ANNALINDA PISANO

PERSONAL INFORMATION
Name: Annalinda Pisano
Nationality: Italy

CURRENT POSITION
Associate Professor, Department of Radiological, Oncological and Pathological Sciences
“Sapienza” University of Rome, Rome, Italy

EDUCATION
2023: Master’s degree in Immuno Oncology, Sapienza University of Rome
2020: ASN - Abilitazione Scientifica Nazionale a Professore di II fascia nel Settore concorsuale
06/N1 – Scienze delle professioni sanitarie e delle tecnologie mediche applicate nella tornata 2018-2020 – Quinto quadrimestre (validità Abilitazione dal 13/11/2020 al 13/11 2032)
2014: Post-doctoral course, 2nd Course in Mitochondrial Medicine, Bertinoro di Romagna (FC)
2014: PhD in Epidemiology and Molecular Pathology, Sapienza University of Rome
Thesis: “Meccanismo di danno nella Neuropatia Ottica Ereditaria di Leber e possibile ruolo terapeutico di sostanze estrogeno-simili”
2012: Course: the micro-oxygraph ‘Seahorse Bioscience’, IRCCS Istituto Neurologico “C. Besta” Milano
2011: Professional qualification: Biologist, Sapienza University of Rome
2009: Master’s degree in Neurobiology, Sapienza University of Rome
2007: Bachelor in Biological Sciences, Sapienza University of Rome

ACADEMIC APPOINTMENTS
2022 – 2025: Assistant Professor (RTDB), Department of Radiology, Oncology and Pathology, Policlinico Umberto I - Sapienza University of Rome
2018 – 2021: Research Fellow, Project: Stabilization of tRNAs as a therapeutic strategy for diseases due to mutations in mt-tRNAs; Department of Radiology, Oncology and Pathology, Policlinico Umberto I - Sapienza University of Rome
2016 – 2018: Research Fellow, Project: Mechanisms and treatment of coronary microvascular disfunction in patients with genetic or secondary left ventricular hypertrophy; Department of Radiology, Oncology and Pathology, Policlinico Umberto I - Sapienza University of Rome
2014 – 2015: Research Fellow, Project: Isolated domains of aminoacyl tRNA syntethases as a possible therapy for mt tRNA mutation associated disease; Department of Radiology, Oncology and Pathology, Policlinico Umberto I - Sapienza University of Rome
2013 – 2014: Post-doctoral fellow, Project: Estrogen mediated regulation of respiratory chain biogenesis and functions: possible therapeutic implications for Leber’s hereditary optic neuropathy; Department of Radiology, Oncology and Pathology, Policlinico Umberto I - Sapienza University of Rome

TEACHING ACTIVITIES
2023 – now: Lecture “Corso di Laurea in Farmacia” Sapienza University of Rome
2023 – now: Lecture “Corso di Laurea in Tecniche di Laboratorio Biomedico” Sapienza University of Rome
2018 – now: Tutor, Master’s Degree Thesis, Medicine and Surgery; Bachelor Thesis, “Tecniche di Laboratorio Biomedico”; Department of Radiology, Oncology and Pathology, Policlinico Umberto I - Sapienza University of Rome
2016 – now: Tutor, Laboratory traineeship for PhD Students; Department of Radiology, Oncology and Pathology, Policlinico Umberto I - Sapienza University of Rome

SOCIETY MEMBERSHIPS, AWARDS AND HONORS
2020 – now: Reviewer for Scientific Reports
2015: Best project award: Telethon Convention 2015
2014: Meet award: 2nd Course in Mitochondrial Medicine - Bertinoro di Romagna (FC)

FUNDING INFORMATION
2025: Progetto di Ricerca di Università-Ateneo 2025; Title: Ischemic/oxidative damage in diverticular disease: set up of an in vitro model.
2022: Progetto di Ricerca di Università-Ateneo 2022; Title: Mitochondrial tRNA related diseases: implementation of cellular models to evaluate the tissue-specific effects and rescuing mechanisms of therapeutic molecules.
2018: “Research Project” Mitocon – Insieme per lo studio e la cura delle malattie mitocondriali Onlus (Grant n° 2018-02); Title: Isolated peptides from mt-leucyl-tRNA synthetase as novel therapeutic instruments against mitochondrial disease caused by mt-tRNA point mutation.

PATENTS
Peptide-mimetic therapeutic for disorders due to point mutations in mitochondrial tRNAs.102021000032930 deposited on December 29, 2021
Patent Cooperation Treaty PCT/IB2022/062354

RESEARCH ACTIVITIES
-Application of cellular and molecular biology techniques to the study of mitochondrial (mt) DNA disease:
Production and characterization of cellular models: trans-mitochondrial cybrids (cybrids), induced pluripotent stem cells, (iPSCs) and iPSC derived cells (cardiomyocytes and neurons) carrying pathogenic mutations in mitochondrial DNA genes to investigate the pathogenic mechanism of disorders due to (mt) DNA point mutations.
Analysis of the effect of therapeutic molecules on cellular models of mt-DNA related disease
Study of the role of mitochondrial biogenesis in the penetrance of mitochondrial disorders.
-Application of morpho-molecular analysis techniques and cellular biology to the study of the pathophysiology of diverticular disease (DD):
Study of the pathogenic role of acute/chronic ischemia in the establishment of oxidative imbalance and investigation of the expression of hypoxic markers in patients with different clinical phenotypes of DD.
Production and characterization of an in vitro model of hypoxia using primary human colonic smooth muscle cells (pHSMCs) and colonic HSMC lines to dissect the role of acute and chronic ischemia in the development of DD.
-Oncological pathology:
Study of prognostic and predictive factors in different neoplastic settings.
-Application of morpho-molecular analysis techniques to the study mitochondrial, cardiac and skeletal muscle diseases:
Evaluation of selective gene expression profiles by Laser Capture Microdissection in conjunction with real time PCR or Next Generation Sequencing.
Analysis of the pathological phenotype of selected diseases by the application of immunohistochemistry, immunofluorescence and histomorphometry techniques on human samples.

PUBLICATIONS
1. Pisano A et al. Peptide-mimetics derived from leucyl-tRNA synthetase are potential agents for the therapy of mt-tRNA related diseases. Front Pharmacol. 2025. doi: 10.3389/fphar.2025.1607343.
2. Leopizzi M et al. Evaluation of immune microenvironment in non-small cell lung carcinoma after neoadjuvant immunotherapy: a case report. Int J Clin Exp Pathol. 2025. doi: 10.62347/NCYZ7977.
3. Carlomagno D et al. Acute diverticulitis in 2024: current evidence to prevent onset and recurrence. Minerva Gastroenterol (Torino). 2025 doi: 10.23736/S2724-5985.25.03882-3.
4. Cappelletti M et al. The Unexplored Role of Mitochondria-Related Oxidative Stress in Diverticular Disease. Int J Mol Sci. 2024. doi: 10.3390/ijms25179680.
5. Botticelli A et al. The role of CD73 in predicting the response to immunotherapy in head and neck cancer patients. Pathol Res Pract. 2024. doi: 10.1016/j.prp.2024.155415.
6. Pallotta L*, Pisano A* et al. From diverticulosis to complicated diverticular disease:Progression of myogenic alterations and oxidative imbalance. Neurogastroenterology & Motility. 2024. doi: 10.1111/nmo.14850. *co-authors.
7. Capirossi G et al. Modelling MERRF in 3D cortical organoids: manipulating patientderived iPSCs to gain insight on prospective pre-clinical therapeutic strategies. Biochimica et Biophysica Acta (BBA) - Bioenergetics 2024. doi: 10.1016/j.bbabio.2024.149469.
8. Burattini M et al. MELAS syndrome: Insights into cardiac mechanics. Vascul Pharmacol. 2024. doi: 10.1016/j.vph.2024.107303.
9. Cerbelli B et al. PD-L1 testing in metastatic triple negative breast cancer: Results of an Italian survey. Tumori. 2024. doi: 10.1177/03008916231196781.
10. Amodeo G et al. The Influence of Bolus of Methylprednisolone on Postorthognathic Surgery Symptoms: A Controlled Clinical Trial. J Craniofac Surg. 2023. doi: 10.1097/SCS.0000000000009492.
11. Cerbelli B*, Pisano A* et al. Overexpression in metastatic breast cancer supports Syndecan-1 as a marker of invasiveness and poor prognosis. Clin Exp Med. 2023. doi: 10.1007/s10238-022-00880-7. *co-authors.
12. Greco N, et al. New Insights and Evidence on "Food Intolerances": Non-Celiac Gluten Sensitivity and Nickel Allergic Contact Mucositis. Nutrients. 2023. doi: 10.3390/nu15102353.
13. Pisano A et al. RNA-seq profiling reveals different pathways between remodeled vessels and myocardium in hypertrophic cardiomyopathy. Microcirculation. 2022. doi: 10.1111/micc.12790.
14. Foglieni C et al. Myosins and MyomiR Network in Patients with Obstructive Hypertrophic Cardiomyopathy. Biomedicines. 2022. doi: 10.3390/biomedicines10092180.
15. Piovesana R et al. Notch Signal Mediates the Cross-Interaction between M2 Muscarinic Acetylcholine Receptor and Neuregulin/ErbB Pathway: Effects on Schwann Cell Proliferation. Biomolecules. 2022. doi: 10.3390/biom12020239.
16. Giordano C et al. Myocardial fibrosis: morphologic patterns and role of imaging in diagnosis and prognostication. Cardiovasc Pathol. 2022. doi: 10.1016/j.carpath.2021.107391.
17. Lombardi M et al. Mitochondrial Energetics and Ca2+-Activated ATPase in Obstructive Hypertrophic Cardiomyopathy. J. Clin. Med. 2020. doi:10.3390/jcm9061799.
18. Perli E*, Pisano A* et al. Exogenous peptides are able to penetrate human cell and mitochondrial membranes, stabilize mitochondrial tRNA structures, and rescue severe mitochondrial defects. FASEB J. 2020. doi: 10.1096/fj.201903270R. *co-authors
19. Cerbelli B et al. CD73 expression and pathologic response to neoadjuvant chemotherapy in triple negative breast cancer. Virchows Arch. 2019. doi: 10.1007/s00428-019-02722-6.
20. Perli E*, Pisano A* et al. Novel compound mutations in the mitochondrial translation elongation factor (TSFM) gene cause severe cardiomyopathy with myocardial fibro-adipose replacement. Sci Rep. 2019. doi: 10.1038/s41598-019-41483-9. *co-authors
21. Musarò A et al. Neuromuscular magnetic stimulation counteracts muscle decline in ALS patients: results of a randomized, double-blind, controlled study. Sci Rep. 2019. doi: 10.1038/s41598-019-39313-z.
22. Cerbelli B et al. Breast cancer subtypes affect the nodal response after neoadjuvant chemotherapy in locally advanced breast cancer: Are we ready to endorse axillary conservation? Breast J. 2019. doi: 10.1111/tbj.13206.
23. Botticelli A et al. Can IDO activity predict primary resistance to anti-PD-1 treatment in NSCLC? J Transl Med. 2018. doi: 10.1186/s12967-018-1595-3.
24. Gramegna LL et al. Cerebral Mitochondrial Microangiopathy Leads to Leukoencephalopathy in Mitochondrial Neurogastrointestinal Encephalopathy. AJNR Am J Neuroradiol. 2018. doi: 10.3174/ajnr. A5507.
25. Cerbelli B et al. Anti-aminoacyl-tRNA synthetase-related myositis and dermatomyositis: clues for differential diagnosis on muscle biopsy. Virchows Arch. 2017. doi: 10.1007/s00428-017-2269-x.
26. Antinozzi C et al. Potential role for the VDR agonist elocalcitol in metabolic control: Evidences in human skeletal muscle cells. J Steroid Biochem Mol Biol. 2016. doi: 10.1016/j.jsbmb.2016.12.010.
27. Di Gioia CR et al. Nonischemic Left Ventricular Scar and Cardiac Sudden Death in the Young. Hum Pathol. 2016. doi: 10.1016/j.humpath.2016.08.004.
28. Perli E et al. Short peptides from leucyl-tRNA synthetase rescue disease-causing mitochondrial tRNA point mutations. Hum Mol Genet. 2016. doi: 10.1093/hmg/ddv619.
29. Pisano A et al. Impaired mitochondrial biogenesis is a common feature to myocardial hypertrophy and end stage ischemic heart failure. Cardiovascular Pathology 2016. doi: 10.1016/j.carpath.2015.09.009.
30. Pippucci T et al. Homozygous NOTCH3 null mutation impairs NOTCH3 signaling and causes recessive early-onset arteriopathy and cavitating leukoencephalopathy. EMBO Mol Med. 2015. doi:10.15252/emmm.201404399.
31. Pisano A et al C. Targeting estrogen receptor β as preventive therapeutic strategy for Leber's hereditary optic neuropathy. Hum Mol Genet. 2015. doi: 10.1093/hmg/ddv396.
32. Perli E et al. The isolated carboxy-terminal domain of human mitochondrial leucyl-tRNA synthetase rescues the pathological phenotype of mitochondrial tRNA mutations in human cells. EMBO Mol Med. 2014. doi: 10.1002/emmm.201303198.
33. Uggenti C et al. M2 muscarinic receptor activation regulates schwann cell differentiation and myelin organization. Dev Neurobiol. 2013. doi: 10.1002/dneu.22161.
34. Giordano C et al. Efficient mitochondrial biogenesis drives incomplete penetrance in Leber’s hereditary optic neuropathy. Brain. 2014. doi: 10.1093/brain/awt343.
35. Giordano G et al. Cardiomyopathies due to homoplasmic mitochondrial Trna mutations: morphologic and molecular features. Human Pathology 2013. doi: 10.1016/j.humpath.2012.10.011.
36. Perli E et al. Isoleucyl-tRNA synthetase levels modulate the penetrance of a homoplasmic m.4277T>C mitochondrial tRNAIle mutation causing hypertrophic cardiomyopathy. Hum Mol Genet. 2012. doi: 10.1093/hmg/ddr440.