Genomics, Epigenomics and Transcriptomics
Transcriptional and post-transcriptional regulation
Data science, machine learning and Complex Systsems
86
Scopus Publications
4121
Scholar Citations
36
Scholar h-index
58
Scholar i10-index
Scopus Publications
Multiple regulatory events contribute to a widespread circular RNA downregulation in precancer and early stage of colorectal cancer development Alessandro Camandona, Amedeo Gagliardi, Nicola Licheri, Sonia Tarallo, Giulia Francescato, et al. Biomarker Research, 2025 Background Early detection of colorectal cancer (CRC) significantly improves its management and patients’ survival. Circular RNAs (circRNAs) are peculiar covalently closed transcripts involved in gene expression modulation whose dysregulation has been extensively reported in CRC cells. However, little is known about their alterations in the early phases of colorectal carcinogenesis. Methods In this study, we performed an integrative analysis of circRNA profiles in RNA-sequencing (RNA-Seq) data of 96 colorectal cancers, 27 adenomas, and matched adjacent mucosa tissues. We also investigated the levels of cognate linear transcripts and those of regulating RNA-binding proteins (RBPs). Levels of circRNA-interacting microRNAs (miRNAs) were explored by integrating data of small RNA-Seq performed on the same samples. Results Our results revealed a significant dysregulation of 34 circRNAs (paired adj. p < 0.05), almost exclusively downregulated in tumor tissues and, prevalently, in early disease stages. This downregulation was associated with decreased expression of circRNA host genes and those encoding for RBPs involved in circRNA biogenesis, including NOVA1, RBMS3, and MBNL1. Guilt-by-association analysis showed that dysregulated circRNAs correlated with increased predicted activity of cell proliferation, DNA repair, and c-Myc signaling pathways. Functional analysis showed interactions among dysregulated circRNAs, RBPs, and miRNAs, which were supported by significant correlations among their expression levels. Findings were validated in independent cohorts and public datasets, and the downregulation of circLPAR1(2,3) and circLINC00632(5) was validated by ddPCR. Conclusions These results support that multiple altered regulatory mechanisms may contribute to the reduction of circRNA levels that characterize early colorectal carcinogenesis.
CircCDYL Association With hnRNPL Modulates CDYL Isoform Switching in Breast Cancer Cells Serena Bernardi, Giorgia Risso, Lorenzo Franchitti, Alessandro Camandona, Jean‐Marie Robbin, et al. Cancer Science, 2025 Circular RNAs (circRNAs) are covalently closed back‐splicing products involved in the regulation of different cellular processes, and their dysregulation has been frequently observed in cancer cells. CircCDYL, a circRNA derived from the back‐splicing of CDYL exon 4, has an emerging role in breast cancer (BC) biology. In this study, we investigated the role of circCDYL in modulating alternative splicing (AS) and isoform switching in MCF‐7 BC cells. The circRNA profiling in MCF‐7 showed circCDYL as the most abundant circRNA, with an expression increasing upon Estrogen Receptor α (ERα) silencing. RNA‐Sequencing analysis of circCDYL knock‐down cells revealed significant alterations in the splicing pattern, with over 2900 AS events significantly affected. Through RNA immunoprecipitation and RNA pull‐down assays, we found evidence of an association between circCDYL and the splicing factor hnRNPL. To explore the consequences of this association, we compared the RNA‐Sequencing of hnRNPL‐silenced cells, unraveling 96 overlapping AS events accompanied by a switching usage of 223 isoforms, including those of CDYL. The self‐loop regulation of circCDYL on its host gene was confirmed by isoform‐specific qRT‐PCR, observing that it was primarily dependent on an alternative promoter usage, rather than an AS regulation. Accordingly, epigenetic changes at CDYL alternative promoters were confirmed in circCDYL and hnRNPL knockdown cells. The confirmation of a chromatin occupancy of hnRNPL and ERα at CDYL‐regulated promoters supported the role of these proteins in CDYL regulation. Our results support a synergic activity of circCDYL and hnRNPL in the regulation of AS and promoter usage in BC cells.
The cGAS-STING pathway is a master regulator of OCT4 expression in persistent sarcoma cells and enhances cellular immunotherapy with NK and CIK lymphocytes Giorgia Giordano, Alessandra Merlini, Federica Capozzi, Giulio Ferrero, Cristina Tucciarello, et al. Cancer Immunology Immunotherapy, 2025 Advanced sarcomas have a poor prognosis and limited therapeutic options. Disease recurrence is caused by persistent cells that survive drug treatments. The alkylating agent trabectedin, when combined with the poly (ADP-ribose) polymerase 1 (PARP1) inhibitor olaparib, exhibits variable antitumor effects in advanced sarcomas. In this study, we demonstrate that the expression of the transcription factor OCT4 is upregulated in persistent cells that survive treatment with trabectedin and olaparib, through the cGAS-STING-IRF3-IFNβ pathway. This route also leads to the upregulation of natural killer (NK) and cytokine-induced killer (CIK) lymphocyte activating ligands. These molecular events enhance the antitumor efficacy of immunotherapy with NK and CIK cells, targeting both the bulk population and residual drug-tolerant cells. In conclusion, the activation of the cGAS-STING pathway has a double-edged effect, enriching the OCT4+ persistent cell population while increasing the expression of NK/CIK ligands. The addition of olaparib to trabectedin potentiates the cGAS-STING pathway activation and the upregulation of NKG2DLs, while simultaneously counteracting the OCT4 overexpression. Therefore, sequential treatment with trabectedin and olaparib followed by NK/CIK immunotherapy represents a promising strategy against advanced sarcomas and warrants further investigation.
Nonproteolytic ubiquitination regulates chromatin occupancy by the NCoR/SMRT/HDAC3 corepressor complex in MCF-7 breast cancer cells Giulio Ferrero, Maria Dafne Cardamone, Francesca Luca, Eliot Bourk, Laura Ricci, et al. Proceedings of the National Academy of Sciences of the United States of America, 2025 Tight regulation of gene expression is achieved through the coordinated action of transcription factors and cofactors that often can act as both repressors and activators in response to regulatory signals, with their activity modulated by context-specific signal transduction pathways that also impinge on their transient and cyclical recruitment to chromatin. However, the mechanisms underlying the intricate interplay between the regulatory strategies controlling cofactors’ activity and localization across subcellar domains remain poorly understood. Here, we investigated the role of G-Protein Pathway Suppressor 2 (GPS2), a transcriptional cofactor critical for maintaining cellular homeostasis via regulation of mitochondrial biogenesis, stress response, lipid metabolism, insulin signaling, and inflammation, in MCF-7 breast cancer cells. By integration of biochemical assays with genome-wide RNA sequencing and Chromatin immunoprecipitation-Seq analyses, we show that nuclear GPS2 is required for licensing histone deacetylase 3 recruitment to chromatin via restricted ubiquitination by tumor necrosis factor receptor-associated factor 6 (TRAF6), an E3 ubiquitin ligase previously shown to regulate the switch from repressive to activating functions of the nuclear receptor corepressor (NCoR)/silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) complex and here unexpectedly found to translocate to the nucleus in response to IL-1β stimulation. Nuclear TRAF6 is recruited to chromatin via direct interaction with the corepressors NCoR/SMRT, and TRAF6-mediated ubiquitination of TGF-beta activated kinase 1 (MAP3K7) binding protein 2 (TAB2), a facultative component of the NCoR/SMRT complex, contributes to corepressor clearance from target regulatory regions. Together, these results reveal an exquisite mechanism for coordinating the local regulation of cofactor activity with proinflammatory signaling pathways.
Leveraging multi-omics data to infer regulators of mRNA 3’ end processing in glioblastoma Aleksei Mironov, Lorenzo Franchitti, Shreemoyee Ghosh, Marie-Francoise Ritz, Gregor Hutter, et al. Frontiers in Molecular Biosciences, 2024 Alterations in mRNA 3’ end processing and polyadenylation are widely implicated in the biology of many cancer types, including glioblastoma (GBM), one the most aggressive tumor types. Although several RNA-binding proteins (RBPs) responsible for alternative polyadenylation (APA) were identified from functional studies in cell lines, their contribution to the APA landscape in tumors in vivo was not thoroughly addressed. In this study we analyzed a large RNA-seq data set of glioblastoma (GBM) samples from The Cancer Genome Atlas (TCGA) to identify APA patterns differentiating the main molecular subtypes of GBM. We superimposed these to RBP footprinting data and to APA events occurring upon depletion of individual RBPs from a large panel tested by the ENCODE Consortium. Our analysis revealed 22 highly concordant and statistically significant RBP-APA associations, whereby changes in RBP expression were accompanied by APA in both TCGA and ENCODE datasets. Among these, we found a previously unknown PTBP1-regulated APA event in the PRRC2B gene and an HNRNPU-regulated event in the SC5D gene. Both of these were further supported by RNA-sequencing data of paired tumor center-periphery GBM samples obtained at the University Hospital of Basel. In addition, we validated the regulation of APA in PRRC2B by PTBP1 in siRNA-knockdown and overexpression experiments followed by RNA-sequencing in two glioblastoma cell lines. The transcriptome analysis workflow that we present here enables the identification of concordant RBP-APA associations in cancers.
A Regulatory Axis between Epithelial Splicing Regulatory Proteins and Estrogen Receptor α Modulates the Alternative Transcriptome of Luminal Breast Cancer Jamal Elhasnaoui, Giulio Ferrero, Valentina Miano, Lorenzo Franchitti, Isabella Tarulli, et al. International Journal of Molecular Sciences, 2022 Epithelial splicing regulatory proteins 1 and 2 (ESRP1/2) control the splicing pattern during epithelial to mesenchymal transition (EMT) in a physiological context and in cancer, including breast cancer (BC). Here, we report that ESRP1, but not ESRP2, is overexpressed in luminal BCs of patients with poor prognosis and correlates with estrogen receptor α (ERα) levels. Analysis of ERα genome-binding profiles in cell lines and primary breast tumors showed its binding in the proximity of ESRP1 and ESRP2 genes, whose expression is strongly decreased by ERα silencing in hormone-deprived conditions. The combined knock-down of ESRP1/2 in MCF-7 cells followed by RNA-Seq, revealed the dysregulation of 754 genes, with a widespread alteration of alternative splicing events (ASEs) of genes involved in cell signaling, metabolism, cell growth, and EMT. Functional network analysis of ASEs correlated with ESRP1/2 expression in ERα+ BCs showed RAC1 as the hub node in the protein–protein interactions altered by ESRP1/2 silencing. The comparison of ERα- and ESRP-modulated ASEs revealed 63 commonly regulated events, including 27 detected in primary BCs and endocrine-resistant cell lines. Our data support a functional implication of the ERα-ESRP1/2 axis in the onset and progression of BC by controlling the splicing patterns of related genes.
The estrogen receptor α signaling pathway controls alternative splicing in the absence of ligands in breast cancer cells Jamal Elhasnaoui, Giulio Ferrero, Valentina Miano, Santina Cutrupi, Michele De Bortoli Cancers, 2021 Background: The transcriptional activity of estrogen receptor α (ERα) in breast cancer (BC) is extensively characterized. Our group has previously shown that ERα controls the expression of a number of genes in its unliganded form (apoERα), among which a large group of RNA-binding proteins (RBPs) encode genes, suggesting its role in the control of co- and post-transcriptional events. Methods: apoERα-mediated RNA processing events were characterized by the analysis of transcript usage and alternative splicing changes in an RNA-sequencing dataset from MCF-7 cells after siRNA-induced ERα downregulation. Results: ApoERα depletion induced an expression change of 681 RBPs, including 84 splicing factors involved in translation, ribonucleoprotein complex assembly, and 3′end processing. ApoERα depletion results in 758 isoform switching events with effects on 3′end length and the splicing of alternative cassette exons. The functional enrichment of these events shows that post-transcriptional regulation is part of the mechanisms by which apoERα controls epithelial-to-mesenchymal transition and BC cell proliferation. In primary BCs, the inclusion levels of the experimentally identified alternatively spliced exons are associated with overall and disease-free survival. Conclusion: Our data supports the role of apoERα in maintaining the luminal phenotype of BC cells by extensively regulating gene expression at the alternative splicing level.
Computational Analysis of circRNA Expression Data Giulio Ferrero, Nicola Licheri, Michele De Bortoli, Raffaele A. Calogero, Marco Beccuti, et al. Methods in Molecular Biology, 2021 Analysis of circular RNA (circRNA) expression from RNA-Seq data can be performed with different algorithms and analysis pipelines, tools allowing the extraction of heterogeneous information on the expression of this novel class of RNAs. Computational pipelines were developed to facilitate the analysis of circRNA expression by leveraging different public tools in easy-to-use pipelines. This chapter describes the complete workflow for a computationally reproducible analysis of circRNA expression starting for a public RNA-Seq experiment. The main steps of circRNA prediction, annotation, classification, sequence reconstruction, quantification, and differential expression are illustrated.
DSCAM-AS1-driven proliferation of breast cancer cells involves regulation of alternative exon splicing and 3′-end usage Jamal Elhasnaoui, Valentina Miano, Giulio Ferrero, Elena Doria, Antonette E. Leon, et al. Cancers, 2020 DSCAM-AS1 is a cancer-related long noncoding RNA with higher expression levels in Luminal A, B, and HER2-positive Breast Carcinoma (BC), where its expression is strongly dependent on Estrogen Receptor Alpha (ERα). DSCAM-AS1 expression is analyzed in 30 public datasets and, additionally, by qRT-PCR in tumors from 93 BC patients, to uncover correlations with clinical data. Moreover, the effect of DSCAM-AS1 knockdown on gene expression and alternative splicing is studied by RNA-Seq in MCF-7 cells. We confirm DSCAM-AS1 overexpression in high grade Luminal A, B, and HER2+ BCs and find a significant correlation with disease relapse. In total, 908 genes are regulated by DSCAM-AS1-silencing, primarily involved in the cell cycle and inflammatory response. Noteworthily, the analysis of alternative splicing and isoform regulation reveals 2085 splicing events regulated by DSCAM-AS1, enriched in alternative polyadenylation sites, 3′UTR (untranslated region) shortening and exon skipping events. Finally, the DSCAM-AS1-interacting splicing factor heterogeneous nuclear ribonucleoprotein L (hnRNPL) is predicted as the most enriched RBP for exon skipping and 3′UTR events. The relevance of DSCAM-AS1 overexpression in BC is confirmed by clinical data and further enhanced by its possible involvement in the regulation of RNA processing, which is emerging as one of the most important dysfunctions in cancer.
p21-ras Expression in Human Breast Cancer M De Bortoli, M Giai, A Piffanelli, P Sismondi Biology and Biochemistry of Normal and Cancer Cell Growth, 203-208 , 2026 2026
CircCDYL Association With hnRNPL Modulates CDYL Isoform Switching in Breast Cancer Cells S Bernardi, G Risso, L Franchitti, A Camandona, JM Robbin, I Tarulli, ... Cancer Science 116 (10), 2750-2762 , 2025 2025
The cGAS-STING pathway is a master regulator of OCT4 expression in persistent sarcoma cells and enhances cellular immunotherapy with NK and CIK lymphocytes G Giordano, A Merlini, F Capozzi, G Ferrero, C Tucciarello, S Majidi, ... Cancer Immunology, Immunotherapy 74 (10), 312 , 2025 2025 Citations: 2
Inhibition of the LINE1-derived MET transcript induces apoptosis and oncoprotein knockdown in cancer cells U Miglio, E Berrino, D Avanzato, I Molineris, V Miano, M Milan, L Lanzetti, ... Molecular Therapy Nucleic Acids 36 (2) , 2025 2025 Citations: 3
Nonproteolytic ubiquitination regulates chromatin occupancy by the NCoR/SMRT/HDAC3 corepressor complex in MCF-7 breast cancer cells G Ferrero, MD Cardamone, F Luca, E Bourk, L Ricci, W Liu, Y Gao, ... Proceedings of the National Academy of Sciences 122 (18), e2502805122 , 2025 2025 Citations: 5
Multiple regulatory events contribute to a widespread circular RNA downregulation in precancer and early stage of colorectal cancer development A Camandona, A Gagliardi, N Licheri, S Tarallo, G Francescato, ... Biomarker research 13 (1), 30 , 2025 2025 Citations: 7
Leveraging multi-omics data to infer regulators of mRNA 3’end processing in glioblastoma A Mironov, L Franchitti, S Ghosh, MF Ritz, G Hutter, M De Bortoli, ... Frontiers in Molecular Biosciences 11, 1363933 , 2024 2024 Citations: 4
Integrative circRNA profiling from RNA-sequencing of colorectal cancer and adenoma tissues shows a downregulation in early stages of the disease A Camandona, A Gagliardi, N Licheri, D Festa, S Tarallo, S Cutrupi, ... -, --- , 2024 2024
The silencing of the L1-MET chimeric transcript activates cancer cell death program and inhibits the expression of crucial oncoproteins in lung cancer cells U Miglio, E Berrino, D Avanzato, I Molineris, V Miano, M Milan, L Lanzetti, ... 2023
A regulatory axis between epithelial splicing regulatory proteins and estrogen receptor α modulates the alternative transcriptome of luminal breast cancer J Elhasnaoui, G Ferrero, V Miano, L Franchitti, I Tarulli, ... International Journal of Molecular Sciences 23 (14), 7835 , 2022 2022 Citations: 14
Int. J. Mol. Sci. 2022, 23, 7835. https://doi. org/10.3390/ijms23147835 www. mdpi. com/journal/ijms Article A Regulatory Axis between Epithelial Splicing Regulatory Proteins … J Elhasnaoui, G Ferrero, V Miano, L Franchitti, I Tarulli, LC Tarrero, ... Int. J. Mol. Sci 23, 7835 , 2022 2022
The estrogen receptor α signaling pathway controls alternative splicing in the absence of ligands in breast cancer cells J Elhasnaoui, G Ferrero, V Miano, S Cutrupi, M De Bortoli Cancers 13 (24), 6261 , 2021 2021 Citations: 13
Computational analysis of circRNA expression data G Ferrero, N Licheri, M De Bortoli, RA Calogero, M Beccuti, F Cordero RNA Bioinformatics, 181-192 , 2021 2021 Citations: 12
DSCAM-AS1-driven proliferation of breast cancer cells involves regulation of alternative exon splicing and 3′-end usage J Elhasnaoui, V Miano, G Ferrero, E Doria, AE Leon, ASC Fabricio, ... Cancers 12 (6), 1453 , 2020 2020 Citations: 31
Docker4Circ: a framework for the reproducible characterization of circRNAs from RNA-Seq Data G Ferrero, N Licheri, L Coscujuela Tarrero, C De Intinis, V Miano, ... International Journal of Molecular Sciences 21 (1), 293 , 2019 2019 Citations: 9
Protocol for a reproducible circRNA analysis using Docker4Circ G Ferrero, N Licheri, LC Tarrero, C De Intinis, V Miano, RA Calogero, ... 2019
Pregnancy epigenetic signature in T helper 17 and T regulatory cells in multiple sclerosis A Iannello, S Rolla, A Maglione, G Ferrero, V Bardina, I Inaudi, ... Frontiers in Immunology 9, 3075 , 2019 2019 Citations: 36
Acknowledgement to Reviewers of Non-Coding RNA in 2018 N Amodio, F Ariel, M Atianand, DH Bach, A Bacolla, M Barteková, ... 2019
The expression of LINE1‐ MET chimeric transcript identifies a subgroup of aggressive breast cancers U Miglio, E Berrino, M Panero, G Ferrero, L Coscujuela Tarrero, V Miano, ... International Journal of Cancer 143 (11), 2838-2848 , 2018 2018 Citations: 39
The new world of RNA biomarkers and explorers’ prudence rules M De Bortoli, V Miano, L Coscujuela Tarrero The International journal of biological markers, 1724600818764071 , 2018 2018
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Genome-wide activity of unliganded estrogen receptor-α in breast cancer cells L Caizzi, G Ferrero, S Cutrupi, F Cordero, C Ballaré, V Miano, S Reineri, ... Proceedings of the National Academy of Sciences 111 (13), 4892-4897 , 2014 2014 Citations: 108
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