Opendata, web and dolomites


Dissecting the role of mitochondrial dynamics in pancreatic carcinogenesis

Total Cost €


EC-Contrib. €






Project "OPEN P-CAN" data sheet

The following table provides information about the project.


Organization address
address: VIA 8 FEBBRAIO 2
city: PADOVA
postcode: 35122

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Italy [IT]
 Total cost 183˙473 €
 EC max contribution 183˙473 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2019
 Funding Scheme MSCA-IF-EF-RI
 Starting year 2020
 Duration (year-month-day) from 2020-04-01   to  2022-03-31


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITA DEGLI STUDI DI PADOVA IT (PADOVA) coordinator 183˙473.00


 Project objective

OPA1 Educates the Nucleus in Pancreatic CANcer. Pancreatic cancer represents an unresolved health burden, showing abysmal chances of survival and refractoriness to conventional and immunological therapies. Significant benefit will be gained from a better understanding of molecular mechanisms leading to cancer formation, with the goal to curtail disease incidence and improve the opportunities to treat it early. The study will describe how mitochondria and nuclei communicate to facilitate pancreatic cancer initiation. Building from my prior research in metabolic-dependent histone acetylation, and leveraging on the host laboratory expertise in mitochondrial dynamics, I designed a roadmap for the study of how mitochondrial activity is altered during pancreatic carcinogenesis and whether that can be exploited for therapeutic purposes. I will decipher the specific role of major cristae-remodeling factor OPA1, which is an unfavorable prognostic factor for pancreatic cancer patients. I will seek how OPA1-altered expression impacts mitochondrial function and metabolite availability in mouse pre-malignant cells, using in vivo models of pancreatic carcinogenesis. My previous experimentation found that metabolite-dependent histone acetylation is critical for the initiation of pancreatic carcinogenesis. I will now investigate whether OPA1-mediated mitochondrial rewiring impacts citrate and acetyl-CoA abundance in a way that alters the levels of histone acetylation. Epigenetic reprogramming will be further investigated in various OPA1 transgenic mice. Finally, the therapeutic potential of OPA1 targeting will be addressed using both genetic and chemical approaches using resources recently developed at the host laboratory. The project represents a career-defying framework for the study of molecular determinants of pancreatic cancer onset.

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "OPEN P-CAN" project.

For instance: the website url (it has not provided by EU-opendata yet), the logo, a more detailed description of the project (in plain text as a rtf file or a word file), some pictures (as picture files, not embedded into any word file), twitter account, linkedin page, etc.

Send me an  email ( and I put them in your project's page as son as possible.

Thanks. And then put a link of this page into your project's website.

The information about "OPEN P-CAN" are provided by the European Opendata Portal: CORDIS opendata.

More projects from the same programme (H2020-EU.1.3.2.)

BiMetaCat (2019)

Two Are Better Than One: Bimetallic Catalysts for the Conversion of Lignin-Derived Aryl-Ethers

Read More  

InProSMod (2021)

Cholinergic and NMDAR-dependent recruitment of Layer 1 Interneuron shapes cortical motor Processing through network States Modulation

Read More  

NeoPur (2019)

New treatments and novel diagnostic tests for neonatal seizures based on purinergic signaling.

Read More