Samantha Donsante

Sapienza University of Rome

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Mara Riminucci

Sapienza University of Rome

Alessandro Corsi

Sapienza University of Rome

Biagio Palmisano

Sapienza University of Rome

Marta Serafini

Wageningen University & Research

Giorgia Farinacci

Sapienza University of Rome

Alice Pievani

University of Milano-Bicocca

Andrea Biondi

University of Milano-Bicocca

Michele Dello Spedale Venti

Sapienza University of Rome

Pamela Gehron Robey

National Institute of Dental and Craniofacial Research

Ilenia Coletta

Sapienza University of Rome

Cooperative Institutions

Istituti di Ricovero e Cura a Carattere Scientifico

Sapienza University of Rome

European Foundation for the Study of Chronic Liver Failure

University of Milano-Bicocca

Charité - Universitätsmedizin Berlin

Bambino Gesù Children's Hospital

Universitat de Barcelona

University College London

Consorci Institut D'Investigacions Biomediques August Pi I Sunyer

University of Milan

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Gene expression profiling in a mouse model of human Fibrous dysplasia reveals a role for matrix remodeling in the physiopathology of the disease

Bone Reports (2022)

Giorgia Farinacci Biagio Palmisano Ilenia Coletta Samantha Donsante Michele Dello Spedale Venti

Pathophysiology

Human disease

10.1016/j.bonr.2022.101562

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Safe and effective off-the-shelf immunotherapy based on CAR.CD123-NK cells for the treatment of acute myeloid leukaemia

Journal of Hematology & Oncology (2022)

Simona Caruso Biagio De Angelis Francesca Del Bufalo Roselia Ciccone Samantha Donsante

Abstract Background Paediatric acute myeloid leukaemia (AML) is characterized by poor outcomes in patients with relapsed/refractory disease, despite the improvements in intensive standard therapy. The leukaemic cells of paediatric AML patients show high expression of the CD123 antigen, and this finding provides the biological basis to target CD123 with the chimeric antigen receptor (CAR). However, CAR.CD123 therapy in AML is hampered by on-target off-tumour toxicity and a long “vein-to-vein” time. Methods We developed an off-the-shelf product based on allogeneic natural killer (NK) cells derived from the peripheral blood of healthy donors and engineered them to express a second-generation CAR targeting CD123 (CAR.CD123). Results CAR.CD123-NK cells showed significant anti-leukaemia activity not only in vitro against CD123 + AML cell lines and CD123 + primary blasts but also in two animal models of human AML-bearing immune-deficient mice. Data on anti-leukaemia activity were also corroborated by the quantification of inflammatory cytokines, namely granzyme B (Granz B), interferon gamma (IFN-γ) and tumour necrosis factor alpha (TNF-α), both in vitro and in the plasma of mice treated with CAR.CD123-NK cells. To evaluate and compare the on-target off-tumour effects of CAR.CD123-T and NK cells, we engrafted human haematopoietic cells (hHCs) in an immune-deficient mouse model. All mice infused with CAR.CD123-T cells died by Day 5, developing toxicity against primary human bone marrow (BM) cells with a decreased number of total hCD45 + cells and, in particular, of hCD34 + CD38 − stem cells. In contrast, treatment with CAR.CD123-NK cells was not associated with toxicity, and all mice were alive at the end of the experiments. Finally, in a mouse model engrafted with human endothelial tissues, we demonstrated that CAR.CD123-NK cells were characterized by negligible endothelial toxicity when compared to CAR.CD123-T cells. Conclusions Our data indicate the feasibility of an innovative off-the-shelf therapeutic strategy based on CAR.CD123-NK cells, characterized by remarkable efficacy and an improved safety profile compared to CAR.CD123-T cells. These findings open a novel intriguing scenario not only for the treatment of refractory/resistant AML patients but also to further investigate the use of CAR-NK cells in other cancers characterized by highly difficult targeting with the most conventional T effector cells.

Interleukin-3 receptor

10.1186/s13045-022-01376-3

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RANKL Inhibition in fibrous dysplasia of bone: A preclinical study in a mouse model of the human disease

Yearbook of pediatric endocrinology (2020)

Biagio Palmisano Emanuela Spica Cristina Remoli Rossella Labella Di Filippo A

In brief: The effect of RANKL inhibition on fibrous dysplasia development is explored here using a mouse model of a fibrous dysplasia-like disorder. Anti-mouse RANKL monoclonal antibody treatment prevented the development and growth of lesions. However, after discontinuation of anti-mouse RANKL antibody treatment, disease progression resumed and newly formed bone was remodelled into fibrous dysplasia.

Discontinuation

Denosumab

10.1530/ey.17.5.7

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Thrombospondin 1 and 2 along with PEDF inhibit angiogenesis and promote lymphangiogenesis in intrahepatic cholangiocarcinoma

Journal of Hepatology (2021)

Guido Carpino Vincenzo Cardinale Alessandra Di Giamberardino Diletta Overi Samantha Donsante

Lymphangiogenesis

PEDF

Thrombospondin 1

Lymphatic Endothelium

10.1016/j.jhep.2021.07.016

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Selective homing of CAR-CIK cells to the bone marrow niche enhances control of the acute myeloid leukemia burden

Carolina Digital Repository (University of North Carolina at Chapel Hill) (2023)

M.L. Biondi Sarah Tettamanti Stefania Galimberti Beatrice Cerina Christophe Tomasoni

Homing (biology)

10.17615/rzxh-h841

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MPSI Manifestations and Treatment Outcome: Skeletal Focus

International Journal of Molecular Sciences (2022)

Giada De Ponti Samantha Donsante Marta Frigeni Alice Pievani Alessandro Corsi

Mucopolysaccharidosis type I (MPSI) (OMIM #252800) is an autosomal recessive disorder caused by pathogenic variants in the IDUA gene encoding for the lysosomal alpha-L-iduronidase enzyme. The deficiency of this enzyme causes systemic accumulation of glycosaminoglycans (GAGs). Although disease manifestations are typically not apparent at birth, they can present early in life, are progressive, and include a wide spectrum of phenotypic findings. Among these, the storage of GAGs within the lysosomes disrupts cell function and metabolism in the cartilage, thus impairing normal bone development and ossification. Skeletal manifestations of MPSI are often refractory to treatment and severely affect patients’ quality of life. This review discusses the pathological and molecular processes leading to impaired endochondral ossification in MPSI patients and the limitations of current therapeutic approaches. Understanding the underlying mechanisms responsible for the skeletal phenotype in MPSI patients is crucial, as it could lead to the development of new therapeutic strategies targeting the skeletal abnormalities of MPSI in the early stages of the disease.

10.3390/ijms231911168

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From Stem Cells to Bone-Forming Cells

International Journal of Molecular Sciences (2021)

Samantha Donsante Biagio Palmisano Marta Serafini Pamela Gehron Robey Alessandro Corsi

Bone formation starts near the end of the embryonic stage of development and continues throughout life during bone modeling and growth, remodeling, and when needed, regeneration. Bone-forming cells, traditionally termed osteoblasts, produce, assemble, and control the mineralization of the type I collagen-enriched bone matrix while participating in the regulation of other cell processes, such as osteoclastogenesis, and metabolic activities, such as phosphate homeostasis. Osteoblasts are generated by different cohorts of skeletal stem cells that arise from different embryonic specifications, which operate in the pre-natal and/or adult skeleton under the control of multiple regulators. In this review, we briefly define the cellular identity and function of osteoblasts and discuss the main populations of osteoprogenitor cells identified to date. We also provide examples of long-known and recently recognized regulatory pathways and mechanisms involved in the specification of the osteogenic lineage, as assessed by studies on mice models and human genetic skeletal diseases.

Bone remodeling

Bone cell

10.3390/ijms22083989

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Scripts used for: THE ENHANCER LANDSCAPE PREDETERMINES THE SKELETAL REGENERATION CAPACITY OF STROMAL CELLS

Zenodo (CERN European Organization for Nuclear Research) (2023)

Sarah Hochmann Kristy Ou Poupardin Rodophe Michaela Mittermeir Martin Textor

10.5281/zenodo.7669457

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Activated Gs⍺ pathway and estrogens reveal different subsets of adiponectin-expressing osteoprogenitors within bone marrow stroma