role of A-Kinase Anchoring Protein 12 in the Central Nervous System.

    Kimura, Shintaro / Lok, Josephine / Gelman, Irwin H / Lo, Eng H / Arai, Ken

    Journal of clinical neurology (Seoul, Korea)

    2023  Volume 19, Issue 4, Page(s) 329–337

    Abstract: A-kinase anchoring protein (AKAP) 12 is a scaffolding protein that anchors various signaling proteins to the plasma membrane. These signaling proteins include protein kinase A, protein kinase C, protein phosphatase 2B, Src-family kinases, cyclins, and ... ...

    Abstract A-kinase anchoring protein (AKAP) 12 is a scaffolding protein that anchors various signaling proteins to the plasma membrane. These signaling proteins include protein kinase A, protein kinase C, protein phosphatase 2B, Src-family kinases, cyclins, and calmodulin, which regulate their respective signaling pathways. AKAP12 expression is observed in the neurons, astrocytes, endothelial cells, pericytes, and oligodendrocytes of the central nervous system (CNS). Its physiological roles include promoting the development of the blood-brain barrier, maintaining white-matter homeostasis, and even regulating complex cognitive functions such as long-term memory formation. Under pathological conditions, dysregulation of AKAP12 expression levels may be involved in the pathology of neurological diseases such as ischemic brain injury and Alzheimer's disease. This minireview aimed to summarize the current literature on the role of AKAP12 in the CNS.
    Language English
    Publishing date 2023-07-05
    Publishing country Korea (South)
    Document type Journal Article ; Review
    ZDB-ID 2500489-X
    ISSN 2005-5013 ; 1738-6586
    ISSN (online) 2005-5013
    ISSN 1738-6586
    DOI 10.3988/jcn.2023.0095
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  6. Article ; Online: Correction: PTEN-regulated PI3K-p110 and AKT isoform plasticity controls metastatic prostate cancer progression.

    Miller, Karina A / Degan, Seamus / Wang, Yanqing / Cohen, Joseph / Ku, Sheng Yu / Goodrich, David W / Gelman, Irwin H

    Oncogene

    2023  Volume 43, Issue 1, Page(s) 76

    Language English
    Publishing date 2023-12-14
    Publishing country England
    Document type Published Erratum
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/s41388-023-02920-2
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  7. Article ; Online: Phosphohistidine signaling promotes FAK-RB1 interaction and growth factor-independent proliferation of esophageal squamous cell carcinoma.

    Zhang, Jianliang / Gelman, Irwin H / Qu, Jun / Hochwald, Steven N

    Oncogene

    2022  Volume 42, Issue 6, Page(s) 449–460

    Abstract: Current clinical therapies targeting receptor tyrosine kinases including focal adhesion kinase (FAK) have had limited or no effect on esophageal squamous cell carcinoma (ESCC). Unlike esophageal adenocarcinomas, ESCC acquire glucose in excess of their ... ...

    Abstract Current clinical therapies targeting receptor tyrosine kinases including focal adhesion kinase (FAK) have had limited or no effect on esophageal squamous cell carcinoma (ESCC). Unlike esophageal adenocarcinomas, ESCC acquire glucose in excess of their anabolic need. We recently reported that glucose-induced growth factor-independent proliferation requires the phosphorylation of FAK
    MeSH term(s) Humans ; Cell Line, Tumor ; Cell Proliferation ; Esophageal Neoplasms/pathology ; Esophageal Squamous Cell Carcinoma/pathology ; Focal Adhesion Protein-Tyrosine Kinases/metabolism ; Glucose ; Intercellular Signaling Peptides and Proteins/metabolism ; Phosphorylation ; Retinoblastoma Binding Proteins/metabolism ; Ubiquitin-Protein Ligases/metabolism
    Chemical Substances Focal Adhesion Protein-Tyrosine Kinases (EC 2.7.10.2) ; Glucose (IY9XDZ35W2) ; Intercellular Signaling Peptides and Proteins ; phosphohistidine (UKY8AGM174) ; RB1 protein, human ; Retinoblastoma Binding Proteins ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; PTK2 protein, human (EC 2.7.10.2)
    Language English
    Publishing date 2022-12-13
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/s41388-022-02568-4
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  8. Article ; Online: PTEN-regulated PI3K-p110 and AKT isoform plasticity controls metastatic prostate cancer progression.

    Miller, Karina A / Degan, Seamus / Wang, Yanqing / Cohen, Joseph / Ku, Sheng Yu / Goodrich, David W / Gelman, Irwin H

    Oncogene

    2023  Volume 43, Issue 1, Page(s) 22–34

    Abstract: PTEN loss, one of the most frequent mutations in prostate cancer (PC), is presumed to drive disease progression through AKT activation. However, two transgenic PC models with Akt activation plus Rb loss exhibited different metastatic development: Pten/ ... ...

    Abstract PTEN loss, one of the most frequent mutations in prostate cancer (PC), is presumed to drive disease progression through AKT activation. However, two transgenic PC models with Akt activation plus Rb loss exhibited different metastatic development: Pten/Rb
    MeSH term(s) Humans ; Male ; Mice ; Animals ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Isoforms/metabolism ; Prostatic Neoplasms/pathology ; Prostatic Intraepithelial Neoplasia ; PTEN Phosphohydrolase/metabolism ; Cell Cycle Proteins/metabolism ; A Kinase Anchor Proteins/metabolism
    Chemical Substances Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Protein Isoforms ; PTEN Phosphohydrolase (EC 3.1.3.67) ; PTEN protein, human (EC 3.1.3.67) ; Akap12 protein, mouse ; Cell Cycle Proteins ; A Kinase Anchor Proteins
    Language English
    Publishing date 2023-10-24
    Publishing country England
    Document type Journal Article
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/s41388-023-02875-4
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  9. Article ; Online: Androgen receptor activation in castration-recurrent prostate cancer: the role of Src-family and Ack1 tyrosine kinases.

    Gelman, Irwin H

    International journal of biological sciences

    2014  Volume 10, Issue 6, Page(s) 620–626

    Abstract: There is growing appreciation that castration-recurrent prostate cancer (CR-CaP) is driven by the continued expression of androgen receptor (AR). AR activation in CR-CaP through various mechanisms, including AR overexpression, expression of AR splice ... ...

    Abstract There is growing appreciation that castration-recurrent prostate cancer (CR-CaP) is driven by the continued expression of androgen receptor (AR). AR activation in CR-CaP through various mechanisms, including AR overexpression, expression of AR splice variants or mutants, increased expression of co-regulator proteins, and by post-translational modification, allows for the induction of AR-regulated genes in response to very low levels of tissue-expressed, so-called intracrine androgens, resulting in pathways that mediate CaP proliferation, anti-apoptosis and oncogenic aggressiveness. The current review focuses on the role played by Src-family (SFK) and Ack1 non-receptor tyrosine kinases in activating AR through direct phosphorylation, respectively, on tyrosines 534 or 267, and how these modifications facilitate progression to CR-CaP. The fact that SFK and Ack1 are central mediators for multiple growth factor receptor signaling pathways that become activated in CR-CaP, especially in the context of metastatic growth in the bone, has contributed to recent therapeutic trials using SFK/Ack1 inhibitors in monotherapy or in combination with antagonists of the AR activation axis.
    MeSH term(s) Androgens/metabolism ; Animals ; Humans ; Male ; Prostatic Neoplasms, Castration-Resistant/metabolism ; Protein-Tyrosine Kinases/metabolism ; Receptors, Androgen/metabolism ; Signal Transduction
    Chemical Substances AR protein, human ; Androgens ; Receptors, Androgen ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; TNK2 protein, human (EC 2.7.10.2)
    Language English
    Publishing date 2014-06-05
    Publishing country Australia
    Document type Journal Article ; Review
    ZDB-ID 2179208-2
    ISSN 1449-2288 ; 1449-2288
    ISSN (online) 1449-2288
    ISSN 1449-2288
    DOI 10.7150/ijbs.8264
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  10. Article ; Online: Suppression of tumor and metastasis progression through the scaffolding functions of SSeCKS/Gravin/AKAP12.

    Gelman, Irwin H

    Cancer metastasis reviews

    2012  Volume 31, Issue 3-4, Page(s) 493–500

    Abstract: Scaffolding proteins such as SSeCKS/Gravin/AKAP12 ("AKAP12") are thought to control oncogenic signaling pathways by regulating key mediators in a spatiotemporal manner. The downregulation of AKAP12 in many human cancers, often associated with promoter ... ...

    Abstract Scaffolding proteins such as SSeCKS/Gravin/AKAP12 ("AKAP12") are thought to control oncogenic signaling pathways by regulating key mediators in a spatiotemporal manner. The downregulation of AKAP12 in many human cancers, often associated with promoter hypermethylation, or the loss of its locus at 6q24-25.2, correlates with progression to malignancy and metastasis. The forced re-expression of AKAP12 in cancer cell lines suppresses in vitro parameters of oncogenic growth, invasiveness, and cell motility through its ability to scaffold protein kinase C (PKC), F-actin, cyclins, Src, and phosphoinositides, and possibly through additional scaffolding domains for PKA, calmodulin, β1,4-galactosyltransferase-polypeptide-1, β2-adrenergic receptors, and cAMP-specific 3',5'-cyclic phosphodiesterase 4D. Moreover, AKAP12 re-expression in tumor models results in metastasis suppression through the inhibition of Src-regulated, VEGF-mediated neovascularization at distal sites. The current review will describe the emerging understanding of how AKAP12 regulates cellular senescence and oncogenic progression at the level of tumor cells and tumor-associated microenvironment via its multiple scaffolding functions.
    MeSH term(s) A Kinase Anchor Proteins/physiology ; Animals ; Cell Cycle Proteins/physiology ; Cellular Senescence ; Disease Progression ; Humans ; Neoplasm Metastasis/prevention & control ; Neoplasms/metabolism ; Neoplasms/pathology ; Signal Transduction ; Tumor Microenvironment
    Chemical Substances A Kinase Anchor Proteins ; AKAP12 protein, human ; Cell Cycle Proteins
    Language English
    Publishing date 2012-06-09
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 604857-2
    ISSN 1573-7233 ; 0167-7659
    ISSN (online) 1573-7233
    ISSN 0167-7659
    DOI 10.1007/s10555-012-9360-1
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