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Ymera Pignochino, PhD (she/her/hers)

Assistant Professor
University of Turin, School of Medicine,Candiolo Cancer Institute, FPO-IRCCS
Candiolo, Turin, Piemonte, Italy

Ymera Pignochino- Biography
• born on October 25, 1977
• gained a Medical Biotechnology Degree (2001), PhD in Oncology (2006), and a Specialization Degree in Laboratory Medicine and Clinical Biochemistry (2011)
• been Assistant Professor of Molecular Biology at the University of Turin, Medical School since 2021
• coordinates the preclinical and translational division of the Sarcoma Unit in the Candiolo Cancer Institute
• is an active member of the FOSTER and the FORTRESS European groups of research on Sarcomas and of the Italian Alliance Against Cancer
• now works on deciphering tumor-stroma interactome and crosstalk mechanisms with tumor microenvironment in sarcoma patient-derived models
Relevant publications:
• Targeting the EphA2 pathway: could it be the way for bone sarcomas? Giordano G et al. Cell Communication and Signaling 2024
• DNA Damage Response and Repair genes in advanced bone and soft tissue sarcomas: an 8-gene Signature as a candidate predictive biomarker of response to trabectedin and olaparib combination. Merlini A, et al. Front. Oncol. 2022
• Pazopanib and trametinib as synergistic strategy against osteosarcoma: preclinical activity and molecular insights. Chiabotto G, et al. Cancers (Basel). 2020
• Trabectedin and olaparib in patients with advanced and non-resectable bone and soft tissue sarcomas (TOMAS trial): a phase 1b study from the Italian Sarcoma Group. Grignani G et al, Lancet Oncol. 2018
• PARP1 expression drives the synergistic antitumor activity of trabectedin and PARP1 inhibitors in sarcoma preclinical models. Pignochino Y et al. Mol Cancer. 2017
• The Combination of Sorafenib and Everolimus Abrogates mTORC1 and mTORC2 upregulation in osteosarcoma preclinical models. Pignochino Y et al, Clin. Cancer Res. 2013
• Sorafenib blocks tumour growth, angiogenesis and metastatic potential in preclinical models of osteosarcoma through a mechanism potentially involving the inhibition of ERK1/2, MCL-1 and ezrin pathways. Pignochino Y et al, Mol. Cancer 2009

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