Meet the Speakers
Keynote Speakers
Prof. Michel Sadelain, Columbia University
Dr. Michel Sadelain, born in Paris in 1960, is a leading genetic engineer and physician-scientist, currently serving as Director of the Columbia Initiative in Cell Engineering & Therapy in New York. He is internationally recognized for pioneering CAR-T cell immunotherapy—a groundbreaking approach that genetically modifies a patient’s T cells into “living drugs” to fight cancer.
Previously at Memorial Sloan Kettering Cancer Center, Dr. Sadelain led the development of CAR-T cells targeting CD19, a marker found in certain blood cancers. His team established the first clinical applications in patients with refractory leukemia in 2007, and their work paved the way for FDA approval of CAR-T therapies in 2017.
His ongoing research focuses on expanding CAR-T therapy to solid tumors and developing off-the-shelf and gene-based treatments. Dr. Sadelain’s contributions have earned him numerous prestigious awards, including the Breakthrough Prize in Life Sciences and the Canada Gairdner Award.
Previously at Memorial Sloan Kettering Cancer Center, Dr. Sadelain led the development of CAR-T cells targeting CD19, a marker found in certain blood cancers. His team established the first clinical applications in patients with refractory leukemia in 2007, and their work paved the way for FDA approval of CAR-T therapies in 2017.
His ongoing research focuses on expanding CAR-T therapy to solid tumors and developing off-the-shelf and gene-based treatments. Dr. Sadelain’s contributions have earned him numerous prestigious awards, including the Breakthrough Prize in Life Sciences and the Canada Gairdner Award.
Prof. Rolf Berger, University of Groningen
Dr. Rolf Berger, MD, PhD, is Professor of Paediatrics and Paediatric Cardiology at the Centre for Congenital Heart Diseases at the University of Groningen in the Netherlands. He is a recognized expert in congenital heart disease and, in addition, all forms of pulmonary vascular disease.
In the Netherlands, the care for children with pulmonary hypertension, high blood pressure in the lung, has been centralized to Groningen. Dr. Berger has played an important role in advancing both clinical care and academic research in the field of paediatric pulmonary vascular disease worldwide.
In the Netherlands, the care for children with pulmonary hypertension, high blood pressure in the lung, has been centralized to Groningen. Dr. Berger has played an important role in advancing both clinical care and academic research in the field of paediatric pulmonary vascular disease worldwide.
Prof. Lotte Bjerre Knudsen, Novo Nordisk
Prof. Lotte Bjerre Knudsen, DMSc, is Chief Scientific Advisor at Novo Nordisk and a leading figure in the field of metabolic drug discovery. With a background in chemical and biotechnology engineering from the Technical University of Denmark and a Doctor of Medical Science degree from the University of Copenhagen, she joined Novo Nordisk in 1989. Her pioneering work has played a central role in the discovery and development of GLP‑1 receptor agonists, including liraglutide (Victoza®/Saxenda®) and semaglutide (Ozempic®/Wegovy®), which have transformed the treatment landscape for type 2 diabetes and obesity worldwide.
Prof. Knudsen has led several research programs expanding the application of GLP‑1–based therapies into cardiovascular, renal, and neurodegenerative diseases. She has held leadership roles at Novo Nordisk for over three decades and currently heads the company’s GLP‑1 Centre of Excellence. In addition to her industrial role, she served as an adjunct professor in translational medicine at Aarhus University from 2015 to 2020.
Her scientific achievements have been widely recognized. She has received numerous international awards, including the Paul Langerhans Medal, the Lasker–DeBakey Clinical Medical Research Award, and the 2025 Breakthrough Prize in Life Sciences. Through her innovative work and leadership, Prof. Knudsen has made an extraordinary impact on global health, positioning Novo Nordisk as a leader in therapies for chronic metabolic diseases.
Prof. Knudsen has led several research programs expanding the application of GLP‑1–based therapies into cardiovascular, renal, and neurodegenerative diseases. She has held leadership roles at Novo Nordisk for over three decades and currently heads the company’s GLP‑1 Centre of Excellence. In addition to her industrial role, she served as an adjunct professor in translational medicine at Aarhus University from 2015 to 2020.
Her scientific achievements have been widely recognized. She has received numerous international awards, including the Paul Langerhans Medal, the Lasker–DeBakey Clinical Medical Research Award, and the 2025 Breakthrough Prize in Life Sciences. Through her innovative work and leadership, Prof. Knudsen has made an extraordinary impact on global health, positioning Novo Nordisk as a leader in therapies for chronic metabolic diseases.
WCMM Talks
Anders Wittrup, WCMM Clinical Researcher
Title: “Moving beyond mRNA vaccines - improved understanding of RNA delivery vehicles to enable next generation RNA drugs”
RNA-based drugs such as siRNA, mRNA, antisense, and CRISPR hold great promise as next-generation precision therapies. However, effective cytosolic delivery remains a major hurdle. While recent years have seen clinical success with mRNA vaccines and liver-targeted siRNA, broader use in areas like regenerative medicine and cancer requires better delivery tools.
In my lab, we’ve developed advanced methods to track and quantify RNA delivery, including a high-throughput assay based on the galectin-9 sensor to detect endosomal escape. This assay is now widely adopted in both academia and industry and has led us to discover novel compounds that enhance delivery across tumor types, including glioblastoma.
We’ve also identified key delivery bottlenecks for lipid nanoparticles—crucial for mRNA and CRISPR therapies—allowing for rational improvements in RNA delivery systems. A deeper understanding of these mechanisms will drive the design of more efficient RNA delivery vehicles, accelerating the development of new treatments in cancer and regenerative medicine.
RNA-based drugs such as siRNA, mRNA, antisense, and CRISPR hold great promise as next-generation precision therapies. However, effective cytosolic delivery remains a major hurdle. While recent years have seen clinical success with mRNA vaccines and liver-targeted siRNA, broader use in areas like regenerative medicine and cancer requires better delivery tools.
In my lab, we’ve developed advanced methods to track and quantify RNA delivery, including a high-throughput assay based on the galectin-9 sensor to detect endosomal escape. This assay is now widely adopted in both academia and industry and has led us to discover novel compounds that enhance delivery across tumor types, including glioblastoma.
We’ve also identified key delivery bottlenecks for lipid nanoparticles—crucial for mRNA and CRISPR therapies—allowing for rational improvements in RNA delivery systems. A deeper understanding of these mechanisms will drive the design of more efficient RNA delivery vehicles, accelerating the development of new treatments in cancer and regenerative medicine.
Gesine Paul-Visse, WCMM Clinical Researcher
Title: “Cell therapy- has a new age come?”
The talk will describe the rational for using cell therapy in brain disorders, in particular Parkinson’s disease, the cell types tested and the ones under development and the results of 2 recent clinical trials performed in Lund, the TransEuro trial using fetal tissue and the STEM-PD trial (ongoing).
The STEM-PD is one of the first academic ATMP trials in Lund and a collaboration between two members of the WCMM (Kirkeby/Paul) showing the successful translation of a cell therapy to the clinic.
The talk will describe the rational for using cell therapy in brain disorders, in particular Parkinson’s disease, the cell types tested and the ones under development and the results of 2 recent clinical trials performed in Lund, the TransEuro trial using fetal tissue and the STEM-PD trial (ongoing).
The STEM-PD is one of the first academic ATMP trials in Lund and a collaboration between two members of the WCMM (Kirkeby/Paul) showing the successful translation of a cell therapy to the clinic.
Camila Consiglio, DDLS Fellow
Title: “Biological influencing immunity”
Why women are more prone to autoimmune diseases while men are more susceptible to severe infections remains a key unanswered question in medicine. Emerging evidence points to sex hormones as critical regulators of the immune system, yet the precise mechanisms underlying these effects remain largely undefined.
The Consiglio Lab at Lund University leverages a combination of in vivo systems-level immunomonitoring and in vitro mechanistic studies to unravel the basis of sexual dimorphism in human immunity. The lab profiles diverse human cohorts and model systems characterized by variations in sex hormone levels—such as individuals undergoing gender-affirming hormone therapy or those with polycystic ovary syndrome—and altered sex hormone signaling, including the antagonism of testosterone pathways, to dissect how hormonal milieu and receptor signaling shape immune cell phenotypes, cytokine responses, and disease susceptibility.
Uncovering the molecular and cellular pathways driving immune sexual dimorphism is a crucial step toward precision medicine, enabling the development of sex-informed therapies for immune-mediated diseases.
Why women are more prone to autoimmune diseases while men are more susceptible to severe infections remains a key unanswered question in medicine. Emerging evidence points to sex hormones as critical regulators of the immune system, yet the precise mechanisms underlying these effects remain largely undefined.
The Consiglio Lab at Lund University leverages a combination of in vivo systems-level immunomonitoring and in vitro mechanistic studies to unravel the basis of sexual dimorphism in human immunity. The lab profiles diverse human cohorts and model systems characterized by variations in sex hormone levels—such as individuals undergoing gender-affirming hormone therapy or those with polycystic ovary syndrome—and altered sex hormone signaling, including the antagonism of testosterone pathways, to dissect how hormonal milieu and receptor signaling shape immune cell phenotypes, cytokine responses, and disease susceptibility.
Uncovering the molecular and cellular pathways driving immune sexual dimorphism is a crucial step toward precision medicine, enabling the development of sex-informed therapies for immune-mediated diseases.
Filipe Pereira, WCMM Fellow
Title: “Humoral Immunity is Required for Dendritic Cell Reprogramming Immunotherapy Uncovering Biomarkers of Response”
The presence of tertiary lymphoid structures (TLS) in tumors correlates with improved responses to immune checkpoint blockade (ICB) therapy. In vivo reprogramming of cancer cells into type 1 conventional dendritic cells (cDC1) elicits a strong antitumor T cell response and synergizes with ICB. We hypothesize that reprogramming drives TLS formation and induces systemic humoral immune responses.
In murine models of breast, lung, melanoma, colon, and bladder cancer, cDC1 reprogramming achieves complete tumor regression at higher rates than anti-PD-1 treatment. TLS formation peaks within 9 days and resolves as tumors regress, correlating with improved survival. Spatial transcriptomics reveal that cDC1 cells near TLS acquire a transient migratory phenotype. Early TLS development is associated with Lymphotoxin A expression, followed by IL-17, IL-21, and LIGHT. Moreover, TLS composition shows reduced Tregs and increased in follicular dendritic cells, stem-like T cells, IgM⁺ B cells, activated B cells and plasma cells. B cells are required for tumor control, as their depletion restores tumor growth in 50% of mice within 21 days. Circulating tumor-specific IgM antibodies emerge by day 14, followed by IgG1 and IgA on day 21, and persist long-term in the blood. Serum transfer from treated mice delays tumor growth in melanoma and lung cancer, demonstrating antibody-mediated antitumor immunity.
Thus, cDC1 reprogramming represents a tumor-agnostic strategy capable of overcoming ICB resistance by inducing TLS formation and tumor-specific antibody responses. These findings support the clinical development of blood-based biomarkers for monitoring treatment efficacy.
The presence of tertiary lymphoid structures (TLS) in tumors correlates with improved responses to immune checkpoint blockade (ICB) therapy. In vivo reprogramming of cancer cells into type 1 conventional dendritic cells (cDC1) elicits a strong antitumor T cell response and synergizes with ICB. We hypothesize that reprogramming drives TLS formation and induces systemic humoral immune responses.
In murine models of breast, lung, melanoma, colon, and bladder cancer, cDC1 reprogramming achieves complete tumor regression at higher rates than anti-PD-1 treatment. TLS formation peaks within 9 days and resolves as tumors regress, correlating with improved survival. Spatial transcriptomics reveal that cDC1 cells near TLS acquire a transient migratory phenotype. Early TLS development is associated with Lymphotoxin A expression, followed by IL-17, IL-21, and LIGHT. Moreover, TLS composition shows reduced Tregs and increased in follicular dendritic cells, stem-like T cells, IgM⁺ B cells, activated B cells and plasma cells. B cells are required for tumor control, as their depletion restores tumor growth in 50% of mice within 21 days. Circulating tumor-specific IgM antibodies emerge by day 14, followed by IgG1 and IgA on day 21, and persist long-term in the blood. Serum transfer from treated mice delays tumor growth in melanoma and lung cancer, demonstrating antibody-mediated antitumor immunity.
Thus, cDC1 reprogramming represents a tumor-agnostic strategy capable of overcoming ICB resistance by inducing TLS formation and tumor-specific antibody responses. These findings support the clinical development of blood-based biomarkers for monitoring treatment efficacy.
Karin Tran Lundmark, WCMM Clinical Researcher
Title: "Synchrotron-based biomedical imaging"
As a pediatric cardiologist I mainly work with heart failure and transplantation, but I also care for children with pulmonary hypertension, high blood pressure in the lung. Pulmonary hypertension will with time cause right heart failure and currently available therapies can reduce symptoms and prolong survival, but there is no cure.
Complex branching structures like the lung are very difficult to fully understand from traditional 2D tissue sections and to cure pulmonary hypertension it is essential to fully understand underlying vascular remodeling processes. When the MAX IV synchrotron opened in Lund in 2016, I and my group got in contact with radiation physicists and have since then had the opportunity to image the pulmonary vasculature in 3D at different synchrotrons around Europe.
By imaging hypertensive lungs explanted at the time of transplantation we have been able to better describe the vascular changes seen in different types of pulmonary hypertension. The next step is to combine the imaging with other methods to decipher molecular mechanisms in search for therapeutic targets. Immunohistochemistry and in situ hybridization can be integrated with 3D tomography volumes and we are now exploring novel multiplex techniques, like in situ-based spatial transcriptomics.
Because of the group’s connection to pediatric cardiology, we have also become involved in studies of heart development and congenital heart disease. In addition, the imaging possibilities are expanding at MAX IV and hopefully this will lead to many successful multidisciplinary biomedical imaging projects in Lund in the future.
As a pediatric cardiologist I mainly work with heart failure and transplantation, but I also care for children with pulmonary hypertension, high blood pressure in the lung. Pulmonary hypertension will with time cause right heart failure and currently available therapies can reduce symptoms and prolong survival, but there is no cure.
Complex branching structures like the lung are very difficult to fully understand from traditional 2D tissue sections and to cure pulmonary hypertension it is essential to fully understand underlying vascular remodeling processes. When the MAX IV synchrotron opened in Lund in 2016, I and my group got in contact with radiation physicists and have since then had the opportunity to image the pulmonary vasculature in 3D at different synchrotrons around Europe.
By imaging hypertensive lungs explanted at the time of transplantation we have been able to better describe the vascular changes seen in different types of pulmonary hypertension. The next step is to combine the imaging with other methods to decipher molecular mechanisms in search for therapeutic targets. Immunohistochemistry and in situ hybridization can be integrated with 3D tomography volumes and we are now exploring novel multiplex techniques, like in situ-based spatial transcriptomics.
Because of the group’s connection to pediatric cardiology, we have also become involved in studies of heart development and congenital heart disease. In addition, the imaging possibilities are expanding at MAX IV and hopefully this will lead to many successful multidisciplinary biomedical imaging projects in Lund in the future.
Nicholas Leigh, WCMM Fellow
Title: “Deciphering evolutionarily innovations of tumor resistance”
Exploiting anti-tumor mechanisms that have arisen via evolution remains an untapped resource for the fight against cancer. Newts are a tumor-resistant species, with their tumor resistance being linked to their remarkable regenerative capacity. How this regenerative capacity endows tumor resistance is unknown.
To investigate how regenerative tissue imparts tumor resistance we have embarked on a CRISPR-based functional assessment of the role of tumor suppressor genes in newt regeneration and cancer resistance. Identifying the means of tumor resistance in newts promises to provide novel solutions to resist and treat human cancers.
Exploiting anti-tumor mechanisms that have arisen via evolution remains an untapped resource for the fight against cancer. Newts are a tumor-resistant species, with their tumor resistance being linked to their remarkable regenerative capacity. How this regenerative capacity endows tumor resistance is unknown.
To investigate how regenerative tissue imparts tumor resistance we have embarked on a CRISPR-based functional assessment of the role of tumor suppressor genes in newt regeneration and cancer resistance. Identifying the means of tumor resistance in newts promises to provide novel solutions to resist and treat human cancers.