ESR1-Activating Mutations Confer Metabolic Vulnerabilities in ER+ Breast Cancer Francesca Bonechi, Marina Bacci, Nicla Lorito, Alfredo Smiriglia, Angela Subbiani, Edoardo Pagliantini, Giuseppina Comito, Giulia Gangarossa, Assia Duatti, Rania El Botty, Laura Sourd, Elisabetta Romano, Gabriele Tani, Ilenia Segatto, Barbara Belletti, Icro Meattini, Lorenzo Livi, Bruna Cerbelli, Andrea Botticelli, Marco Fiorillo, Elisabetta Marangoni, Andrea Morandi Cancer Research, 2026 Endocrine therapy (ET) is the standard of care for estrogen receptor (ER)–positive breast cancer. Point mutations in the ligand-binding domain of the gene encoding the estrogen receptor (ESR1) are rare in naïve ER+ breast cancer while becoming common in the ET-resistant setting. In this study, we found that ESR1 mutations expose breast cancers to critical vulnerabilities related to lipid metabolism. Particularly, ESR1 mutations that induce constitutive ER activation drove aberrant lipid biogenesis and lipid upload in parallel with increased expression of acyl-CoA synthetase long-chain family member 4 (ACSL4), which plays a crucial role in fatty acid activation and has been shown to correlate with increased ferroptosis susceptibility. Although ER+ breast cancer cells displayed ferroptosis resistance, the presence of ESR1 mutations rendered tumor cells sensitive to ferroptosis induction. Importantly, ferroptosis inducers potentiated the effects of the selective ER degraders fulvestrant and elacestrant, which are the standard of care for breast cancers carrying ESR1 mutations. These findings, validated both in preclinical models and in patient-derived material, identify a combinatory therapeutic approach in the setting of ET resistance and establish ACSL4 as an important biomarker to recognize ER+ breast cancers susceptible to ferroptosis induction. Significance: ESR1 mutations in breast cancer induce metabolic changes that trigger ferroptosis sensitivity, enabling ferroptosis inducers to enhance selective ER degraders' efficacy and positioning ACSL4 as a biomarker for guiding therapy in endocrine-resistant disease.
Under pressure: peroxisomes in cancer therapy resistance Nicla Lorito, Francesca Bonechi, Elisabetta Romano, Alfredo Smiriglia, Andrea Morandi Trends in Molecular Medicine, 2026 Therapy resistance is a major obstacle to durable clinical responses. While genetic alterations and signalling rewiring are primary drivers of resistance, metabolic adaptation, which is closely intertwined with these processes, enables tumour persistence under therapeutic pressure and directly contributes to resistance. Peroxisomes are metabolic organelles with a role in controlling lipid metabolism, together with redox signalling and homeostasis-processes that intersect with pathways governing cancer behaviour and therapy response. Indeed, peroxisomal functions are remodelled to support metabolic plasticity and redox buffering under therapeutic stress. In this review, we synthesise emerging evidence linking peroxisome biology to resistance to chemotherapy, targeted therapies, radiotherapy, and immunotherapy and discuss how peroxisomal pathways may be exploited therapeutically or as biomarkers to overcome cancer therapy resistance.
Cell Cycle Control of Nuclear Metabolism Couples Phosphatidylinositol Signaling to Histone Methylation Antoni Gañez‐Zapater, Savvas Kourtis, Camilla Reiter Elbæk, Lorena Espinar, Carolina Toro‐Márquez, Albert Coll‐Manzano, Alfredo Smiriglia, Laura García‐López, Laura Wiegand, Maria Guirola, Frédéric Fontaine, Andrea Morandi, André C. Müller, Sara Sdelci Advanced Science, 2026 Progression through the cell cycle requires coordinated regulation of transcription, chromatin state, and cellular metabolism. While metabolic enzymes are known to localize the nucleus and influence chromatin states, how nuclear metabolism itself oscillates during the cell cycle remains unexplored. Here, we combine a customized FUCCI‐3 reporter with chromatome mass spectrometry and high‐throughput imaging to systematically resolve nuclear and chromatin‐associated metabolic changes across cell cycle phases. We identify phosphatidylinositol metabolism as a nuclear pathway that oscillates with the cell cycle, with PIP5K1A, PLCD3, and PLD2 showing phase‐specific nuclear and chromatin dynamics. Nuclear PIP2 levels redistribute within the nucleus depending on cell cycle stage. Downregulation of PIP5K1A reduces nuclear PIP2 levels, whereas nuclear enrichment of PIP5K1A increases PIP2 abundance in the nucleus and nucleolus, functionally linking PIP5K1A nuclear localization to nuclear PIP2 synthesis. Moreover, perturbation of nuclear PIP2 synthesis alters chromatin methylation, with a pronounced impact on H4K20 monomethylation. Together, our results reveal that nuclear phosphatidylinositol metabolism is cell cycle regulated and functionally linked to chromatin methylation, establishing nuclear lipid metabolism as a previously unrecognized layer of cell cycle control.
MAPK15 controls intracellular lipid uptake and protects mammalian liver from steatotic disease Giovanni Inzalaco, Sara Gargiulo, Denise Bonente, Lisa Gherardini, Lorenzo Franci, Nicla Lorito, Serena Del Turco, Danilo Tatoni, Tiziana Tamborrino, Federico Galvagni, Eugenio Bertelli, Romina D’Aurizio, Maria Grazia Andreassi, Giuseppina Basta, Amalia Gastaldelli, Andrea Morandi, Virginia Barone, Mario Chiariello Hepatology Communications, 2026 Background: Accumulation of lipids in the liver characterizes metabolic dysfunction–associated steatotic liver disease (MASLD), the most prevalent chronic liver disease worldwide. Methods: To explore the role of mitogen-activated protein kinase 15 (MAPK15) in mammalian lipid homeostasis, we created and characterized the first knockout mouse model for this gene. Hepatocellular in vitro models were also used to further investigate molecular mechanisms underlying MAPK15-dependent regulation of lipid metabolism in the liver. Results: We observed that Mapk15-/- mice exhibited liver steatosis in the context of a MASLD-like phenotype while hepatocellular in vitro models allowed to demonstrate that dysregulated accumulation of lipids was due to increased expression and membrane localization of the CD36 fatty acid translocase. Consistently, Mapk15-/- mice exhibited elevated hepatic levels of CD36 and feeding them with a western-type diet significantly accelerated their progression to a steatohepatitis-like phenotype. Importantly, transcriptomic analysis of human cohorts revealed increased liver expression of MAPK15 in MASLD patients, suggesting a compensatory role in disease progression. In this context, overexpression of this kinase efficiently opposed lipid accumulation in a MASLD hepatocellular model, opening to the possibility of counteracting hepatic steatosis in humans by pharmacologically or genetically activating this MAP kinase. Conclusions: Presented data highlight a critical role for MAPK15 in liver physiopathology, by contributing to maintaining physiological intracellular levels of lipids in this tissue.
Estrogen-dependent activation of TRX2 reverses oxidative stress and metabolic dysfunction associated with steatotic disease Alfredo Smiriglia, Nicla Lorito, Marina Bacci, Angela Subbiani, Francesca Bonechi, Giuseppina Comito, Marta Anna Kowalik, Andrea Perra, Andrea Morandi Cell Death and Disease, 2025 Metabolic dysfunction-associated steatotic liver disease (MASLD) encompasses a spectrum of hepatic disorders, ranging from simple steatosis to steatohepatitis, with the most severe outcomes including cirrhosis, liver failure, and hepatocellular carcinoma. Notably, MASLD prevalence is lower in premenopausal women than in men, suggesting a potential protective role of estrogens in mitigating disease onset and progression. In this study, we utilized preclinical in vitro models—immortalized cell lines and hepatocyte-like cells derived from human embryonic stem cells—exposed to clinically relevant steatotic-inducing agents. These exposures led to lipid droplet (LD) accumulation, increased reactive oxygen species (ROS) levels, and mitochondrial dysfunction, along with decreased expression of markers associated with hepatocyte functionality and differentiation. Estrogen treatment in steatotic-induced liver cells resulted in reduced ROS levels and LD content while preserving mitochondrial integrity, mediated by the upregulation of mitochondrial thioredoxin 2 (TRX2), an antioxidant system regulated by the estrogen receptor. Furthermore, disruption of TRX2, either pharmacologically using auranofin or through genetic interference, was sufficient to counteract the protective effects of estrogens, highlighting a potential mechanism through which estrogens may prevent or slow MASLD progression.
Lead induces cell-autonomous proliferation and metabolic reprogramming of hepatocytes Marina Serra, Alfredo Smiriglia, Cristina Migliore, Andrea Caddeo, Nicla Lorito, Gabriele Tani, Giorgia Zedda, Amedeo Columbano, Andrea Perra, Silvia Giordano, Marta Anna Kowalik, Andrea Morandi Cell Death and Disease, 2025 Reprogramming of energy metabolism is widely recognized as a hallmark of cancer cells. However, recent evidence indicates that metabolic reprogramming also occurs in vivo in differentiated rat hepatocytes following administration of the primary mitogen lead nitrate (LN). It remains unclear whether this phenomenon results from a direct action of LN on hepatocytes or is mediated by non-parenchymal liver cells. In our study, we investigated the cell-autonomous effects of LN using immortalized non-tumorigenic rat (RNT) and human (THLE-2) hepatocytes. LN treatment induced cancer-like metabolic features in non-tumorigenic hepatocytes, including increased glycolysis, activation of both oxidative and non-oxidative pentose phosphate pathways (PPP), and reduced oxidative phosphorylation (OXPHOS). Additionally, LN increased several targets of the transcription factor nuclear factor (erythroid-derived 2)-like 2 (NRF2), a key regulator of cellular defense against stress. We found that activation of the Kelch-like ECH-associated protein 1 (KEAP1)-NRF2 pathway was associated with increased hepatocyte proliferation. Importantly, silencing NRF2 completely abolished the LN-induced metabolic reprogramming. In contrast, triiodothyronine (T3), a liver mitogen that does not activate NRF2, failed to trigger metabolic reprogramming. Overall, our findings demonstrate that LN directly drives both proliferation and metabolic reprogramming in hepatocytes, independently of microenvironmental or immune signals. NRF2 plays a central role as a key driver of these cancer-like metabolic shifts, even in non-tumorigenic cells.
In vivo imaging of the spatial heterogeneity of intratumoral acidosis (pH) as a marker of the metastatic phenotype in breast cancer Alessia Corrado, Nicla Lorito, Annasofia Anemone, Antonella Carella, Daisy Villano, Elisa Pirotta, Francesco Gammaraccio, Angela Subbiani, Marina Bacci, Walter Dastrù, Andrea Morandi, Dario Livio Longo Breast Cancer Research, 2025 Background Metabolic alterations, including acidosis in the tumor microenvironment, have been extensively linked to more aggressive phenotypes and increased therapy resistance. However, current imaging techniques are limited in their ability to capture extracellular tumor acidosis precisely and assess spatial heterogeneity in vivo, making its association with augmented malignancy poorly understood. In this study, we investigated whether Magnetic Resonance Imaging– Chemical Exchange Saturation Transfer (MRI-CEST) technique for tumor pH imaging of intratumoral acidosis could differentiate between metastatic and non-metastatic breast cancers. Methods Isogenic metastatic (4T1) and non-metastatic (67NR) breast cancer cell lines were characterized for their metabolic and acidosis features, including LDH-A/PDK-1 expression, glucose consumption, extracellular acidification rate (ECAR) and oxygen consumption rate (OCR). Potential relationship between tumor acidosis, vascularization and hypoxia with metastatic potential was assessed in vivo by MRI-based imaging approaches in orthotopic breast tumors. Validation of MRI findings was assessed ex vivo by western blot, immunohistochemistry and immunofluorescence assays for a multiparametric characterization of tumor microenvironment and metabolic properties. Results We observed a higher energetic profile of the 4T1 cells compared to the 67NR cells, alongside elevated glycolytic (LDH-A, PDK-1), hypoxia (CAIX, Pimonidazole), and vascularization (CD31) markers in 4T1 orthotopic primary tumors, which were associated with a greater metastatic propensity. MRI-CEST tumor pH imaging revealed increased extracellular tumor acidity in 4T1 tumors, along with marked spatial intratumoral heterogeneity, in contrast to the more homogenous 67NR tumors, as further confirmed by LAMP-2 staining. Notably, this spatial intratumor heterogeneity in acidosis enables clear differentiation between high- and low-malignancy tumors. Conclusions These findings underscore the role of tumor acidosis and its spatial heterogeneity in promoting aggressive phenotypes and highlight the potential of in vivo tumor pH imaging as a marker of malignancy in breast cancers.
CD44 and SLC1A2 are commonly regulated but do not form a fusion transcript in ER+ breast cancer Francesca Bonechi, Marina Bacci, Nicla Lorito, Alfredo Smiriglia, Edoardo Pagliantini, Matteo Benelli, Icro Meattini, Andrea Morandi Molecular and Cellular Biochemistry, 2025 Endocrine therapy (ET) is essential for managing ER+ HER2− breast cancer; however, resistance remains a significant clinical challenge. This study investigated whether CD44-SLC1A2 gene fusions, reported in gastrointestinal malignancies, contribute to ET resistance mechanisms in breast cancer. Although no CD44-SLC1A2 fusions were detected, high expression of CD44 and SLC1A2 was associated with poor survival outcomes and identified a therapy-resistant subpopulation sustained by aspartate and glutamate metabolism, highlighting potential metabolic vulnerabilities for future therapeutic intervention.
Targeting carbonic anhydrase IX/XII prevents the anti-ferroptotic effect of stromal lactic acid in prostate carcinoma Elisa Pardella, Giuseppina Comito, Luigi Ippolito, Erica Pranzini, Marta Iozzo, Giulia Gangarossa, Francesca Virgilio, Silvia Bua, Alessio Nocentini, Giada Sandrini, Nicla Lorito, Marina Bacci, Gabriella Nesi, Pietro Spatafora, Sergio Serni, Claudiu T. Supuran, Andrea Morandi, Paola Chiarugi, Elisa Giannoni Molecular Oncology, 2025 Ferroptosis is a form of regulated cell death dependent on iron‐driven phospholipid peroxidation and is controlled by both cell autonomous and non‐cell autonomous mechanisms. In prostate cancer (PCa), tumor cells engage in a metabolic crosstalk with cancer‐associated fibroblasts (CAFs), resulting in increased utilization of CAF‐secreted lactic acid, that ultimately supports cancer aggressiveness. In this context, the effect of the prostate tumor microenvironment in modulating ferroptosis sensitivity has not yet been extensively investigated. Here, we demonstrate that CAF‐secreted lactic acid protects PCa cells from ferroptosis induction and supports the upregulation of the antioxidant enzyme glutathione peroxidase 4 (GPX4). Interestingly, targeting carbonic anhydrase IX/XII (CA IX/XII), the main regulators of microenvironmental acidosis, in tumor and stromal compartments hinders lactic acid shuttle within the tumor–stroma interplay and thus, prevents ferroptosis resistance induced by lactic acid. Analyses of tissue samples from PCa patients also revealed that GPX4, CA IX, and CA XII expression levels increase during PCa progression. Overall, these findings support a role for stromal lactic acid in mediating ferroptosis resistance in PCa, identifying CA IX/XII as potential therapeutic targets regulating ferroptosis sensitivity.
Cardioprotection in patients with anthracycline-treated breast cancer: final analysis from the 2 × 2 randomized, placebo-controlled, double-blind SAFE trial I. Meattini, C. Becherini, F. Martella, M.R. Del Bene, C. Saieva, C. Bacci, L. Coltelli, G. Pilato, L. Visani, V. Salvestrini, G. Francolini, L. Marrazzo, M. Bernini, L. Orzalesi, J. Nori, S. Bianchi, I. Olivotto, A. Morandi, G. Curigliano, G. Barletta, L. Livi ESMO Open, 2025 BACKGROUND: Anthracycline-based chemotherapy is a cornerstone in breast cancer treatment but is associated with cardiotoxicity, including subclinical cardiac damage. This study evaluates the efficacy of ramipril and bisoprolol in preventing subclinical cardiac impairment in patients with nonmetastatic breast cancer undergoing anthracycline-based chemotherapy. PATIENTS AND METHODS: The SAFE trial is a multicenter, 2 × 2 factorial, randomized, placebo-controlled, double-blind study involving 262 patients. Participants were allocated to one of four groups: placebo-placebo, ramipril-placebo, bisoprolol-placebo, or ramipril-bisoprolol, administered concurrently with chemotherapy. Subclinical cardiac damage was assessed at 24 months using echocardiographic measures, specifically a ≥10% reduction in three-dimensional left ventricular ejection fraction (3D-LVEF) or global longitudinal strain (GLS). RESULTS: At 24 months, patients receiving ramipril, bisoprolol, or their combination experienced significantly smaller declines in 3D-LVEF compared with placebo (-2.1%, -2.2%, and -3.4%, respectively; all P < 0.001). GLS results were consistent with these findings (P < 0.001). Subclinical cardiac damage occurred in 11.4% of patients receiving ramipril versus 39.3% without ramipril (P < 0.001), and in 9.6% of patients receiving bisoprolol versus 43.5% without bisoprolol (P < 0.001). CONCLUSIONS: Ramipril and bisoprolol significantly reduce the incidence of subclinical cardiac damage in patients with breast cancer undergoing anthracycline-based chemotherapy, thus supporting their use as early prevention cardioprotective strategies.
Metabolic reprogramming in Nrf2-driven proliferation of normal rat hepatocytes Marta A. Kowalik, Keiko Taguchi, Marina Serra, Andrea Caddeo, Elisabetta Puliga, Marina Bacci, Seizo Koshiba, Jin Inoue, Eiji Hishinuma, Andrea Morandi, Silvia Giordano, Andrea Perra, Masayuki Yamamoto, Amedeo Columbano Hepatology, 2024
Acetyl-CoA carboxylase 1 controls a lipid droplet–peroxisome axis and is a vulnerability of endocrine-resistant eR+ breast cancer Marina Bacci, Nicla Lorito, Alfredo Smiriglia, Angela Subbiani, Francesca Bonechi, Giuseppina Comito, Ludivine Morriset, Rania El Botty, Matteo Benelli, Joanna I. López-Velazco, Maria M. Caffarel, Ander Urruticoechea, George Sflomos, Luca Malorni, Michela Corsini, Luigi Ippolito, Elisa Giannoni, Icro Meattini, Vittoria Matafora, Kristina Havas, Angela Bachi, Paola Chiarugi, Elisabetta Marangoni, Andrea Morandi Science Translational Medicine, 2024
International multidisciplinary consensus on the integration of radiotherapy with new systemic treatments for breast cancer: European Society for Radiotherapy and Oncology (ESTRO)-endorsed recommendations Icro Meattini, Carlotta Becherini, Saverio Caini, Charlotte E Coles, Javier Cortes, Giuseppe Curigliano, Evandro de Azambuja, Clare M Isacke, Nadia Harbeck, Orit Kaidar-Person, Elisabetta Marangoni, Birgitte V Offersen, Hope S Rugo, Viola Salvestrini, Luca Visani, Andrea Morandi, Matteo Lambertini, Philip Poortmans, Lorenzo Livi, Sara Alkner, Indrani S. Bhattacharya, Liesbeth Boersma, Maurizio Callari, Robert B. Clarke, Lucia Del Mastro, Maria Ekholm, Alessandra Gennari, Anna M. Kirby, Stephanie Kroeze, Marcos Malumbres, Maja Vestmø Maraldo, Gustavo Nader Marta, Ingvil Mjaaland, Gilberto Morgan, Barbara Pistilli, Shani Paluch-Shimon, Sofia Rivera, Sven Rottenberg, Cristina Saura, Tanja Skyttä, Tanja Spanic Lancet Oncology, 2024
Oxidative phosphorylation is a metabolic vulnerability of endocrine therapy and palbociclib resistant metastatic breast cancers Rania El-Botty, Ludivine Morriset, Elodie Montaudon, Zakia Tariq, Anne Schnitzler, Marina Bacci, Nicla Lorito, Laura Sourd, Léa Huguet, Ahmed Dahmani, Pierre Painsec, Heloise Derrien, Sophie Vacher, Julien Masliah-Planchon, Virginie Raynal, Sylvain Baulande, Thibaut Larcher, Anne Vincent-Salomon, Guillaume Dutertre, Paul Cottu, Géraldine Gentric, Fatima Mechta-Grigoriou, Scott Hutton, Keltouma Driouch, Ivan Bièche, Andrea Morandi, Elisabetta Marangoni Nature Communications, 2023
Safety profile of cyclin-dependent kinase (CDK) 4/6 inhibitors with concurrent radiation therapy: A systematic review and meta-analysis Carlotta Becherini, Luca Visani, Saverio Caini, Indrani S. Bhattacharya, Anna M. Kirby, Gustavo Nader Marta, Gilberto Morgan, Viola Salvestrini, Charlotte E. Coles, Javier Cortes, Giuseppe Curigliano, Evandro de Azambuja, Nadia Harbeck, Clare M. Isacke, Orit Kaidar-Person, Elisabetta Marangoni, Birgitte Offersen, Hope S. Rugo, Andrea Morandi, Matteo Lambertini, Philip Poortmans, Lorenzo Livi, Icro Meattini Cancer Treatment Reviews, 2023
Safety profile of trastuzumab-emtansine (T-DM1) with concurrent radiation therapy: A systematic review and meta-analysis Viola Salvestrini, Kyubo Kim, Saverio Caini, Sara Alkner, Maria Ekholm, Tanja Skyttä, Carlotta Becherini, Charlotte E. Coles, Orit Kaidar-Person, Birgitte Offersen, Evandro de Azambuja, Luca Visani, Javier Cortes, Nadia Harbeck, Hope S. Rugo, Clare M. Isacke, Elisabetta Marangoni, Andrea Morandi, Matteo Lambertini, Philip Poortmans, Lorenzo Livi, Icro Meattini Radiotherapy and Oncology, 2023
Lysosomal lipid switch sensitises to nutrient deprivation and mTOR targeting in pancreatic cancer Maria Chiara De Santis, Luca Gozzelino, Jean Piero Margaria, Andrea Costamagna, Edoardo Ratto, Federico Gulluni, Enza Di Gregorio, Erica Mina, Nicla Lorito, Marina Bacci, Rossano Lattanzio, Gianluca Sala, Paola Cappello, Francesco Novelli, Elisa Giovannetti, Caterina Vicentini, Silvia Andreani, Pietro Delfino, Vincenzo Corbo, Aldo Scarpa, Paolo Ettore Porporato, Andrea Morandi, Emilio Hirsch, Miriam Martini Gut, 2023
Lactate Rewires Lipid Metabolism and Sustains a Metabolic-Epigenetic Axis in Prostate Cancer Luigi Ippolito, Giuseppina Comito, Matteo Parri, Marta Iozzo, Assia Duatti, Francesca Virgilio, Nicla Lorito, Marina Bacci, Elisa Pardella, Giada Sandrini, Francesca Bianchini, Roberta Damiano, Lavinia Ferrone, Giancarlo la Marca, Sergio Serni, Pietro Spatafora, Carlo V. Catapano, Andrea Morandi, Elisa Giannoni, Paola Chiarugi Cancer Research, 2022
A novel phage display based platform for exosome diversity characterization Domenico Maisano, Selena Mimmi, Vincenzo Dattilo, Fabiola Marino, Massimo Gentile, Eleonora Vecchio, Giuseppe Fiume, Nancy Nisticò, Annamaria Aloisio, Maria Penelope de Santo, Giovanni Desiderio, Vincenzo Musolino, Saverio Nucera, Francesca Sbrana, Sebastiano Andò, Simone Ferrero, Andrea Morandi, Francesco Bertoni, Ileana Quinto, Enrico Iaccino Nanoscale, 2022
Thyroid hormone inhibits hepatocellular carcinoma progression via induction of differentiation and metabolic reprogramming Marta Anna Kowalik, Elisabetta Puliga, Lavinia Cabras, Pia Sulas, Annalisa Petrelli, Andrea Perra, Giovanna Maria Ledda-Columbano, Andrea Morandi, Simone Merlin, Claudia Orrù, Carlos Sanchez-Martin, Francesca Fornari, Laura Gramantieri, Matteo Parri, Andrea Rasola, Sara Erika Bellomo, Carlos Sebastian, Antonia Follenzi, Silvia Giordano, Amedeo Columbano Journal of Hepatology, 2020
Compartmentalized activities of the pyruvate dehydrogenase complex sustain lipogenesis in prostate cancer Jingjing Chen, Ilaria Guccini, Diletta Di Mitri, Daniela Brina, Ajinkya Revandkar, Manuela Sarti, Emiliano Pasquini, Abdullah Alajati, Sandra Pinton, Marco Losa, Gianluca Civenni, Carlo V. Catapano, Jacopo Sgrignani, Andrea Cavalli, Rocco D’Antuono, John M. Asara, Andrea Morandi, Paola Chiarugi, Sara Crotti, Marco Agostini, Monica Montopoli, Ionica Masgras, Andrea Rasola, Ramon Garcia-Escudero, Nicolas Delaleu, Andrea Rinaldi, Francesco Bertoni, Johann de Bono, Arkaitz Carracedo, Andrea Alimonti Nature Genetics, 2018
Metabolic reprogramming identifies the most aggressive lesions at early phases of hepatic carcinogenesis Marta Anna Kowalik, Giulia Guzzo, Andrea Morandi, Andrea Perra, Silvia Menegon, Ionica Masgras, Elena Trevisan, Maria Maddalena Angioni, Francesca Fornari, Luca Quagliata, Giovanna Maria Ledda-Columbano, Laura Gramantieri, Luigi Terracciano, Silvia Giordano, Paola Chiarugi, Andrea Rasola, Amedeo Columbano Oncotarget, 2016
Senescent stroma promotes prostate cancer progression: The role of miR-210 Maria Letizia Taddei, Lorenzo Cavallini, Giuseppina Comito, Elisa Giannoni, Marco Folini, Alberto Marini, Paolo Gandellini, Andrea Morandi, Gianfranco Pintus, Maria Rosaria Raspollini, Nadia Zaffaroni, Paola Chiarugi Molecular Oncology, 2014
