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EBMT 2025 Annual Meeting - Greetings from Chiara Nozzoli

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Chiara Nozzoli, Careggi University Hospital, Florence, Italy; 51st Annual Meeting of the EBMT Scientific Committee Co-Chair.

Can you begin by telling us a bit about your background and what your current role as Head of the Transplant Unit at the Careggi University Hospital, Florence, Italy, entails?

In 2002, I started working in the Blood and Marrow Transplant (BMT) unit at Careggi University Hospital. There, I followed the evolution of transplant procedures and assisted patients affected by both onco-haematological and autoimmune diseases.

For many years now, I have focused my scientific interests on multiple myeloma (MM) through participation and promotion of clinical studies in autologous and allogeneic transplantation. Following the passing of Riccardo Saccardi, I was appointed as Director of the Transplant Unit at the Careggi University Hospital in March 2024, where we perform procedures of autologous and allogeneic stem cell transplantation and CAR-T therapy. 

You have been actively involved in haematopoietic cell transplantation (HCT), particularly in relation to MM. What initially drew you to focus on this condition?

MM is a disease that has seen significant progress in biological knowledge and the therapeutic scenario in recent years. In particular, this is thanks to the use of new proteasome inhibitor drugs, immunomodulators, and immunotherapy, in particular monoclonal antibodies, up to bispecific antibodies, CAR-T, and CAR-NK. 

I believe that, particularly in high-risk patients, we can still imagine a role for allogeneic transplantation with the long-lasting graft versus myeloma effect of the donor's immune system, which can represent a treatment platform with immunomodulatory drugs and monoclonal antibodies both in post-transplant maintenance and in relapse.

How do you see the evolving landscape of personalised medicine impacting the future of MM treatment?

The increasingly in-depth biological knowledge of the disease leads us to the possibility of stratifying patients based on risk and on personalisation of therapy through the identification of cellular antigenic targets for monoclonal antibodies, bispecifics, and cellular therapy, with CAR-T today and CAR-NK cells and trispecific antibodies in the future. It will be important to define an algorithm for the treatment of the disease that identifies the correct sequence of all available therapies. It would be valuable to consider the possibility of anticipating the most effective therapies in the first line of treatment to obtain a significant outcome advantage.

In the 51st Annual Meeting of the EBMT, you are set to chair an oral workshop and an oral session centred on MM. What treatment innovations for MM that are just over the horizon are you most excited about?

The most interesting innovation in MM, in my opinion, will be treatment with trispecific antibodies (TsAb), which can either target two different MM-associated antigens to prevent antigen escape or provide an additional co-stimulatory signal for T cells to prevent CD28-mediated effector cell exhaustion. 

What potential does CAR-T therapy hold for patients with MM, and what challenges persist?

The success of autologous CAR-T cells has changed the treatment landscape in relapsed and refractory MM, resulting in the potential movement of CAR-T cells to the frontline treatment setting. However, one of the greatest weaknesses of this therapy is its autologous nature, which makes it time-consuming, labour intensive, and dependent on the patient’s T cell fitness. The development of allogeneic CARs, including CAR-T, CAR-NK, and CAR-iNKT cells, is critical to overcome these challenges and provide patients with an off-the-shelf alternative.

Are there any other sessions or speakers at the EBMT 2025 Annual Meeting that you're particularly looking forward to? 

In my opinion, there are many interesting speakers and sessions, but the ones that I’m particularly interested in are ‘New frontiers in acute and chronic GVHD (E03)’ and ‘Relapse in acute leukemia (P01)’.


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