Federica Scotto di Carlo

@igb.cnr.it

Temporary Researcher at the Institute of Genetics and Biophysics (IGB) - National Research Council (CNR) of Italy
National Research Council of Italy

Federica Scotto di Carlo


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https://researchid.co/f_scottodicarlo

RESEARCH, TEACHING, or OTHER INTERESTS

Cell Biology, Biochemistry, Genetics and Molecular Biology, Cancer Research
13

Scopus Publications

261

Scholar Citations

10

Scholar h-index

10

Scholar i10-index

Scopus Publications

  • ADAR2 induces the differentiation of osteosarcoma cells by editing activity on IGFBP7: new implications for therapy
    Michela Rossi, Federica Scotto di Carlo, Jacopo Di Gregorio, Sharon Russo, Laura Di Giuseppe, Giulia Battafarano, Sara Terreri, Olivia Pagliarosi, Domenico Alessandro Silvestris, Marco Corona, Adriano Barra, Marco Pezzullo, Cristiano De Stefanis, Simone Pelle, Pier Francesco Costici, Salvatore Minisola, Jessica Pepe, Franco Locatelli, Fernando Gianfrancesco, Angela Gallo, Andrea Del Fattore
    Bone Research, 2026
    Osteosarcoma is a highly malignant bone tumor which primarily affects the juvenile population and is characterized by high rate of recurrence and metastasis. RNA editing has emerged as a key process in cancer progression. Herein, we investigated the role of RNA editing enzyme ADAR2 (Adenosine Deaminase Acting on RNA 2) in osteosarcoma. We demonstrated that ADAR2 expression increases during osteoblast differentiation and inversely correlates with the aggressiveness of osteosarcoma cells. Interestingly, the overexpression of ADAR2 in osteosarcoma cell lines reduces their tumoral properties and promotes their differentiation in osteoblast-like cells, as shown by gene expression analysis and mineralization assays. These results were also confirmed by in vivo experiments; indeed, intratibial injection of ADAR2-overexpressing osteosarcoma cells in NSG mice resulted in less aggressive tumors compared to mice injected with pEmpty or pInactive ADAR2 E/A vector-transfected cells. To elucidate the mechanisms by which ADAR2 overexpression induces osteogenic terminal differentiation of osteosarcoma cells, we performed RNA-seq analysis of Saos-2 cells and identified IGFBP7 (Insulin-like Growth Factor Binding Protein 7) as the most highly edited transcript in ADAR2-overexpressing cells. We showed that the editing activity of ADAR2 on IGFBP7 abolishes its proliferative effect on osteosarcoma cells and triggers terminal differentiation. Overall, our results indicate that ADAR2 acts as a tumor suppressor in osteosarcoma and may represent a novel therapeutic target for this aggressive pediatric tumor.
  • From bone alterations to tumours: Genetic drivers linking Paget’s disease of bone to cancer
    Fernando Gianfrancesco, Federica Scotto di Carlo
    Critical Reviews in Oncology Hematology, 2026
  • A mutation in the ZNF687 gene that is responsible for the severe form of Paget’s disease of bone causes severely altered bone remodeling and promotes hepatocellular carcinoma onset in a knock-in mouse model
    Sharon Russo, Federica Scotto di Carlo, Antonio Maurizi, Giorgio Fortunato, Anna Teti, Danilo Licastro, Carmine Settembre, Tommaso Mello, Fernando Gianfrancesco
    Bone Research, 2023
    Paget’s disease (PDB) is a late-onset bone remodeling disorder with a broad spectrum of symptoms and complications. One of the most aggressive forms is caused by the P937R mutation in the ZNF687 gene. Although the genetic involvement of ZNF687 in PDB has been extensively studied, the molecular mechanisms underlying this association remain unclear. Here, we describe the first Zfp687 knock-in mouse model and demonstrate that the mutation recapitulates the PDB phenotype, resulting in severely altered bone remodeling. Through microcomputed tomography analysis, we observed that 8-month-old mutant mice showed a mainly osteolytic phase, with a significant decrease in the trabecular bone volume affecting the femurs and the vertebrae. Conversely, osteoblast activity was deregulated, producing disorganized bone. Notably, this phenotype became pervasive in 16-month-old mice, where osteoblast function overtook bone resorption, as highlighted by the presence of woven bone in histological analyses, consistent with the PDB phenotype. Furthermore, we detected osteophytes and intervertebral disc degeneration, outlining for the first time the link between osteoarthritis and PDB in a PDB mouse model. RNA sequencing of wild-type and Zfp687 knockout RAW264.7 cells identified a set of genes involved in osteoclastogenesis potentially regulated by Zfp687, e.g., Tspan7, Cpe, Vegfc, and Ggt1, confirming its role in this process. Strikingly, in this mouse model, the mutation was also associated with a high penetrance of hepatocellular carcinomas. Thus, this study established an essential role of Zfp687 in the regulation of bone remodeling, offering the potential to therapeutically treat PDB, and underlines the oncogenic potential of ZNF687.
  • Profilin 1 deficiency drives mitotic defects and reduces genome stability
    Federica Scotto di Carlo, Sharon Russo, Francesc Muyas, Maria Mangini, Lorenza Garribba, Laura Pazzaglia, Rita Genesio, Flavia Biamonte, Anna Chiara De Luca, Stefano Santaguida, Katia Scotlandi, Isidro Cortés-Ciriano, Fernando Gianfrancesco
    Communications Biology, 2023
    Profilin 1—encoded by PFN1—is a small actin-binding protein with a tumour suppressive role in various adenocarcinomas and pagetic osteosarcomas. However, its contribution to tumour development is not fully understood. Using fix and live cell imaging, we report that Profilin 1 inactivation results in multiple mitotic defects, manifested prominently by anaphase bridges, multipolar spindles, misaligned and lagging chromosomes, and cytokinesis failures. Accordingly, next-generation sequencing technologies highlighted that Profilin 1 knock-out cells display extensive copy-number alterations, which are associated with complex genome rearrangements and chromothripsis events in primary pagetic osteosarcomas with Profilin 1 inactivation. Mechanistically, we show that Profilin 1 is recruited to the spindle midzone at anaphase, and its deficiency reduces the supply of actin filaments to the cleavage furrow during cytokinesis. The mitotic defects are also observed in mouse embryonic fibroblasts and mesenchymal cells deriving from a newly generated knock-in mouse model harbouring a Pfn1 loss-of-function mutation. Furthermore, nuclear atypia is also detected in histological sections of mutant femurs. Thus, our results indicate that Profilin 1 has a role in regulating cell division, and its inactivation triggers mitotic defects, one of the major mechanisms through which tumour cells acquire chromosomal instability.
  • The Osteoclast Traces the Route to Bone Tumors and Metastases
    Sharon Russo, Federica Scotto di Carlo, Fernando Gianfrancesco
    Frontiers in Cell and Developmental Biology, 2022
    Osteoclasts are highly specialized cells of the bone, with a unique apparatus responsible for resorption in the process of bone remodeling. They are derived from differentiation and fusion of hematopoietic precursors, committed to form mature osteoclasts in response to finely regulated stimuli produced by bone marrow–derived cells belonging to the stromal lineage. Despite a highly specific function confined to bone degradation, emerging evidence supports their relevant implication in bone tumors and metastases. In this review, we summarize the physiological role of osteoclasts and then focus our attention on their involvement in skeletal tumors, both primary and metastatic. We highlight how osteoclast-mediated bone erosion confers increased aggressiveness to primary tumors, even those with benign features. We also outline how breast and pancreas cancer cells promote osteoclastogenesis to fuel their metastatic process to the bone. Furthermore, we emphasize the role of osteoclasts in reactivating dormant cancer cells within the bone marrow niches for manifestation of overt metastases, even decades after homing of latent disseminated cells. Finally, we point out the importance of counteracting tumor progression and dissemination through pharmacological treatments based on a better understanding of molecular mechanisms underlying osteoclast lytic activity and their recruitment from cancer cells.
  • Modulation of endocannabinoid tone in osteoblastic differentiation of mc3t3-e1 cells and in mouse bone tissue over time
    Magdalena Kostrzewa, Ali Mokhtar Mahmoud, Roberta Verde, Federica Scotto di Carlo, Fernando Gianfrancesco, Fabiana Piscitelli, Alessia Ligresti
    Cells, 2021
    Bone is a highly complex and metabolically active tissue undergoing a continuous remodeling process, which endures throughout life. A complex cell-signaling system that plays role in regulating different physiological processes, including bone remodeling, is the endocannabinoid system (ECS). Bone mass expresses CB1 and CB2 cannabinoid receptors and enzymatic machinery responsible for the metabolism of their endogenous ligands, endocannabinoids (AEA and 2-AG). Exogenous AEA is reported to increase the early phase of human osteoblast differentiation in vitro. However, regarding this cell context little is known about how endocannabinoids and endocannabinoid-related N-acylethanolamines like PEA and OEA are modulated, in vitro, during cell differentiation and, in vivo, over time up to adulthood. Here we characterized the endocannabinoid tone during the different phases of the osteoblast differentiation process in MC3T3-E1 cells, and we measured endocannabinoid levels in mouse femurs at life cycle stages characterized by highly active bone growth (i.e., of juvenile, young adult, and mature adult bone). Endocannabinoid tone was significantly altered during osteoblast differentiation, with substantial OEA increment, decline in 2-AG and AEA, and consistent modulation of their metabolic enzymes in maturing and mineralized MC3T3-E1 cells. Similarly, in femurs, we found substantial, age-related, decline in 2-AG, OEA, and PEA. These findings can expand existing knowledge underlying physiological bone cell function and contribute to therapeutic strategies for preventing bone-related metabolic changes accruing through lifespan.
  • Rare variants in autophagy and non-autophagy genes in late-onset pompe disease: Suggestions of their disease-modifying role in two Italian families
    Filomena Napolitano, Giorgia Bruno, Chiara Terracciano, Giuseppina Franzese, Nicole Palomba, Federica Scotto di Carlo, Elisabetta Signoriello, Paolo De Blasiis, Stefano Navarro, Alessandro Gialluisi, Mariarosa Melone, Simone Sampaolo, Teresa Esposito
    International Journal of Molecular Sciences, 2021
    Pompe disease is an autosomal recessive disorder caused by a deficiency in the enzyme acid alpha-glucosidase. The late-onset form of Pompe disease (LOPD) is characterized by a slowly progressing proximal muscle weakness, often involving respiratory muscles. In LOPD, the levels of GAA enzyme activity and the severity of the clinical pictures may be highly variable among individuals, even in those who harbour the same combination of GAA mutations. The result is an unpredictable genotype–phenotype correlation. The purpose of this study was to identify the genetic factors responsible for the progression, severity and drug response in LOPD. We report here on a detailed clinical, morphological and genetic study, including a whole exome sequencing (WES) analysis of 11 adult LOPD siblings belonging to two Italian families carrying compound heterozygous GAA mutations. We disclosed a heterogeneous pattern of myopathic impairment, associated, among others, with cardiac defects, intracranial vessels abnormality, osteoporosis, vitamin D deficiency, obesity and adverse response to enzyme replacement therapy (ERT). We identified deleterious variants in the genes involved in autophagy, immunity and bone metabolism, which contributed to the severity of the clinical symptoms observed in the LOPD patients. This study emphasizes the multisystem nature of LOPD and highlights the polygenic nature of the complex phenotype disclosed in these patients.
  • The two faces of giant cell tumor of bone
    Federica Scotto di Carlo, Michael P. Whyte, Fernando Gianfrancesco
    Cancer Letters, 2020
  • ZNF687 Mutations in an Extended Cohort of Neoplastic Transformations in Paget's Disease of Bone: Implications for Clinical Pathology
    Federica Scotto di Carlo, Laura Pazzaglia, Steven Mumm, Maria S Benassi, Annarosaria De Chiara, Alessandro Franchi, Antonina Parafioriti, Alberto Righi, Teresa Esposito, Michael P Whyte, Fernando Gianfrancesco
    Journal of Bone and Mineral Research, 2020
    Neoplastic transformation is a rare but serious complication of Paget's disease of bone (PDB), occurring in fewer than 1% of individuals with polyostotic disease. Their prognosis is poor, with less than 50% surviving 5 years. In 2016, the genetic alteration of giant cell tumor (GCT) complicating PDB was identified as a founder germline mutation (P937R) in the ZNF687 gene. However, the study population was exclusively of Italian descent, and patients of different ethnic origins were not studied. To fill this gap, herein we performed mutation analysis of ZNF687 in a GCT in the pelvis of a 45-year-old black American woman with polyostotic PDB. The P937R mutation in ZNF687 was found in her tumor but, as expected, the ancestral haplotype that characterizes the Italian GCT/PDB patients was not found. Furthermore, we identified two additional Italian GCT/PDB patients with this ZNF687 mutation, now constituting a cohort of 18 GCT/PDB cases, all harboring the identical mutation. We also searched for ZNF687 mutations in a unique collection of tumor tissues derived from Italian PDB patients, including 28 osteosarcomas (OS/PDB), 8 undifferentiated sarcomas (SRC/PDB), 1 fibrosarcoma (FS/PDB), and 1 chondrosarcoma (CS/PDB). We identified the P937R mutation in one SRC/PDB and a different ZNF687 mutation (R331W) in 1 of 28 pagetic osteosarcomas. Thus, whereas GCT/PDB pathogenesis globally seems to involve the P937R mutation in ZNF687, other neoplasms associated with PDB seem to be less related to mutations in this gene. Finally, we identified the G34W mutation in the H3F3A gene in the maxillary tumor masses of two PDB patients, defining them as conventional GCT rather than GCT/PDB. Thus, combined molecular analysis of H3F3A and ZNF687 is essential to clarify the origin and diagnosis of tumors in PDB. © 2020 American Society for Bone and Mineral Research.
  • The Loss of Profilin 1 Causes Early Onset Paget's Disease of Bone
    Federica Scotto di Carlo, Laura Pazzaglia, Teresa Esposito, Fernando Gianfrancesco
    Journal of Bone and Mineral Research, 2020
    Paget's disease of bone (PDB) is a late-onset disorder frequently caused by mutations in the SQSTM1 gene, leading to hyperactive osteoclasts and resulting in bone pain, deformities, and fractures. However, some more severe forms of PDB—negative for SQSTM1 mutations—have been described, in which the disease degenerates into bone cancers and shows a poor prognosis. Osteosarcoma is the most frequent and aggressive tumor arising in PDB (OS/PDB), with a 5-year survival rate almost nil, but the underlying molecular mechanism is unknown. Here, we investigated an extended pedigree with 11 individuals affected by early onset and polyostotic PDB, mainly interesting the appendicular skeleton. Interestingly, three members also developed secondary osteosarcoma. We performed exome sequencing and identified a 4-bp deletion in the PFN1 gene, resulting in the degradation of the mutant protein. Copy number screening on 218 PDB individuals of our biobank disclosed that four of them (~2%) carry a germline heterozygous deletion of PFN1. The identification of these subjects, who exhibit a particularly severe form of disease, emphasizes the diagnostic value of this genetic screening to identify PDB individuals predisposed to develop osteosarcoma. In fact, we detected allelic imbalance at PFN1 locus also in 8 of 14 (57%) sporadic OS/PDB, further proving its causative role. in vitro experiments also confirmed PFN1 involvement in this form of PDB. Indeed, CRISPR-Cas9-mediated Pfn1 knockout in pre-osteoclasts resulted into enhanced osteoclast differentiation and resorption, with the formation of large osteoclasts never described before in PDB. In addition, Pfn1 lacking pre-osteoblasts lost their differentiation capability and failed to efficiently mineralize bone. Moreover, they acquired features of malignant transformation, including loss of focal adhesions and increased invasion ability. In conclusion, these findings disclose PFN1 haploinsufficiency as the pathological mechanism in OS/PDB. © 2020 American Society for Bone and Mineral Research.
  • ZNF687 mutations are frequently found in pagetic patients from South Italy: implication in the pathogenesis of Paget's disease of bone
    G. Divisato, F. Scotto di Carlo, N. Petrillo, T. Esposito, F. Gianfrancesco
    Clinical Genetics, 2018
  • The identification of H3F3A mutation in giant cell tumour of the clivus and the histological diagnostic algorithm of other clival lesions permit the differential diagnosis in this location
    Federica Scotto di Carlo, Giuseppina Divisato, Maurizio Iacoangeli, Teresa Esposito, Fernando Gianfrancesco
    BMC Cancer, 2018
  • The distinct clinical features of giant cell tumor of bone in pagetic and non-pagetic patients are associated with genetic, biochemical and histological differences
    Giuseppina Divisato, Federica Scotto di Carlo, Laura Pazzaglia, Riccardo Rizzo, Domenico A. Coviello, Maria Serena Benassi, Piero Picci, Teresa Esposito, Fernando Gianfrancesco
    Oncotarget, 2017

RECENT SCHOLAR PUBLICATIONS

  • ADAR2 induces the differentiation of osteosarcoma cells by editing activity on IGFBP7: new implications for therapy: The role of ADAR2 in osteosarcoma
    M Rossi, F Scotto di Carlo, J Di Gregorio, S Russo, L Di Giuseppe, ...
    Bone Research 14 (1), 38 , 2026
    2026
  • Profilin 1 maintains cell cycle fidelity to prevent unscheduled genome doubling and polyploidy in cancer
    F Scotto di Carlo, S Russo, S Gemble, N Vitale, AS Mace, IJ Harmsen, ...
    bioRxiv, 2026.05. 12.724607 , 2026
    2026
  • Mitotic slippage causes nuclear instability in polyploid cells
    S Gemble, M Budzyk, A Simon, R Lambuta, N Weiss, A Forest, ...
    bioRxiv, 2025.07. 21.665898 , 2025
    2025
    Citations: 1
  • A mutation in the ZNF687 gene that is responsible for the severe form of Paget’s disease of bone causes severely altered bone remodeling and promotes …
    S Russo, F Scotto di Carlo, A Maurizi, G Fortunato, A Teti, D Licastro, ...
    Bone Research 11 (1), 16 , 2023
    2023
    Citations: 12
  • Profilin 1 deficiency drives mitotic defects and reduces genome stability
    F Scotto di Carlo, S Russo, F Muyas, M Mangini, L Garribba, L Pazzaglia, ...
    Communications Biology 6 (1), 9 , 2023
    2023
    Citations: 16
  • The osteoclast traces the route to bone tumors and metastases
    S Russo, F Scotto di Carlo, F Gianfrancesco
    Frontiers in Cell and Developmental Biology, 788 , 2022
    2022
    Citations: 43
  • Modulation of Endocannabinoid Tone in Osteoblastic Differentiation of MC3T3-E1 Cells and in Mouse Bone Tissue over Time
    M Kostrzewa, AM Mahmoud, R Verde, F Scotto di Carlo, F Gianfrancesco, ...
    Cells 10 (5), 1199 , 2021
    2021
    Citations: 12
  • Rare Variants in Autophagy and Non-Autophagy Genes in Late-Onset Pompe Disease: Suggestions of Their Disease-Modifying Role in Two Italian Families
    F Napolitano, G Bruno, C Terracciano, G Franzese, NP Palomba, ...
    International Journal of Molecular Sciences 22 (7), 3625 , 2021
    2021
    Citations: 6
  • The two faces of giant cell tumor of bone
    F Scotto di Carlo, MP Whyte, F Gianfrancesco
    Cancer Letters , 2020
    2020
    Citations: 52
  • ZNF687 mutations in an extended cohort of neoplastic transformations in Paget's disease of bone: implication for clinical pathology
    F Scotto di Carlo, L Pazzaglia, S Mumm, MS Benassi, A De Chiara, ...
    Journal of Bone and Mineral Research , 2020
    2020
    Citations: 15
  • The loss of Profilin 1 causes early-onset Paget's disease of bone
    F Scotto di Carlo, L Pazzaglia, T Esposito, F Gianfrancesco
    Journal of Bone and Mineral Research , 2020
    2020
    Citations: 37
  • The identification of H3F3A mutation in giant cell tumour of the clivus and the histological diagnostic algorithm of other clival lesions permit the differential diagnosis in …
    F Scotto di Carlo, G Divisato, M Iacoangeli, T Esposito, F Gianfrancesco
    BMC cancer 18 (1), 358 , 2018
    2018
    Citations: 23
  • ZNF687 mutations are frequently found in pagetic patients from South Italy: implication in the pathogenesis of Paget's disease of bone
    G Divisato, F Scotto di Carlo, N Petrillo, T Esposito, F Gianfrancesco
    Clinical genetics 93 (6), 1240-1244 , 2018
    2018
    Citations: 21
  • The distinct clinical features of giant cell tumor of bone in pagetic and non-pagetic patients are associated with genetic, biochemical and histological differences
    G Divisato, F Scotto di Carlo, L Pazzaglia, R Rizzo, DA Coviello, ...
    Oncotarget 8 (38), 63121 , 2017
    2017
    Citations: 23

MOST CITED SCHOLAR PUBLICATIONS

  • The two faces of giant cell tumor of bone
    F Scotto di Carlo, MP Whyte, F Gianfrancesco
    Cancer Letters , 2020
    2020
    Citations: 52
  • The osteoclast traces the route to bone tumors and metastases
    S Russo, F Scotto di Carlo, F Gianfrancesco
    Frontiers in Cell and Developmental Biology, 788 , 2022
    2022
    Citations: 43
  • The loss of Profilin 1 causes early-onset Paget's disease of bone
    F Scotto di Carlo, L Pazzaglia, T Esposito, F Gianfrancesco
    Journal of Bone and Mineral Research , 2020
    2020
    Citations: 37
  • The identification of H3F3A mutation in giant cell tumour of the clivus and the histological diagnostic algorithm of other clival lesions permit the differential diagnosis in …
    F Scotto di Carlo, G Divisato, M Iacoangeli, T Esposito, F Gianfrancesco
    BMC cancer 18 (1), 358 , 2018
    2018
    Citations: 23
  • The distinct clinical features of giant cell tumor of bone in pagetic and non-pagetic patients are associated with genetic, biochemical and histological differences
    G Divisato, F Scotto di Carlo, L Pazzaglia, R Rizzo, DA Coviello, ...
    Oncotarget 8 (38), 63121 , 2017
    2017
    Citations: 23
  • ZNF687 mutations are frequently found in pagetic patients from South Italy: implication in the pathogenesis of Paget's disease of bone
    G Divisato, F Scotto di Carlo, N Petrillo, T Esposito, F Gianfrancesco
    Clinical genetics 93 (6), 1240-1244 , 2018
    2018
    Citations: 21
  • Profilin 1 deficiency drives mitotic defects and reduces genome stability
    F Scotto di Carlo, S Russo, F Muyas, M Mangini, L Garribba, L Pazzaglia, ...
    Communications Biology 6 (1), 9 , 2023
    2023
    Citations: 16
  • ZNF687 mutations in an extended cohort of neoplastic transformations in Paget's disease of bone: implication for clinical pathology
    F Scotto di Carlo, L Pazzaglia, S Mumm, MS Benassi, A De Chiara, ...
    Journal of Bone and Mineral Research , 2020
    2020
    Citations: 15
  • A mutation in the ZNF687 gene that is responsible for the severe form of Paget’s disease of bone causes severely altered bone remodeling and promotes …
    S Russo, F Scotto di Carlo, A Maurizi, G Fortunato, A Teti, D Licastro, ...
    Bone Research 11 (1), 16 , 2023
    2023
    Citations: 12
  • Modulation of Endocannabinoid Tone in Osteoblastic Differentiation of MC3T3-E1 Cells and in Mouse Bone Tissue over Time
    M Kostrzewa, AM Mahmoud, R Verde, F Scotto di Carlo, F Gianfrancesco, ...
    Cells 10 (5), 1199 , 2021
    2021
    Citations: 12
  • Rare Variants in Autophagy and Non-Autophagy Genes in Late-Onset Pompe Disease: Suggestions of Their Disease-Modifying Role in Two Italian Families
    F Napolitano, G Bruno, C Terracciano, G Franzese, NP Palomba, ...
    International Journal of Molecular Sciences 22 (7), 3625 , 2021
    2021
    Citations: 6
  • Mitotic slippage causes nuclear instability in polyploid cells
    S Gemble, M Budzyk, A Simon, R Lambuta, N Weiss, A Forest, ...
    bioRxiv, 2025.07. 21.665898 , 2025
    2025
    Citations: 1
  • ADAR2 induces the differentiation of osteosarcoma cells by editing activity on IGFBP7: new implications for therapy: The role of ADAR2 in osteosarcoma
    M Rossi, F Scotto di Carlo, J Di Gregorio, S Russo, L Di Giuseppe, ...
    Bone Research 14 (1), 38 , 2026
    2026
  • Profilin 1 maintains cell cycle fidelity to prevent unscheduled genome doubling and polyploidy in cancer
    F Scotto di Carlo, S Russo, S Gemble, N Vitale, AS Mace, IJ Harmsen, ...
    bioRxiv, 2026.05. 12.724607 , 2026
    2026