@article{%a1.%Y_230,

title = {In vitro study of cold atmospheric plasma-induced proliferation inhibition and morphological changes in head and neck carcinoma cell lines},

author = {Maravic T and Petrucci G and Giacomo VD and Mazzitelli C and Acharya TR and Kaushik NK and Choi EH and Rapino M and D'Urso D and Josic U and Caponio VCA and Micaroni M and Edoardo M and Russo LL and Muzio LL and Breschi L and Perotti V},

url = {https://www.sciencedirect.com/science/article/pii/S0300571225004518?via%3Dihub},

doi = {10.1016/j.jdent.2025.106007},

year  = {2025},

date = {2025-09-03},

journal = {Journal of dentistry},

volume = {161},

pages = {106007},

abstract = {Objectives: The use of cold atmospheric plasma (CAP) has been growing in medical field. Since limited data exist on the influence of CAP exposure on head and neck cancer (HNC) cells, we aimed to investigate in vitro its impact on proliferation and morphology of HNC (HSC2, HSC3, and FaDu) cells, as well as healthy gingival fibroblasts (hGF). Methods: A CAP gas air jet was applied directly on the HSC2, HSC3, FaDu and hGF cells for 30 and 60 s; doxorubicin has been used as positive control. Inhibition of cell proliferation at different time points (24, 48, and 72 h) was investigated through MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium]. Morphological alterations were observed using scanning electron microscope (SEM) and transmission electron microscope (TEM). Data were statistically analyzed (p < 0.05). Results: CAP exposure of 60 s showed the highest proliferation inhibitory effects in all investigated cancer cell lines (p < 0.001). While HSC2 had the highest proliferation inhibition at 24 h, HSC3, and FaDu exhibited a positive, time-dependent inhibitory effect (24 < 48 < 72 h) after CAP exposure. Interestingly, effects of CAP in the hGF were minimal. SEM observations revealed morphological changes in HNC cells treated with CAP at 30 and 60 s. Moreover, TEM showed stressed conditions in the survived HNC cells at 48 h after CAP exposure demonstrated by the presence of multilamellar and multi-vesicular bodies. Conclusions: CAP treatment induced proliferation inhibition, morphologic changes and stressed conditions in HNC cell lines (HSC2, HSC3, and FaDu), while demonstrating limited effects on hGF cells. Clinical significance: This work characterized early cellular responses of HSC2, HSC3, and FaDu to CAP exposure, including proliferation, and morphology, as foundational data before progressing to more clinically representative models.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_229,

title = {In vitro study of cold atmospheric plasma-induced proliferation inhibition and morphological changes in head and neck carcinoma cell lines},

author = {Maravic T and Petrucci G and Giacomo VD and Mazzitelli C and Acharya TR and Kaushik NK and Choi EH and Rapino M and D'Urso D and Josic U and Caponio VCA and Micaroni M and Edoardo M and Russo LL and Muzio LL and Breschi L and Perotti V},

url = {https://www.sciencedirect.com/science/article/pii/S0300571225004518?via%3Dihub},

doi = {10.1016/j.jdent.2025.106007},

year  = {2025},

date = {2025-09-03},

journal = {Journal of dentistry},

volume = {161},

pages = {106007},

abstract = {Objectives: The use of cold atmospheric plasma (CAP) has been growing in medical field. Since limited data exist on the influence of CAP exposure on head and neck cancer (HNC) cells, we aimed to investigate in vitro its impact on proliferation and morphology of HNC (HSC2, HSC3, and FaDu) cells, as well as healthy gingival fibroblasts (hGF). Methods: A CAP gas air jet was applied directly on the HSC2, HSC3, FaDu and hGF cells for 30 and 60 s; doxorubicin has been used as positive control. Inhibition of cell proliferation at different time points (24, 48, and 72 h) was investigated through MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium]. Morphological alterations were observed using scanning electron microscope (SEM) and transmission electron microscope (TEM). Data were statistically analyzed (p < 0.05). Results: CAP exposure of 60 s showed the highest proliferation inhibitory effects in all investigated cancer cell lines (p < 0.001). While HSC2 had the highest proliferation inhibition at 24 h, HSC3, and FaDu exhibited a positive, time-dependent inhibitory effect (24 < 48 < 72 h) after CAP exposure. Interestingly, effects of CAP in the hGF were minimal. SEM observations revealed morphological changes in HNC cells treated with CAP at 30 and 60 s. Moreover, TEM showed stressed conditions in the survived HNC cells at 48 h after CAP exposure demonstrated by the presence of multilamellar and multi-vesicular bodies. Conclusions: CAP treatment induced proliferation inhibition, morphologic changes and stressed conditions in HNC cell lines (HSC2, HSC3, and FaDu), while demonstrating limited effects on hGF cells. Clinical significance: This work characterized early cellular responses of HSC2, HSC3, and FaDu to CAP exposure, including proliferation, and morphology, as foundational data before progressing to more clinically representative models.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_228,

title = {Human Helicase DDX5 is Hijacked by SARS-CoV‑2 Nsp13 Helicase to Enhance RNA Unwinding},

author = {Barra G and Ruggiero A and Napolitano V and Lodola C and Secchi M and Pallotta MM and Benincasa V and Leone F and Maga G and Berisio R},

url = {https://pmc.ncbi.nlm.nih.gov/articles/PMC12355267/},

doi = {10.1021/acsomega.5c04271},

year  = {2025},

date = {2025-09-03},

urldate = {2025-09-03},

journal = {ACS omega},

volume = {10},

issue = {31},

pages = {34941-34950},

abstract = {DEAD-box protein (DDX) 5 plays important roles in multiple aspects of cellular processes that require modulation of the RNA structure. Alongside the canonical role in RNA metabolism, numerous studies have demonstrated that DDX5 influences viral infections by directly interacting with viral proteins. However, the precise functional role of DDX5 during viral infection remains largely unclear. Here, we explore the previously undiscovered ability of DDX5 to interact and synergize with the Nsp13 helicase of SARS-CoV-2. We show that DDX5 exhibits a nanomolar binding affinity to Nsp13. Also, by dissecting DDX5 in its individual domains, we show that the Nsp13-DDX5 interaction is mediated by the RecA1 domain of DDX5. Importantly, we show that DDX5 and Nsp13 synergize in unwinding double-stranded RNA. Consistent with its ability to bind Nsp13, the RecA1 domain of DDX5 acts as a weak inhibitor of the synergic action of the two helicases in the RNA unwinding process. Modeling of the DDX5-Nsp13 complex provides a plausible explanation for the synergic action of the two helicases, in a mechanism that is likely instrumental in the early stage of infection, when the concentration of Nsp13 is still low.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_228,

title = {Weaponizing CRISPR/Cas9 for selective elimination of cells with an aberrant genome},

author = {Tavella S and di Lillo A and Conti A and Iannelli F and Mancheno-Ferris A and Matti V and Di Micco R and {d’Adda di Fagagna F}},

url = {https://www.sciencedirect.com/science/article/pii/S1568786425000369?via%3Dihub},

doi = {10.1016/j.dnarep.2025.103840},

year  = {2025},

date = {2025-08-11},

urldate = {2025-08-11},

journal = {DNA Repair},

volume = {149},

pages = {103840},

abstract = {The CRISPR/Cas9 technology is a powerful and versatile tool to disrupt genes' functions by introducing sequence-specific DNA double-strand breaks (DSBs). Here, we repurpose this technology to eradicate aberrant cells by specifically targeting silent and non-functional genomic sequences present only in target cells to be eliminated. Indeed, an intrinsic challenge of most current therapies against cancer and viral infections is the non-specific toxicity that they can induce in normal tissues because of their impact on important cellular mechanisms shared, to different extents, between unhealthy and healthy cells. The CRISPR/Cas9 technology has potential to overcome this limitation; however, so far effectiveness of these approaches was made dependent on the targeting and inactivation of a functional gene product. Here, we generate proof-of-principle evidence by engineering HeLa and RKO cells with a promoterless Green Fluorescent Protein (GFP) construct. The integration of this construct simulates either a genomic alteration, as in cancer cells, or a silent proviral genome. Cas9-mediated DSBs in the GFP sequence activate the DNA damage response (DDR), reduce cell viability and increase mortality. This is associated with increased cell size, multinucleation, cGAS-positive micronuclei accumulation and the activation of an inflammatory response. Pharmacological inhibition of the DNA repair factor DNA-PK enhances cell death. These results demonstrate the therapeutic potential of the CRISPR/Cas9 system in eliminating cells with an aberrant genome, regardless of the expression or the function of the target DNA sequence.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_227,

title = {Transcription: friend or foe of genome stability},

author = {Compe E and Orioli D},

url = {https://febs.onlinelibrary.wiley.com/doi/10.1002/1873-3468.15091},

doi = {10.1002/1873-3468.15091},

year  = {2025},

date = {2025-08-11},

urldate = {2025-08-11},

journal = {FEBS letters},

volume = {599},

issue = {2},

pages = {143-146},

abstract = {No abstract available},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_226,

title = {Sex Disparities in P53 Regulation and Functions: Novel Insights for Personalized Cancer Therapies},

author = {Cardano M and Buscemi G and Zannini L},

url = {https://www.mdpi.com/2073-4409/14/5/363},

doi = {10.3390/cells14050363},

year  = {2025},

date = {2025-08-11},

journal = {Cells},

volume = {14},

issue = {5},

pages = {363},

abstract = {Epidemiological studies have revealed significant sex differences in the incidence of tumors unrelated to reproductive functions, with females demonstrating a lesser risk and a better response to therapy than males. However, the reasons for these disparities are still unknown and cancer therapies are generally sex-unbiased. The tumor-suppressor protein p53 is a transcription factor that can activate the expression of multiple target genes mainly involved in the maintenance of genome stability and tumor prevention. It is encoded by TP53, which is the most-frequently mutated gene in human cancers and therefore constitutes an attractive target for therapy. Recently, evidence of sex differences has emerged in both p53 regulations and functions, possibly providing novel opportunities for personalized cancer medicine. Here, we will review and discuss current knowledge about sexual disparities in p53 pathways, their role in tumorigenesis and cancer progression, and their importance in the therapy choice process, finally highlighting the importance of considering sex contribution in both basic research and clinical practice.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_225,

title = {Effect of Spiroplasma infection on the mating behavior of Glossina fuscipes fuscipes},

author = {Fiorenza G and Piccinno R and Bruzzese DJ and Scolari F and Milanesi G and Casali C and Gomulski LM and Lescai F and Forneris F and Gasperi G and Dera KM and de Beer C and Abd-Alla AMM and Aksoy S and Malacrida AR},

url = {https://onlinelibrary.wiley.com/doi/10.1111/1744-7917.70042},

doi = {10.1111/1744-7917.70042},

year  = {2025},

date = {2025-08-11},

journal = {Insect science},

abstract = {Tsetse flies are insects of significant public health and zoonotic importance as they are the main vectors of African trypanosomes. To date, an effective vaccine is unavailable and efforts to limit the spread of the disease primarily rely on controlling the tsetse populations. The discovery of Spiroplasma (class Mollicutes) in Glossina fuscipes fuscipes (Gff) (palpalis subgroup), offers promising insights into its potential use as a biological control agent to hinder trypanosomes infection in tsetse flies. Indeed, a negative correlation between Spiroplasma and trypanosome co-infection has been observed. Using a laboratory strain of Gff, we provide fundamental biological insights into the effects of Spiroplasma infection on the mating behavior of the fly. We found a sex-biased Spiroplasma infection, with males exhibiting a higher infection rate. Mass mating experiments revealed a higher mating propensity in Spiroplasma-infected flies. Additionally, the presence of Spiroplasma influenced premating isolation, leading to nonrandom mating patterns that favored the pairing of individuals with matching infection statuses. Moreover, we present evidence of Spiroplasma vertical paternal transmission. By analyzing female reproductive tissues at 2 and 24 h postmating, we confirmed that an infected male can transfer Spiroplasma to the female via the spermatophore, which can subsequently migrate to the spermathecae. This study provides foundational insights into the role of Spiroplasma in tsetse fly mating behavior and provides supporting evidence for vertical transmission from infected males.},

keywords = {},

pubstate = {forthcoming},

tppubtype = {article}

}

@article{%a1.%Y_224,

title = {Circulating MicroRNAs in Patients with Psoriasis Treated with Anti-IL-23: A Cohort Study},

author = {Diotallevi F and Matacchione G and Campanati A and Marinelli Busilacchi E and Viola N and Pace I and Fontana B and Roncarati R and Bonafe' M and Ferracin M and Sabbatinelli J and Olivieri F},

url = {https://link.springer.com/article/10.1007/s13555-024-01331-9},

doi = {10.1007/s13555-024-01331-9},

year  = {2025},

date = {2025-08-11},

urldate = {2025-08-11},

journal = {Dermatology and therapy},

volume = {15},

issue = {1},

pages = {125-140},

abstract = {Introduction: Psoriasis is characterized by aberrant keratinocyte activity and immune cell infiltration, driven by immune-mediated pathways. MicroRNAs (miRNAs) play crucial roles in regulating these processes, offering insights into disease mechanisms and therapeutic targets. Objectives: This study aimed to investigate changes in circulating miRNAs in psoriasis patients undergoing risankizumab therapy, an anti-IL-23 monoclonal antibody, to understand its impact on disease pathogenesis and treatment response. Methods: Plasma samples from 12 psoriasis patients were collected before (T0) and after 1 year (T1) of risankizumab treatment and analyzed using small RNA sequencing. Findings were validated in a separate cohort of 23 patients using quantitative real-time PCR (qRT-PCR). T-regulatory cell (Treg) numbers and pro-inflammatory cytokine levels were also assessed. Results: Significant clinical improvement was observed in all patients after 1 year of treatment, accompanied by increased Treg counts and reduced levels of pro-inflammatory cytokines. Twenty-four miRNAs exhibited differential expression post-treatment; 9 were downregulated and 15 upregulated. Notably, miR-200a-3p showed a significant correlation with baseline Psoriasis Area Severity Index (PASI), indicating its potential as a severity marker. Risankizumab therapy also decreased peripheral blood levels of IL-23, IL-1β, and IL-8. Conclusions: This study identifies specific circulating miRNAs, including miR-200a-3p, as potential biomarkers for monitoring treatment responses in psoriasis patients. The findings underscore the therapeutic efficacy of risankizumab in modulating miRNA profiles and immune pathways associated with psoriasis pathogenesis. Overall, these results provide new insights into the mechanisms of risankizumab action and highlight miRNAs as promising candidates for personalized medicine approaches in psoriasis management.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_223,

title = {Chemical Analysis of Plasma-Activated Culture Media by Ion Chromatography},

author = {Locatelli M and Perrucci M and Balaha M and Acharya TR and Kaushik NK and Choi EH and Rapino M and Perrotti V},

url = {https://www.mdpi.com/1424-8247/18/2/199},

doi = {10.3390/ph18020199},

year  = {2025},

date = {2025-08-11},

journal = {Pharmaceuticals (Basel)},

volume = {18},

issue = {2},

pages = {199},

abstract = {Background: Currently, the procedures and methods applied in biological and medical fields for the determination of reactive oxygen and nitrogen species (RONS), primarily rely on spectrophotometric techniques, which involve the use of colorimetric reagents. While these methods are widely accepted, they exhibit significant limitations from an analytical standpoint, particularly due to potential inaccuracies, artifacts, and pronounced susceptibility to matrix effects. The purpose of this Technical Note is to demonstrate the application of ion chromatography-a robust and well-established analytical technique-for the quantification of RONS produced in cell culture media through the exposure to cold atmospheric plasma (CAP), an innovative therapeutic approach for cancer treatment, known as CAP indirect treatment. In addition, the present protocol proposes to apply the pharmacokinetics principles to the RONS generated in plasma-treated liquids (PTLs) following CAP exposure. Methods: The strategy involves elucidating the kinetic profiles of certain characteristic species by evaluating their half-life in the specific media used for cell cultures and investigating their "pharmacokinetic" (PK) profile. In this approach the drug dose is represented by the plasma power and the infusion time corresponds to the exposure time of the culture medium to CAP. Volume-dependent results were shown, focusing on nitrites and nitrates activities, justifying cellular inhibition. Results: This methodology enables the correlation of the PTL biological effects on different cell lines with the PK profiles (dose/time) obtained via ion chromatography. Conclusions: In conclusion, being a simple and green method, it could be used as an alternative to toxic reactions and analytical techniques with higher detection limits, while achieving good resolution.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_222,

title = {ANKRD2 Knockdown as a Therapeutic Strategy in Osteosarcoma: Effects on Proliferation and Drug Response in U2OS and HOS Cells},

author = {Cenni V and Bavelloni A and Capanni C and Mattioli E and Bortolozzo F and Kojic S and Orlandi G and Bertacchini J and Blalock WL},

url = {https://www.mdpi.com/1422-0067/26/4/1736},

doi = {10.3390/ijms26041736},

year  = {2025},

date = {2025-08-11},

urldate = {2025-08-11},

journal = {International journal of molecular sciences},

volume = {26},

issue = {4},

pages = {1736},

abstract = {Ankrd2, a mechanoresponsive protein primarily studied in muscle physiology, is emerging as a player in cancer progression. This study investigates the functional role of Ankrd2 in osteosarcoma cells, revealing its critical involvement in cell proliferation and response to chemotherapeutic drugs. We showed that Ankrd2 knockdown impairs the activation of PI3K/Akt and ERK1/2 pathways, reduces levels of cell cycle regulators including cyclin D1 and cyclin B, and counteracts the expression of nuclear lamin A and lamin B, disrupting nuclear morphology and DNA integrity. Strikingly, the loss of Ankrd2 enhances the sensitivity of osteosarcoma cells to doxorubicin and cisplatin, highlighting Ankrd2 potential as a therapeutic target to improve chemotherapeutic efficacy. Defining a novel mechanistic role for Ankrd2 in promoting tumor progression, we propose that Ankrd2 reduction could be exploited as an adjuvant strategy to enhance the efficacy of chemotherapy, offering new therapeutic opportunities for OS treatment.},

keywords = {},

pubstate = {forthcoming},

tppubtype = {article}

}

@article{%a1.%Y_223,

title = {FACILITY: feeding the family-the intergenerational approach to fight obesity, a cross-sectional study protocol},

author = {Vincenti and Calcaterra V and Santero S and Viroli G and Di Napoli I and Biino G and Daconto L and Cusumano M and Zuccotti G and Cena H},

url = {https://www.frontiersin.org/journals/pediatrics/articles/10.3389/fped.2025.1450324/full},

doi = {1450324},

year  = {2025},

date = {2025-08-11},

urldate = {2025-08-11},

journal = {Frontiers in pediatrics},

volume = {13},

pages = {1450324},

abstract = {Introduction: Paediatric obesity has been described by the World Health Organization as one of the most serious health challenges of the 21st century. Over the past four decades, the number of children and adolescents with obesity has increased between 10 and 12-fold worldwide. Methods: Childhood obesity is a complex and multifactorial outcome which can be attributed to factors such as socioeconomic status, ethnicity, lifestyle and eating habits. Beside personal-children-related factors, maternal (education, food knowledge, income) and environmental ones (food environment's features and accessibility) have been proven but their influences are still worth discussion. The cross-sectional study of the "FACILITY: feeding the family-the intergenerational approach to fight obesity" project aims at estimating children prevalence of overweight and obesity and assessing the impacts of lifestyle and of socio-economic-cultural and environmental factors on overweight and obesity. Results: Due to the current importance of developing multidisciplinary mother-child centred prevention programs, FACILITY cross-sectional study will investigate maternal and child socio-cultural, economic, environmental, health and lifestyle-related risk factors for the development of obesity. Discussion: The knowledge gained will provide the basis to develop a "primordial prevention program" to early tackle childhood obesity. Clinical trial registration: ClinicalTrials.gov, identifier (NCT06179381).},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_222,

title = {Polygenic prediction of body mass index and obesity through the life course and across ancestries},

author = {Smit RAJ and …… and Biino G and …… and Loos RJF},

url = {https://www.nature.com/articles/s41591-025-03827-z},

doi = {10.1038/s41591-025-03827-z},

year  = {2025},

date = {2025-08-11},

urldate = {2025-08-11},

abstract = {Polygenic scores (PGSs) for body mass index (BMI) may guide early prevention and targeted treatment of obesity. Using genetic data from up to 5.1 million people (4.6% African ancestry, 14.4% American ancestry, 8.4% East Asian ancestry, 71.1% European ancestry and 1.5% South Asian ancestry) from the GIANT consortium and 23andMe, Inc., we developed ancestry-specific and multi-ancestry PGSs. The multi-ancestry score explained 17.6% of BMI variation among UK Biobank participants of European ancestry. For other populations, this ranged from 16% in East Asian-Americans to 2.2% in rural Ugandans. In the ALSPAC study, children with higher PGSs showed accelerated BMI gain from age 2.5 years to adolescence, with earlier adiposity rebound. Adding the PGS to predictors available at birth nearly doubled explained variance for BMI from age 5 onward (for example, from 11% to 21% at age 8). Up to age 5, adding the PGS to early-life BMI improved prediction of BMI at age 18 (for example, from 22% to 35% at age 5). Higher PGSs were associated with greater adult weight gain. In intensive lifestyle intervention trials, individuals with higher PGSs lost modestly more weight in the first year (0.55 kg per s.d.) but were more likely to regain it. Overall, these data show that PGSs have the potential to improve obesity prediction, particularly when implemented early in life.},

keywords = {},

pubstate = {forthcoming},

tppubtype = {article}

}

@article{%a1.%Y_221,

title = {Anti-myogenic and profibrotic effect of serum from patients affected by muscular laminopathies},

author = {Schena E and Pini A and Cavalcante P and Siciliano G and Ricci G},

url = {https://www.actamyologica.it/article/view/1126},

doi = {10.36185/2532-1900-1126},

year  = {2025},

date = {2025-08-11},

journal = {Acta myologica: myopathies and cardiomyopathies: official journal of the Mediterranean Society of Myology },

abstract = {Emery-Dreifuss Muscular Dystrophy type 2 (EDMD2) and LMNA-related congenital muscular dystrophy (L-CMD) are caused by mutations in LMNA gene. Both pathologies are characterized by joint contractures, muscle weakness and wasting and cardiac involvement. In the last few years, circulating factors have been proposed to play a critical role in the pathogenesis of these diseases. Based on this consideration, we studied the effect of laminopathic serum on the myogenic differentiation in healthy human myoblasts in culture. We observed impaired myogenesis and increased fibrosis in myoblast cultures conditioned with laminopathic serum and a dramatic increase in the level of profibrotic and proinflammatory cytokines in the cell culture supernatants. These results strongly support the pathogenic role of circulating factors in muscular laminopathies and pave the way to a possible therapeutic strategy.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_220,

title = {DNA damage response defects induced by the formation of TDP-43 and mutant FUS cytoplasmic inclusions and their pharmacological rescue},

author = {Modafferi S and Farina S and Esposito F and Brandi O and Di Salvio M and Della Valle I and D'Uva S and Scarian E and Cicio G and Riccardi A and Pisati F and Garbelli A and Santini T and Pansarasa O and Morlando M and D'Ambrosi N and Cozzolino M and Cestra G and {d'Adda di Fagagna F} and Gioia U and Francia S},

url = {https://www.nature.com/articles/s41418-025-01530-7},

doi = {10.1038/s41418-025-01530-7},

year  = {2025},

date = {2025-08-11},

journal = {Cell death and differentiation},

abstract = {Formation of cytoplasmic inclusions (CIs) of TDP-43 and FUS, along with DNA damage accumulation, is a hallmark of affected motor neurons in Amyotrophic Lateral Sclerosis (ALS). However, the impact of CIs on DNA damage response (DDR) and repair in this pathology remains unprobed. Here, we show that CIs of TDP-43 and FUSP525L, co-localizing with stress granules, lead to a dysfunctional DDR activation associated with physical DNA breakage. Inhibition of the activity of the DDR kinase ATM, but not of ATR, abolishes DDR signaling, indicating that DNA double-strand breaks (DSBs) are the primary source of DDR activation. In addition, cells with TDP-43 and FUSP525L CIs exhibit reduced DNA damage-induced RNA synthesis at DSBs. We previously showed that the two endoribonucleases DROSHA and DICER, also known to interact with TDP-43 and FUS during small RNA processing, contribute to DDR signaling at DSBs. Treatment with enoxacin, which stimulates DDR and repair by boosting the enzymatic activity of DICER, restores a proficient DDR and reduces DNA damage accumulation in cultured cells with CIs and in vivo in a murine model of ALS. In Drosophila melanogaster, Dicer-2 overexpression rescues TDP-43-mediated retinal degeneration. In summary, our results indicate that the harmful effects caused by TDP-43 and FUS CIs include genotoxic stress and that the pharmacological stimulation of the DNA damage signaling and repair counteracts it.},

keywords = {},

pubstate = {forthcoming},

tppubtype = {article}

}

@article{%a1.%Y_219,

title = {Myopathic Ehlers-Danlos Syndrome (mEDS) Related to COL12A1: Two Novel Families and Literature Review},

author = {Merlini L and Sabatelli P and Cenni V and Zanobio M and Di Martino A and Traina F and Faldini C and Nigro V and Torella A},

url = {https://www.mdpi.com/1422-0067/26/11/5387},

doi = {10.3390/ijms26115387},

year  = {2025},

date = {2025-08-11},

journal = {International journal of molecular sciences},

volume = {26},

issue = {11},

pages = {5387},

abstract = {Myopathic Ehlers-Danlos syndrome (RmEDS) is an emerging hybrid phenotype that combines connective and muscle tissue abnormalities. It has been associated with variants of the COL12A1 gene, which are known as Ullrich congenital muscular dystrophy-2 (UCMD2; 616470) and Bethlem myopathy-2 (BTHLM2; 616471). Here, we report two splicing mutations of COL12A1 identified in three patients from two unrelated families who present a combination of joint hypermobility and axial, distal, and proximal weakness. The muscular strength of their neck and limb muscles was assessed at 4/5 (MRC); however, when measured with a myometer, the expected percentage by age and sex ranged from 35% to 40% for elbow flexion, 37% to 75% for knee extension, and was 50% for neck flexion. In addition to confirming the characteristic atrophy of the rectus femoris, we presented evidence of involvement of the neck and lumbar muscles through MRI and CT imaging. In vitro studies revealed filamentous disorganization and an altered pattern of collagen XII alpha 1 chain migration due to the skipping of exons 55 and 56 of collagen XII. Additionally, we review the myopathic involvement of COL12-RM in 30 patients across 18 families with dominant mutations and 15 patients from 13 families with recessive mutations.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_218,

title = {In vitro study of cold atmospheric plasma-induced proliferation inhibition and morphological changes in head and neck carcinoma cell lines},

author = {Maravic T and Petrucci G and Giacomo VD and Mazzitelli C and Acharya TR and Kaushik NK and Choi EH and Rapino M and D'Urso D and Josic U and Caponio VCA and Micaroni M and Edoardo M and Russo LL and Muzio LL and Breschi L and Perotti V},

url = {https://www.sciencedirect.com/science/article/pii/S0300571225004518?via%3Dihub},

doi = {10.1016/j.jdent.2025.106007},

year  = {2025},

date = {2025-08-11},

journal = {Journal of dentistry},

abstract = {"Objectives: The use of cold atmospheric plasma (CAP) has been growing in medical field. Since limited data exist on the influence of CAP exposure on head and neck cancer (HNC) cells, we aimed to investigate in vitro its impact on proliferation and morphology of HNC (HSC2, HSC3, and FaDu) cells, as well as healthy gingival fibroblasts (hGF).

Methods: A CAP gas air jet was applied directly on the HSC2, HSC3, FaDu and hGF cells for 30 and 60 s; doxorubicin has been used as positive control. Inhibition of cell proliferation at different time points (24, 48, and 72 h) was investigated through MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium]. Morphological alterations were observed using scanning electron microscope (SEM) and transmission electron microscope (TEM). Data were statistically analyzed (p < 0.05). Results: CAP exposure of 60 s showed the highest proliferation inhibitory effects in all investigated cancer cell lines (p < 0.001). While HSC2 had the highest proliferation inhibition at 24 h, HSC3, and FaDu exhibited a positive, time-dependent inhibitory effect (24 < 48 < 72 h) after CAP exposure. Interestingly, effects of CAP in the hGF were minimal. SEM observations revealed morphological changes in HNC cells treated with CAP at 30 and 60 s. Moreover, TEM showed stressed conditions in the survived HNC cells at 48 h after CAP exposure demonstrated by the presence of multilamellar and multi-vesicular bodies. Conclusions: CAP treatment induced proliferation inhibition, morphologic changes and stressed conditions in HNC cell lines (HSC2, HSC3, and FaDu), while demonstrating limited effects on hGF cells.Clinical significance: This work characterized early cellular responses of HSC2, HSC3, and FaDu to CAP exposure, including proliferation, and morphology, as foundational data before progressing to more clinically representative models."},

keywords = {},

pubstate = {forthcoming},

tppubtype = {article}

}

@article{%a1.%Y,

title = {Exploring structure-activity relationships of pyrrolyl diketo acid derivatives as non-nucleoside inhibitors of terminal deoxynucleotidyl transferase enzyme},

author = {Madia VN and Garibaldi N and Ialongo D and Patacchini E and Tudino V and Ruggieri G and Zarbo L and Cara E and Coluccia A and Artico M and Scipione L and Messore A and Saccoliti F and Mentegari E and Maga G and Di Santo R and Crespan E and Costi R},

url = {https://www.tandfonline.com/doi/full/10.1080/14756366.2025.2496782?rfr_dat=cr_pub++0pubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org},

doi = {10.1080/14756366.2025.2496782},

year  = {2025},

date = {2025-08-11},

journal = {Journal of enzyme inhibition and medicinal chemistry},

volume = {40},

number = {1},

abstract = {Terminal deoxynucleotidyl transferase (TdT) is overexpressed in some cancer types, where it drives the mutagenic repair of double strand breaks through non canonical non-homologous end joining pathway. The TdT enzyme belongs to the X family of polymerases, together with the DNA polymerase λ (pol λ) and β (pol β). However, TdT exclusively displays template-independent nucleotide polymerisation. Pursuing our studies in developing TdT inhibitors, herein we deepened the structure-activity relationships of new structural analogues of our previously identified hit compounds. The diketo hexenoic acid derivatives here analysed showed high selectivity towards TdT and inhibition potencies spanning from the low micromolar range to the nanomolar. Docking studies highlighted the chemical features involved in the TdT binding, well contributing to the rationalisation of the structural requirements needed for the enzymatic inhibition.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_216,

title = {Mapping of RORγt+ dendritic cells in human tissues establishes their preferential niche in adult lymph nodes},

author = {Lonardi S and Bianchetto-Aguilera FM and Monti M and {Di Matteo A} and Missale F and Picinoli S and Bugatti M and Benedetti M and Ferrari G and Cassatella MA and Moratto D and Zini S and Agostini V and Savoldi V and Lorenzi L and Chiarini M and Facchetti F and Wu S and Antonova AU and Liu YA and Cella M and Ghigna C and Colonna M and Vermi W},

url = {https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2025.1527499/full},

doi = {1527499},

year  = {2025},

date = {2025-08-11},

urldate = {2025-08-11},

journal = {Frontiers in immunology},

volume = {16},

pages = {1527499},

abstract = {Background: The retinoic-acid-receptor-related orphan receptor gamma t (RORγt) isoform is required for the development of lymphoid organs, T-helper 17 cells (Th17), and innate lymphoid cells (ILC3s). Recent data in mouse and human have revealed non-T, non-ILC3 cell populations with antigen presenting features that express RORγt. This study maps the presence of RORγt cells with dendritic cell (DC) features in human adult and fetal lymphoid tissues. Methods: By combining multicolor flow cytometry, RNAseq of peripheral blood cells, analysis of lymph node scRNAseq datasets, and microscopic analysis on human tissue sections and single-cell suspensions, this study maps the presence of RORγt cells with DC features in human tissues. Results: RORγt-DCs are found in human lymphoid organs, particularly in lymph nodes. Lymph node RORγt-DCs are located in the interfollicular area surrounding high endothelial venules and in the marginal sinuses. In terms of phenotype, RORγt-DCs are distinct from other nodal dendritic cells. They express PRDM16 and PIGR as well as transcripts supporting the antigen presentation machinery, while lacking stromal markers. A significant fraction of RORγt-DCs is proliferating, suggesting local self-renewal. Moreover, most of them lack autoimmune regulator (AIRE) expression. Comparison with mouse RORγt Thetis cells (TC) and Janus cells (JC) shows more similarity with group II TC than group I and III TC or JC, all of which are tolerogenic and express AIRE. Conclusion: Overall, this study identifies human lymph nodes as a relevant niche for RORγt-DCs and establishes tools for their microscopic mapping in human disease states},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_215,

title = {Sammy Basso, his life and message, and the importance of progeria research},

author = {Lattanzi G},

url = {https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehaf355/8160766?login=true#google_vignette},

doi = {10.1093/eurheartj/ehaf355},

year  = {2025},

date = {2025-08-11},

journal = {European heart journal},

abstract = {not available},

keywords = {},

pubstate = {forthcoming},

tppubtype = {article}

}

@article{nokey,

title = {Trichothiodystrophy: Molecular insights and mechanisms of pathogenicity},

author = {Lanzafame M and Brevi F and Veniali G and Botta E},

url = {https://www.sciencedirect.com/science/article/pii/S1383574225000262?via%3Dihub},

doi = {10.1016/j.mrrev.2025.108555},

year  = {2025},

date = {2025-08-11},

journal = {Mutation research. Reviews in mutation research},

abstract = {Trichothiodystrophy (TTD) is a rare hereditary disease characterized by brittle, sulphur deficient hair associated with a wide and varied spectrum of clinical features which include skin alterations, neurodevelopmental defects, and immune dysfunction. The presence of hypersensitivity to UV light defines the two main forms of TTD: photosensitive (PS-TTD) and non-photosensitive (NPS-TTD). The disease arises from mutations in a variety of genes involved in different biological processes. Affected processes include DNA repair, transcription as well as translation. This review provides the latest vision of TTD: from up-to-date mutational spectra and genotype-phenotype relationships to our current understanding of the pathogenic mechanisms that underlie the complex etiology of this multi-faceted disease.},

keywords = {},

pubstate = {forthcoming},

tppubtype = {article}

}

@article{%a1.%Y_214,

title = {Trichothiodystrophy-causative pathogenic variants impair a cooperative action of TFIIH and DDX1 in R-loop processing},

author = {Ferri D and Branca G and Lanzafame M and Gandolfi E and Riva V and Maga G and Nardo T and Landi C and Bini L and Arseni L and Peverali FA and Compe E and Orioli D},

url = {https://academic.oup.com/nar/article/53/14/gkaf745/8221718?login=true},

doi = {10.1093/nar/gkaf745},

year  = {2025},

date = {2025-08-11},

journal = {Nucleic Acids Research},

volume = {53},

issue = {14},

pages = {gkaf745},

abstract = {The transcription factor IIH (TFIIH) is a key player in transcription and DNA repair by nucleotide excision repair. It is made of 10 subunits organized in core-TFIIH and CAK sub-complexes bridged by XPD. Pathogenic variants in the ERCC2/XPD gene give rise to xeroderma pigmentosum (XP) or trichothiodystrophy (TTD), two distinct clinical entities with opposite skin cancer proneness. Here, we show that TTD variants cause a partial dissociation of the CAK from the chromatin and from the core-TFIIH. Mass spectrometry analysis reveals that the chromatin-bound CAK, as a component of the entire TFIIH, participates in a protein assembly containing the RNA-binding proteins DDX1, SFPQ, NONO as well as RNA polymerase II (Pol II). Gene silencing experiments demonstrate that the protein assembly is required to process the DNA:RNA hybrids formed during Pol II extension and to protect the cell from transcriptional stress. TTD-specific variants in ERCC2/XPD result in TFIIH instability, altered interaction of the CAK with DDX1-SFPQ-NONO, and R-loop accumulation. Therefore, the limited amount of TFIIH that distinguishes TTD from XP gives rise to transcriptional stress and extensive gene expression deregulations, thus accounting for the wide spectrum of TTD clinical features.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_213,

title = {Defective collagen VI-NG2 axis impairs pericyte balance between proliferation and quiescence in COLVI-related myopathies},

author = {Fazio A and Sabatelli P and Faldini C and {Di Martino A} and Marvi MV and Neri I and Koufi FD and Merlini L and Manzoli L and Ratti S and Evangelisti C},

url = {https://www.sciencedirect.com/science/article/pii/S0925443925003606?via%3Dihub},

doi = {10.1016/j.bbadis.2025.168012},

year  = {2025},

date = {2025-08-11},

journal = {Biochimica et biophysica acta. Molecular basis of disease},

volume = {168012},

abstract = {Collagen VI-related myopathies (COLVI-RMs) are rare genetic disorders caused by impaired assembly and secretion of COLVI, a key extracellular matrix (ECM) protein. COLVI deficiency alters ECM architecture and biomechanics, leading to progressive muscle fiber damage and connective tissue abnormalities. While pericytes are emerging as key players in muscle regeneration due to their myogenic potential, their role in COLVI-RMs remains unclear. This study investigates pericyte involvement in COLVI-RMs, focusing on the interaction between COLVI and neural/glial antigen 2 (NG2), a proteoglycan expressed on pericyte membranes. Muscle biopsies from COLVI-RMs patients revealed abnormal pericyte distribution, reduced vessel coverage, and thickened capillary basement membranes. In vitro, healthy pericytes formed a dense COLVI network, while COLVI-RM-derived pericytes displayed a disrupted matrix and impaired cell-ECM interaction. Proximity ligation assays demonstrated a significant reduction in COLVI-NG2 binding in COLVI-RM pericytes, correlating with altered balance between proliferative and quiescent states. In turn, defects in signaling pathways related to proliferation (Akt/mTOR and Wnt/β-catenin pathways) and quiescence (N-cadherin, Notch3, FOXO3A) were identified, revealing a marked quiescent state. In vitro inhibition of the COLVI-NG2 binding in healthy pericytes reproduced these pathological features, underscoring the functional relevance of this molecular axis. Taken together, the data here reported revealed an unexpected role of NG2-COLVI binding on pericytes status. It follows that the impairment of functional binding between NG2 and COLVI could have important consequences on the pericytes myogenic potential in COLVI-RMs, and consequently on the muscle regeneration. Finally, targeting defective pericytes could provide potential therapeutic strategies for these debilitating diseases.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_212,

title = {Fatty acid binding protein 1 (FABP1) depletion promotes an oxidative metabolic shift in Caco-2 colorectal cancer cells},

author = {Borus DL and Zadra G and Minsky D and Costa ML and Corsico B and Storch J and Scaglia N},

url = {https://www.sciencedirect.com/science/article/pii/S1388198125000691?via%3Dihub},

doi = {10.1016/j.bbalip.2025.159661},

year  = {2025},

date = {2025-08-11},

journal = {Biochimica et biophysica acta. Molecular and cell biology of lipids},

abstract = {Lipid metabolism reprogramming is a well-established hallmark of many cancer types, including colorectal cancer (CRC). Nevertheless, a clear understanding on how fatty acid (FA) metabolism is fine-tuned during CRC development and progression is still missing. Given that CRC is the second leading cause of cancer-related death, addressing these critical aspects may provide the rationale for new therapeutic approaches and early biomarker identification. Fatty acid binding protein 1 (FABP1) is a small protein that binds FA and other lipophilic compounds, acting as a lipid transporter in the intestine. Little is currently known about the function of FABP1 in CRC. Here we show that the knockdown of FABP1 in CRC cells impairs de novo FA and cholesterol synthesis, specifically, via altering the transcriptional regulation of lipid metabolism genes. FABP1 depletion suppresses the expression of FA and cholesterol synthesis-associated genes while promoting that of FA oxidation genes and mitochondrial oxidative pathways. The latter is associated with increased oxygen consumption rate and activation of the energy sensor 5' AMP-activated kinase (AMPK). Taken together, our results show that FABP1 orchestrates the balance between FA synthesis and oxidation, most likely to prevent the cytotoxic effects of circulating unbound free fatty acids. Thus, targeting FABP1 function may represent a potential therapeutic strategy in advanced CRC.},

keywords = {},

pubstate = {forthcoming},

tppubtype = {article}

}

@article{%a1.%Y_209,

title = {Combining prelamin A accumulation and oxidative stress: A strategy to target glioblastoma},

author = {Marvi MV and Evangelisti C and Cerchier CB and Fazio A and Neri I and Koufi FD and Blalock WL and Cenni V and Zoli M and Asioli S and Morandi L and Franceschi E and Manzoli L and Capanni C and Ratti S},

url = {https://www.sciencedirect.com/science/article/pii/S0171933525000160?via%3Dihub},

doi = {10.1016/j.ejcb.2025.151491},

year  = {2025},

date = {2025-06-10},

urldate = {2025-06-10},

journal = {European journal of cell biology},

volume = {104},

issue = {2},

pages = {151491},

abstract = {Glioblastoma is the most aggressive and prevalent tumor of the Central Nervous System (CNS) with limited treatment options and poor patient outcomes. Standard therapies, including surgery, radiation, and chemotherapy, provide only modest survival benefits, highlighting the need for innovative therapeutic approaches. This study investigates a novel strategy targeting prelamin A processing in glioblastoma cells. By inhibiting the farnesyltransferase enzyme using SCH66336 (Lonafarnib), we promote the accumulation of lamin A precursor (prelamin A) in glioblastoma cells, thereby increasing their susceptibility to oxidative stress induced by Menadione administration, while sparing normal human astrocytes. Notably, the combined SCH66336-Menadione treatment reduced cell proliferation, modified the expression of stemness markers, and decreased viability in patient-derived glioblastoma stem cells, which represent the population responsible for tumor aggressiveness and recurrence. These findings indicate that inhibiting prelamin A processing could be a potential strategy to reduce glioblastoma aggressiveness and enhance therapeutic outcomes, particularly for treatment-resistant glioblastoma stem cell populations. This approach shows potential for integrating prelamin A processing disruption as a complementary strategy in glioblastoma therapy.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_208,

title = {A Novel Cognitive Frailty Index for Geriatric Mice},

author = {Marcozzi S and Bigossi G and Giuliani ME and Lai G and Bartozzi B and Balietti M and Casoli T and Orlando F and Amoroso A and Giacconi R and Cardelli M and Piacenza F and Lattanzio F and Olivieri F and de Keizer PLJ and {d'Adda di Fagagna F} and Malavolta M},

url = {https://onlinelibrary.wiley.com/doi/10.1111/acel.70056},

doi = {10.1111/acel.70056},

year  = {2025},

date = {2025-06-10},

journal = {Aging Cell},

abstract = {Loss of cognitive function is a significant challenge in aging, and developing models to understand and target cognitive decline is crucial for the development of Geroscience-based interventions. Aged mice offer a valuable model as they share features of cognitive decline with humans. Despite numerous studies, knowledge of longitudinal age-related cognitive changes and cognitive frailty in naturally aging mice is limited, particularly in cohorts exceeding 30 months of age, where cognitive decline is more pronounced. Moreover, the impaired physical function of aged mice is known to affect latency-based strategies to measure cognitive performances. Here, we show a comprehensive longitudinal assessment using the Barnes Maze test in a large cohort of 424 aged (≥ 21 months) C57BL/6J mice. We introduced a new metric, the Cognitive Frailty Index (CoFI), which summarizes different age-associated Barnes Maze parameters into a unique function. CoFI strongly associates with advancing age and mortality, offering a reliable ability to discriminate long- and short-lived mice. We also established a CoFI cut-off and a physically adjusted CoFI, both of which can distinguish between physical and cognitive frailty. This is further supported by the enhanced predictive power when physical and cognitive frailty are combined to assess short-term mortality. Moreover, the computation method for CoFI is adaptable to various cognitive assessment tests, leveraging procedures akin to those used for calculating other frailty indices. In conclusion, through robust longitudinal tracking, CoFI has the potential to become an important ally in assessing the effectiveness of Geroscience-based interventions to counteract age-related cognitive impairment.},

keywords = {},

pubstate = {forthcoming},

tppubtype = {article}

}

@article{%a1.%Y_207,

title = {Amy and Friends: improving the lives of individuals affected by DNA repair disorders},

author = {Hughes J and Orioli D and Arseni L},

url = {https://febs.onlinelibrary.wiley.com/doi/10.1002/1873-3468.70049},

doi = {10.1002/1873-3468.70049},

year  = {2025},

date = {2025-06-10},

journal = {FEBS letters},

volume = {599},

issue = {10},

pages = {1339-1345},

abstract = {DNA repair disorders are rare genetic conditions characterized by defects in the mechanisms responsible for repairing damaged DNA. DNA damage occurs frequently due to environmental factors, and in healthy cells, repair systems fix this damage to maintain genomic integrity. In individuals with DNA repair disorders, these mechanisms are impaired, leading to accumulated damage, cellular dysfunction, premature aging, and cell death. Symptoms vary depending on the specific repair pathway defect, with examples including Cockayne syndrome (CS), trichothiodystrophy (TTD), and xeroderma pigmentosum. Amy and Friends was founded by Jayne Hughes in the UK in 2007 to support children/young adults and families suffering from CS, TTD, and linked DNA repair disorders. In this second of a new series on patient advocacy, FEBS Letters interviews Founder and CEO Jayne Hughes and molecular geneticist and specialist team member Prof. Donata Orioli on the aims, achievements, and activities of Amy and Friends.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_206,

title = {Surface Charge Overrides Protein Corona Formation in Determining the Cytotoxicity, Cellular Uptake, and Biodistribution of Silver Nanoparticles},

author = {Barbalinardo M and Chiarini F and Teti G and Paganelli F and Mercadelli E and Bartoletti A and Migliori A and Piazzi M and Bertacchini J and Sena P and Sanson A and Falconi M and Palumbo C and Cavallini M and Gentili D},

url = {https://pubs.acs.org/doi/10.1021/acsabm.5c00392},

doi = {10.1021/acsabm.5c00392},

year  = {2025},

date = {2025-06-10},

urldate = {2025-06-10},

journal = {ACS applied bio materials},

volume = {8},

issue = {6},

pages = {5032-5043},

abstract = {Silver nanoparticles (AgNPs) hold great promise in biomedical applications due to their unique properties and potential for specific tissue targeting. However, the clinical translation of nanoparticle-based therapeutics remains challenging, primarily due to an incomplete understanding of how nanoparticle properties influence interactions at the nano-bio interface, as well as the role of surface-adsorbed proteins (i.e., protein corona) in modulating nanoparticle-cell interactions. This study demonstrates that the surface charge has a greater influence than protein corona formation in determining the cytotoxicity, cellular uptake, and biodistribution of AgNPs. Using negatively and positively charged AgNPs, we show that while protein corona formation is essential for ensuring nanoparticle availability for cellular interactions, the adsorption of biomolecules is nonspecific and independent of surface charge. Conversely, the surface charge significantly influences the interactions of AgNPs with cells. Positively charged nanoparticles exhibit enhanced cellular uptake, preferential accumulation in lysosomes, and pronounced mitochondrial damage compared to their negatively charged counterparts, resulting in greater cytotoxic effects. This effect is particularly evident in human breast cancer cells, where negatively charged nanoparticles show minimal uptake and cytotoxicity. These findings demonstrate that surface charge is the primary factor governing nanoparticle-cell interactions rather than protein corona formation. Nonetheless, the protein corona plays a critical role in stabilizing nanoparticles in physiological environments.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y__198,

title = {The complex interplay between aging and cancer},

author = {Trastus LA and {d'Adda di Fagagna F}},

url = {https://www.nature.com/articles/s43587-025-00827-z},

doi = {10.1038/s43587-025-00827-z},

year  = {2025},

date = {2025-04-09},

journal = {Nature aging},

volume = {5},

issue = {3},

pages = {350-365},

abstract = {Cancer is an age-related disease, but the interplay between cancer and aging is complex and their shared molecular drivers are deeply intertwined. This Review provides an overview of how different biological pathways affect cancer and aging, leveraging evidence mainly derived from animal studies. We discuss how genome maintenance and accumulation of DNA mutations affect tumorigenesis and tissue homeostasis during aging. We describe how age-related telomere dysfunction and cellular senescence intricately modulate tumor development through mechanisms involving genomic instability and inflammation. We examine how an aged immune system and chronic inflammation shape tumor immunosurveillance, fueling DNA damage and cellular senescence. Finally, as animal models are important to untangling the relative contributions of these aging-modulated pathways to cancer progression and to test interventions, we discuss some of the limitations of physiological and accelerated aging models, aiming to improve experimental designs and enhance translation.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y__197,

title = {V-ATPase in glioma stem cells: a novel metabolic vulnerability},

author = {Storaci AM and Bertolini I and Martelli C and De Turris G and Mansour N and Crosti M and De Filippo MR and Ottobrini L and Valenti L and Polledri E and Fustinoni S and Caroli M and Fanizzi C and Bosari S and Ferrero S and Zadra G and Vaira V},

url = {https://jeccr.biomedcentral.com/articles/10.1186/s13046-025-03280-3},

doi = {10.1186/s13046-025-03280-3},

year  = {2025},

date = {2025-04-09},

urldate = {2025-04-09},

journal = {Journal of experimental & clinical cancer research},

volume = {44},

issue = {1},

pages = {17},

abstract = {Background: Glioblastoma (GBM) is a lethal brain tumor characterized by the glioma stem cell (GSC) niche. The V-ATPase proton pump has been described as a crucial factor in sustaining GSC viability and tumorigenicity. Here we studied how patients-derived GSCs rely on V-ATPase activity to sustain mitochondrial bioenergetics and cell growth.,Methods: V-ATPase activity in GSC cultures was modulated using Bafilomycin A1 (BafA1) and cell viability and metabolic traits were analyzed using live assays. The GBM patients-derived orthotopic xenografts were used as in vivo models of disease. Cell extracts, proximity-ligation assay and advanced microscopy was used to analyze subcellular presence of proteins. A metabolomic screening was performed using Biocrates p180 kit, whereas transcriptomic analysis was performed using Nanostring panels. Results: Perturbation of V-ATPase activity reduces GSC growth in vitro and in vivo. In GSC there is a pool of V-ATPase that localize in mitochondria. At the functional level, V-ATPase inhibition in GSC induces ROS production, mitochondrial damage, while hindering mitochondrial oxidative phosphorylation and reducing protein synthesis. This metabolic rewiring is accompanied by a higher glycolytic rate and intracellular lactate accumulation, which is not exploited by GSCs for biosynthetic or survival purposes. Conclusions: V-ATPase activity in GSC is critical for mitochondrial metabolism and cell growth. Targeting V-ATPase activity may be a novel potential vulnerability for glioblastoma treatment.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y__196,

title = {Synthesis and biological investigation of peptidomimetic SARS-CoV-2 main protease inhibitors bearing quinoline-based heterocycles at P3},

author = {Rossi S and Deidda G and Fiaschi L and Ibba R and Pieroni M and Dichiara M and Carullo G and Butini S and Ramunno A and Brogi S and Lolicato M and Arrigoni C and Cabella N and Bavagnoli L and Maga G and Varasi I and Biba C and Vicenti I and Gemma S and Crespan E and Zazzi M and Campiani G},

url = {https://onlinelibrary.wiley.com/doi/10.1002/ardp.202400812},

doi = {10.1002/ardp.202400812},

year  = {2025},

date = {2025-04-09},

journal = {Archiv der Pharmazie},

volume = {358},

issue = {1},

pages = {e240081},

abstract = {In the last few years, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been the cause of a worldwide pandemic, highlighting the need for novel antiviral agents. The main protease (Mpro) of SARS-CoV-2 was immediately identified as a crucial enzyme for viral replication and has been validated as a drug target. Here, we present the design and synthesis of peptidomimetic Mpro covalent inhibitors characterized by quinoline-based P3 moieties. Structure-activity relationships (SARs) were also investigated at P1 and P2, as well as for different warheads. The binding modes of the designed inhibitors were assessed using X-ray crystallographic and molecular docking studies. The identified Mpro inhibitors were tested for their antiviral activities in cell-based assays, and the results were encouraging. The SAR studies presented here can contribute to the future design of improved inhibitors by addressing some of the current or prospective issues regarding Mpro inhibitors currently used in therapy.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y__195,

title = {Angiogenic Events Positively Modulated by Complex Magnetic Fields in an In Vitro Endothelial Cell Model},

author = {Ricci A and Cataldi A and Gallorini M and di Giacomo V and Rapino M and Di Pietro N and Mantarro M and Piattelli A and Zara S},

url = {https://www.mdpi.com/2073-4409/14/5/332},

doi = {10.3390/cells14050332},

year  = {2025},

date = {2025-04-08},

journal = {Cells},

volume = {14},

issue = {5},

pages = {332},

abstract = {The vascular system is primarily responsible for orchestrating the underlying healing processes to achieve tissue regeneration, thus the promotion of angiogenic events could be a useful strategy to repair injured tissues. Among several approaches to stimulate tissue regeneration, non-invasive devices are currently widely diffused. Complex Magnetic Fields (CMFs) are innovative pulsed multifrequency electromagnetic fields used for their promising results in clinical applications, such as diabetic foot treatment or edema resorption. Nevertheless, few papers are available demonstrating the biological mechanisms involved. In this paper, in order to understand CMFs' capability to promote angiogenic events, Regenerative Tissue Program (RTP) was applied to an in vitro Endothelial Cells (ECs) model. ECs were stimulated with (I) 2 RTP consecutive cycles, (II) with an interval of 8 h (T0 + T8), or (III) 24 h (T0 + T24) from one cycle to another. Results demonstrate that (I) extracellular matrix degradation is promoted through matrix metalloproteinases 2 and 9 modulation, leading to an increased cell migratory capability; (II) CMFs support EC growth, activating Integrin β1-Erk-Cdk2 pathway and sustaining G1/S transition; (III) vessel morphogenesis is promoted when CMFs are applied. In conclusion, the promising clinical results are supported by in vitro analyses which evidence that main angiogenic events are stimulated by CMFs.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y__194,

title = {On the tracks of an uninvited guest, the Asian tiger mosquito, Aedes albopictus in Cyprus},

author = {Piccinno R and Fiorenza G and Vasquez MI and Bouyer J and Notarides G and Gomulski LM and Meletiou S and Akiner M and Michaelakis A and Forneris F and Maga G and Gasperi G and Malacrida AR},

url = {https://parasitesandvectors.biomedcentral.com/articles/10.1186/s13071-024-06651-5},

doi = {10.1186/s13071-024-06651-5},

year  = {2025},

date = {2025-04-08},

urldate = {2025-04-08},

journal = {Parasites & vectors},

volume = {18},

issue = {1},

pages = {39},

abstract = {Background: Aedes albopictus, the Asian tiger mosquito, which is listed among the world's 100 most dangerous invasive species, is the main vector of chikungunya, dengue and Zika viruses. This mosquito species has rapidly dispersed and invaded much of the globe assisted by its life history traits and high propagule pressure driven by human activities. Aedes albopictus is currently widespread across mainland Europe and the Mediterranean region, including the islands. Cyprus remained free of Ae. albopictus until October 2022, when specimens were recorded for the first time in Limassol district, including the port area. Understanding the processes associated with the introduction, expansion and establishment of this vector in Cyprus is of primary importance to mitigate its dispersal on the island, and to implement control methods to prevent disease outbreaks. A genetic analysis of these invasive specimens collected in Limassol district and in areas from the Central Mediterranean was performed to obtain a genetic portrait of the demographic history of the invasive mosquitoes on Cyprus. Methods: We applied highly polymorphic simple sequence repeat (SSR) markers to the Ae. albopictus mosquitoes collected in Cyprus and to specimens from Italy, France, Switzerland, the Balkans, Greece and Turkey to construct an SSR individual genotype dataset that would enable the invasion pattern of Ae. albopictus in Cyprus to be traced. Bayesian clustering analyses using STRUCTURE and BayesAss version 3 were employed to derive information on the degree of ancestry among Cypriot and Mediterranean mosquitoes and on recent mosquito movements both within Cyprus and between Cyprus and the Central Mediterranean areas. Results: The Cypriot mosquitoes appear to be highly polymorphic with no signs of genetic drift due to recent founder effects. An ongoing mosquito dispersal within the Limassol district was detected, suggesting the presence of established, hidden adventive populations. These mosquitoes share a high degree of ancestry with those in the Balkans and parts of northern Italy that border the Adriatic Sea. Conclusions: Considering the trade connections of Limassol port, Cyprus with the Balkans and the Adriatic Italian region, we hypothesise that these areas may be involved in the incursion of Ae. albopictus into Cyprus. As the Balkan and Italian mosquitoes display high competence for CHIKV, questions arise about possible arbovirus outbreaks in Cyprus and highlight the need to implement surveillance and control measures.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y__193,

title = {At the nucleus of cancer: how the nuclear envelope controls tumor progression},

author = {Paganelli F and Poli A and Truocchio S and Martelli AM and Palumbo C and Lattanzi G and Chiarini F},

url = {https://pmc.ncbi.nlm.nih.gov/articles/PMC11758262/},

doi = {10.1002/mco2.70073},

year  = {2025},

date = {2025-04-08},

journal = {MedComm},

volume = {6},

issue = {2},

pages = {e70073},

abstract = {Historically considered downstream effects of tumorigenesis-arising from changes in DNA content or chromatin organization-nuclear alterations have long been seen as mere prognostic markers within a genome-centric model of cancer. However, recent findings have placed the nuclear envelope (NE) at the forefront of tumor progression, highlighting its active role in mediating cellular responses to mechanical forces. Despite significant progress, the precise interplay between NE components and cancer progression remains under debate. In this review, we provide a comprehensive and up-to-date overview of how changes in NE composition affect nuclear mechanics and facilitate malignant transformation, grounded in the latest molecular and functional studies. We also review recent research that uses advanced technologies, including artificial intelligence, to predict malignancy risk and treatment outcomes by analyzing nuclear morphology. Finally, we discuss how progress in understanding nuclear mechanics has paved the way for mechanotherapy-a promising cancer treatment approach that exploits the mechanical differences between cancerous and healthy cells. Shifting the perspective on NE alterations from mere diagnostic markers to potential therapeutic targets, this review calls for further investigation into the evolving role of the NE in cancer, highlighting the potential for innovative strategies to transform conventional cancer therapies.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y__192,

title = {Non-canonical NF-κB signaling in dendritic cells is required for ATP-driven indoleamine 2,3-dioxygenase 1 induction through P2Y11 receptor},

author = {Ocadlikova D and Fiordi B and Trabanelli S and Salvestrini V and Ciciarello M and Forte D and Campazzi E and Vitali L and Cipollitta SC and Pegoraro A and Jandus C and Di Virgilio F and Adinolfi E and Cavo M and Curti A},

url = {https://academic.oup.com/jleukbio/advance-article/doi/10.1093/jleuko/qiaf010/7997481?login=true},

doi = {10.1093/jleuko/qiaf010},

year  = {2025},

date = {2025-04-08},

journal = {Journal of leukocyte biology},

abstract = {Extracellular ATP released from dying cells, including tumor cells, is a key mediator of inflammation and tolerance by binding to purinergic receptors on dendritic cells, resulting in inflammasome activation (via P2X7R), dendritic cell maturation (via P2Y11R), and Indoleamine-2,3-dioxygenase 1 upregulation. However, the regulation of ATP-driven Indoleamine-2,3-dioxygenase 1 expression in human dendritic cells has been poorly investigated. In this work we aimed to investigate the ATP-driven molecular regulation of Indoleamine-2,3-dioxygenase 1 expression via purinergic receptors and to provide an in-depth characterization of ATP-driven T regulatory cells induced by Indoleamine-2,3-dioxygenase 1-expressing dendritic cells. We identified P2Y11R as being responsible for ATP-driven Indoleamine-2,3-dioxygenase 1 upregulation, and non-canonical NF-kB as a molecular pathway associated with ATP-dependent Indoleamine-2,3-dioxygenase 1 induction through P2Y11R. Then we investigated - but did not confirm - an involvement of inflammasome machinery through P2X7R in Indoleamine-2,3-dioxygenase 1 upregulation. Finally, we evaluated the role of ATP catabolism via ATP ectonucleotidases, i.e. CD39 and CD73 and its main product adenosine, in regulating the generation of Indoleamine-2,3-dioxygenase 1-driven T regulatory cells. We found that ATP-driven Indoleamine-2,3-dioxygenase 1 upregulation is associated with CD73 upregulation and adenosine production. Additionally, ATP-treated Indoleamine-2,3-dioxygenase 1-positive mature dendritic cells induce PD-1-expressing bone fide suppressive T regulatory cells via adenosine A2AR. Collectively, a more in-depth understanding of ATP-driven immune-regulatory mechanisms through Indoleamine-2,3-dioxygenase 1 regulation in human dendritic cells leading to the induction of T regulatory cells can have clinical implications for the development of Indoleamine-2,3-dioxygenase 1 inhibitors in cancer patients, especially in combination with immunotherapy such as an anti-CD73 or adenosine receptor agonist and immunogenic chemotherapy.},

keywords = {},

pubstate = {forthcoming},

tppubtype = {article}

}

@article{%a1.%Y__191,

title = {Suppression of Spry1 reduces HIF1α-dependent glycolysis and impairs angiogenesis in BRAF-mutant cutaneous melanoma},

author = {Montico B and Giurato G and Guerrieri R and Colizzi F and Salvati A and Nassa G and Lamberti J and Memoli D and Sabatelli P and Comelli M and Bellazzo A and Fejza A and Camicia L and Baboci L and Dal Bo M and Covre A and Nyman TA and Weisz A and Steffan A and Maio M and Sigalotti L and Mongiat M and Andreuzzi E and Fratta E},

url = {https://jeccr.biomedcentral.com/articles/10.1186/s13046-025-03289-8},

doi = {10.1186/s13046-025-03289-8},

year  = {2025},

date = {2025-04-08},

journal = {Journal of experimental & clinical cancer research},

volume = {44},

number = {53},

issue = {1},

abstract = {Background: About 50% of cutaneous melanoma (CM) harbors the activating BRAFV600 mutation which exerts most of the oncogenic effects through the MAPK signaling pathway. In the last years, a number of MAPK modulators have been identified, including Spry1. In this context, we have recently demonstrated that knockout of Spry1 (Spry1KO) in BRAFV600-mutant CM led to cell cycle arrest and apoptosis, repressed cell proliferation in vitro, and reduced tumor growth in vivo. Despite these findings, however, the precise molecular mechanism linking Spry1 to BRAFV600-mutant CM remains to be elucidated. Materials and methods: Immunoprecipitation coupled to mass spectrometry was employed to gain insight into Spry1 interactome. Spry1 gene was knocked-out using the CRISPR strategy in the BRAF-mutant cell lines. Transmission electron microscopy was used to assess the relationship between Spry1 expression and mitochondrial morphology. By using in vitro and in vivo models, the effects of Spry1KO were investigated through RNA-sequencing, quantitative real-time PCR, Western blot, and immunofluorescence analyses. The Seahorse XF24 assay allowed real-time measurement of cellular metabolism in our model. Angiogenic potential was assessed through in vitro tube formation assays and in vivo CD31 staining. Results: Spry1 was mainly located in mitochondria in BRAFV600-mutant CM cells where it interacted with key molecules involved in mitochondrial homeostasis. Spry1 loss resulted in mitochondrial shape alterations and dysfunction, which associated with increased reactive oxygen species production. In agreement, we found that nuclear hypoxia-inducible factor-1 alpha (HIF1α) protein levels were reduced in Spry1KO clones both in vitro and in vivo along with the expression of its glycolysis related genes. Accordingly, Ingenuity Pathway Analysis identified "HIF1α Signaling" as the most significant molecular and cellular function affected by Spry1 silencing, whereas the glycolytic function was significantly impaired in Spry1 depleted BRAFV600-mutant CM cells. In addition, our results indicated that the expression of the vascular endothelial growth factor A was down-regulated following Spry1KO, possibly as a result of mitochondrial dysfunction. Consistently, we observed a substantial impairment of angiogenesis, as assessed by the tube formation assay in vitro and the immunofluorescence staining of CD31 in vivo. Conclusions: Altogether, these findings identify Spry1 as a potential regulator of mitochondrial homeostasis, and uncover a previously unrecognized role for Spry1 in regulating nuclear HIF1α expression and angiogenesis in BRAFV600-mutant CM. Significance: Spry1KO profoundly impacts on mitochondria homeostasis, while concomitantly impairing HIF1α-dependent glycolysis and reducing angiogenesis in BRAF-mutant CM cells, thus providing a potential therapeutic target to improve BRAFV600-mutant CM treatment.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_182,

title = {Traffic light at DSB-transit regulation between gene transcription and DNA repair},

author = {Modafferi S and Esposito F and Tavella S and Gioia U and Francia S},

url = {https://febs.onlinelibrary.wiley.com/doi/10.1002/1873-3468.15024},

doi = {10.1002/1873-3468.15024},

year  = {2025},

date = {2025-01-16},

urldate = {2024-10-21},

journal = {FEBS letters},

volume = {599},

issue = {2},

pages = {177-189},

abstract = {Transcription of actively expressed genes is dampened for kilobases around DNA lesions via chromatin modifications. This is believed to favour repair and prevent genome instability. Nonetheless, mounting evidence suggests that transcription may be induced by DNA breakage, resulting in the local de novo synthesis of non-coding RNAs (ncRNAs). Such transcripts have been proposed to play important functions in both DNA damage signalling and repair. Here, we review the recently identified mechanistic details of transcriptional silencing at damaged chromatin, highlighting how post-translational histone modifications can also be modulated by the local synthesis of DNA damage-induced ncRNAs. Finally, we envision that these entangled transcriptional events at DNA breakages can be targeted to modulate DNA repair, with potential implications for locus-specific therapeutic strategies},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y__184,

title = {CRISPR/Cas9 screens identify LIG1 as a sensitizer of PARP inhibitors in castration-resistant prostate cancer},

author = {Fracassi G and Lorenzin F and Orlando F and Gioia U and D'Amato G and Casaramona AS and Cantore T and Prandi D and Santer FR and Klocker H and {d'Adda di Fagagna F} and Mateo J and Demichelis F},

url = {https://www.jci.org/articles/view/179393},

doi = {10.1172/JCI179393},

year  = {2024},

date = {2024-12-12},

journal = {Journal of clinical investigation},

volume = {135},

issue = {4},

pages = {e179393},

abstract = {PARP inhibitors (PARPi) have received regulatory approval for the treatment of several tumors, including prostate cancer (PCa), and demonstrate remarkable results in the treatment of castration-resistant prostate cancer (CRPC) patients characterized by defects in homologous recombination repair (HRR) genes. Preclinical studies showed that DNA repair genes (DRG) other than HRR genes may have therapeutic value in the context of PARPi. To this end, we performed multiple CRISPR/Cas9 screens in PCa cell lines using a custom sgRNA library targeting DRG combined with PARPi treatment. We identified LIG1, EME1, and FAAP24 losses as PARPi sensitizers and assessed their frequencies from 3 to 6% among CRPC patients. We showed that concomitant inactivation of LIG1 and PARP induced replication stress and DNA double-strand breaks, ultimately leading to apoptosis. This synthetic lethality (SL) is conserved across multiple tumor types (e.g., lung, breast, and colorectal), and its applicability might be extended to LIG1-functional tumors through a pharmacological combinatorial approach. Importantly, the sensitivity of LIG1-deficient cells to PARPi was confirmed in vivo. Altogether, our results argue for the relevance of determining the status of LIG1, and potentially other non-HRR DRG for CRPC patient stratification and provide evidence to expand their therapeutic options.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y__180,

title = {A multiparametric screen uncovers FDA-approved small molecules that potentiate the nuclear mechano-dysfunctions in ATR-defective cells},

author = {Cera MR and Bastianello G and Purushothaman D and Andronache A and Ascione F and Robusto M, Faga' G and Pasi M and Meroni G and Li Q and Choudhary R and Varasi M and Foiani M and Mercurio C},

url = {https://www.nature.com/articles/s41598-024-80837-w},

doi = {10.1038/s41598-024-80837-w},

year  = {2024},

date = {2024-12-12},

urldate = {2024-12-12},

journal = {Scientific reports},

volume = {14},

issue = {1},

pages = {30786},

abstract = {Targeting nuclear mechanics is emerging as a promising therapeutic strategy for sensitizing cancer cells to immunotherapy. Inhibition of the mechano-sensory kinase ATR leads to mechanical vulnerability of cancer cells, causing nuclear envelope softness and collapse and activation of the cGAS-STING-mediated innate immune response. Finding novel compounds that interfere with the non-canonical role of ATR in controlling nuclear mechanics presents an intriguing therapeutic opportunity. We carried out a multiparametric high-content screen to identify small molecules that affect nuclear envelope shape and to uncover novel players that could either ameliorate or further compromise the nuclear mechanical abnormalities of ATR-defective cells. The screen was performed in HeLa cells genetically depleted for ATR. Candidate hits were also tested in combination with the chemical inhibition of ATR by AZD6738, and their efficacy was further validated in the triple-negative breast cancer cell lines BT549 and HCC1937. We show that those compounds enhancing the abnormal nuclear shape of ATR-defective cells also synergize with AZD6738 to boost the expression of interferon-stimulated genes, highlighting the power of multiparametric screens to identify novel combined therapeutic interventions targeting nuclear mechanics for cancer immunotherapy.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y__190,

title = {A Novel G-Quadruplex Structure within Apolipoprotein E Promoter: A New Promising Target in Cancer and Dementia Fight?},

author = {Pirota V and Stritto AD and Magnaghi LR and Biesuz R and Doria F and Mella M and Freccero M and Crespan E},

url = {https://pmc.ncbi.nlm.nih.gov/articles/PMC11561760/},

doi = {10.1021/acsomega.4c06430},

year  = {2024},

date = {2024-12-11},

journal = {ACS omega},

volume = {9},

issue = {45},

pages = {45203-45213},

abstract = {Human apolipoprotein E (APOE) is a crucial lipid transport glycoprotein involved in various biological processes, including lipid metabolism, immune response, and neurodegeneration. Elevated APOE levels are linked to poor prognosis in several cancers and increased risk of Alzheimer's disease (AD). Therefore, modulating APOE expression presents a promising therapeutic strategy for both cancer and AD. Considering the pivotal role of G-quadruplex (G4) structures in medicinal chemistry as modulators of gene expression, here, we present a newly discovered G-quadruplex (G4) structure within the ApoE gene promoter. Bioinformatic analysis identified 21 potential G4-forming sequences in the ApoE promoter, with the more proximal to the transcription start site, pApoE, showing the highest G-score. Biophysical studies confirmed the folding of pApoE into a stable parallel G4 under physiological conditions, supported by circular dichroism, NMR spectroscopy, UV-melting, and a quantitative PCR stop assay. Moreover, the ability to modulate pApoE-G4 folding was demonstrated by using G4-stabilizing ligands (HPHAM, Braco19, and PDS), which increased the thermal stability of pApoE-G4. In contrast, peptide nucleic acid conjugates were synthesized to disrupt G4 formation, effectively hybridizing with pApoE sequences, and confirming the potential to unfold G4 structures. Overall, our findings provide a mainstay for future therapeutic approaches targeting ApoE-G4s to regulate APOE expression, offering potential advancements in cancer and AD treatment.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y__187,

title = {Aging research from bench to bedside and beyond: What we learned from Sammy Basso},

author = {Lattanzi G and Lanzuolo C and Cugudda E and Maggi L and Politano L and Santiago-Fernández O and Ricci G and Squarzoni S and Lopez-Otin C},

url = {https://onlinelibrary.wiley.com/doi/10.1111/acel.14414},

doi = {10.1111/acel.14414},

year  = {2024},

date = {2024-12-11},

journal = {Aging Cell},

volume = {23},

issue = {12},

pages = {e14414},

keywords = {},

pubstate = {published},

tppubtype = {article}

}