Roberta Santarelli

Associate Professor

Università degli Studi di Roma La Sapienza Dipartimento di Scienze Statistiche

Italy

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About

Roberta Santarelli is an Associate Professor at Università degli Studi di Roma La Sapienza in the Dipartimento di Scienze Statistiche, Italy. Her research focuses on the interactions between various molecular mechanisms and cancer cell behavior, particularly in pancreatic and colon cancers, as evidenced by her recent publications. Areas of interest include the modulation of cell cycle regulators, the effects of curcumin on gene expression, and therapeutic strategies targeting lymphoma cells.

Articles (10)

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2025

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2025

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2025

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2024

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2023

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2023

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2023

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2022

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2022

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2021

Collaborators (3)

Michele Di Crosta

Sapienza University of Rome

ITALY

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Mara Cirone

ITALY

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Gabriella D'ORAZI

Associate Professor

Saint Camillus International University of Health Sciences

ITALY

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Roberta Santarelli

Research Interests

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Articles (10)

Valemetostat–SAHA-Driven Acetylation of p53 via SET/TAF-Iβ Displacement and p300 Activation Modulates Cell Cycle Regulators in Pancreatic Cancer Cells

Modulatory Effect of Curcumin on Expression of Methyltransferase/Demethylase in Colon Cancer Cells: Impact on wt p53, mutp53 and c-Myc

Changes in Lysine Methylation Contribute to the Cytotoxicity of Curcumin in Colon Cancer Cells

EZH2 Inhibition by DS3201 Triggers the Kaposi’s Sarcoma-Associated Herpesvirus Lytic Cycle and Potentiates the Effects Induced by SAHA in Primary Effusion Lymphoma Cells

NFE2L2 and STAT3 Converge on Common Targets to Promote Survival of Primary Lymphoma Cells

HSPs/STAT3 Interplay Sustains DDR and Promotes Cytokine Release by Primary Effusion Lymphoma Cells

HSP110 Inhibition in Primary Effusion Lymphoma Cells: One Molecule, Many Pro-Survival Targets

Concomitant Inhibition of IRE1α/XBP1 Axis of UPR and PARP: A Promising Therapeutic Approach against c-Myc and Gammaherpesvirus-Driven B-Cell Lymphomas

Mechanisms of Sensitivity and Resistance of Primary Effusion Lymphoma to Dimethyl Fumarate (DMF)

Lovastatin reduces PEL cell survival by phosphorylating ERK1/2 that blocks the autophagic flux and engages a cross‐talk with p53 to activate p21

Collaborators (3)

Michele Di Crosta

Mara Cirone

Gabriella D'ORAZI

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