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  1. Article ; Online: Metastatic colorectal cancer: mechanisms and emerging therapeutics.

    Shin, Alice E / Giancotti, Filippo G / Rustgi, Anil K

    Trends in pharmacological sciences

    2023  Volume 44, Issue 4, Page(s) 222–236

    Abstract: Metastatic colorectal cancer (mCRC) remains a lethal disease with an approximately 14% 5-year survival rate. While early-stage colorectal cancer (CRC) can be cured by surgery with or without adjuvant chemotherapy, mCRC cannot be eradicated due to a large ...

    Abstract Metastatic colorectal cancer (mCRC) remains a lethal disease with an approximately 14% 5-year survival rate. While early-stage colorectal cancer (CRC) can be cured by surgery with or without adjuvant chemotherapy, mCRC cannot be eradicated due to a large burden of disseminated cancer cells comprising therapy-resistant metastasis-competent cells. To address this gap, recent studies have focused on further elucidating the molecular mechanisms underlying colorectal metastasis and recognizing the limitations of available therapeutic interventions. In this review, we discuss newfound factors that regulate CRC cell dissemination and colonization of distant organs, such as genetic mutations, identification of metastasis-initiating cells (MICs), epithelial-mesenchymal transition (EMT), and the tumor microenvironment (TME). We also review current treatments for mCRC, therapeutic regimens undergoing clinical trials, and trending preclinical studies being investigated to target treatment-resistant mCRC.
    MeSH term(s) Humans ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Epithelial-Mesenchymal Transition ; Tumor Microenvironment
    Language English
    Publishing date 2023-02-23
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 282846-7
    ISSN 1873-3735 ; 0165-6147
    ISSN (online) 1873-3735
    ISSN 0165-6147
    DOI 10.1016/j.tips.2023.01.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1513: Show issues Location:
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  2. Article ; Online: Integrin Signaling in Cancer: Mechanotransduction, Stemness, Epithelial Plasticity, and Therapeutic Resistance.

    Cooper, Jonathan / Giancotti, Filippo G

    Cancer cell

    2019  Volume 35, Issue 3, Page(s) 347–367

    Abstract: Integrins mediate cell adhesion and transmit mechanical and chemical signals to the cell interior. Various mechanisms deregulate integrin signaling in cancer, empowering tumor cells with the ability to proliferate without restraint, to invade through ... ...

    Abstract Integrins mediate cell adhesion and transmit mechanical and chemical signals to the cell interior. Various mechanisms deregulate integrin signaling in cancer, empowering tumor cells with the ability to proliferate without restraint, to invade through tissue boundaries, and to survive in foreign microenvironments. Recent studies have revealed that integrin signaling drives multiple stem cell functions, including tumor initiation, epithelial plasticity, metastatic reactivation, and resistance to oncogene- and immune-targeted therapies. Here, we discuss the mechanisms leading to the deregulation of integrin signaling in cancer and its various consequences. We place emphasis on novel functions, determinants of context dependency, and mechanism-based therapeutic opportunities.
    MeSH term(s) Cell Plasticity ; Drug Resistance, Neoplasm ; Gene Expression Regulation, Neoplastic ; Humans ; Integrins/metabolism ; Mechanotransduction, Cellular ; Neoplasms/metabolism ; Neoplastic Stem Cells/metabolism ; Signal Transduction
    Chemical Substances Integrins
    Language English
    Publishing date 2019-03-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 2078448-X
    ISSN 1878-3686 ; 1535-6108
    ISSN (online) 1878-3686
    ISSN 1535-6108
    DOI 10.1016/j.ccell.2019.01.007
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  3. Article: Noncanonical Activity of Med4 as a Gatekeeper of Metastasis through Epigenetic Control of Integrin Signaling.

    Bae, Seong-Yeon / Chen, Yi / Chen, Hong / Kumar, Dhiraj / Karaiskos, Spyros / Xu, Jane / Lu, Chao / Viny, Aaron D / Giancotti, Filippo G

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Breast cancer metastatic relapse after a latency period, known as metastatic dormancy. Through genetic screening in mice, we identified the mediator complex subunit 4 ( ...

    Abstract Breast cancer metastatic relapse after a latency period, known as metastatic dormancy. Through genetic screening in mice, we identified the mediator complex subunit 4 (
    Language English
    Publishing date 2024-01-10
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.11.18.566087
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  4. Article ; Online: Deregulation of cell signaling in cancer.

    Giancotti, Filippo G

    FEBS letters

    2014  Volume 588, Issue 16, Page(s) 2558–2570

    Abstract: Oncogenic mutations disrupt the regulatory circuits that govern cell function, enabling tumor cells to undergo de-regulated mitogenesis, to resist to pro-apoptotic insults, and to invade through tissue boundaries. Cancer cell biology has played a crucial ...

    Abstract Oncogenic mutations disrupt the regulatory circuits that govern cell function, enabling tumor cells to undergo de-regulated mitogenesis, to resist to pro-apoptotic insults, and to invade through tissue boundaries. Cancer cell biology has played a crucial role in elucidating the signaling mechanisms by which oncogenic mutations sustain these malignant behaviors and thereby in identifying rational targets for cancer drugs. The efficacy of such targeted therapies illustrate the power of a reductionist approach to the study of cancer.
    MeSH term(s) Animals ; Cell Proliferation ; Humans ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplastic Stem Cells/pathology ; Signal Transduction
    Language English
    Publishing date 2014-02-20
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 212746-5
    ISSN 1873-3468 ; 0014-5793
    ISSN (online) 1873-3468
    ISSN 0014-5793
    DOI 10.1016/j.febslet.2014.02.005
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  5. Article ; Online: Editorial overview: Cell signalling: Signal transduction to the nucleus, cytoskeleton, and organelles.

    Thompson, Barry J / Giancotti, Filippo G

    Current opinion in cell biology

    2018  Volume 51, Page(s) iv–vii

    Language English
    Publishing date 2018-05-11
    Publishing country England
    Document type Editorial
    ZDB-ID 1026381-0
    ISSN 1879-0410 ; 0955-0674
    ISSN (online) 1879-0410
    ISSN 0955-0674
    DOI 10.1016/j.ceb.2018.04.005
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  6. Article ; Online: Mechanisms governing metastatic dormancy and reactivation.

    Giancotti, Filippo G

    Cell

    2013  Volume 155, Issue 4, Page(s) 750–764

    Abstract: Many cancer patients suffer from metastatic relapse several years after they have undergone radical surgery. Early cancer cell dissemination followed by a protracted period of dormancy potentially explains this prevalent clinical behavior. Increasing ... ...

    Abstract Many cancer patients suffer from metastatic relapse several years after they have undergone radical surgery. Early cancer cell dissemination followed by a protracted period of dormancy potentially explains this prevalent clinical behavior. Increasing evidence suggests that the metastasis-initiating cells are cancer stem cells or revert to this functional state upon infiltrating a target organ. Their entry into dormancy and subsequent reactivation are governed by intrinsic programs and by contextual cues, which resemble those regulating the self-renewal capability of adult stem cells. In addition, metastatic cells undergoing reactivation are nursed by specialized extracellular matrix niches, which support positive signals, such as Wnt and Notch, and attenuate negative signals, such as BMP. In spite of significant remaining uncertainties, these findings provide a framework to understand the logic of metastatic dormancy and reactivation and open new avenues for therapeutic intervention.
    MeSH term(s) Animals ; Extracellular Matrix/metabolism ; Extracellular Matrix/pathology ; Humans ; Neoplasm Metastasis/pathology ; Neoplasms/pathology ; Neoplasms/therapy ; Neoplastic Stem Cells/pathology
    Language English
    Publishing date 2013-11-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2013.10.029
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  7. Article ; Online: Cancer: a new role for non-canonical Hippo signaling.

    Cooper, Jonathan / Giancotti, Filippo G

    Cell research

    2017  Volume 27, Issue 4, Page(s) 459–460

    Abstract: The molecular mechanisms governing self-renewal and differentiation of the mammary epithelium are incompletely defined; a better understanding of the events implicated in the specification and expansion of luminal progenitors is of particular importance ... ...

    Abstract The molecular mechanisms governing self-renewal and differentiation of the mammary epithelium are incompletely defined; a better understanding of the events implicated in the specification and expansion of luminal progenitors is of particular importance as many breast cancers originate from their transformation. Britschgi et al. found that, in addition to phosphorylating and inactivating YAP, LATS functions as a scaffold to facilitate estrogen receptor-α ubiquitylation by the E3 ligase CRL4 and consequently suppresses luminal progenitor specification and expansion.
    MeSH term(s) Breast ; Cell Differentiation ; Estrogen Receptor alpha ; Humans ; Protein-Serine-Threonine Kinases ; Signal Transduction
    Chemical Substances Estrogen Receptor alpha ; LATS1 protein, human (EC 2.7.1.-) ; Hippo protein, human (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2017-02-28
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 1319303-x
    ISSN 1748-7838 ; 1001-0602
    ISSN (online) 1748-7838
    ISSN 1001-0602
    DOI 10.1038/cr.2017.27
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    Zs.A 5283: Show issues Location:
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  8. Article ; Online: Clonal Evolution and Epithelial Plasticity in the Emergence of AR-Independent Prostate Carcinoma.

    Laudato, Sara / Aparicio, Ana / Giancotti, Filippo G

    Trends in cancer

    2019  Volume 5, Issue 7, Page(s) 440–455

    Abstract: In spite of an initial clinical response to androgen deprivation therapy (ADT), the majority of prostate cancer patients eventually develop castration-resistant prostate cancer (CRPC). Recent studies have highlighted the role of epithelial plasticity, ... ...

    Abstract In spite of an initial clinical response to androgen deprivation therapy (ADT), the majority of prostate cancer patients eventually develop castration-resistant prostate cancer (CRPC). Recent studies have highlighted the role of epithelial plasticity, including transdifferentiation and epithelial-to-mesenchymal transition (EMT), in the development of AR pathway-negative CRPC, a form of the disease that has increased in incidence after the introduction of potent AR inhibitors. In this review, we will discuss the switches between different cell fates that occur in response to AR blockade or acquisition of specific oncogenic mutations, such as those in TP53 and RB1, during the evolution to CRPC. We highlight the urgent need to dissect the mechanistic underpinnings of these transitions and identify novel vulnerabilities that can be targeted therapeutically.
    MeSH term(s) Antineoplastic Agents, Hormonal/pharmacology ; Antineoplastic Agents, Hormonal/therapeutic use ; Cell Plasticity ; Clonal Evolution ; Drug Resistance, Neoplasm/genetics ; Epithelial-Mesenchymal Transition/genetics ; Epithelium/metabolism ; Epithelium/pathology ; Humans ; Male ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/etiology ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Receptors, Androgen/metabolism
    Chemical Substances Antineoplastic Agents, Hormonal ; Receptors, Androgen
    Language English
    Publishing date 2019-06-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2852626-0
    ISSN 2405-8025 ; 2405-8033 ; 2405-8033
    ISSN (online) 2405-8025 ; 2405-8033
    ISSN 2405-8033
    DOI 10.1016/j.trecan.2019.05.008
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  9. Article: Deregulation of cell signaling in cancer

    Giancotti, Filippo G

    Federation of European Biochemical Societies FEBS letters. 2014 Aug. 19, v. 588, no. 16

    2014  

    Abstract: Oncogenic mutations disrupt the regulatory circuits that govern cell function, enabling tumor cells to undergo de-regulated mitogenesis, to resist to pro-apoptotic insults, and to invade through tissue boundaries. Cancer cell biology has played a crucial ...

    Abstract Oncogenic mutations disrupt the regulatory circuits that govern cell function, enabling tumor cells to undergo de-regulated mitogenesis, to resist to pro-apoptotic insults, and to invade through tissue boundaries. Cancer cell biology has played a crucial role in elucidating the signaling mechanisms by which oncogenic mutations sustain these malignant behaviors and thereby in identifying rational targets for cancer drugs. The efficacy of such targeted therapies illustrate the power of a reductionist approach to the study of cancer.
    Keywords apoptosis ; drugs ; mitogenesis ; mutation ; neoplasm cells ; neoplasms
    Language English
    Dates of publication 2014-0819
    Size p. 2558-2570.
    Publishing place Elsevier B.V.
    Document type Article
    ZDB-ID 212746-5
    ISSN 1873-3468 ; 0014-5793
    ISSN (online) 1873-3468
    ISSN 0014-5793
    DOI 10.1016/j.febslet.2014.02.005
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  10. Article ; Online: Guido Tarone, Ph.D. (1951-2015).

    Giancotti, Filippo G / Fässler, Reinhard

    Journal of cell science

    2015  Volume 128, Issue 16, Page(s) 2955–2956

    MeSH term(s) Cell Biology/history ; History, 20th Century ; History, 21st Century ; Humans
    Language English
    Publishing date 2015-10-23
    Publishing country England
    Document type Biography ; Historical Article ; Journal Article
    ZDB-ID 2993-2
    ISSN 1477-9137 ; 0021-9533
    ISSN (online) 1477-9137
    ISSN 0021-9533
    DOI 10.1242/jcs.175919
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