My group studies how different populations of immune cells in the tumour microenvironment cross-talk in order to establish a tumour-supportive niche in metastasis. This research aims to identify more effective therapeutic targets in metastatic cancers.
The interplay between the cancer cells and the cells in the tumour microenvironment (TME) is critical for the metastatic growth. Our knowledge of how the metastatic “niches” support tumour growth is still very limited, particularly at the early stage of the disease, due to the technical challenge to discriminate TME cells within the whole metastatic tissue.
Cherry-niche, a novel labelling system I developed, allows cancer cells to directly identify their surrounding cells in the metastatic microenvironment (Ombrato et al., Nature 2019). Labelled tissue cells, which represent the local metastatic niche, can be spatially discriminated, isolated from and compared to the entire tissue. Now we have the opportunity to understand how these cells change in the local niche environment.
My lab studies how different immune cell populations interact in metastasis to identify the key events required to establish a favourable “niche” to support tumour growth, in order to propose new therapeutic approaches.
To address these issues, my research aims to answer the following questions:
1. How does the immune-niche evolve in metastasis?
My lab studies how the composition of the “immune-niche” changes, both quantitatively and qualitatively during metastatic disease progression.
2. What makes a niche pro-metastatic?
Several changes occur at the distant tissue when tumour cells colonise it. However, only some of these changes will be critically required for metastatic progression.
We aim to identify the key changes in the metastatic microenvironment that support tumour growth and find potential therapeutic strategies to prevent them.
In vivo labelling system to study cell neighbourhoods Ombrato L Nature Reviews Cancer (2022) 22(7) 661
Early functional mismatch between breast cancer cells and their tumour microenvironment suppresses long term growth Perdrix Rosell A, Maiques O, Martin JAJ et al. Cancer Letters (2022) 544(7)
Disrupted control of origin activation compromises genome integrity upon destabilization of Polε and dysfunction of the TRP53-CDKN1A/P21 axis Borel V, Boeing S, Van Wietmarschen N et al. Cell Reports (2022) 39(7)
Author Correction: Radiation exposure elicits a neutrophil-driven response in healthy lung tissue that enhances metastatic colonization (Nature Cancer, (2022), 3, 2, (173-187), 10.1038/s43018-022-00336-7) Nolan E, Bridgeman VL, Ombrato L et al. Nature Cancer (2022) 3(7) 519
Radiation exposure elicits a neutrophil-driven response in healthy lung tissue that enhances metastatic colonization Nolan E, Bridgeman VL, Ombrato L et al. Nature Cancer (2022) 3(7) 173-187
Integrated OMICs unveil the bone-marrow microenvironment in human leukemia Passaro D, Garcia-Albornoz M, Diana G et al. Cell Reports (2021) 35(7)
Generation of neighbor-labeling cells to study intercellular interactions in vivo Ombrato L, Nolan E, Passaro D et al. Nature Protocols (2021) 16(7) 872-892
Early functional mismatch between breast cancer cells and their tumour microenvironment suppresses long term growth Rosell AP, Maiques O, Chakravarty P et al. (2021) (18)
Technical Advancements for Studying Immune Regulation of Disseminated Dormant Cancer Cells Ombrato L, Montagner M Frontiers in Oncology (2020) 10(1) 594514-594514
Inducing cancer indolence by targeting mitochondrial Complex I is potentiated by blocking macrophage-mediated adaptive responses Kurelac I, Iommarini L, Vatrinet R et al. Nature Communications (2019) 10(7)For additional publications, please click here