David Lane talks at the IFOM-Kyoto University Joint Symposium in Milan about an inhibitor of the p53 pathway, which was previously thought to be impossible to develop. Dr Lane also discusses the advances in the use of antibodies for imaging and a shift to more biologics due to recent clinical success.

Discussing his talk on the mechanisms linking inflammation and cancer, Dr Mantovani highlights the importance of the tumour microenvironment at the IFOM-Kyoto University Joint Symposium in Milan. Dr Mantovani notes that a tumour is not only made up tumour cells, but also normal cells that provide structure, blood vessels and defense cells, such as macrophages. The key to fighting the tumour cells and inflammation is reprogramming the defense cells to recognise the tumour cells as negative.

Michiyuki Matsuda talks to ecancer at the IFOM-Kyoto University Joint Symposium in Milan about his talk, 'Roles of Rho-family GTPases in glioma invasion as visualised by FRET biosensors'. While this process can also take place in breast and lung cancer, Dr Matsuda highlights the process in glioma and the potential effects visualising this process will have on cancer therapy.

Satyajit Mayor talks about the development of the National Centre for Biological Sciences in India and their multi-disciplinary approach combining cell biology with Physics and Chemistry to study how a cell may locally regulate membrane composition and control shape to engage in fundamental cellular processes such as signaling and endocytosis, respectively.

Nagahiro Minato talks at the IFOM-Kyoto University Joint Symposium in Milan about his work on cancer immunology and how the immune system can cope with tumour cells, particularly leukaemia cells. Dr Minato’s research centres on the development of lymphocytes and how they become malignant.

Luigi Naldini talks at the IFOM-Kyoto University Joint Symposium in Milan about his talk on the recent advances in haematopoietic stem cell gene therapy. Dr Naldini explains the process off modifying stem cells with genes and replacing the mutated ones. These stem cells are then corrected and infused into the problem area, creating a potential permanent solution as they are self-regenerating in the patient.

Giorgio Scita talks about the trafficking of cell membranes and the plasma membrane receptor and the reasons why previous attempts to understand metastasis have been unsuccessful. New developments in research show that due to tumour cell's flexibility to use different vessels to spread, stopping one pathway can stimulate a different type of metastasis.

Shunichi Takeda explains the explored molecules responsible for the extraordinary efficient gene-targeting in DT40 cells at the IFOM-Kyoto University Symposium in Milan and how this gene can be manipulated in order progress cancer treatment.

Makoto Mark Taketo talks at the IFOM-Kyoto University Joint Symposium about his talk on the microenvironment of colon cancer using mouse models. Dr Taketo recently began identifying the proteases, MMP9 and MMP2, which can be inhibited; however, there is no compound yet which has had success in clinical trials.

Recent findings support the concept that cells with the properties of stem cells (SC) are integral to the development and perpetuation of several forms of human cancer, and that eradication of cancer stem cells (CSC) may be essential to achieve cancer cure. However, direct proof of these concepts is still lacking, mainly due the scarcity of appropriate model systems. We are characterizing the biological differences between normal and transformed SCs. SCs are defined by their abilities to generate more SCs (‘self-renewal’) and to produce cells that differentiate. One mechanism by which SCs accomplish these two tasks is asymmetric cell division, whereby each SC divides to generate one daughter with SC fate and one that differentiates. SCs, however, possess the ability to expand in number, as it occurs during development and in adulthood after injury or disease. This increase is not accounted by asymmetric divisions, in which only one daughter cell maintains SC identity. Recent findings in C.elegans and Drosophila indicate that SCs can also generate daughter cells that are destined to acquire the same fate (symmetric cell division). On the other hand, SC quiescence is critical to maintain tissue homeostasis after injury. We will discuss our recent findings showing increased symmetric divisions of CSCs in breast tumors (due to inactivation of the p53 tumor suppressor) and dependency of leukemia development on quiescent leukemia SCs (due to transcriptional up-regulation of the cell cycle inhibitor p21 by leukemia-associated fusion proteins). Our findings suggest that that asymmetric divisions of stem cells function as a mechanism of tumor suppression, that SC quiescence is critical to the maintenance of the transformed clone and that symmetric divisions of SCs permits its geometric expansion. Finally, I will discuss downstream mechanisms of regulation of SC divisions by p53 and implications of these findings for the mechanisms regulating checkpoint activation in tissue stem cells. Speaker affiliation: IEO - Universuty of Milan, IT