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  1. Article ; Online: Bioengineered 'mini-colons' shed light on cancer progression.

    Riggi, Nicolò / de Sousa E Melo, Felipe

    Nature

    2024  

    Language English
    Publishing date 2024-04-24
    Publishing country England
    Document type News
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/d41586-024-01018-3
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  2. Article ; Online: Necrotic debris and STING exert therapeutically relevant effects on tumor cholesterol homeostasis.

    Katakam, Sampath / Anand, Santosh / Martin, Patricia / Riggi, Nicolo / Stamenkovic, Ivan

    Life science alliance

    2022  Volume 5, Issue 3

    Abstract: Malignant tumors commonly display necrosis, which invariably triggers an inflammatory response that supports tumor growth. However, the effect on tumor cells of necrotic debris, or damage-associated molecular patterns (DAMPs) released by dying cells is ... ...

    Abstract Malignant tumors commonly display necrosis, which invariably triggers an inflammatory response that supports tumor growth. However, the effect on tumor cells of necrotic debris, or damage-associated molecular patterns (DAMPs) released by dying cells is unknown. Here, we addressed the effect of DAMPs on primary Ewing sarcoma (EwS) cells and cell lines grown in 3D (spheroids) and 2D culture. We show that DAMPs promote the growth of EwS spheroids but not 2D cultures and that the underlying mechanism implicates an increase in cholesterol load in spheroids. In contrast, stimulation of the nucleic acid sensor signaling platform STING by its ligand cyclic GMP-AMP decreases the tumor cell cholesterol load and reduces their tumor initiating ability. Overexpression of STING or stimulation with cyclic GMP-AMP opposes the growth stimulatory effect of DAMPs and synergizes with the cholesterol synthesis inhibitor simvastatin to inhibit tumor growth. Our observations show that modulation of cholesterol homeostasis is a major effect of necrotic cell debris and STING and suggest that combining STING agonists with statins may help control tumor growth.
    MeSH term(s) Alarmins/metabolism ; Apoptosis ; Biomarkers ; Cell Line, Tumor ; Cholesterol/metabolism ; Disease Management ; Disease Susceptibility ; Gene Expression Regulation, Neoplastic ; Homeostasis ; Humans ; Lipid Metabolism ; Membrane Proteins/metabolism ; Necrosis/metabolism ; Neoplasms/etiology ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/therapy ; Spheroids, Cellular ; Tumor Cells, Cultured
    Chemical Substances Alarmins ; Biomarkers ; Membrane Proteins ; STING1 protein, human ; Cholesterol (97C5T2UQ7J)
    Language English
    Publishing date 2022-01-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2575-1077
    ISSN (online) 2575-1077
    DOI 10.26508/lsa.202101256
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  3. Article ; Online: Ewing's Sarcoma.

    Riggi, Nicolò / Suvà, Mario L / Stamenkovic, Ivan

    The New England journal of medicine

    2021  Volume 384, Issue 2, Page(s) 154–164

    MeSH term(s) Antineoplastic Agents/therapeutic use ; Bone Neoplasms/genetics ; Bone Neoplasms/therapy ; Combined Modality Therapy ; DNA Methylation ; DNA, Neoplasm/metabolism ; Gene Expression Regulation ; Humans ; Mutation ; Oncogene Proteins, Fusion/metabolism ; Polymorphism, Genetic ; Prognosis ; Proto-Oncogene Protein c-fli-1/metabolism ; RNA-Binding Protein EWS/metabolism ; Sarcoma, Ewing/genetics ; Sarcoma, Ewing/therapy ; Suppression, Genetic ; Translocation, Genetic
    Chemical Substances Antineoplastic Agents ; DNA, Neoplasm ; EWS-FLI fusion protein ; Oncogene Proteins, Fusion ; Proto-Oncogene Protein c-fli-1 ; RNA-Binding Protein EWS
    Language English
    Publishing date 2021-01-26
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMra2028910
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  4. Article ; Online: Ewing's Sarcoma. Reply.

    Riggi, Nicolò / Suvà, Mario L / Stamenkovic, Ivan

    The New England journal of medicine

    2021  Volume 384, Issue 15, Page(s) 1477–1478

    MeSH term(s) Bone Neoplasms ; Humans ; Sarcoma, Ewing/therapy ; Tumor Cells, Cultured
    Language English
    Publishing date 2021-04-14
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMc2102423
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  5. Article ; Online: Clear cell sarcoma: state-of-the art and perspectives.

    Wetterwald, Laureline / Riggi, Nicolò / Kyriazoglou, Anastasios / Dei Tos, Giovanni / Dei Tos, Angelo / Digklia, Antonia

    Expert review of anticancer therapy

    2023  Volume 23, Issue 3, Page(s) 235–242

    Abstract: Introduction: Clear cell sarcoma (CCS) is an ultrarare soft tissue sarcoma (STS) with a poor prognosis due to its propensity to metastasize and its low chemosensitivity. The standard treatment of localized CCS consists of wide surgical excision with or ... ...

    Abstract Introduction: Clear cell sarcoma (CCS) is an ultrarare soft tissue sarcoma (STS) with a poor prognosis due to its propensity to metastasize and its low chemosensitivity. The standard treatment of localized CCS consists of wide surgical excision with or without additive radiotherapy. However, unresectable CCS is generally treated with conventional systemic therapies available for treatment of STS despite the weak scientific evidence to support its use.
    Areas covered: In this review, we discuss the clinicopathologic characteristics of CSS, as well as the current treatment landscape and future therapeutic approaches.
    Expert opinion: The current treatment strategy of advanced CCSs, based on STSs regimens, shows a lack of effective options. Combination therapiesin particular, the association of immunotherapy and TKIs, represent a promising approach. Translational studies are needed in order to decipher the regulatory mechanisms involved in the oncogenesis of this ultrarare sarcoma and identify potential molecular targets.
    MeSH term(s) Humans ; Sarcoma, Clear Cell/therapy ; Immunotherapy ; Soft Tissue Neoplasms/drug therapy
    Language English
    Publishing date 2023-02-27
    Publishing country England
    Document type Review ; Journal Article
    ZDB-ID 2112544-2
    ISSN 1744-8328 ; 1473-7140
    ISSN (online) 1744-8328
    ISSN 1473-7140
    DOI 10.1080/14737140.2023.2183846
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  6. Article: 5-Hydroxymethylcytosine Loss in Conjunctival Melanoma.

    Stahl, Alexandre / Riggi, Nicolo / Nardou, Katya / Nicolas, Michael / Kaya, Gurkan / Moulin, Alexandre

    Dermatopathology (Basel, Switzerland)

    2021  Volume 8, Issue 2, Page(s) 176–184

    Abstract: Aims: Conjunctival and cutaneous melanoma partially share similar clinical and molecular backgrounds. As 5-hydroxymethylcytosine (5-hmC) loss has been demonstrated in cutaneous melanoma, we decided to assess if similar changes were occurring in ... ...

    Abstract Aims: Conjunctival and cutaneous melanoma partially share similar clinical and molecular backgrounds. As 5-hydroxymethylcytosine (5-hmC) loss has been demonstrated in cutaneous melanoma, we decided to assess if similar changes were occurring in conjunctival melanoma.
    Methods: 5-methylcytosine (5-mC), 5-hmC and TET2 were respectively identified by immunohistochemistry and RNA ISH in 40 conjunctival nevi and 37 conjunctival melanomas. Clinicopathological correlations were established.
    Results: 5-mC, TET2 and 5-hmC were respectively identified in 67.5%, 95% and 100% of conjunctival nevi and in 81.1%, 35.1% and 54% of conjunctival melanomas. A significant 5-hmC and TET2 loss was identified in conjunctival melanoma comparing to nevus, as well as a significant correlation between TET2 and 5-hmC expression. In the melanomas, 5-hmC expression was only significantly associated with local lymphatic invasion, but not with other clinicopathological parameters. There was a correlation between TET2 expression and the localization of the tumors. 5-mC expression was not associated with any clinicopathological parameters.
    Conclusions: We identified a significant 5-hmC loss in conjunctival melanoma similar to cutaneous melanoma. This loss may possibly be attributed to TET2 loss or IDH1 mutations. 5-hmC loss in conjunctival melanoma may help in the differential diagnosis between atypical conjunctival nevus and conjunctival melanoma.
    Language English
    Publishing date 2021-06-05
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2777118-0
    ISSN 2296-3529
    ISSN 2296-3529
    DOI 10.3390/dermatopathology8020023
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  7. Article ; Online: Synovial sarcoma: when epigenetic changes dictate tumour development.

    Riggi, Nicolo / Cironi, Luisa / Stamenkovic, Ivan

    Swiss medical weekly

    2018  Volume 148, Page(s) w14667

    Abstract: Synovial sarcoma is a highly aggressive soft tissue malignancy that often affects adolescents and young adults. It is associated with a unique chromosomal translocation that results in the formation and expression of the fusion gene SS18-SSX, which ... ...

    Abstract Synovial sarcoma is a highly aggressive soft tissue malignancy that often affects adolescents and young adults. It is associated with a unique chromosomal translocation that results in the formation and expression of the fusion gene SS18-SSX, which underlies its pathogenesis. Although SS18-SSX provides a potentially unique therapeutic target, all attempts to neutralise it have been unsuccessful thus far. When complete surgical removal of the tumour fails, therapy is limited to largely ineffective cytotoxic drug regimens. Nevertheless, recent discoveries about the mechanisms of SS18-SSX protein function have provided insight into potential alternative therapeutic strategies. SS18-SSX displays oncogenic activity through protein-protein interactions and participation in chromatin remodelling complexes. This review summarises our current understanding of the function of SS18-SSX and the mechanisms by which it alters the epigenetic landscape of permissive cells to induce transformation and the subsequent development of synovial sarcoma.
    MeSH term(s) Cell Transformation, Neoplastic/genetics ; Chromatin/genetics ; Epigenesis, Genetic ; Humans ; Neoplasm Proteins/genetics ; Proto-Oncogene Proteins/genetics ; Repressor Proteins/genetics ; Sarcoma, Synovial/genetics ; Sarcoma, Synovial/pathology ; Translocation, Genetic/genetics
    Chemical Substances Chromatin ; Neoplasm Proteins ; Proto-Oncogene Proteins ; Repressor Proteins ; SS18 protein, human ; synovial sarcoma X breakpoint proteins (164289-47-8)
    Language English
    Publishing date 2018-12-02
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2036179-8
    ISSN 1424-3997 ; 1424-7860
    ISSN (online) 1424-3997
    ISSN 1424-7860
    DOI 10.4414/smw.2018.14667
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  8. Article ; Online: Cancer Metastasis: A Reappraisal of Its Underlying Mechanisms and Their Relevance to Treatment.

    Riggi, Nicolo / Aguet, Michel / Stamenkovic, Ivan

    Annual review of pathology

    2017  Volume 13, Page(s) 117–140

    Abstract: Metastases are responsible for the vast majority of cancer-related deaths, but, despite intense efforts to understand their underlying mechanisms with the goal of uncovering effective therapeutic targets, treatment of metastatic cancer has progressed ... ...

    Abstract Metastases are responsible for the vast majority of cancer-related deaths, but, despite intense efforts to understand their underlying mechanisms with the goal of uncovering effective therapeutic targets, treatment of metastatic cancer has progressed minimally. In this review, we examine the biological programs currently proposed to be key drivers of metastasis. On the basis of evidence from a growing body of research, we discuss to what extent the cellular and molecular mechanisms that are suggested to underlie cancer cell dissemination are specific to the metastatic process, as opposed to representing natural primary tumor progression. Our review highlights the contrast between the abundance of insight gained into the events that constitute the metastatic cascade and the paucity of therapeutic options.
    MeSH term(s) Humans ; Neoplasm Invasiveness/pathology ; Neoplasm Metastasis/pathology ; Neoplasms/pathology ; Neoplastic Stem Cells/pathology
    Language English
    Publishing date 2017-10-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2227429-7
    ISSN 1553-4014 ; 1553-4006
    ISSN (online) 1553-4014
    ISSN 1553-4006
    DOI 10.1146/annurev-pathol-020117-044127
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  9. Article ; Online: Pan-Cancer Landscape of Aberrant DNA Methylation across Human Tumors.

    Saghafinia, Sadegh / Mina, Marco / Riggi, Nicolo / Hanahan, Douglas / Ciriello, Giovanni

    Cell reports

    2018  Volume 25, Issue 4, Page(s) 1066–1080.e8

    Abstract: The discovery of cancer-associated alterations has primarily focused on genetic variants. Nonetheless, altered epigenomes contribute to deregulate transcription and promote oncogenic pathways. Here, we designed an algorithmic approach (RESET) to identify ...

    Abstract The discovery of cancer-associated alterations has primarily focused on genetic variants. Nonetheless, altered epigenomes contribute to deregulate transcription and promote oncogenic pathways. Here, we designed an algorithmic approach (RESET) to identify aberrant DNA methylation and associated cis-transcriptional changes across >6,000 human tumors. Tumors exhibiting mutations of chromatin remodeling factors and Wnt signaling displayed DNA methylation instability, characterized by numerous hyper- and hypo-methylated loci. Most silenced and enhanced genes coalesced in specific pathways including apoptosis, DNA repair, and cell metabolism. Cancer-germline antigens (CG) were frequently epigenomically enhanced and their expression correlated with response to anti-PD-1, but not anti-CTLA4, in skin melanoma. Finally, we demonstrated the potential of our approach to explore DNA methylation changes in pediatric tumors, which frequently lack genetic drivers and exhibit epigenomic modifications. Our results provide a pan-cancer map of aberrant DNA methylation to inform functional and therapeutic studies.
    MeSH term(s) Cell Line, Tumor ; Child ; DNA Methylation/genetics ; Epigenesis, Genetic ; Gene Silencing ; Humans ; Neoplasms/genetics
    Language English
    Publishing date 2018-10-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2018.09.082
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  10. Article ; Online: DisP-seq reveals the genome-wide functional organization of DNA-associated disordered proteins.

    Xing, Yu-Hang / Dong, Rui / Lee, Lukuo / Rengarajan, Shruthi / Riggi, Nicolò / Boulay, Gaylor / Rivera, Miguel N

    Nature biotechnology

    2023  Volume 42, Issue 1, Page(s) 52–64

    Abstract: Intrinsically disordered regions (IDRs) in DNA-associated proteins are known to influence gene regulation, but their distribution and cooperative functions in genome-wide regulatory programs remain poorly understood. Here we describe DisP-seq (disordered ...

    Abstract Intrinsically disordered regions (IDRs) in DNA-associated proteins are known to influence gene regulation, but their distribution and cooperative functions in genome-wide regulatory programs remain poorly understood. Here we describe DisP-seq (disordered protein precipitation followed by DNA sequencing), an antibody-independent chemical precipitation assay that can simultaneously map endogenous DNA-associated disordered proteins genome-wide through a combination of biotinylated isoxazole precipitation and next-generation sequencing. DisP-seq profiles are composed of thousands of peaks that are associated with diverse chromatin states, are enriched for disordered transcription factors (TFs) and are often arranged in large lineage-specific clusters with high local concentrations of disordered proteins and different combinations of histone modifications linked to regulatory potential. We use DisP-seq to analyze cancer cells and reveal how disordered protein-associated islands enable IDR-dependent mechanisms that control the binding and function of disordered TFs, including oncogene-dependent sequestration of TFs through long-range interactions and the reactivation of differentiation pathways upon loss of oncogenic stimuli in Ewing sarcoma.
    MeSH term(s) DNA ; Chromatin ; Sequence Analysis, DNA
    Chemical Substances DNA (9007-49-2) ; Chromatin
    Language English
    Publishing date 2023-04-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1311932-1
    ISSN 1546-1696 ; 1087-0156
    ISSN (online) 1546-1696
    ISSN 1087-0156
    DOI 10.1038/s41587-023-01737-4
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