This spring Barncancerfonden, the Swedish Childhood Cancer Foundation, awarded SEK 64 million to 29 researchers across the country. The funding includes positions of up to six years for scientists studying the most common forms of childhood cancer, such as leukemia and brain tumors, and how complications after treatment can be prevented or reduced.
Among this year's recipients are three researchers at Lund University’s Lund Stem Cell Center, each working to find new answers about how infant and childhood leukemia develops. Below, they tell us more about their research:
Maria Jassinskaja,
a research associate at the Division of Molecular Medicine and Gene Therapy, was awarded a four-year pediatric cancer research grant for the project 'Mapping the molecular networks behind MLL::AF4-driven childhood leukemia.’
Congratulations! What can you tell us about the project:
“The goal is to establish an in vitro model that mimics what happens during infant leukemia driven by the KMT2A::AFF1 fusion oncogene. We will then use this model to characterize the molecular and cellular events that cause the disease to develop and progress.”
What inspired you to pursue this specific area of research?
“My PhD focused on explaining the differences between fetal and adult hematopoiesis in normal development and in the context of leukemia. During my postdoctoral training, I performed ex vivo modelling of hematopoiesis in normal settings and in the presence of mutations associated with blood diseases. For this project, I wanted to go back to my scientific roots and to apply what I learned during my postdoc to hopefully contribute to advancing treatment options for infant leukemia.”
What do you hope this research will lead to?
“Infant KMT2A-rearranged leukemias are rare but highly aggressive with few treatment options and a very poor prognosis. I hope that by being able to recreate the conditions of disease initiation and progression in the lab, we will be able to pinpoint the underlying molecular mechanisms and dynamics of the disease and use this knowledge to guide future studies aimed at developing efficient and targeted therapies.”
Do you have any advice for early-career researchers?
“I am incredibly grateful for the support I have received from my mentors throughout my career – Jenny Hansson during my PhD, David Kent during my postdoc, and now Jonas Larsson who convinced me to apply for this grant. I’d also like to say to my fellow early career researchers who might feel they’re “too junior” to apply for bigger grants – just go for it! The worst that can happen is that you get a no, and the best is that you get to pursue research you’re truly passionate about, which is a fantastic opportunity worth all the hard work.”
Keiki Nagaharu,
a postdoctoral fellow in the Developmental Lymphopoiesis and Leukemia research group, was awarded a two-year postdoctoral research grant for the project 'Identifying key factors for the initiation of infant leukemia.’
What is the main goal of the project?
“Our project aims to clarify the nature of infant leukemia. Leukemia is the most commonly diagnosed cancer in children across all ethnicities and countries. Medical advancement makes prognosis better year by year. However, some types of childhood leukemias still have a poor prognosis. One of the reasons for this is the lack of appropriate models for evaluating how leukemia initiates in the fetal period. Our research will provide a powerful method to advance our understanding of leukemia initiation. As a final goal of this project, we aim to discover the critical factor for infant leukemia development.”
What inspired you to pursue this area of research?
“My background is in clinical medicine. As a licensed medical doctor in Japan, I have treated leukemia patients from teenagers to individuals in their 90s. During my clinical experience, I wondered why these patients developed the disease. During my PhD research in Japan, I focused on how lymphocytes—one type of blood cell—are generated. I found that some populations in cord blood possess distinct characteristics which are lacking in adult blood systems. This led me to hypothesize that a distinct hematopoietic system operates during fetal development and may contribute to infant leukemia.
Here in Lund, discussions with my supervisor provided me with valuable insights to extend my research perspectives. And I sincerely want to acknowledge my supervisor and lab colleagues who support my lab work every day.”
What do you hope this research will lead to?
“This study consists of two main steps: first, the establishment of an embryonic hematopoietic model using human induced pluripotent stem cells; and second, the application of this model to investigate infant leukemia.
From a scientific perspective, I believe our work will advance the understanding of not only leukemia but also embryonic hematopoiesis, the process of creating new blood cells. Moreover, our in vitro model could potentially be applied to other developmental blood disorders, such as congenital immunodeficiencies characterized by the absence of specific immune cell populations at birth.
For patients, we are focusing on identifying key molecules involved in disease progression. Our approach may uncover critical, previously unknown mechanisms underlying leukemia initiation—mechanisms that could potentially serve as new therapeutic targets in the future.”
Joanna Watral,
a postdoctoral fellow in the Proteomic Hematology research group, was awarded a two-year postdoctoral research grant for the project 'Mapping and disruption of proteomic vulnerabilities in the microenvironment of infant leukemia.’
What can you tell us about the project?
“The main goal is to better understand how pre-leukemic cells in the fetus and infants communicate with their surrounding microenvironment, or niche, and, conversely, how the niche may support leukemia development during fetal and infant life. We focus specifically on the communication through proteins. By mapping these interactions, we aim to identify new cellular and molecular vulnerabilities that could be targeted by future therapies to improve outcomes for children with aggressive forms of leukemia.”
What inspired you to pursue this area of research?
“While researching fetal- and adult-origin leukemia, I found an interesting ability of pre-leukemic cells to communicate with their surroundings by secreted proteins. I was surprised by how much remains unknown about the mechanisms of molecular communication between leukemic cells and their surrounding microenvironment in the context of infant biology.
I was particularly inspired by the idea that leukemia-initiating cells not only respond to signals from nearby cells but can also actively change their environment to support disease development. Working in Jenny Hansson’s group helped me see this topic from new perspective.Rather than focusing solely on destroying leukemic cells, I am motivated by the possibility of developing therapies that target the broader cellular ecosystem—disrupting the supportive interactions between malignant and non-malignant cells.”
What do you hope this research will lead to?
“I hope this work will help fill a key knowledge gap about the molecular crosstalk between leukemic cells and their specific environment. In the long term, our ambition is to evaluate the therapeutic potential of disrupting these supportive interactions. This could lead to a new class of anti-leukemic agents that work fundamentally differently from current treatments. Such therapies may offer better precision and cause less harm to healthy, developing tissues – something that’s especially important for infants.”