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  1. Article: The CRISP(Y) Future of Pediatric Soft Tissue Sarcomas.

    Pomella, Silvia / Rota, Rossella

    Frontiers in chemistry

    2020  Volume 8, Page(s) 178

    Abstract: The RNA-guided clustered regularly interspaced palindromic repeats (CRISPR)/associated nuclease 9 (Cas9)-based genome editing technology has increasingly become a recognized method for translational research. In oncology, the ease and versatility of ... ...

    Abstract The RNA-guided clustered regularly interspaced palindromic repeats (CRISPR)/associated nuclease 9 (Cas9)-based genome editing technology has increasingly become a recognized method for translational research. In oncology, the ease and versatility of CRISPR/Cas9 has made it possible to obtain many results in the identification of new target genes and in unravel mechanisms of resistance to therapy. The majority of the studies have been made on adult tumors so far. In this mini review we present an overview on the major aspects of CRISPR/Cas9 technology with a focus on a group of rare pediatric malignancies, soft tissue sarcomas, on which this approach is having promising results.
    Language English
    Publishing date 2020-03-13
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2711776-5
    ISSN 2296-2646
    ISSN 2296-2646
    DOI 10.3389/fchem.2020.00178
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  2. Article ; Online: The CRISP(Y) Future of Pediatric Soft Tissue Sarcomas

    Silvia Pomella / Rossella Rota

    Frontiers in Chemistry, Vol

    2020  Volume 8

    Abstract: The RNA-guided clustered regularly interspaced palindromic repeats (CRISPR)/associated nuclease 9 (Cas9)-based genome editing technology has increasingly become a recognized method for translational research. In oncology, the ease and versatility of ... ...

    Abstract The RNA-guided clustered regularly interspaced palindromic repeats (CRISPR)/associated nuclease 9 (Cas9)-based genome editing technology has increasingly become a recognized method for translational research. In oncology, the ease and versatility of CRISPR/Cas9 has made it possible to obtain many results in the identification of new target genes and in unravel mechanisms of resistance to therapy. The majority of the studies have been made on adult tumors so far. In this mini review we present an overview on the major aspects of CRISPR/Cas9 technology with a focus on a group of rare pediatric malignancies, soft tissue sarcomas, on which this approach is having promising results.
    Keywords CRISPR/Cas9 ; sarcoma ; enhancers ; chromosomal translocation ; mice models ; Chemistry ; QD1-999
    Language English
    Publishing date 2020-03-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: DNA repair in tumor radioresistance: insights from fruit flies genetics.

    Porrazzo, Antonella / Cassandri, Matteo / D'Alessandro, Andrea / Morciano, Patrizia / Rota, Rossella / Marampon, Francesco / Cenci, Giovanni

    Cellular oncology (Dordrecht)

    2023  

    Abstract: Background: Radiation therapy (RT) is a key anti-cancer treatment that involves using ionizing radiation to kill tumor cells. However, this therapy can lead to short- and long-term adverse effects due to radiation exposure of surrounding normal tissue. ... ...

    Abstract Background: Radiation therapy (RT) is a key anti-cancer treatment that involves using ionizing radiation to kill tumor cells. However, this therapy can lead to short- and long-term adverse effects due to radiation exposure of surrounding normal tissue. The type of DNA damage inflicted by radiation therapy determines its effectiveness. High levels of genotoxic damage can lead to cell cycle arrest, senescence, and cell death, but many tumors can cope with this damage by activating protective mechanisms. Intrinsic and acquired radioresistance are major causes of tumor recurrence, and understanding these mechanisms is crucial for cancer therapy. The mechanisms behind radioresistance involve processes like hypoxia response, cell proliferation, DNA repair, apoptosis inhibition, and autophagy.
    Conclusion: Here we briefly review the role of genetic and epigenetic factors involved in the modulation of DNA repair and DNA damage response that promote radioresistance. In addition, leveraging our recent results on the effects of low dose rate (LDR) of ionizing radiation on Drosophila melanogaster we discuss how this model organism can be instrumental in the identification of conserved factors involved in the tumor resistance to RT.
    Language English
    Publishing date 2023-12-14
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 2595109-9
    ISSN 2211-3436 ; 1875-8606 ; 2211-3428
    ISSN (online) 2211-3436
    ISSN 1875-8606 ; 2211-3428
    DOI 10.1007/s13402-023-00906-6
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  4. Article ; Online: New Insights on the Nuclear Functions and Targeting of FAK in Cancer.

    Pomella, Silvia / Cassandri, Matteo / Braghini, Maria Rita / Marampon, Francesco / Alisi, Anna / Rota, Rossella

    International journal of molecular sciences

    2022  Volume 23, Issue 4

    Abstract: Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase over-expressed and activated in both adult and pediatric cancers, where it plays important roles in the regulation of pathogenesis and progression of the malignant phenotype. FAK exerts its ... ...

    Abstract Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase over-expressed and activated in both adult and pediatric cancers, where it plays important roles in the regulation of pathogenesis and progression of the malignant phenotype. FAK exerts its functions in cancer by two different ways: a kinase activity in the cytoplasm, mainly dependent on the integrin signaling, and a scaffolding activity into the nucleus by networking with different gene expression regulators. For this reason, FAK has to be considered a target with high therapeutic values. Indeed, evidence suggests that FAK targeting could be effective, either alone or in combination, with other already available treatments. Here, we propose an overview of the novel insights about FAK's structure and nuclear functions, with a special focus on the recent findings concerning the roles of this protein in cancer. Additionally, we provide a recent update on FAK inhibitors that are currently in clinical trials for patients with cancer, and discuss the challenge and future directions of drug-based anti-FAK targeted therapies.
    MeSH term(s) Animals ; Cell Nucleus/metabolism ; Focal Adhesion Protein-Tyrosine Kinases/metabolism ; Gene Expression Regulation/genetics ; Humans ; Neoplasms/metabolism ; Signal Transduction/physiology
    Chemical Substances Focal Adhesion Protein-Tyrosine Kinases (EC 2.7.10.2)
    Language English
    Publishing date 2022-02-11
    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/ijms23041998
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  5. Article ; Online: DNA Damage Response Gene Signature as Potential Treatment Markers for Oral Squamous Cell Carcinoma.

    Pomella, Silvia / Cassandri, Matteo / Melaiu, Ombretta / Marampon, Francesco / Gargari, Marco / Campanella, Vincenzo / Rota, Rossella / Barillari, Giovanni

    International journal of molecular sciences

    2023  Volume 24, Issue 3

    Abstract: Oral squamous cell carcinoma (OSCC) is a rapidly progressive cancer that often develops resistance against DNA damage inducers, such as radiotherapy and chemotherapy, which are still the standard of care regimens for this tumor. Thus, the identification ... ...

    Abstract Oral squamous cell carcinoma (OSCC) is a rapidly progressive cancer that often develops resistance against DNA damage inducers, such as radiotherapy and chemotherapy, which are still the standard of care regimens for this tumor. Thus, the identification of biomarkers capable of monitoring the clinical progression of OSCC and its responsiveness to therapy is strongly required. To meet this need, here we have employed Whole Genome Sequencing and RNA-seq data from a cohort of 316 patients retrieved from the TCGA Pan-Cancer Atlas to analyze the genomic and transcriptomic status of the DNA damage response (DDR) genes in OSCC. Then, we correlated the transcriptomic data with the clinical parameters of each patient. Finally, we relied on transcriptomic and drug sensitivity data from the CTRP v2 portal, performing Pearson's correlation analysis to identify putative vulnerabilities of OSCC cell lines correlated with DDR gene expression. Our results indicate that several DDR genes show a high frequency of genomic and transcriptomic alterations and that the expression of some of them correlates with OSCC grading and infection by the human papilloma virus. In addition, we have identified a signature of eight DDR genes (namely
    MeSH term(s) Humans ; Carcinoma, Squamous Cell/drug therapy ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/metabolism ; Squamous Cell Carcinoma of Head and Neck ; Mouth Neoplasms/drug therapy ; Mouth Neoplasms/genetics ; Mouth Neoplasms/metabolism ; DNA Damage ; Head and Neck Neoplasms
    Language English
    Publishing date 2023-01-31
    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/ijms24032673
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  6. Article ; Online: Gamma-Secretase Inhibitors Downregulate the Profibrotic NOTCH Signaling Pathway in Recessive Dystrophic Epidermolysis Bullosa.

    Condorelli, Angelo Giuseppe / Nobili, Rebecca / Muglia, Anita / Scarpelli, Giorgia / Marzuolo, Elisa / De Stefanis, Cristiano / Rota, Rossella / Diociaiuti, Andrea / Alaggio, Rita / Castiglia, Daniele / Odorisio, Teresa / El Hachem, May / Zambruno, Giovanna

    The Journal of investigative dermatology

    2024  

    Abstract: Recessive dystrophic epidermolysis bullosa (RDEB) is a rare skin fragility disorder caused by mutations in COL7A1. RDEB is hallmarked by trauma-induced unremitting blistering, chronic wounds with inflammation, and progressive fibrosis, leading to severe ... ...

    Abstract Recessive dystrophic epidermolysis bullosa (RDEB) is a rare skin fragility disorder caused by mutations in COL7A1. RDEB is hallmarked by trauma-induced unremitting blistering, chronic wounds with inflammation, and progressive fibrosis, leading to severe disease complications. There is currently no cure for RDEB-associated fibrosis. Our previous studies and increasing evidence highlighted the profibrotic role of NOTCH pathway in different skin disorders, including RDEB. In this study, we further investigated the role of NOTCH signaling in RDEB pathogenesis and explored the effects of its inhibition by γ-secretase inhibitors DAPT and PF-03084014 (nirogacestat). Our analyses demonstrated that JAG1 and cleaved NOTCH1 are upregulated in primary RDEB fibroblasts (ie, RDEB-derived fibroblasts) compared with controls, and their protein levels are further increased by TGF-β1 stimulation. Functional assays unveiled the involvement of JAG1/NOTCH1 axis in RDEB fibrosis and demonstrated that its blockade counteracts a variety of fibrotic traits. In particular, RDEB-derived fibroblasts treated with PF-03084014 showed (i) a significant reduction of contractility, (ii) a diminished secretion of TGF-β1 and collagens, and (iii) the downregulation of several fibrotic proteins. Although less marked than PF-03084014-treated cells, RDEB-derived fibroblasts exhibited a reduction of fibrotic traits also upon DAPT treatment. This study provides potential therapeutic strategies to antagonize RDEB fibrosis onset and progression.
    Language English
    Publishing date 2024-01-17
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80136-7
    ISSN 1523-1747 ; 0022-202X
    ISSN (online) 1523-1747
    ISSN 0022-202X
    DOI 10.1016/j.jid.2023.10.045
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    In stock of ZB MED Cologne/Königswinter

    Ui VI Zs.124: Show issues Location:
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  7. Article ; Online: New Insights on the Nuclear Functions and Targeting of FAK in Cancer

    Silvia Pomella / Matteo Cassandri / Maria Rita Braghini / Francesco Marampon / Anna Alisi / Rossella Rota

    International Journal of Molecular Sciences, Vol 23, Iss 1998, p

    2022  Volume 1998

    Abstract: Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase over-expressed and activated in both adult and pediatric cancers, where it plays important roles in the regulation of pathogenesis and progression of the malignant phenotype. FAK exerts its ... ...

    Abstract Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase over-expressed and activated in both adult and pediatric cancers, where it plays important roles in the regulation of pathogenesis and progression of the malignant phenotype. FAK exerts its functions in cancer by two different ways: a kinase activity in the cytoplasm, mainly dependent on the integrin signaling, and a scaffolding activity into the nucleus by networking with different gene expression regulators. For this reason, FAK has to be considered a target with high therapeutic values. Indeed, evidence suggests that FAK targeting could be effective, either alone or in combination, with other already available treatments. Here, we propose an overview of the novel insights about FAK’s structure and nuclear functions, with a special focus on the recent findings concerning the roles of this protein in cancer. Additionally, we provide a recent update on FAK inhibitors that are currently in clinical trials for patients with cancer, and discuss the challenge and future directions of drug-based anti-FAK targeted therapies.
    Keywords FAK ; adult cancers ; pediatric cancers ; targeted therapy ; combination therapy ; PROTACs ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 616
    Language English
    Publishing date 2022-02-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: DNA Damage Response Gene Signature as Potential Treatment Markers for Oral Squamous Cell Carcinoma

    Silvia Pomella / Matteo Cassandri / Ombretta Melaiu / Francesco Marampon / Marco Gargari / Vincenzo Campanella / Rossella Rota / Giovanni Barillari

    International Journal of Molecular Sciences, Vol 24, Iss 2673, p

    2023  Volume 2673

    Abstract: Oral squamous cell carcinoma (OSCC) is a rapidly progressive cancer that often develops resistance against DNA damage inducers, such as radiotherapy and chemotherapy, which are still the standard of care regimens for this tumor. Thus, the identification ... ...

    Abstract Oral squamous cell carcinoma (OSCC) is a rapidly progressive cancer that often develops resistance against DNA damage inducers, such as radiotherapy and chemotherapy, which are still the standard of care regimens for this tumor. Thus, the identification of biomarkers capable of monitoring the clinical progression of OSCC and its responsiveness to therapy is strongly required. To meet this need, here we have employed Whole Genome Sequencing and RNA-seq data from a cohort of 316 patients retrieved from the TCGA Pan-Cancer Atlas to analyze the genomic and transcriptomic status of the DNA damage response (DDR) genes in OSCC. Then, we correlated the transcriptomic data with the clinical parameters of each patient. Finally, we relied on transcriptomic and drug sensitivity data from the CTRP v2 portal, performing Pearson’s correlation analysis to identify putative vulnerabilities of OSCC cell lines correlated with DDR gene expression. Our results indicate that several DDR genes show a high frequency of genomic and transcriptomic alterations and that the expression of some of them correlates with OSCC grading and infection by the human papilloma virus. In addition, we have identified a signature of eight DDR genes (namely CCNB1 , CCNB2 , CDK2 , CDK4 , CHECK1 , E2F1 , FANCD2 , and PRKDC ) that could be predictive for OSCC response to the novel antitumor compounds sorafenib and tipifarnib-P1. Altogether, our data demonstrate that alterations in DDR genes could have an impact on the biology of OSCC. Moreover, here we propose a DDR gene signature whose expression could be predictive of OSCC responsiveness to therapy.
    Keywords oral squamous cell carcinoma ; DNA damage response ; The Cancer Genome Atlas ; DepMap ; bioinformatics ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 612
    Language English
    Publishing date 2023-01-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Pitfalls in the quantitative imaging of glutathione in living cells.

    Cossetti, Cristina / Di Giovamberardino, Gianna / Rota, Rossella / Pastore, Anna

    Nature communications

    2018  Volume 9, Issue 1, Page(s) 1588

    MeSH term(s) Glutathione ; Single-Cell Analysis
    Chemical Substances Glutathione (GAN16C9B8O)
    Language English
    Publishing date 2018-04-23
    Publishing country England
    Document type Letter ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-018-04035-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: CDK9 as a Valuable Target in Cancer: From Natural Compounds Inhibitors to Current Treatment in Pediatric Soft Tissue Sarcomas.

    Cassandri, Matteo / Fioravanti, Rossella / Pomella, Silvia / Valente, Sergio / Rotili, Dante / Del Baldo, Giada / De Angelis, Biagio / Rota, Rossella / Mai, Antonello

    Frontiers in pharmacology

    2020  Volume 11, Page(s) 1230

    Abstract: Cyclin-Dependent Kinases (CDKs) are well-known reliable targets for cancer treatment being often deregulated. Among them, since the transcription-associated CDK9 represents the sentry of cell transcriptional homeostasis, it can be a valuable target for ... ...

    Abstract Cyclin-Dependent Kinases (CDKs) are well-known reliable targets for cancer treatment being often deregulated. Among them, since the transcription-associated CDK9 represents the sentry of cell transcriptional homeostasis, it can be a valuable target for managing cancers in which the transcriptional machinery is dysregulated by tumor-driver oncogenes. Here we give an overview of some natural compounds identified as CDK inhibitors with reported activity also against CDK9, that were taken as a model for the development of highly active synthetic anti-CDK9 agents. After, we summarize the data on CDK9 inhibition in a group of rare pediatric solid tumors such as rhabdomyosarcoma, Ewing's sarcoma, synovial sarcoma and malignant rhabdoid tumors (soft tissue sarcomas), highlighting the more recent results in this field. Finally, we discuss the perspective and challenge of CDK9 modulation in cancer.
    Language English
    Publishing date 2020-08-13
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2020.01230
    Database MEDical Literature Analysis and Retrieval System OnLINE

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