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Article: Primary Ovarian Leiomyosarcoma Is a Very Rare Entity: A Narrative Review of the Literature.

Mandato, Vincenzo Dario / Torricelli, Federica / Mastrofilippo, Valentina / Palicelli, Andrea / Costagliola, Luigi / Aguzzoli, Lorenzo

Cancers

2023 Volume 15, Issue 11

Abstract: Background: Primary ovarian leiomyosarcoma is a very rare malignancy characterized by unclear management and poor survival. We reviewed all the cases of primary ovarian leiomyosarcoma to identify prognostic factors and the best treatment.: Methods: ... ...

Abstract	Background: Primary ovarian leiomyosarcoma is a very rare malignancy characterized by unclear management and poor survival. We reviewed all the cases of primary ovarian leiomyosarcoma to identify prognostic factors and the best treatment. Methods: We collected and analyzed the articles published in the English literature regarding primary ovarian leiomyosarcoma from January 1951 to September 2022, using PubMed research. Clinical and pathological characteristics, different treatments and outcomes were analyzed. Results: 113 cases of primary ovarian leiomyosarcoma were included. Most patients received surgical resection, associated with lymphadenectomy in 12.5% of cases. About 40% of patients received chemotherapy. Follow-up information was available for 100/113 (88.5%) patients. Stage and mitotic count were confirmed to affect survival, and lymphadenectomy and chemotherapy were associated with a better survival rate. A total of 43.4% of patients relapsed, and their mean disease-free survival was 12.5 months. Conclusions: Primary ovarian leiomyosarcomas are more common in women in their 50s (mean age 53 years). Most of them are at an early stage at presentation. Advanced stage and mitotic count showed a detrimental effect on survival. Surgical excision associated with lymphadenectomy and chemotherapy are associated with increased survival. An international registry could help collect clear and reliable data to standardize the diagnosis and treatment.
Language	English
Publishing date	2023-05-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers15112953
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Article: Molecular Fingerprints of Malignant Pleural Mesothelioma: Not Just a Matter of Genetic Alterations.

Lorenzini, Eugenia / Ciarrocchi, Alessia / Torricelli, Federica

Journal of clinical medicine

2021 Volume 10, Issue 11

Abstract: Malignant pleural mesothelioma (MPM) is a clinical emergency of our time. Being strongly associated with asbestos exposure, incidence of this cancer is ramping up these days in many industrialized countries and it will soon start to increase in many ... ...

Abstract	Malignant pleural mesothelioma (MPM) is a clinical emergency of our time. Being strongly associated with asbestos exposure, incidence of this cancer is ramping up these days in many industrialized countries and it will soon start to increase in many developing areas where the use of this silicate derivate is still largely in use. Deficiency of reliable markers for the early identification of these tumors and the limited efficacy of the currently available therapeutic options are the basis of the impressive mortality rate of MPM. These shortcomings reflect the very poor information available about the molecular basis of this disease. Results of the recently released deep profiling studies point to the epigenome as a central element in MPM development and progression. First, MPM is characterized by a low mutational burden and a highly peculiar set of mutations that hits almost exclusively epigenetic keepers or proteins controlling chromatin organization and function. Furthermore, asbestos does not seem to be associated with a distinctive mutational signature, while the precise mapping of epigenetic changes caused by this carcinogen has been defined, suggesting that alterations in epigenetic features are the driving force in the development of this disease. Last but not least, consistent evidence also indicates that, in the setting of MPM, chromatin rewiring and epigenetic alterations of cancer cells heavily condition the microenvironment, including the immune response. In this review we aim to point to the relevance of the epigenome in MPM and to highlight the dependency of this tumor on chromatin organization and function. We also intend to discuss the opportunity of targeting these mechanisms as potential therapeutic options for MPM.
Language	English
Publishing date	2021-06-02
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2662592-1
ISSN	2077-0383
ISSN	2077-0383
DOI	10.3390/jcm10112470
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Article ; Online: A multimodal integrative approach to model transcriptional addiction of thyroid cancer on RUNX2.

Vitale, Emanuele / Sauta, Elisabetta / Gugnoni, Mila / Torricelli, Federica / Manicardi, Veronica / Ciarrocchi, Alessia

Cancer communications (London, England)

2022 Volume 42, Issue 9, Page(s) 892–896

MeSH term(s)	Core Binding Factor Alpha 1 Subunit/genetics ; Core Binding Factor Alpha 1 Subunit/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Thyroid Neoplasms/genetics
Chemical Substances	Core Binding Factor Alpha 1 Subunit ; RUNX2 protein, human
Language	English
Publishing date	2022-04-22
Publishing country	United States
Document type	Letter ; Research Support, Non-U.S. Gov't
ISSN	2523-3548
ISSN (online)	2523-3548
DOI	10.1002/cac2.12292
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Article ; Online: An Innovative Drug Repurposing Approach to Restrain Endometrial Cancer Metastatization.

Torricelli, Federica / Sauta, Elisabetta / Manicardi, Veronica / Mandato, Vincenzo Dario / Palicelli, Andrea / Ciarrocchi, Alessia / Manzotti, Gloria

Cells

2023 Volume 12, Issue 5

Abstract: Background: Endometrial cancer (EC) is the most common gynecologic tumor and the world's fourth most common cancer in women. Most patients respond to first-line treatments and have a low risk of recurrence, but refractory patients, and those with ... ...

Abstract	Background: Endometrial cancer (EC) is the most common gynecologic tumor and the world's fourth most common cancer in women. Most patients respond to first-line treatments and have a low risk of recurrence, but refractory patients, and those with metastatic cancer at diagnosis, remain with no treatment options. Drug repurposing aims to discover new clinical indications for existing drugs with known safety profiles. It provides ready-to-use new therapeutic options for highly aggressive tumors for which standard protocols are ineffective, such as high-risk EC. Methods: Here, we aimed at defining new therapeutic opportunities for high-risk EC using an innovative and integrated computational drug repurposing approach. Results: We compared gene-expression profiles, from publicly available databases, of metastatic and non-metastatic EC patients being metastatization the most severe feature of EC aggressiveness. A comprehensive analysis of transcriptomic data through a two-arm approach was applied to obtain a robust prediction of drug candidates. Conclusions: Some of the identified therapeutic agents are already successfully used in clinical practice to treat other types of tumors. This highlights the potential to repurpose them for EC and, therefore, the reliability of the proposed approach.
MeSH term(s)	Humans ; Female ; Drug Repositioning/methods ; Reproducibility of Results ; Endometrial Neoplasms/pathology ; Gene Expression Profiling ; Transcriptome
Language	English
Publishing date	2023-03-03
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12050794
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Article ; Online: BET inhibitors drive Natural Killer activation in non-small cell lung cancer via BRD4 and SMAD3.

Reggiani, Francesca / Talarico, Giovanna / Gobbi, Giulia / Sauta, Elisabetta / Torricelli, Federica / Manicardi, Veronica / Zanetti, Eleonora / Orecchioni, Stefania / Falvo, Paolo / Piana, Simonetta / Lococo, Filippo / Paci, Massimiliano / Bertolini, Francesco / Ciarrocchi, Alessia / Sancisi, Valentina

Nature communications

2024 Volume 15, Issue 1, Page(s) 2567

Abstract: Non-small-cell lung carcinoma (NSCLC) is the most common lung cancer and one of the pioneer tumors in which immunotherapy has radically changed patients' outcomes. However, several issues are emerging and their implementation is required to optimize ... ...

Abstract	Non-small-cell lung carcinoma (NSCLC) is the most common lung cancer and one of the pioneer tumors in which immunotherapy has radically changed patients' outcomes. However, several issues are emerging and their implementation is required to optimize immunotherapy-based protocols. In this work, we investigate the ability of the Bromodomain and Extra-Terminal protein inhibitors (BETi) to stimulate a proficient anti-tumor immune response toward NSCLC. By using in vitro, ex-vivo, and in vivo models, we demonstrate that these epigenetic drugs specifically enhance Natural Killer (NK) cell cytotoxicity. BETi down-regulate a large set of NK inhibitory receptors, including several immune checkpoints (ICs), that are direct targets of the transcriptional cooperation between the BET protein BRD4 and the transcription factor SMAD3. Overall, BETi orchestrate an epigenetic reprogramming that leads to increased recognition of tumor cells and the killing ability of NK cells. Our results unveil the opportunity to exploit and repurpose these drugs in combination with immunotherapy.
MeSH term(s)	Humans ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/pathology ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Cell Cycle Proteins/metabolism ; Cell Line, Tumor ; Antineoplastic Agents/pharmacology ; Killer Cells, Natural ; Smad3 Protein/genetics ; Smad3 Protein/metabolism ; Bromodomain Containing Proteins
Chemical Substances	Nuclear Proteins ; Transcription Factors ; Cell Cycle Proteins ; Antineoplastic Agents ; SMAD3 protein, human ; Smad3 Protein ; BRD4 protein, human ; Bromodomain Containing Proteins
Language	English
Publishing date	2024-03-22
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-46778-8
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Article ; Online: Selinexor in multiple myeloma.

Martino, Enrica Antonia / Vigna, Ernesto / Bruzzese, Antonella / Labanca, Caterina / Mendicino, Francesco / Lucia, Eugenio / Olivito, Virginia / Zimbo, Annamaria / Torricelli, Federica / Neri, Antonino / Morabito, Fortunato / Gentile, Massimo

Expert opinion on pharmacotherapy

2024 Volume 25, Issue 4, Page(s) 421–434

Abstract: Introduction: Selinexor, an XPO1 inhibitor, has emerged as a promising therapeutic option in the challenging landscape of relapsed/refractory multiple myeloma (RRMM).: Areas covered: This article provides a review of selinexor, with a focus on ... ...

Abstract	Introduction: Selinexor, an XPO1 inhibitor, has emerged as a promising therapeutic option in the challenging landscape of relapsed/refractory multiple myeloma (RRMM). Areas covered: This article provides a review of selinexor, with a focus on available clinical studies involving MM patients and its safety profile. Clinical trials, such as STORM and BOSTON, have demonstrated its efficacy, particularly in combination regimens, showcasing notable overall response rates (ORR) and prolonged median progressionfree survival (mPFS). Selinexor's versatility is evident across various combinations, including carfilzomibdexamethasone (XKd), lenalidomidedexamethasone (XRd), and pomalidomidedexamethasone (XPd), with efficacy observed even in tripleclass refractory and highrisk patient populations. However, challenges, including resistance mechanisms and adverse events, necessitate careful management. Realworld evidence also underscores selinexor's effectiveness in RRMM, though dose adjustments and supportive measures remain crucial. Ongoing trials are exploring selinexor in diverse combinations and settings, including pomalidomidenaïve patients and postautologous stem cell transplant (ASCT) maintenance. Expert opinion: The evolving landscape of selinexor's role in the sequencing of treatment for RRMM, its potential in highrisk patients, including those with extramedullary disease, as revealed in the most recent international meetings, and ongoing investigations signal a dynamic era in myeloma therapeutics. Selinexor emerges as a pivotal component in multidrug strategies and innovative combinations.
MeSH term(s)	Multiple Myeloma/drug therapy ; Humans ; Hydrazines/therapeutic use ; Hydrazines/adverse effects ; Triazoles/therapeutic use ; Triazoles/adverse effects ; Karyopherins/antagonists & inhibitors ; Exportin 1 Protein ; Receptors, Cytoplasmic and Nuclear/antagonists & inhibitors ; Antineoplastic Agents/therapeutic use ; Antineoplastic Agents/adverse effects ; Antineoplastic Agents/pharmacology ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/adverse effects ; Progression-Free Survival
Chemical Substances	selinexor (31TZ62FO8F) ; Hydrazines ; Triazoles ; Karyopherins ; Exportin 1 Protein ; Receptors, Cytoplasmic and Nuclear ; Antineoplastic Agents
Language	English
Publishing date	2024-03-25
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2001535-5
ISSN	1744-7666 ; 1465-6566
ISSN (online)	1744-7666
ISSN	1465-6566
DOI	10.1080/14656566.2024.2333376
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Article ; Online: Linc00941 fuels ribogenesis and protein synthesis by supporting robust cMYC translation in malignant pleural mesothelioma.

Gugnoni, Mila / Lorenzini, Eugenia / Torricelli, Federica / Donati, Benedetta / Manicardi, Veronica / Vitale, Emanuele / Muccioli, Silvia / Piana, Simonetta / Lococo, Filippo / Zamponi, Raffaella / Gandellini, Paolo / Ciarrocchi, Alessia

Cancer letters

2024 Volume 592, Page(s) 216950

Abstract: Malignant pleural mesothelioma is a rare and lethal cancer caused by exposure to asbestos. The highly inflammatory environment caused by fibers accumulation forces cells to undergo profound adaptation to gain survival advantages. Prioritizing the ... ...

Abstract	Malignant pleural mesothelioma is a rare and lethal cancer caused by exposure to asbestos. The highly inflammatory environment caused by fibers accumulation forces cells to undergo profound adaptation to gain survival advantages. Prioritizing the synthesis of essential transcripts is an efficient mechanism coordinated by multiple molecules, including long non-coding RNAs. Enhancing the knowledge about these mechanisms is an essential weapon in combating mesothelioma. Linc00941 correlates to bad prognosis in various cancers, but it is reported to partake in distinct and apparently irreconcilable processes. In this work, we report that linc00941 supports the survival and aggressiveness of mesothelioma cells by influencing protein synthesis and ribosome biogenesis. Linc00941 binds to the translation initiation factor eIF4G, promoting the selective protein synthesis of cMYC, which, in turn, enhances the expression of key genes involved in translation. We analyzed a retrospective cohort of 97 mesothelioma patients' samples from our institution, revealing that linc00941 expression strongly correlates with reduced survival probability. This discovery clarifies linc00941's role in mesothelioma and proposes a unified mechanism of action for this lncRNA involving the selective translation of essential oncogenes, reconciling the discrepancies about its function.
Language	English
Publishing date	2024-05-08
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2024.216950
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Article ; Online: Long Noncoding RNA

Pistoni, Mariaelena / Rossi, Teresa / Donati, Benedetta / Torricelli, Federica / Polano, Maurizio / Ciarrocchi, Alessia

Molecular cancer research : MCR

2021 Volume 19, Issue 5, Page(s) 799–811

Abstract: BRD4 is an epigenome reader known to exert key roles at the interface between chromatin remodeling and transcriptional regulation, and is primarily known for its role in promoting gene expression. In selective contexts, however, BRD4 may work as negative ...

Abstract	BRD4 is an epigenome reader known to exert key roles at the interface between chromatin remodeling and transcriptional regulation, and is primarily known for its role in promoting gene expression. In selective contexts, however, BRD4 may work as negative regulator of transcription. Here, we reported that BRD4 binds several long noncoding RNAs (lncRNA). Among these, the lncRNA
MeSH term(s)	Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Line, Tumor ; Humans ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Melanoma/genetics ; Melanoma/metabolism ; Melanoma/pathology ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcriptional Activation
Chemical Substances	BRD4 protein, human ; Cell Cycle Proteins ; Intracellular Signaling Peptides and Proteins ; NEAT1 long non-coding RNA, human ; RNA, Long Noncoding ; Transcription Factors ; WDR5 protein, human
Language	English
Publishing date	2021-02-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-20-0324
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Article ; Online: Expression levels of NONO, a nuclear protein primarily involved in paraspeckles function, are associated with several deregulated molecular pathways and poor clinical outcome in multiple myeloma.

Ronchetti, Domenica / Favasuli, Vanessa Katia / Silvestris, Ilaria / Todoerti, Katia / Torricelli, Federica / Bolli, Niccolò / Ciarrocchi, Alessia / Taiana, Elisa / Neri, Antonino

Discover. Oncology

2022 Volume 13, Issue 1, Page(s) 124

Abstract: Purpose: The NONO protein belongs to the multifunctional family of proteins that can bind DNA, RNA and proteins. It is located in the nucleus of most mammalian cells and can affect almost every step of gene regulation. Dysregulation of NONO has been ... ...

Abstract	Purpose: The NONO protein belongs to the multifunctional family of proteins that can bind DNA, RNA and proteins. It is located in the nucleus of most mammalian cells and can affect almost every step of gene regulation. Dysregulation of NONO has been found in many types of cancer; however, data regarding its expression and relevance in Multiple Myeloma (MM) are virtually absent. Methods: We took advantage of a large cohort of MM patients enrolled in the Multiple Myeloma Research Foundation CoMMpass study to elucidate better the clinical and biological relevance of NONO expression in the context of the MM genomic landscape and transcriptome. Results: NONO is overexpressed in pathological samples compared to normal controls. In addition, higher NONO expression levels are significant independent prognostic markers of worse clinical outcome in MM. Our results indicate that NONO deregulation may play a pathogenetic role in MM by affecting cell cycle, DNA repair mechanisms, and influencing translation by regulating ribosome biogenesis and assembly. Furthermore, our data suggest NONO involvement in the metabolic reprogramming of glucose metabolism from respiration to aerobic glycolysis, a phenomenon known as the 'Warburg Effect' that supports rapid cancer cell growth, survival, and invasion. Conclusion: These findings strongly support the need of future investigations for the understanding of the mechanisms of deregulation and the biological role and activity of NONO in MM.
Language	English
Publishing date	2022-11-11
Publishing country	United States
Document type	Journal Article
ISSN	2730-6011
ISSN (online)	2730-6011
DOI	10.1007/s12672-022-00582-2
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Article ; Online: OVOL2 impairs RHO GTPase signaling to restrain mitosis and aggressiveness of Anaplastic Thyroid Cancer.

Gugnoni, Mila / Manzotti, Gloria / Vitale, Emanuele / Sauta, Elisabetta / Torricelli, Federica / Reggiani, Francesca / Pistoni, Mariaelena / Piana, Simonetta / Ciarrocchi, Alessia

Journal of experimental & clinical cancer research : CR

2022 Volume 41, Issue 1, Page(s) 108

Abstract: Background: Anaplastic Thyroid Cancer (ATC) is an undifferentiated and aggressive tumor that often originates from well-Differentiated Thyroid Carcinoma (DTC) through a trans-differentiation process. Epithelial-to-Mesenchymal Transition (EMT) is ... ...

Abstract	Background: Anaplastic Thyroid Cancer (ATC) is an undifferentiated and aggressive tumor that often originates from well-Differentiated Thyroid Carcinoma (DTC) through a trans-differentiation process. Epithelial-to-Mesenchymal Transition (EMT) is recognized as one of the major players of this process. OVOL2 is a transcription factor (TF) that promotes epithelial differentiation and restrains EMT during embryonic development. OVOL2 loss in some types of cancers is linked to aggressiveness and poor prognosis. Here, we aim to clarify the unexplored role of OVOL2 in ATC. Methods: Gene expression analysis in thyroid cancer patients and cell lines showed that OVOL2 is mainly associated with epithelial features and its expression is deeply impaired in ATC. To assess OVOL2 function, we established an OVOL2-overexpression model in ATC cell lines and evaluated its effects by analyzing gene expression, proliferation, invasion and migration abilities, cell cycle, specific protein localization through immunofluorescence staining. RNA-seq profiling showed that OVOL2 controls a complex network of genes converging on cell cycle and mitosis regulation and Chromatin Immunoprecipitation identified new OVOL2 target genes. Results: Coherently with its reported function, OVOL2 re-expression restrained EMT and aggressiveness in ATC cells. Unexpectedly, we observed that it caused G2/M block, a consequent reduction in cell proliferation and an increase in cell death. This phenotype was associated to generalized abnormalities in the mitotic spindle structure and cytoskeletal organization. By RNA-seq experiments, we showed that many pathways related to cytoskeleton and migration, cell cycle and mitosis are profoundly affected by OVOL2 expression, in particular the RHO-GTPase pathway resulted as the most interesting. We demonstrated that RHO GTPase pathway is the central hub of OVOL2-mediated program in ATC and that OVOL2 transcriptionally inhibits RhoU and RhoJ. Silencing of RhoU recapitulated the OVOL2-driven phenotype pointing to this protein as a crucial target of OVOL2 in ATC. Conclusions: Collectively, these data describe the role of OVOL2 in ATC and uncover a novel function of this TF in inhibiting the RHO GTPase pathway interlacing its effects on EMT, cytoskeleton dynamics and mitosis.
MeSH term(s)	Epithelial-Mesenchymal Transition/genetics ; Female ; Humans ; Mitosis ; Pregnancy ; Thyroid Carcinoma, Anaplastic/genetics ; Thyroid Neoplasms/genetics ; Thyroid Neoplasms/pathology ; Transcription Factors/genetics ; rho GTP-Binding Proteins/genetics
Chemical Substances	Ovol2 protein, human ; Transcription Factors ; RHOJ protein, human (EC 3.6.1.-) ; rho GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2022-03-25
Publishing country	England
Document type	Journal Article
ZDB-ID	803138-1
ISSN	1756-9966 ; 0392-9078
ISSN (online)	1756-9966
ISSN	0392-9078
DOI	10.1186/s13046-022-02316-2
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Zs.A 2065: Show issues

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