Tag: #JournalClub

#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

#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

#JournalClubwithRabia: How Can Fish Help Us Study Anticancer Drugs?

Hi all! Rabia here, I came across an intriguing paper highly relevant to my work on the rapid in vivo validation of HDAC inhibitor-based treatments using neuroblastoma zebrafish xenografts. The study outlines a zebrafish neuroblastoma yolk sac model specifically designed to evaluate both the effectiveness and toxicity of histone deacetylase (HDAC) inhibitors.

HDAC inhibitors are drugs that target specific enzymes involved in gene regulation. This study tested broad-spectrum HDAC inhibitors as standalone treatments and combined them with doxorubicin, a well-known chemotherapy drug.

But why on Zebrafish? The zebrafish model provides a rapid and efficient means of testing these treatments, offering valuable insights into their potential use in combating neuroblastoma. This model allows for assessing drug efficacy and helps understand the associated toxicities quickly, making it a powerful tool for developing new anti-cancer therapies.

In the study, fish larvae were implanted with fluorescently labelled, well-established neuroblastoma cell line (SK-N-BE(2)-C) and patient samples (HD-N33, NB-S-124) to grow tumours. Non-cancerous cells (VH7 fibroblasts) were utilized to verify that tumour progression in zebrafish was specific to tumour cells. The engraftment of human cells into fish larvae was confirmed by immunohistochemistry (IHC) staining on zebrafish sections injected with neuroblastoma cells (SK-N-BE). This was achieved using a STEM121 antibody that reacts specifically with a human cytoplasmic protein. The findings showed that pediatric tumour cells survive and grow in the zebrafish model at rates like those observed in human tumours.

Before testing drug efficacy in zebrafish xenografts, optimal drug concentrations and maximal tolerated doses (MTD) were determined. Toxicity tests were conducted by treating fish larvae cells for three days without tumour cell injection to identify the maximum tolerated dose that did not cause observable morbidity, changes in morphology, or severe aberrations in larval behaviour. and lethal dose (LD) for each compound. To find optimal drug concentrations, larvae with xenografted tumour cells were incubated with increasing drug doses 24 hours post-implantation to the maximally tolerated dose (MTD). The relative IC50 values were then determined based on changes in tumour mass volume.

To evaluate the treatment, SK-N-BE(2)- cells were used to test the broad-spectrum HDAC inhibitors, including panobinostat, vorinostat, and tubastatin A, both alone and combined with doxorubicin. The partial response rate (PR) was measured to see how well different drug combinations work to shrink tumours in the zebrafish model. Here’s what they found: Doxorubicin combined with panobinostat resulted in a 23% PR, Doxorubicin combined with tubastatin A showed a 31% PR, and Doxorubicin combined with vorinostat achieved the best result with a 36% PR.

To test the effectiveness of the HDAC inhibitor treatment, they monitored the tumour growth using a confocal microscope before and 48 hours after giving the drug. The test revealed that a 48-hour treatment of SK-N-BE (2)-C zebrafish xenografts with vorinostat and doxorubicin alone, `and in combination, increased cell death. The combination of these two drugs was the most effective, causing a significant increase in cancer cell death (apoptosis) by decreasing cell proliferation, as indicated by reduced PPH3 marker and activating the number of Cleaved caspase-3 (Figure 1).

Figure 1: Treatment for 48 h with Vorinostat, doxorubicin, or a combination of both increased the amount of cleaved caspase-3 and reduced mitotic tumour cells. Adapted from Pharmaceuticals 2020, 13(11), 345

In essence, this study validates the use of HDAC inhibitors in treating neuroblastoma and paves the way for broader applications of zebrafish models in cancer research. As we look to the future, these innovative models could significantly enhance our ability to develop effective cancer therapies, making strides towards better treatments and, ultimately, more effective cures.

Written by Rabia Saleem

#JournalClub with Shreya: Modelling Brain Tumour Spread

This article by Krieger et al. discusses the most common form of brain cancer called glioblastoma. Due to its highly aggressive nature, research must be conducted consistently and rapidly to develop new treatments. This has proven challenging due to primary tumours being resected before further research can be done, as well as the lack of current technologies to fully explore relationships between GBM and surrounding brain tissues. This study aimed to study the aforementioned interactions in under 4 weeks, accounting for the rapid progression of the disease in real life.  

GBM cells were first derived from four patients and treated with glutamine, heparin, epidermal and fibroblast growth factors, then underwent a sequence of manipulations, such as second-generation replication lentivirus infection of GBM cells, iPSC line 409b2 inoculation in Aggrewell plates and later manipulation with invasion assays, and scRNA sequencing, which, along with the Aggrewell cells, produced neural progenitor cell spheroids for analysis. Confocal microscopy and the developed image processing algorithm allowed for visualization of these cells following fluoroscopy and depicted consistent growth of tumour cells. There was also the growth of microtubules. Any dissociated organoids were then co-cultured with GBM cells again, promoting interaction between the two. Further analysis revealed the upregulation of 45 genes, including PAX6, GJA1, GPC3, and others involved in cell regulation.  

Credit to Teresa G Krieger, Stephan M Tirier, Jeongbin Park, Katharina Jechow, Tanja Eisemann, Heike Peterziel, Peter Angel, Roland Eils, Christian Conrad, Modeling glioblastoma invasion using human brain organoids and single-cell transcriptomics, Neuro-Oncology, Volume 22, Issue 8, August 2020, Pages 1138–1149

In conclusion, this novel mechanism of analysis of GBM cells using Aggrewell plates provided fruitful results, indicating intricate relationships between GBM cells and organoids, providing crucial insight for treatments by elucidating specific gene expression, heterogeneity of cells, and offering new targets based on ligand-receptor interactions. The particular relevance of this study to my work is regarding the usage of Aggrewell plates, which I am currently studying to determine how best to keep cells growing successfully within the wells. This article proves the usability and efficiency of Aggrewell and establishes its crucial role in the realm of brain cancer treatment research.  

Written by Shreya Sankar

#JournalClub with Alysia: How exosomes can promote cancer spread?

Hi, it’s Alysia, here to give you some insight on exosomes’ impact on tumor metastatic niche formation! I found an interesting paper related to my work that I want to share with you: Tumour-derived exosomes drive immunosuppressive macrophages in a pre-metastatic niche through glycolytic dominant metabolic reprogramming.

Exosomes have been a groundbreaking field of research due to their hypothesized ability to create a pre-metastatic niche through non-cancerous cell manipulation. They achieve this by relaying oncogenes and proteins from cancer cells in their molecular “cargo”. In this study, Morrissey et al. examined the role of tumor-derived exosomes (TDEs) in increasing programmed death ligand-1 (PDL-1) expression in macrophages. In pre-metastatic tumour microenvironments, there is an increase in inflammation and an immunosuppressive response, thus promoting tumorigenesis. PDL-1 is increased by TDEs manipulating the signalling of toll-like receptor 2 (TLR2) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB), which increases lactate production and glucose uptake in an event called the “Warburg Effect”, which is common in tumour microenvironments. TDEs taken from lung cancer samples were injected into mice, and PDL-1 expression levels of macrophages were higher than in healthy lung samples.

To accomplish this, Lewis lung carcinoma tumour cells (derived from mice) labelled with a green fluorescent protein (LLC-GFP+) were injected into mice with tumours; seven days later, they were injected with either non-GFP LLC exosomes or control mouse lung epithelial cell exosomes (MLE-12). The mice injected with non-GFP LLC exosomes had no metastatic difference compared to the control mice. However, the mice injected with LLC-GFP+ exosomes had an increase in micro-metastases, which was confirmed using fluorescent microscopy to observe LLC-GFP+ occurrence. With confocal microscopy, they observed an increase in PDL-1 expression in lung tissue compared to the control mice. These findings suggest that PDL-1 expression is preferentially increased in lung tumour tissue by injecting LLC-GFP+ exosomes.

Figure A. Schematic of experimental design. Figure B. Micro-metastatic burden quantified by LLC-GFP% in the lungs of s.c. GFP-LLC tumour-bearing mice treated intravenously (i.v.) with MLE-12 or LLC exosomes. Representative dot plots of GFP expression in the lungs and summarized data of LLC-GFP% are shown. Each dot represents data from one mouse. *p < 0.05, one-way ANOVA with multiple comparisons. Figure C. Confocal microscopic analysis of lung GFP+ micro-metastases from primary s.c. LLC tumor-bearing mice. Figure D. Confocal microscopic analysis of PD-L1 expression in LLC Exo- or LLC Exo+ -treated lungs. Adapted from Morrissey et al.

Researchers also examined the clinical significance of human TDEs and their manipulation of macrophages in the lymph nodes of non-small-cell lung cancer (NSCLC) patients. They found that there was increased expression of PDL-1 in the lymph nodes of these patients. To further study this, the researchers treated macrophages with either MLE-12 or LLC exosomes and then put them in a co-culture with OVA transgenic T-cells (a type of immune cell). The T-cells had a decrease in cell proliferation, which was later reversed by adding neutralizing α-PD-1 to the co-culture. This led them to think that PDL-1 had an inhibitory effect on T-cell function through macrophage stimulation. In summary, this study found that TDEs have an impact on PDL-1 expression found in tumour tissue and pre-metastatic tissue, resulting in creating an immunosuppressed environment for cancer cell growth. In my project, I’m interested in what cargo exosomes can carry from parental tumour cells to non-cancerous cells when creating a pre-metastatic niche. Knowing that there has been documented manipulation of the cellular makeup by exosomes encourages me to continue my research using neuroblastoma cells to elucidate the oncogenic markers relayed by exosomes. This research is very exciting, and I hope to shed some light on exosome impact in neuroblastoma tumour microenvironments with my own work!

Written by Alysia Scott

#JournalClub with Ronja: What can we learn from other cancers?

In this row of journal club blog posts, I’ve decided to look at this study: A Tumor Microenvironment Model of Pancreatic Cancer to Elucidate Responses toward Immunotherapy.

In this study, researchers developed an advanced model to simulate the environment surrounding pancreatic cancer cells. Using a specialized hydrogel matrix, they encapsulated pancreatic cancer cells, patient-derived stromal cells (non-cancerous cells that influence tumour behaviour), and immune cells. Within this matrix, the cells grew and formed spheroids, closely resembling the structure of tumours in the body. By fine-tuning the hydrogel’s properties, they controlled the stiffness and adhesion, optimizing conditions for cell growth and interaction, thereby enhancing the model’s resemblance to real-life pancreatic cancer. The researchers tested this model to evaluate its effectiveness in assessing new treatments, particularly immunotherapies. They treated the 3D cultures with a combination of immune and chemotherapy drugs and monitored the cells’ responses (See Figure). Notably, they focused on the novel drug ADH-503. Their findings revealed that the model accurately mirrored the responses observed in actual pancreatic cancer patients, confirming its validity for preclinical drug testing.

Furthermore, they explored the impact of these treatments on the secretion of cytokines—proteins crucial for immune regulation and tumour progression. They observed changes in the levels of specific cytokines (IL6 and IL8), indicating that the treatments could alter the tumour microenvironment and potentially improve therapeutic outcomes.

Figure 1 Multicellular spheroids of pancreatic cancer, patient-derived fibroblasts and immune cells stained for cell nuclei(blue), cytoskeleton and proliferating cells. From left to right, (i) untreated control, (ii) ADH-503 and immunotherapeutic, (iii) ADH-503 and chemotherapeutics and (iv) ADH-503 and both immuno- and chemotherapeutics. Modified from Adv Healthcare Materials, Volume: 12, Issue: 14, First published: 23 November 2022, DOI: (10.1002/adhm.202201907)

Overall, this study highlights the utility of their model for testing new therapies and gaining insights into the complex interactions within pancreatic tumours. It provides a robust platform for further research to develop more effective treatments for pancreatic cancer. While the study primarily focuses on pancreatic cancer, its findings and methodology have significant relevance to neuroblastoma research. Like pancreatic cancer, neuroblastoma is a solid tumour with a complex microenvironment that influences its growth and response to therapy. Thus, the model developed in this study, which accurately mimics the tumour microenvironment and allows for the testing of immunotherapies and combination treatments, could be adapted for neuroblastoma research. More directly relevant is the combination therapy of ADH-503 with immunotherapy and chemotherapy, underscoring the potential for this approach in treating other types of solid tumours like neuroblastoma. For my project, specifically, this study is helpful because it shows the relevance of immunotherapeutics on the immune cells present and their behaviour, which I plan to investigate for neuroblastoma in the future.

Written by Ronja Struck

#JournalClub: Anti-Cancer Immunotherapy

Hi there, Federica here! In the fast-paced world of scientific research, staying informed about the latest studies and breakthroughs is crucial. It enables researchers to build upon existing knowledge, avoid redundant efforts, and discover new directions for their work. That’s why we’ve started a new series of blog posts highlighting recent papers and explaining their significance for our research.

Recently, a fascinating study explored an innovative method to boost the effectiveness of cancer immunotherapy: “A combination of a TLR7/8 agonist and an epigenetic inhibitor suppresses triple-negative breast cancer through triggering anti-tumour immune“.

The researchers investigated a combination of immune checkpoint blockade (ICB) and other drugs to turn “immune-cold” tumours (which evade the immune system) into “immune-hot” tumours (which the immune system can attack). They developed a special delivery system using nanoparticles called metal-organic frameworks (MOFs). These nanoparticles were loaded with two types of drugs—a TLR7/8 agonist and an epigenetic inhibitor (BRD4 inhibitor). To make the nanoparticles even more effective, they were coated with vesicles from the cancer cells themselves. This coating helps the nanoparticles specifically target cancer cells.

But how does it work?

The nanoparticles are designed to find and enter triple-negative breast cancer (TNBC) cells. Once inside, the drugs prompt the cancer cells to break apart and release signals that alert the immune system. These signals attract dendritic cells, which then activate CD8+ T cells—the body’s natural cancer fighters. The TLR7/8 agonist further enhances this immune response, making the treatment more powerful.

In both laboratory tests and animal models, this method showed significant promise. It not only slowed down tumour growth but also improved the body’s immune response to cancer. Importantly, the study found that this approach could remodel the tumour environment, making it more hostile to cancer cells. For example, they wanted to verify that their combined delivery system could really boost the body’s ability to fight tumours. They focused on a protein called calreticulin (CRT) that, when it shows up on the surface of tumour cells, helps the immune system spot and remove them. They found that when they used their special delivery system (CM@UN and MCM@UN), the levels of CRT on the surface of tumour cells went way up. This was especially true for the MCM@UN group, showing just how powerful their method was in getting the immune system to attack the tumours.

The original image was published in J Nanobiotechnology. 2024; 22: 296.

So, why is this study important for my work?

The principles of enhancing the immune system’s ability to fight cancer are central to both the research in the study and in my project. Like the nanoparticles in the study, mRNA vaccines can be designed to specifically target cancer cells, ensuring that the treatment reaches its intended destination. Another similarity is how the drugs activate the immune system, which parallels how mRNA vaccines work—by training the immune system to recognise and attack cancer cells.

I find this study really interesting as it sheds light on innovative strategies for cancer treatment and provides valuable insights that can inform and inspire our research on developing mRNA vaccines for childhood neuroblastoma!

Written by Federica Cottone