Our Laboratory focuses on identifying more effective cancer treatments for pancreatic ductal adenocarcinoma (PDA) patients that are based on the biological mechanisms that drive cancer.

In particular, our research focuses on:

  1. Characterizing fibroblast and immune cell heterogeneity in normal, inflamed and malignant states.
  2. Pharmacologically and genetically dissecting cancer/fibroblast signaling interactions.
  3. Developing therapeutic strategies that target tumor-promoting stromal components of PDA.
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About Giulia Biffi

I received my Master’s degree in Biomolecular Sciences and Genetics from the University of Pavia, Italy. My Ph.D. dissertation was completed with Sir Shankar Balasubramanian at the Cancer Research UK Cambridge Institute. During my doctoral training, I demonstrated the existence of RNA and DNA secondary structures called G-quadruplexes in human cells by developing a G-quadruplex-specific antibody. This antibody has become a standard tool for the study of these structures in homeostasis and cancer.

During my post-doctoral training, I furthered my interest in characterizing the biochemical differences between normal and malignant cells by studying the signaling pathways active in the microenvironment of pancreatic ductal adenocarcinoma (PDA). In particular, using organoid and mouse models, I investigated the crosstalk between cancer cells and cancer-associated fibroblasts (CAFs). I co-led the establishment of a three-dimensional co-culture system of PDA organoids and fibroblasts, which recapitulated the extracellular matrix deposition and symbiotic interactions observed in vivo. Using this co-culture system and mouse models of PDA, I helped to identify two distinct CAF subtypes, with potentially different roles in PDA progression. I also demonstrated that these cell populations dynamically interconvert, depending upon spatial and tropic cues. Importantly, this cell plasticity represents a therapeutic opportunity as it may be more beneficial to convert, rather than just ablate, tumor-promoting CAFs into potentially tumor-restraining populations. In addition, I determined the critical ligands and receptors responsible for specifying these CAF subtypes in vitro and in vivo, laying the groundwork for the generation of new models that will allow to genetically dissect the roles of these populations.

Contact: Giulia.Biffi@cruk.cam.ac.uk

Tracing the Origin of Fibroblasts in Pancreatic Cancer.

E-pub date: 1 Aug 2020
Journal name: Cell Mol Gastroenterol Hepatol

Diversity and Biology of Cancer-Associated Fibroblasts.

E-pub date: 1 Jan 2021
Journal name: Physiol Rev

Organoid models of human and mouse ductal pancreatic cancer.

E-pub date: 15 Jan 2015
Journal name: Cell

Distinct populations of inflammatory fibroblasts and myofibroblasts in pancreatic cancer.

E-pub date: 6 Mar 2017
Journal name: J Exp Med

Cancer: Double trouble for tumours.

E-pub date: 2 Feb 2017
Journal name: Nature

Deciphering cancer fibroblasts.

E-pub date: 3 Dec 2018
Journal name: J Exp Med

A FATal Combination: Fibroblast-Derived Lipids and Cancer-Derived Autotaxin Promote Pancreatic Cancer Growth.

E-pub date: 1 May 2019
Journal name: Cancer Discov

Cross-Species Single-Cell Analysis of Pancreatic Ductal Adenocarcinoma Reveals Antigen-Presenting Cancer-Associated Fibroblasts.

E-pub date: 31 Aug 2019
Journal name: Cancer Discov