My group studies how different populations of immune cells in the tumour microenvironment cross-talk in order to establish a “favourable” niche in metastasis.
Metastatic-niche labelling reveals parenchymal cells with stem features. Nature (2019) 572(7771):603-608. PMID: 31462798
Mesenchymal cancer cell-stroma crosstalk promotes niche activation, epithelial reversion, and metastatic colonization. Cell Reports (2015) 13(11):2456-69. PMID: 26670048
The EMT universe: space between cancer cell dissemination and metastasis initiation. Critical reviews in oncogenesis (2014) 19(5):349-61. PMID: 25404150
T-cell factor 3 (Tcf3) deletion increases somatic cell reprogramming by inducing epigenome modifications. PNAS (2011) 108(29):11912-7. PMID: 21730189
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.
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
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)
Author Correction: Metastatic-niche labelling reveals parenchymal cells with stem features (Nature, (2019), 572, 7771, (603-608), 10.1038/s41586-019-1487-6) Ombrato L, Nolan E, Kurelac I et al. Nature (2019) 575(7) E8
Metastatic-niche labelling reveals parenchymal cells with stem features Ombrato L, Nolan E, Kurelac I et al. Nature (2019) 572(7) 603-608
Subclonal cooperation rewrites metastasis Ombrato L, Malanchi I Nature Cell Biology (2019) 21(7) 797-798
Mesenchymal Cancer Cell-Stroma Crosstalk Promotes Niche Activation, Epithelial Reversion, and Metastatic Colonization del Pozo Martin Y, Park D, Ramachandran A et al. Cell Reports (2015) 13(7) 2456-2469
Temporal perturbation of the Wnt signaling pathway in the control of cell reprogramming is modulated by TCF1 Aulicino F, Theka I, Ombrato L et al. Stem Cell Reports (2014) 2(7) 707-720
The EMT universe: Space between cancer cell dissemination and metastasis initiation Ombrato L, Malanchi I Critical Reviews in Oncogenesis (2014) 19(7) 349-361
Regulation of self-renewal and reprogramming by TCF factors Ombrato L, Lluis F, Cosma MP Cell Cycle (2012) 11(7) 39-47For additional publications, please click here