Since cholesterol is essential for cell growth, proliferation and membrane integrity, I was interested in the lipid composition of different ALCL models and whether interaction with macrophages can alter the lipid profile of ALK-positive ALCL cells. For this, I used the Folch method to extract lipids from human cells and then analyzed them using thin-layer chromatography (TLC), a method that separates lipids based on their polarity. I analyzed Karpas299 and SupM2 cells after co-culture with THP-1-derived M2-like macrophages. In addition, I compared untreated different ALCL cell lines, ALK-positive as well as ALK-negative.

To verify that THP-1 macrophages provide cholesterol to ALK-positive ALCL cells through secretion, THP-1-derived macrophages were fed with fluorescently labelled cholesterol and subsequently co-cultured with ALK-positive ALCL cells. After only a few hours, fluorescent cholesterol had been taken up by the ALK-positive ALCL cells, located mostly in.

Beyond the scientific work, I really enjoyed the change of routine and learning a new technique in a different laboratory environment. Moreover, I had the chance to meet and collaborate with colleagues from the FANTOM network and the former ALKATRAS network, as well as to reconnect with researchers I had met during my first secondment in Gerda Eggers lab.

The initiative provided participants with practical experience in presenting their research to a wider audience. Listen to Rebekka discussing her research project in a conversation with Rachael. 

ABOUT: 

Rebekka Johanna Sabine Salzmann (UNIPD)  

Identification of New Biomarkers of Disease Resistance in ALCL of childhood: the role of exosomes.  

My research focuses on why patients with the same type of cancer can respond very differently to the same treatment. One key reason appears to be the body’s own defense system, which is meant to fight cancer but can sometimes be manipulated by it.  

Cancer cells can “hack” immune cells by sending signals that confuse them, slow them down, or prevent them from functioning properly. As a result, instead of attacking the tumor, some immune cells may become dysfunctional or even support tumor growth.  

The goal of my work is to understand these mechanisms in detail and to find ways to prevent cancer from disrupting immune function, so that the immune system can effectively eliminate cancer cells again. 

The initiative provided participants with practical experience in presenting their research to a wider audience. Listen to Aiindrila discussing her research project in a conversation with Rachael. 

ABOUT: 

Aiindrila Dhara (MUNI)  

Investigating the effects on the tumoral heterogeneity of ALCL in treatment resistance development  

My PhD research focuses on understanding how cancer cells evolve during treatment, particularly how they become resistant to targeted therapies over time. I study a type of childhood cancer called ALK-positive Anaplastic Large Cell Lymphoma, and I’m interested in why treatment responses vary so much from patient to patient. 

This disease is a T-cell lymphoma, diagnosed by the presence of hallmark cells that express the CD30 marker. It is broadly classified into ALK-positive and ALK-negative types, depending on the expression of a protein called Anaplastic Lymphoma Kinase (ALK). In ALK-positive cases, the ALK gene fuses with another gene called Nucleophosmin (NPM). Since NPM is normally expressed in T cells but ALK is not, this fusion leads to constitutive expression of ALK. 

This is critical because ALK acts as a driver oncogene. The NPM–ALK fusion protein sits at the top of several key signalling pathways, such as JAK–STAT and continuously activates them. This sustained signalling transforms normal T cells into malignant ones by increasing proliferation and disrupting their normal functions. 

Because of this, targeting ALK has become a highly effective treatment strategy, with more than 90% of patients achieving a cure. However, around 10% of patients either do not respond, relapse, or eventually become resistant despite initially responding well. 

The central question I am trying to address is: why do we see such heterogeneous treatment responses? 

To approach this, I think of cancer as an evolving ecosystem. Within a tumour, different cells can have distinct traits—such as genetic mutations, transcriptional states, or epigenetic modifications—similar to diversity within a natural population. When exposed to treatment, this system is subjected to selective pressure. 

Working in Professor Lena Illert’s laboratory and closely alongside Magdalena, I worked with clinical ALK+ ALCL patient samples using the PhenoCycler-Fusion 2.0 system (Akoya Biosciences). Applying a multiplex staining protocol with a panel of more than 45 markers, I was able to comprehensively characterize the cellular composition of the tumor microenvironment and investigate the spatial relationships between malignant and immune cell populations. This approach provided detailed insight into the organization and interaction of cells within the tissue context and supported the identification of features potentially associated with relapse and patient outcomes.

Magdalena’s expertise and guidance throughout the project were invaluable, allowing me to develop practical skills in the multiplex staining protocol, operation of the PhenoCycler-Fusion 2.0 system, image acquisition, and the downstream bioinformatics pipeline used to process and analyze high-dimensional spatial proteomics data. Our discussions also provided an opportunity to exchange ideas and perspectives from our respective PhD projects.

Beyond the laboratory, the secondment also gave me the opportunity to explore Munich and experience life in a new city. During my stay, I visited the English Garden, explored the historic city centre, and spent time at the BMW Museum. These activities allowed me to learn more about Munich while enjoying its unique atmosphere, making the secondment a rewarding experience both scientifically and personally.

Overall, this secondment significantly enhanced my technical expertise and broadened my scientific perspective, while generating valuable data contributing to the identification of prognostic markers for relapse in ALK+ ALCL patients. In addition, the stay allowed me to explore Munich, which further enhanced the overall experience.

The initiative provided participants with practical experience in presenting their research to a wider audience. Listen to Carla discussing her research project in a conversation with Rachael. 

ABOUT: 

Carla Vázquez Amos (UCAM – UKRI associate)  

Investigating the role of the T cell receptor (TCR) in ALCL pathogenesis towards the development of an innovative therapeutic approach  

My research focuses on understanding how and why people get cancer. Specifically, I study two subtypes of a rare immune cell cancer called Anaplastic Large Cell Lymphoma (ALCL). In this disease, T cells that are usually protecting the body from cancer have become cancer. In the first subtype I study, these T cells have a protein called ALK that they’re not supposed to, because two genes have been chopped and stuck together by accident in the patients’ DNA. Constant ALK activity can cause uncontrolled cell growth. However, we do sometimes find these two genes fused together in the blood of healthy people and from umbilical cords of healthy babies. Therefore, we think another event might be required to trigger the cancer. To investigate this, I am using mice with genetic modifications that mimic the disease, genetically modified human cells, patient samples and bioinformatic approaches. My findings suggest the second essential event in the creation of this cancer is linked to a signalling pathway important in how T cells are educated to protect the body. Interestingly, in mature T cells, this pathway is also important in sensing the environment for foreign agents.  

The other subtype I study is called Breast Implant Associated ALCL, which arises in some people who have textured breast implants. Although this cancer looks broadly similar to the other subtype under the microscope, it doesn’t have the ALK protein. We think there is a chemical present on the implants that causes T cells to become cancerous. I’m working with chemists, materials scientists and a masters student to identify which chemicals are on implants and how they affect our cells. Overall, we hope that increasing our understanding of how these cancers start will help us improve treatments for ALK+ ALCL and avoid more cases of BIA-ALCL happening in the future.  

This experience has been incredibly valuable both scientifically and professionally. During my time at Suzanne Turner’s Lab in the Department of Pathology, University of Cambridge, I had the opportunity to work closely with researchers in the field of translational cancer research, with a major focus on applying WILDseq in ALCL PDX models to better understand tumour heterogeneity and its role in treatment resistance development.

A key outcome of this secondment was the successful development of DNA-barcoded ALCL PDX models using the WILDseq lineage tracing system, which is a major focus of my PhD research at Masaryk University, funded through the EU Horizon MSCA FANTOM Fellowship programme.

Beyond the research itself, this experience allowed me to exchange ideas, learn new techniques, and build meaningful collaborations in such an inspiring academic environment. I cannot thank Prof. Suzanne Turner, Dr. Lucy Hare, Dr. Marta Ferraresso, and Dr. Perla Pucci and all other members enough for their warm welcome throughout this journey.

I’m also grateful to be part of the FANTOM Doctoral Network, which has made international collaboration opportunities like this possible and continues to support my growth and development as an early-career researcher.

Looking forward to continuing these collaborations and translating these learnings into the next phase of my research.

The initiative provided participants with practical experience in presenting their research to a wider audience. Listen to Nicola discussing his research project in a conversation with Rachael. 

ABOUT: 

Nicola Mora (MUW) 

STAT1 as tumor suppressor and potential therapy target in Anaplastic Large Cell Lymphoma  

My research is about a cancer called ALCL, which affects immune cells known as T-cells. These cells normally help your body fight infections, but in this disease they accumulate genetic errors and start multiplying uncontrollably, crowding out the healthy ones and compromising the ability of the immune system to work properly.  

The type of ALCL I study is caused by a genetic accident where two genes accidentally fuse together, generating a defective protein that constantly pushes the cell to grow and divide. But like any living cell, even cancer cells need to maintain a delicate balance — too little signal and they die, but too much signal and they also die.   

There are already drugs called ALK inhibitors that work by cutting off the growth signal at the source, starving the cancer cells until they die. The drug I am testing works in the completely opposite way. Instead of reducing the signal, it destroys the protein responsible for keeping that balance in check, causing the signals to go out of control. The cancer cells then receive too much stimulation than they can handle and end up destroying themselves. 

I am also looking at whether this destruction then triggers the immune system to jump in and clear out whatever is left — so instead of just using the drug alone, the body becomes part of the treatment too.  

On top of that, since the same genetic accident shows up in other cancers as well, we are testing whether this drug could be useful beyond ALCL too. 

The initiative provided participants with practical experience in presenting their research to a wider audience. Listen to Magdalena discussing her research project in a conversation with Rachael.

ABOUT:

Magdalena Kršić (TUM)

Development of a TME-based Immunoscore as a prognostic and predictive biomarker for ALCL – Most people think cancer is just about the tumor itself, a mass of “bad” cells growing out of control. But that’s only part of the story. What I study is everything around the tumor – the immune cells trying to fight it, the surrounding support cells, and the signals they all send to each other. This environment is called the tumor microenvironment, and it can actually decide whether cancer grows, spreads, or gets stopped. To understand this hidden world, I use cutting-edge technologies that let me zoom in at an incredible level of detail. I can measure dozens of proteins and hundreds of genes in a single piece of tissue, while also seeing exactly where each cell is located, almost like a high-resolution map of a tiny city. And that’s important, because it’s not just about which cells are there. It’s about how they interact. Some cells help the immune system attack the tumor, while others can actually protect it. These cellular “conversations” might explain why some cancers respond to treatment and others don’t. The exciting part? Scientists are now developing new therapies that don’t just target the tumor itself, but this entire surrounding environment. By understanding it better, we could unlock new ways to make treatments work more effectively. So in a way, I’m not just studying cancer. I’m studying the ecosystem it lives in. And that ecosystem might hold the key to beating it.

The initiative provided participants with practical experience in presenting their research to a wider audience. Listen to Stefania discussing her research project in a conversation with Rachael.

ABOUT:

Stefania Massari (MUW) 

STAT proteins as (de)regulators of metabolism in ALCL – My research focuses on a type of cancer called anaplastic large cell lymphoma (ALCL), which comes from T cells—immune cells that normally protect the body from infections. In healthy conditions, T cells only grow and divide when they are activated to fight something. In ALCL, however, these cells seem to get stuck in a constantly “on” mode, growing and dividing when they shouldn’t. I study how this happens by looking at how these cancer cells produce and use energy, since growing cells need a lot of fuel. In particular, I’m interested in a signalling system called JAK–STAT, which acts like an internal switch that tells cells how to behave. I want to understand whether this system is forcing the cancer cells to keep using energy in a way that supports their uncontrolled growth. By figuring this out, we hope to find ways to target how these cells fuel themselves and potentially stop the cancer from growing..

The initiative provided participants with practical experience in presenting their research to a wider audience. Listen to Will discussing her research project in a conversation with Rachael.

ABOUT:

Will Shepheard (UKE) 

Establishment of ALK-autoantibodies, T cell responses against ALK and cell-free DNA as biomarkers and for response monitoring of patients with ALCL  My research focuses on developing smarter, less invasive ways to monitor childhood cancer using blood samples. Instead of relying only on scans or more invasive tests, this work looks for signals in the blood. One approach involves analysing cell-free DNA (cfDNA), which are tiny fragments of DNA released by cancer cells, to detect the disease, see if it is still present, and spot any new changes in the cancer over time. I also study the immune system, including T cells, which can attack cancer, and autoantibodies, which can give clues about how well treatment is working and whether the cancer might come back. Overall, the goal is to combine these signals to detect cancer earlier, track treatment more accurately, and make testing easier for young patients.