Research – Blog about neuroblastoma research

Beyond the Bench: Inside EACR 2025

The European Association for Cancer Research (EACR) is a registered charity and scientific community that has been holding conferences since 1968. EACR’s annual four-day congress is dedicated to basic, preclinical and translational cancer research. It brings together the cancer research community, including PhD students, postdocs, PIs, and commercial sponsors, for the opportunity to network and collaborate to progress cancer therapeutics.

I was fortunate enough to receive the Breakthrough Cancer Research Education and Travel Award, which made it possible for me to attend this year’s EACR conference held in Lisbon, Portugal. Breakthrough Cancer Research is an Irish Medical research charity focused on improving the outcomes of patients diagnosed with rare and poor prognosis cancers, like neuroblastoma.

When I first arrived at the congress center in Lisbon, I was immediately impressed by how well organized and put together the conference was. A schedule of four full days included speakers, poster presentations, industry talks, a technology exhibition, giveaways, networking rounds, and early-career talks. I checked in, received my “goodie bag” and was on my way to the first talk. For the duration of the conference, you were encouraged to move freely between all the available presentations within several auditoriums and pavilions. They even had screens and speakers set up outside the auditoriums if there was no more space inside to make sure that the research presented was accessible to everyone. The lunch breaks were the perfect time to enjoy the sunshine, walk along the Tagus River, and have a picnic with views of the Ponte 25 de Abril bridge (similar in style to the Golden Gate Bridge in San Francisco, California).

Exhibitors showcase with over 100 companies available to talk about their technology. QR codes were at each booth to scan for participants to be entered into a drawing for an iPad and free entry to next year’s conference in Budapest, Hungary.

Throughout the conference, I listened to talks that ranged from how estrogen levels in breast cancer are related to the loss of bone density to how we can detect cancer in circulating cells for a diagnosis three years earlier than previous tests. One of the talks began with the necessity for physiologically relevant in vitro to 3D models and then the conclusion of the talk discussed how there’s a bridge needed between academia and industry for treatments to be more streamlined and accessible. Most importantly, I was able to read quite a few posters with research that other PhD students were doing related to small extracellular vesicles (sEVs). My work specifically looks at the relationship between sEVs shared from cancerous to non-cancerous cells and what their functional impact is. A lot of the work I saw was optimization of sEV isolation and characterization, which can be quite tricky to do but was helpful to see what complications others were running into and their troubleshooting results.

Presentation by Cindrilla Chumduri during EACR – EMBO Symposium: Advanced in vitro Models. Chumduri highlights the “valley of death” where there is a gap between academic and industry research that impedes the progression of scientific breakthroughs in cancer research.

By the time it got to my poster defense, I was excited to talk about my work and looking forward to meeting others who might be doing research similar to mine. There were a handful of people that came to speak to me about my work and ask questions. One thing about the PhD journey is that sometimes you can be so deeply involved in your own work and what isn’t going right that you lose sight of how impactful your work can be. When several people approached me about the co-culture model I was using, they were so curious and wanted to implement something like that into their work. Hearing positive feedback on my efforts was a refreshing way to end the conference. At the end of the day, there was a celebration dinner where a traditional Portuguese Fado band played music while we were able to unwind and network with other PhD students. My time spent in Lisbon at EACR was one of the best conference experiences I’ve had. I’m looking forward to heading back into the lab, making progress with my project, and presenting at the next conference.

My poster defense during the Tumor Biology poster sessions.

Special thanks to Breakthrough Cancer Research for supporting my research and providing me with this fantastic opportunity.

Written by Alysia Scott

Mac4Me project kicks off with a meeting in Rotterdam and the first doctoral training session

The European doctoral network Mac4Me (Macrophage Targets for Metastatic Treatment) has officially commenced its action with a successful kick-off meeting held in Rotterdam on June 25-26, 2025. The event, organised by the Erasmus University Medical Centre (the project coordinator), brought together the project’s core partners to harmonise efforts and set the stage for the next four years of research.

Mac4Me goes beyond technical expertise, striving to ensure each doctoral candidate has the tools to flourish both professionally and personally. This commitment was evident in the first training, which covered clinical aspects and requirements related to the three metastatic cancer types Mac4Me is focusing on. Besides advanced scientific methodologies, including single-cell mechanics and organ-on-chip technology, the students gained insights into fundamental biological mechanisms such as tumour formation, immune evasion, and DNA repair deficiency in age-related diseases. The training also explored the ethics of cancer research and included an activity in which the communication team produced short introductory videos featuring each doctoral candidate on the website. A significant part of the training focused on Patient and Public Involvement in Research (PPI). This session, led by patient advocates from Dublin and the US, fostered an immediate connection with the doctoral candidates, emphasising the importance of collaboration and direct patient engagement at every step in the research process. A profound mutual interest in the project’s success was shared.

With nearly all doctoral candidates and principal investigators meeting in person for the very first time, the training and the meeting were marked by a palpable spirit of eagerness and enjoyment. This initial gathering fostered strong team-building among the doctoral candidates and across the various subprojects, laying a crucial foundation for their scientific and technical collaboration. The meeting proved to be a success in promoting the exchange of expertise and significantly strengthening networking opportunities, thereby setting a precedent for ongoing collaboration.

Mac4Me is a Horizon Europe MSCA (Marie Skłodowska-Curie Actions) Doctoral Network. The project is led by a core consortium of 14 partners and supported by an additional 11 associated partners. For more information about the consortium and the project, visit the Mac4Me website.

For media inquiries, please contact: mac4me@upf.edu.

My little lab story

I’m Ronja, a final-year PhD student navigating the final stretch of lab work, attempting to weave a cohesive narrative from the experiments—and occasional failures—that I’ve genuinely enjoyed over the past three and a half years. With just four months to go until my submission deadline, the calendar is dotted with wedding invitations, visits from friends eager to see me in Dublin while I’m still here, and one last Irish summer that I’m determined to savour—despite the ever-present stress and a slow, persistent creep of anxiety.

At long last, I’m learning to let go of perfection. I can no longer afford to chase down every loose thread left behind by past experiments. Time is no longer elastic, and what remains must be used with ruthless efficiency. It’s time to channel the inner German: go in, do the work with precision, make it count, and don’t let standards slip.

After years spent crafting a PhD through chapters of optimisation—each concluding with an arbitrary line drawn in the sand, because there’s always room for refinement—it’s a hard lesson to internalise. Eventually, the improvements stop justifying the time and resources they demand. Knowing where to stop might be the hardest skill of all.

Perhaps that, in the end, will be the life lesson my PhD leaves me with: learning how to spend my time in ways that truly matter—ways that serve my goals, whether they’re professional, in service of others, or deeply personal. And with that lesson in hand, I’m quietly hopeful that what comes next will be shaped not just by ambition, but by intention.

Written by Ronja Struck

Mac4Me MSCA Doctoral Network

We are delighted to provide training and contribute to neuroblastoma research through the Mac4Me Doctoral Network Programme. Mac4Me is a 48-month project that addresses both technical and social challenges in cancer metastasis. It focuses on three tumour types that show poor response to current immunotherapies: neuroblastoma, breast, and prostate cancer. These tumour types reflect cancer development across a person’s lifetime and share metastatic disease spreading to the brain, bone, and liver.

Working alongside researchers and patients, the network will train 18 Doctoral Candidates to study the tumour microenvironment at metastatic sites, with a particular focus on the macrophage immune cell population. It will combine organ-on-chip technology with microfluidic systems to investigate early cell-cell and cell-matrix interactions during tumour invasion. Mac4Me will move beyond traditional “thinking in boxes” approaches by integrating bioinformatics and Artificial Intelligence solutions with real-world clinical data. The project will focus on patient experiences and translate scientific advances into meaningful outcomes.

The kick-off meeting of Mac4Me partners, Feb 2025

We are very proud to train two out of 18 Doctoral Candidates, building upon the expertise of Drs Ian Woods, Adrian Dervan and Prof Fergal O’Brien in biomaterials and 3D bioprinting and Dr Olga Piskareva in neuroblastoma biology and 3D in vitro cancer models.

#JournalClubwithRabia: “New Advances in Targeted Cancer Treatments: Targeting Neuroblastoma with miR-34a-Loaded Nanoparticles”

I’m excited to kick off my second-year PhD journey with a deeper dive into cancer research. This is my first blog post of the year, and I’m eager to share what’s sparking my curiosity. So, I came across a paper by Tivnan et al. (2012), which focused on the targeted delivery of microRNA-34a (miR-34a) using nanoparticles. What intrigued me most was how these nanoparticles are designed to deliver therapies straight to cancer cells. Neuroblastoma is a highly aggressive and difficult-to-treat tumour, so finding a way to target it without affecting healthy cells could be a breakthrough.

Here’s what makes this study so exciting: the team developed a nanoparticle system coated with anti-GD2, a molecule that recognizes and binds to GD2, a marker commonly found on neuroblastoma cells. Think of these GD2-coated nanoparticles as specialized delivery trucks with a precise address—they’re designed to deliver miR-34a.

Now, let’s dive into the details of miR-34a’s role. MiR-34a isn’t just any therapeutic agent—it’s a master regulator capable of influencing multiple genes involved in cell growth, survival, and blood vessel formation. By releasing miR-34a into tumour cells, this study activated pathways that induced cell death and suppressed angiogenesis, preventing the tumour from forming new blood vessels. It’s almost as if miR-34a is a conductor orchestrating a complex, multi-step attack on cancer, using the tumour’s own cellular mechanisms against it.

The Results? A Direct and Multi-Layered Attack on Tumor’s

In their mouse model, the GD2-targeted nanoparticles packed with miR-34a significantly reduced tumour growth. These “smart” nanoparticles didn’t just shrink tumors by inducing apoptosis (cell death); they also cut off the tumor’s blood supply by promoting the expression of TIMP2, an anti-angiogenic protein. Essentially, the tumor cells were directly targeted and deprived of the resources they needed to survive—a powerful one-two punch.

Where Do We Go From Here?

This study is an excellent example of how targeted therapies could evolve to tackle other types of cancer. Traditional therapies, like chemotherapy, often affect both healthy and cancerous cells, leading to significant side effects. In contrast, this targeted approach delivers miR-34a specifically to neuroblastoma cells, which could be especially beneficial for pediatric patients who need treatments that minimize harm to developing bodies. Imagine pairing nanoparticles like these with different therapeutic targets, such as GPC2, ALK, or PDL1, or even combining them with existing treatments to boost effectiveness while minimizing side effects. For those in the field, the potential here feels like a breakthrough waiting to happen.

Written By Rabia Saleem

#JournalClubwithFederica:How small RNAs contribute to neuroblastoma biology

We’ve recently started a new journal club series focusing on papers published by our research group over the past few years. The paper I chose is titled “A Context-Dependent Role for MiR-124-3p on Cell Phenotype, Viability and Chemosensitivity in Neuroblastoma in vitro“. It explores the anti-cancer potential of miR-124-3p in neuroblastoma.

Neuroblastoma is particularly challenging to treat, especially when tumours become resistant to chemotherapy. This resistance is compounded by tumour heterogeneity—these cancers comprise different cell types, specifically adrenergic and mesenchymal cells. This variability affects treatment responses and plays a role in metastasis and how aggressively the cancer can spread.

MicroRNAs (miRNAs) are small RNA molecules that regulate gene expression, and miR-124-3p has emerged as a promising player in cancer research. A Kaplan–Meier plot in the study (Figure 1) shows a strong association between low miR-124-3p levels and poorer survival rates in neuroblastoma patients, underscoring its potential impact on patient outcomes.

Our group’s study specifically examined how miR-124-3p might help reverse chemotherapy resistance and inhibit tumour cell growth in neuroblastoma. Excitingly, it has the potential to reduce cancer cell survival and increase their sensitivity to chemotherapy—an important breakthrough for treating resistant neuroblastomas.

The study found that miR-124-3p directly targets genes involved in the epithelial-to-mesenchymal transition (EMT), a process that makes cancer cells more invasive and treatment-resistant. By suppressing these genes, miR-124-3p can reverse EMT, shifting cells to a less aggressive, more treatment-sensitive state. Our group observed that increased miR-124-3p significantly reduced neuroblastoma cell invasion (Figure 2). In SK-N-AS cells and their drug-resistant form, invasion dropped by 50% and 70%. In Kelly cells and their resistant form, invasion decreased by 10% and 30%. The most invasive of all, the drug-resistant SK-N-ASCis24 cells, showed the most substantial decrease in invasion after miR-124-3p treatment. This suggests that miR-124-3p could help limit neuroblastoma spread, highlighting its therapeutic potential.

While miR-124-3p isn’t part of my project, seeing how different molecular mechanisms can be harnessed to develop cancer therapies is always inspiring. Using miRNAs to sensitize resistant cancer cells to treatment could complement approaches like immunotherapies or vaccines, like the one I’m working on. Understanding these molecular pathways brings fresh perspectives on weakening cancer cells and making treatments more effective.

Written by Federica Cottone

National PPI Festival 2024: Let’s Talk About Childhood Cancer Research

The RCSI Cancer Bioengineering Group hosted an in-person event during the National PPI Festival 2024 to share their childhood cancer research and connect with the public and patients.

We welcomed members of the public, family members of children with cancer, researchers, clinicians, and patient/community organisations on October 17th. Our past lab members and students paid a visit, too! Our group shared ongoing research on neuroblastoma biology and finding new treatments. Prof Cormac Owens from CHI brought us through the journey of clinical trials in neuroblastoma patients. We heard the heartbreaking story of the brave young man who lost his life to neuroblastoma and his parents who never gave up. This truly inspirational family founded a charity – the Conor Foley Neuroblastoma Cancer Research Foundation, to support curiosity-driven and translationally-focused research. The Foleys know very well how important it is to return happy days to kids and their families.

We thank RCSI PPI Ignite for supporting us!

Stay in touch!

#JournalClubwithEve: Unraveling Neuroblastoma Metastasis – My Exciting PhD Journey into 3D Models

As a new PhD student, I’m incredibly excited to dive into cancer research, and what better way to kick off this journey than by exploring 3D models to study neuroblastoma metastasis? Neuroblastoma is one of the most common childhood cancers, and about 50% of patients have metastatic disease at diagnosis. Understanding how these cells spread is key to developing better therapies, which is why this recent study by Gavin et al. (2021) caught my eye.

So, what did the researchers do? They used something called patient-derived xenografts (PDX) and cell lines to grow organoids (tiny mini-tumors) in a 3D extracellular matrix (ECM). This ECM mimics the environment these cells would encounter in the body, which is super important because cells behave very differently in 3D than in the typical 2D Petri dishes. It’s like giving the cells an entire landscape to explore rather than just a flat road—suddenly, they have mountains to climb and valleys to cross, allowing them to behave much more like they would inside the body!

One of the coolest things about this study is how the neuroblastoma cells developed various invasion strategies based on their environment. Some stayed in tightly knit groups, while others decided to go full-on lone wolf, sending out long, thin projections to explore the surrounding matrix. These cells are smart-adapting to different ECM compositions like Matrigel (which is rich in laminin and collagen), made them change their behaviour entirely. It’s like they’re navigating an obstacle course, with each new challenge requiring a different tactic!

Let’s Talk Actin Filaments!

Now, this is where it gets super cool (and nerdy in the best way!). The images captured by confocal microscopy are stunning. They show actin filaments—the internal skeleton of the cells—as they help the cancer cells move and invade new areas. The actin filaments form these amazing, intricate networks that shape the cells and allow them to stretch and invade. It’s almost like watching tiny construction workers build bridges and tunnels as they move forward. Check out this confocal image showing the red filaments—how awesome is that?!

Written by Eve O’Donoghue

#JournalClubwithRonja: Reaping the benefits of PhDs past

It’s the second round of journal club blog posts, and this time around, we’ll be looking at papers published by this very lab. I’ll be focussing on the paper in which the cell line I am currently working with (KellyCis83) was developed: “The development of cisplatin resistance in neuroblastoma is accompanied by epithelial to mesenchymal transition in vitro” This research addresses a critical challenge in cancer treatment: drug resistance, of course focusing on neuroblastoma, pediatric cancer notorious for its aggressive nature and poor prognosis that this lab has been studying for years.

Neuroblastoma is typically treated with cisplatin, a potent chemotherapy drug that induces DNA damage in cancer cells, leading to their death. The issue is that over time and particularly during relapse, some neuroblastoma cells develop resistance to cisplatin, rendering the treatment ineffective. Understanding the mechanisms behind this resistance is crucial for developing new therapeutic strategies.

In this study, neuroblastoma cell lines resistant to cisplatin were created by gradually exposing the cells to increasing drug concentrations over 6 months. This approach mimics the clinical scenario where tumours are exposed to chemotherapy over an extended period, eventually leading to resistance. The resistant cell lines were then characterized to uncover the molecular changes that had occurred alongside or as part of the increased drug-resistance.

The cisplatin-resistant neuroblastoma cells exhibited significant disruptions in their cell cycle regulation, as highlighted by the most altered pathways identified by mass spectrometry. Cisplatin typically causes DNA damage that halts the cell cycle, leading to cell death. However, the researchers found upregulated pathways in resistant cells that allowed these cells to bypass this damage-induced arrest. One key finding was the identification of Vimentin upregulation in the upstream regulator analysis. Vimentin is a marker typically associated with epithelial-to-mesenchymal transition (EMT).

EMT is a process where epithelial cells acquire mesenchymal, fibroblast-like properties, including enhanced motility and apoptosis resistance. The link between EMT and cancer progression is well-established, as EMT not only facilitates metastasis but also contributes to drug resistance. In the context of neuroblastoma, the upregulation of Vimentin and dysregulation of related EMT proteins found in two of the resistant cell lines (specifically SNAI1 and TWIST1) suggests that these cells are not only evading cisplatin-induced cell cycle arrest but are also acquiring more aggressive, invasive characteristics. This links back to their findings on invasiveness, which showed greater levels in the two resistant cell lines that also had greater changes in EMT-related proteins (Figure 1).

Figure 1 A Relative invasiveness of the parental cell lines compared to the cisplatin resistant daughter cell lines. Graphed data represent mean values ± SD of three independent experiments. Asterisks indicate statistical significance obtained using a paired Student’s t-test. * p < 0.05, ** p < 0.01, ***p < 0.001, n = 3 for all experiments. B The fold change in protein expression of drug resistant cells compared to their parental counterparts was quantified by densitometric analysis of two biological repeat experiments, normalised against endogenous control ACTB. (Adapted from (Piskareva et al., 2015).

Understanding the role of EMT in cisplatin-resistance opens up new avenues for therapeutic intervention. Targeting EMT-related pathways Vimentin could potentially restore the sensitivity of these resistant neuroblastoma cells to cisplatin, by targeting the evasive mechanisms the cells developed to bypass the cell-cycle disruption. Such therapies would offer a new strategy to tackle drug-resistant relapse cases, which currently have very poor outcomes.

Overall, this study provides a valuable model for investigating drug resistance in neuroblastoma and highlights the crucial role of EMT and its associated pathways in finding ways to treat drug-resistant tumours. As we continue to explore these avenues, these models will serve us as a strong foundation facilitating the research currently taking place in our lab towards finding such combination therapies and hopefully improving outcomes for children battling this devastating cancer in the future.

Written By Ronja Struck

September – Childhood Cancer Awareness Month, 2024

Cancer is the 2nd most common cause of death among children after accidents.

Childhood cancer is an umbrella term for many other types of this disease. Every September, many charities, researchers and parents of children with cancer work hard to raise awareness of this cancer. You may learn more about kids with cancer, their loving families, the doctors and caregivers who look after them and treat them, the young survivors of cancer and those kids and teens who lost their battle, and the scientists who work hard to find a way to stop childhood cancer.

This year, our research team will run the Pub Quiz on September 18th, 2024, in honour of Childhood Cancer Awareness Month. All donations will go to the Conor Foley Neuroblastoma Research Foundation (CFNRF).

If you would like to get involved in this amazing challenge and help us raise vital funds for childhood cancers, you can contribute to our fundraising page: