Ilaria Malanchi

Tumour-Host Interaction Laboratory

Each cell, constituting tissues of each organ, has a very specific task; this ensures the entire body functions altogether. Cancer arises when a cell of a certain tissue loses its specialised function, stops contributing to organ activity and importantly starts breaking the rules limiting its growth within the tissue.

A cancer-initiating cell restarts the embryonic program of 'construction', activates extensive proliferation and builds new interactions with the surrounding healthy cells of the tissue influencing their behaviour.

Consequently the normal cells of a tissue surrounding tumourigenic cells start building a stromal structure and a blood vessels network to support and become part of the tumour growth. If the tumourigenic cells are not cleared early by the immune system, they lead to an abnormal mass that continues to evolve and 'corrupt' the normal host cells locally as well as systemically at distal sites. The powerful growth program is sustained by this crosstalk with host-derived cells, which make the tumour constantly evolve and spread to the entire body. Indeed cancer cells cannot grow without their 'corrupted' surrounded stroma. Therefore, when cancer cells spread from the organ of origin to a distant tissue they must first create a favourable microenvironment (or niche) supporting the growth of a secondary mass.

The lab studies the strategies adopted by cancer cells to establish these crucial interactions with their microenvironment (local tissue cells or inflammatory cells) during the process of tumour initiation as well as metastatic spreading. Our final aim is to find approaches to interfere with the tumour-host crosstalk, a fist step toward novel, more effective anti-cancer therapies.

Figure 1

Metastatic cancer cell (green) "changing" the adjacent cells of the invading tissue (red) when seeding in the lung. Nuclei of all cells are shown in blue. (Click to view larger image)

Selected publications

1. Wculek SK, Malanchi I. (2015) Neutrophils support lung colonization of metastasis-initiating breast cancer cells. Nature. 528(7582):413-7

2. Del Pozo Martin Y, Park D, Ramachandran A, Ombrato L, Calvo F, Chakravarty P, Spencer-Dene B, Derzsi S, Hill CS, Sahai E, Malanchi I.
(2015) Mesenchymal Cancer Cell-Stroma Crosstalk Promotes Niche Activation, Epithelial Reversion, and Metastatic Colonization. Cell Rep. 13(11):2456-69

3. Ombrato, L and Malanchi, I (2014) The EMT universe: space between cancer cell dissemination and metastasis initiation.Critical Reviews in Oncogenesis 19, 349-361

4. Malanchi I, Santamaria MA, Susanto E, Peng H, Lehr HA, Delaloye JF, Huelsken J. (2012) Interactions between cancer stem cells and their niche govern metastatic colonization. Nature 481(7379):85-89

5. Malanchi I, Peinado H, Kassen D, Hussenet T, Metzger D, Chambon P, Huber M, Hohl D, Cano A, Birchmeier W, Huelsken J. Cutaneous cancer stem cell maintenance is dependent on Beta-catenin signalling. Nature. 2008;452(7187):650-653

 

Ilaria Malanchi

ilaria.malanchi@crick.ac.uk
+44 (0)20 379 61282

  • Qualifications and History
  • 2002 PhD, University of Heidelberg, Germany
  • 2003 Postdoctoral Fellow, World Health Organization, France
  • 2004 Postdoctoral Fellow, Swiss Federal Institute of Technology Lausanne, Switzerland
  • 2011 Established lab at the London Research Institute, Cancer Research UK
  • 2015 Group Leader, the Francis Crick Institute, London, UK