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  1. Article: Professor Maurizio D'Incalci interviewed by Emma Cannell.

    D'Incalci, Maurizio

    European journal of cancer (Oxford, England : 1990)

    2002  Volume 38, Issue 12, Page(s) 1559

    MeSH term(s) Career Choice ; Humans ; Italy ; Medical Oncology
    Language English
    Publishing date 2002-08
    Publishing country England
    Document type Interview
    ZDB-ID 82061-1
    ISSN 1879-0852 ; 0959-8049 ; 0277-5379 ; 0964-1947
    ISSN (online) 1879-0852
    ISSN 0959-8049 ; 0277-5379 ; 0964-1947
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Editorial: Trabectedin, lurbinectedin, and other marine-derived anticancer alkaloids on solid cancer: Mechanisms of action, clinical impact, and future perspectives.

    Zambelli, Alberto / D'Incalci, Maurizio

    Frontiers in oncology

    2023  Volume 12, Page(s) 1115342

    Language English
    Publishing date 2023-01-25
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2022.1115342
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: In-Silico Identification of Novel Pharmacological Synergisms: The Trabectedin Case.

    Mannarino, Laura / Ravasio, Nicholas / D'Incalci, Maurizio / Marchini, Sergio / Masseroli, Marco

    International journal of molecular sciences

    2024  Volume 25, Issue 4

    Abstract: The in-silico strategy of identifying novel uses for already existing drugs, known as drug repositioning, has enhanced drug discovery. Previous studies have shown a positive correlation between expression changes induced by the anticancer agent ... ...

    Abstract The in-silico strategy of identifying novel uses for already existing drugs, known as drug repositioning, has enhanced drug discovery. Previous studies have shown a positive correlation between expression changes induced by the anticancer agent trabectedin and those caused by irinotecan, a topoisomerase I inhibitor. Leveraging the availability of transcriptional datasets, we developed a general in-silico drug-repositioning approach that we applied to investigate novel trabectedin synergisms. We set a workflow allowing the identification of genes selectively modulated by a drug and possible novel drug interactions. To show its effectiveness, we selected trabectedin as a case-study drug. We retrieved eight transcriptional cancer datasets including controls and samples treated with trabectedin or its analog lurbinectedin. We compared gene signature associated with each dataset to the 476,251 signatures from the Connectivity Map database. The most significant connections referred to mitomycin-c, topoisomerase II inhibitors, a PKC inhibitor, a Chk1 inhibitor, an antifungal agent, and an antagonist of the glutamate receptor. Genes coherently modulated by the drugs were involved in cell cycle, PPARalpha, and Rho GTPases pathways. Our in-silico approach for drug synergism identification showed that trabectedin modulates specific pathways that are shared with other drugs, suggesting possible synergisms.
    MeSH term(s) Trabectedin/pharmacology ; Trabectedin/therapeutic use ; Tetrahydroisoquinolines/pharmacology ; Dioxoles/pharmacology ; Antineoplastic Agents ; Drug Synergism
    Chemical Substances Trabectedin (ID0YZQ2TCP) ; Tetrahydroisoquinolines ; Dioxoles ; Antineoplastic Agents
    Language English
    Publishing date 2024-02-08
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms25042059
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Liquid Biopsy in the Clinical Management of High-Grade Serous Epithelial Ovarian Cancer-Current Use and Future Opportunities.

    Paracchini, Lara / D'Incalci, Maurizio / Marchini, Sergio

    Cancers

    2021  Volume 13, Issue 10

    Abstract: The lack of a sensitive and specific biomarker and the limits relating to the single primary tumor sampling make it difficult to monitor high-grade serous epithelial ovarian cancer (HGS-EOC) over time and to capture those alterations that are potentially ...

    Abstract The lack of a sensitive and specific biomarker and the limits relating to the single primary tumor sampling make it difficult to monitor high-grade serous epithelial ovarian cancer (HGS-EOC) over time and to capture those alterations that are potentially useful in guiding clinical decisions. To overcome these issues, liquid biopsy has emerged as a very promising tool for HGS-EOC. The analysis of circulating tumor DNA appears to be feasible and studies assessing specific pathogenic mutations (i.e.,
    Language English
    Publishing date 2021-05-14
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers13102386
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: DNA Damage Response and Immune Defense.

    Nastasi, Claudia / Mannarino, Laura / D'Incalci, Maurizio

    International journal of molecular sciences

    2020  Volume 21, Issue 20

    Abstract: DNA damage is the cause of numerous human pathologies including cancer, premature aging, and chronic inflammatory conditions. The DNA damage response (DDR), in turn, coordinates DNA damage checkpoint activation and promotes the removal of DNA lesions. In ...

    Abstract DNA damage is the cause of numerous human pathologies including cancer, premature aging, and chronic inflammatory conditions. The DNA damage response (DDR), in turn, coordinates DNA damage checkpoint activation and promotes the removal of DNA lesions. In recent years, several studies have shown how the DDR and the immune system are tightly connected, revealing an important crosstalk between the two of them. This interesting interplay has opened up new perspectives in clinical studies for immunological diseases as well as for cancer treatment. In this review, we provide an overview, from cellular to molecular pathways, on how DDR and the immune system communicate and share the crucial commitment of maintaining the genomic fitness.
    MeSH term(s) Animals ; Biomarkers ; DNA Damage ; Disease Susceptibility ; Host-Pathogen Interactions/genetics ; Host-Pathogen Interactions/immunology ; Humans ; Immunity ; Immunity, Innate ; Inflammation/etiology ; Inflammation/metabolism ; Molecular Targeted Therapy ; Neoplasms/drug therapy ; Neoplasms/etiology ; Neoplasms/radiotherapy ; Oxidative Stress ; Signal Transduction
    Chemical Substances Biomarkers
    Language English
    Publishing date 2020-10-12
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms21207504
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Effects of the Anti-Tumor Agents Trabectedin and Lurbinectedin on Immune Cells of the Tumor Microenvironment.

    Allavena, Paola / Belgiovine, Cristina / Digifico, Elisabeth / Frapolli, Roberta / D'Incalci, Maurizio

    Frontiers in oncology

    2022  Volume 12, Page(s) 851790

    Abstract: Immune cells in the tumor micro-environment (TME) establish a complex relationship with cancer cells and may strongly influence disease progression and response to therapy. It is well established that myeloid cells infiltrating tumor tissues favor cancer ...

    Abstract Immune cells in the tumor micro-environment (TME) establish a complex relationship with cancer cells and may strongly influence disease progression and response to therapy. It is well established that myeloid cells infiltrating tumor tissues favor cancer progression. Tumor-Associated Macrophages (TAMs) are abundantly present at the TME and actively promote cancer cell proliferation and distant spreading, as well as contribute to an immune-suppressive milieu. Active research of the last decade has provided novel therapeutic approaches aimed at depleting TAMs and/or at reprogramming their functional activities. We reported some years ago that the registered anti-tumor agent trabectedin and its analogue lurbinectedin have numerous mechanisms of action that also involve direct effects on immune cells, opening up new interesting points of view. Trabectedin and lurbinectedin share the unique feature of being able to simultaneously kill cancer cells and to affect several features of the TME, most notably by inducing the rapid and selective apoptosis of monocytes and macrophages, and by inhibiting the transcription of several inflammatory mediators. Furthermore, depletion of TAMs alleviates the immunosuppressive milieu and rescues T cell functional activities, thus enhancing the anti-tumor response to immunotherapy with checkpoint inhibitors. In view of the growing interest in tumor-infiltrating immune cells, the availability of antineoplastic compounds showing immunomodulatory effects on innate and adaptive immunity deserves particular attention in the oncology field.
    Language English
    Publishing date 2022-03-01
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2022.851790
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Trabectedin suppresses escape from therapy-induced senescence in tumor cells by interfering with glutamine metabolism.

    Pacifico, Francesco / Mellone, Stefano / D'Incalci, Maurizio / Stornaiuolo, Mariano / Leonardi, Antonio / Crescenzi, Elvira

    Biochemical pharmacology

    2022  Volume 202, Page(s) 115159

    Abstract: Conventional and targeted cancer therapies may induce a cellular senescence program termed therapy-induced senescence. However, unlike normal cells, cancer cells are able to evade the senescence cell cycle arrest and to resume proliferation, driving ... ...

    Abstract Conventional and targeted cancer therapies may induce a cellular senescence program termed therapy-induced senescence. However, unlike normal cells, cancer cells are able to evade the senescence cell cycle arrest and to resume proliferation, driving tumor recurrence after treatments. Cells that escape from therapy-induced senescence are characterized by a plastic, cancer stem cell-like phenotype, and recent studies are beginning to define their unique metabolic features, such as glutamine dependence. Here, we show that the antineoplastic drug trabectedin suppresses escape from therapy-induced senescence in all cell lines studied, and reduces breast cancer stem-like cells, at concentrations that do not affect the viability of senescent tumor cells. We demonstrate that trabectedin downregulates both the glutamine transporter SLC1A5 and glutamine synthetase, thereby interfering with glutamine metabolism. On the whole, our results indicate that trabectedin targets a glutamine-dependent cancer stem-like cell population involved in evasion from therapy-induced senescence and suggest a therapeutic potential for trabectedin combined with pro-senescence chemotherapy in tumor treatment.
    MeSH term(s) Amino Acid Transport System ASC/genetics ; Amino Acid Transport System ASC/metabolism ; Cell Cycle Checkpoints ; Cell Line, Tumor ; Cellular Senescence/physiology ; Glutamine/metabolism ; Humans ; Minor Histocompatibility Antigens/genetics ; Neoplasms/metabolism ; Neoplastic Stem Cells/pathology ; Trabectedin
    Chemical Substances Amino Acid Transport System ASC ; Minor Histocompatibility Antigens ; SLC1A5 protein, human ; Glutamine (0RH81L854J) ; Trabectedin (ID0YZQ2TCP)
    Language English
    Publishing date 2022-06-30
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 208787-x
    ISSN 1873-2968 ; 0006-2952
    ISSN (online) 1873-2968
    ISSN 0006-2952
    DOI 10.1016/j.bcp.2022.115159
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Book ; Conference proceedings: Heterogeneity of cancer cells

    D'Incalci, Maurizio

    [papers presented at the International Symposium on Heterogeneity of Cancer Cells in June 1992, held ... in Milan]

    (Serono Symposia publications from Raven Press ; 95)

    1993  

    Event/congress International Symposium on Heterogeneity of Cancer Cells (1992, Mailand)
    Author's details ed. Maurizio d'Incalci
    Series title Serono Symposia publications from Raven Press ; 95
    Collection
    Keywords Neoplasms / pathology / congresses
    Language English
    Size XII, 142 S. : Ill., graph. Darst.
    Publisher Raven Press
    Publishing place New York
    Publishing country United States
    Document type Book ; Conference proceedings
    HBZ-ID HT006266428
    ISBN 0-88167-907-0 ; 978-0-88167-907-6
    Database Catalogue ZB MED Medicine, Health

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  9. Article ; Online: DNA Damage Response and Immune Defense

    Claudia Nastasi / Laura Mannarino / Maurizio D’Incalci

    International Journal of Molecular Sciences, Vol 21, Iss 7504, p

    2020  Volume 7504

    Abstract: DNA damage is the cause of numerous human pathologies including cancer, premature aging, and chronic inflammatory conditions. The DNA damage response (DDR), in turn, coordinates DNA damage checkpoint activation and promotes the removal of DNA lesions. In ...

    Abstract DNA damage is the cause of numerous human pathologies including cancer, premature aging, and chronic inflammatory conditions. The DNA damage response (DDR), in turn, coordinates DNA damage checkpoint activation and promotes the removal of DNA lesions. In recent years, several studies have shown how the DDR and the immune system are tightly connected, revealing an important crosstalk between the two of them. This interesting interplay has opened up new perspectives in clinical studies for immunological diseases as well as for cancer treatment. In this review, we provide an overview, from cellular to molecular pathways, on how DDR and the immune system communicate and share the crucial commitment of maintaining the genomic fitness.
    Keywords DNA damage response ; DNA repair ; immune defense ; immune signalling ; innate immunity ; cancer ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Language English
    Publishing date 2020-10-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: Trabectedin for the treatment of breast cancer.

    D'Incalci, Maurizio / Zambelli, Alberto

    Expert opinion on investigational drugs

    2016  Volume 25, Issue 1, Page(s) 105–115

    Abstract: Introduction: Trabectedin is an anti-tumor compound registered in Europe and in several other countries, for the second-line treatment of soft tissue sarcoma (STS) and for ovarian cancer in combination with liposomal doxorubicin. Trabectedin inhibits ... ...

    Abstract Introduction: Trabectedin is an anti-tumor compound registered in Europe and in several other countries, for the second-line treatment of soft tissue sarcoma (STS) and for ovarian cancer in combination with liposomal doxorubicin. Trabectedin inhibits cancer cell proliferation mainly affecting the transcription regulation. Trabectedin also acts as a modulator of tumor microenvironment by reducing the number of tumor associated macrophages (TAM). Because of its unique mechanism of action, trabectedin has the potential to act as antineoplastic agent also in several solid malignancies, including breast cancer (BC).
    Areas covered: This article reviews the preclinical and clinical data of trabectedin focusing on development in metastatic BC (mBC). Comments regarding the nature and the results of these trials are included.
    Expert opinion: Trabectedin is thought to have a crucial activity with defective DNA-repair machinery and also in modulating the tumor micro-environment and the immune-system of cancer patients. From the current available data, we recognize a potential activity of trabectedin in mBC and support the renewed efforts to better elucidate the value of trabectedin in this indication.
    MeSH term(s) Animals ; Antineoplastic Agents, Alkylating/pharmacology ; Antineoplastic Agents, Alkylating/therapeutic use ; Breast Neoplasms/drug therapy ; Breast Neoplasms/pathology ; DNA Repair/drug effects ; Dioxoles/pharmacology ; Dioxoles/therapeutic use ; Female ; Humans ; Neoplasm Metastasis ; Tetrahydroisoquinolines/pharmacology ; Tetrahydroisoquinolines/therapeutic use ; Tumor Microenvironment/drug effects
    Chemical Substances Antineoplastic Agents, Alkylating ; Dioxoles ; Tetrahydroisoquinolines ; trabectedin (ID0YZQ2TCP)
    Language English
    Publishing date 2016
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1182884-5
    ISSN 1744-7658 ; 0967-8298 ; 1354-3784
    ISSN (online) 1744-7658
    ISSN 0967-8298 ; 1354-3784
    DOI 10.1517/13543784.2016.1124086
    Database MEDical Literature Analysis and Retrieval System OnLINE

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