Margareta Wilhelm
About me
Margareta Wilhelm is an Associate Professor of Tumor Biology and a Research Group Leader at the Department of Microbiology, Tumor and Cell biology (MTC). Currently she is the Head of the Tumor Biology Division and Vice Prefekt at MTC.
She graduated from Umeå University with a M.Sc. in Molecular Biology and received her Ph.D. in Experimental Oncology in 2003 from Karolinska Institutet, followed by post-doctoral training at the Campbell Family Cancer Research Institute, Toronto, Canada. Dr. Wilhelm has been awarded an Assistant Professor position from the Swedish Research Council and a Young Investigator Award from the Swedish Cancer Society, a Faculty funded senior researcher position from Karolinska Institutet and currently holds a senior childhood cancer research position from the Swedish Childhood Cancer Foundation.
Research
The Wilhelm lab focuses on understanding mechanisms regulating tumor
initiation and progression with a specific interest in the tumor
microenvironment and infiltrating immune cells. The lab is using transgenic
models, cellular reprogramming, stem cells, and brain organoids to model tumor
development.
Teaching
- Docent in Tumor Biology
- Program Director Research Education program in Tumor Biology and Oncology (FoTO)
- Study Director elective track in Tumor Biology, Biomedicine Master program
- Course Organizer and Teacher Biomedicine Master program
- Teacher Biomedicine Bachelor program
Selected publications
- Article: ONCOIMMUNOLOGY. 2025;14(1):2485535Boutin L; Liu M; Merville JD; Bedoya-Reina O; Wilhelm MT
- Preprint: BIORXIV. 2025Zhang F; Boutin L; Das I; Melief J; Singh M; Stantic M; Alzrigat M; Azimi A; Baldran L; Bazzar W; Da Silva Liberio M; Goodwin J; Tuominen R; Höiom V; Jerhammar F; Brage SE; Hansson J; Kiessling R; Selivanova G; Wiman KG; Wilhelm M; Larsson L-G
- Article: NEURO-ONCOLOGY. 2025;27(3):779-794van Bree N; Oppelt A-S; Lindstroem S; Zhou L; Boutin L; Coyle B; Swartling FJ; Johnsen JI; Braeutigam L; Wilhelm M
- Article: NEURO-ONCOLOGY. 2024;26(9):1685-1699Zhou L; van Bree N; Boutin L; Ryu J; Moussaud S; Liu M; Otrocka M; Olsson M; Falk A; Wilhelm M
- Review: CANCERS. 2022;14(20):5009van Bree NFHN; Wilhelm M
- Article: CELLULAR AND MOLECULAR LIFE SCIENCES. 2022;79(10):535Maeso-Alonso L; Alonso-Olivares H; Martinez-Garcia N; Lopez-Ferreras L; Villoch-Fernandez J; Puente-Santamaria L; Colas-Algora N; Fernandez-Corona A; Lorenzo-Marcos ME; Jimenez B; Holmgren L; Wilhelm M; Millan J; del Peso L; Claesson-Welsh L; Marques MM; Marin MC
- Article: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 2021;118(10):e2017089118Wolfsberger J; Sakil HAM; Zhou L; van Bree N; Baldisseri E; Ferreira SDS; Zubillaga V; Stantic M; Fritz N; Hartman J; Rolny C; Wilhelm MT
- Article: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 2020;117(33):20127-20138Susanto E; Navarro AM; Zhou L; Sundstrom A; van Bree N; Stantic M; Moslem M; Tailor J; Rietdijk J; Zubillaga V; Huebner J-M; Weishaupt H; Wolfsberger J; Alafuzoff I; Nordgren A; Magnaldo T; Siesjo P; Johnsen JI; Kool M; Tammimies K; Darabi A; Swartling FJ; Falk A; Wilhelm M
- Article: CELL DEATH & DISEASE. 2020;11(1):52Navarro AM; Pronk RJ; van der Geest AT; Oliynyk G; Nordgren A; Arsenian-Henriksson M; Falk A; Wilhelm M
- Article: STEM CELL RESEARCH. 2019;34:101356Navarro AM; Day K; Kogner P; Wilhelm M; Falk A
- Article: ONCOGENE. 2018;37(27):3729-3739Stantic M; Wolfsberger J; Sakil HAM; Wilhelm MT
- Review: CELL DEATH DISCOVERY. 2018;4:7Navarro AM; Susanto E; Falk A; Wilhelm M
- Article: CELLULAR ONCOLOGY. 2017;40(6):631-638Sakil HAM; Stantic M; Wolfsberger J; Brage SE; Hansson J; Wilhelm MT
- Article: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 2015;112(1):220-225Stantic M; Sakil HAM; Zirath H; Fang T; Sanz G; Fernandez-Woodbridge A; Marin A; Susanto E; Mak TW; Henriksson MA; Wilhelm MT
Articles
- Article: FRONTIERS IN MOLECULAR BIOSCIENCES. 2022;9:823195Grinkevich VV; Vema A; Fawkner K; Issaeva N; Andreotti V; Dickinson ER; Hedstrom E; Spinnler C; Inga A; Larsson L-G; Karlen A; Wilhelm M; Barran PE; Okorokov AL; Selivanova G; Zawacka-Pankau JE
- Article: CANCERS. 2021;13(21):5493Milosevic J; Fransson S; Gulyas M; Olsen TK; Gallo-Oller G; Treis D; Elfman LHM; Wilhelm M; Martinsson T; Baryawno N; Kogner P; Johnsen JI
- Article: CELL DEATH & DISEASE. 2019;10(9):663Das I; Wilhelm M; Hoiom V; Marquez RF; Svedman FC; Hansson J; Tuominen R; Brage SE
- Article: CELL DEATH & DISEASE. 2014;5(10):e1484Kostecka A; Sznarkowska A; Meller K; Acedo P; Shi Y; Sakil HAM; Kawiak A; Lion M; Krolicka A; Wilhelm M; Inga A; Zawacka-Pankau J
- Article: EMBO REPORTS. 2014;15(4):383-391Zinin N; Adameyko I; Wilhelm M; Fritz N; Uhlen P; Ernfors P; Henriksson MA
- Article: CELL DEATH AND DIFFERENTIATION. 2013;20(2):293-301Tomasini R; Secq V; Pouyet L; Thakur AK; Wilhelm M; Nigri J; Vasseur S; Berthezene P; Calvo E; Melino G; Mak TW; Iovanna JL
- Article: PHYSICS IN MEDICINE AND BIOLOGY. 2012;57(22):7431-7441Lundstrom U; Larsson DH; Burvall A; Scott L; Westermark UK; Wilhelm M; Henriksson MA; Hertz HM
- Article: ONCOGENE. 2010;29(49):6442-6451Rokaeus N; Shen J; Eckhardt I; Bykov VJN; Wiman KG; Wilhelm MT
- Article: GENES & DEVELOPMENT. 2010;24(6):549-560Wilhelm MT; Rufini A; Wetzel MK; Tsuchihara K; Inoue S; Tomasini R; Itie-Youten A; Wakeham A; Arsenian-Henriksson M; Melino G; Kaplan DR; Miller FD; Mak TW
- Article: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 2009;106(37):15756-15761Vilborg A; Glahder JA; Wilhelm MT; Bersani C; Corcoran M; Mahmoudi S; Rosenstierne M; Grander D; Farnebo M; Norrild B; Wiman KG
- Article: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 2009;106(3):797-802Tomasini R; Tsuchihara K; Tsuda C; Lau SK; Wilhelm M; Ruffini A; Tsao M-S; Iovanna JL; Jurisicova A; Melino G; Mak TW
- Article: GENES & DEVELOPMENT. 2008;22(19):2677-2691Tomasini R; Tsuchihara K; Wilhelm M; Fujitani M; Rufini A; Cheung CC; Khan F; Itie-Youten A; Wakeham A; Tsao M-S; Iovanna JL; Squire J; Jurisica I; Kaplan D; Melino G; Jurisicova A; Mak TW
- Article: EUROPEAN JOURNAL OF IMMUNOLOGY. 2008;38(1):64-72Hall HTL; Wilhelm MT; Saibil SD; Mak TW; Flavell RA; Ohashi PS
All other publications
- Preprint: BIORXIV. 2024Boutin L; Liu M; Merville JD; Bedoya-Reina O; Wilhelm M
- Preprint: BIORXIV. 2024van Bree N; Oppelt A-S; Lindström S; Zhou L; Boutin L; Johnsen JI; Bräutigam L; Wilhelm M
- Preprint: BIORXIV. 2024Zhou L; van Bree N; Boutin L; Moussaud S; Otrocka M; Falk A; Wilhelm M
- Review: SEMINARS IN CANCER BIOLOGY. 2011;21(4):256-266Westermark UK; Wilhelm M; Frenzel A; Henriksson MA
- Review: CELL DEATH AND DIFFERENTIATION. 2011;18(9):1434-1440Vilborg A; Bersani C; Wilhelm MT; Wiman KG
- Review: JOURNAL OF MOLECULAR MEDICINE-JMM. 2010;88(7):645-652Vilborg A; Wilhelm MT; Wiman KG
Grants
- Swedish Research Council1 January 2024 - 31 December 2026Medulloblastoma and Neuroblastoma are among the most common neural tumors in children. Neural tumors constitute around one third of all childhood cancers, but almost half of the mortalities. In Sweden most children affected by cancer survives, however, many survivors experience late complications in life, with one third getting life threatening conditions including secondary cancers, heart failure, and stroke. Taken together, this shows not only a need for increasing our understanding of molecular mechanisms operating during neural tumor formation, but furthermore, it highlights the importance of developing targeted therapies that will spare the developing child while specifically eradicating tumor cells. To achieve this, we have developed new cancer models using human disease-relevant cell types. By somatic cell reprogramming to induced pluripotent stem (iPS) cells and differentiation to neural stem cells, we have generated new orthotopic cancer models with cells from patients with familial driver mutations known to cause medulloblastoma and neuroblastoma. We show that our models mimic the human disease on histology and transcriptome. Using our new models, we aim to understand molecular mechanisms important for tumor initiation and progression, identify tumor-specific targets for precision medicine, and for screening and testing purposes. Our studies will provide better models where therapeutics can be discovered and evaluated.
- Swedish Cancer Society1 January 2023Medulloblastoma and Neuroblastoma are among the most common malignant neural tumors in children. Neural tumors make up about a third of all childhood cancers, but cause almost half of all deaths. In Sweden, 85% of children affected by cancer survive, but many of the survivors suffer from severe side effects and complications late in life. Taken together, this not only demonstrates a need to increase our understanding of molecular mechanisms leading to neural tumorigenesis, it also underscores the importance of developing targeted therapies that spare the growing child while eliminating tumor cells. We have developed new cancer models by reprogramming patient cells into neural stem cells, which are the cell type in which the disease arises. We use our models to investigate how certain mutations lead to the development of disease in normal cells and how the surrounding healthy cells affect the course of the disease. Since our models are based on disease-relevant cells, we can use them to identify new target proteins that can be used to develop precision medicine as well as to test the effectiveness of already known drugs that have not previously been tested on these cancer types. We want to develop good models for medulloblastoma and neuroblastoma that represent the course of the disease in patients to try to explain how the cancer arises and spreads. We also want to understand how the cancer responds to treatment and how recurrences occur, in order to be able to develop more individualized treatment for patients.
- Swedish Research Council1 January 2021 - 31 December 2023
- Barncancerfonden1 January 2021 - 31 December 2021
- Swedish Cancer Society1 January 2020Tumor diseases affect just over 50,000 people in Sweden every year. Despite improvements in cancer treatment, there are still many who can not be cured. A greater understanding of the molecular mechanisms behind the formation of tumors can provide new biologically based treatment methods, which are more specific and provide fewer side effects than those used today. Studies have shown that the growth and spread of tumors is not only due to the ability of cancer cells to constantly divide, but their interaction with the tumor environment is equally important for their progress. We want to study the complex interaction between tumor cells and their environment, to investigate how the tumor cells' energy production is controlled, and to study mechanisms that control how tumor cells are recognized by their own immune system. We have also established a completely new type of cancer model by using cell reprogramming technology. With cellular reprogramming technology, we can take normal skin cells from individuals diagnosed with a disease and / or have a hereditary mutation and reprogram them into iPS cells. We can then control the iPS cells to become the cell type where the disease occurs to study how the cancer starts. Our research will provide a better insight into basic mechanisms during tumor development, which may lead to new tools for diagnosis and treatment methods for cancer patients.
- Identification of mechanisms regulating tumor development, and generation of next-generation cancer models using cellular reprogrammingSwedish Cancer Society1 January 2019Tumor diseases affect just over 50,000 people in Sweden every year. Despite improvements in cancer treatment, there are still many who can not be cured. A greater understanding of the molecular mechanisms behind the formation of tumors can provide new biologically based treatment methods, which are more specific and provide fewer side effects than those used today. Studies have shown that the growth and spread of tumors is not only due to the ability of cancer cells to constantly divide, but their interaction with the tumor environment is equally important for their progress. We want to study the complex interaction between tumor cells and their environment, to investigate how the tumor cells' energy production is controlled, and to study mechanisms that control how tumor cells are recognized by their own immune system. We have also established a completely new type of cancer model by using cell reprogramming technology. With cellular reprogramming technology, we can take normal skin cells from individuals diagnosed with a disease and / or have a hereditary mutation and reprogram them into iPS cells. We can then control the iPS cells to become the cell type where the disease occurs to study how the cancer starts. Our research will provide a better insight into basic mechanisms during tumor development, which may lead to new tools for diagnosis and treatment methods for cancer patients.
- Mechanisms controlled by p73 isoforms during tumor developmentSwedish Cancer Society1 January 2018Despite improvements in cancer treatment, there are still many who cannot be cured. Therefore, a greater understanding of the molecular mechanisms underlying the formation of tumors is required. My research group wants to understand how the p73 gene controls tumor emergence. The special feature of the p73 gene is that it encodes two different types of protein, TAp73 and DNp73. TAp73 prevents the onset of tumors, while DNp73 instead accelerates tumor growth. In tumors, the balance between TAp73 and DNp73 shifts, and high levels of DNp73 lead to inability to respond to chemotherapy, poorer prognosis and survival in patients. To clarify the function of the various p73 variants in tumor development, we have produced genetic models that lack either TAp73 or DNp73. We now want to investigate in more detail how the balance between TAp73 and DNp73 affects normal cells during the actual initiation to become a cancer cell and how they affect the energy levels of tumors, blood supply and the spread of established tumors. By studying p73 we hope to gain a better insight into basic mechanisms that prevent or increase tumor development. The importance of this is reflected in the fact that overexpression of DNp73 in tumors has been correlated with inability to respond to chemotherapy with reduced survival in cancer patients. Our discoveries will provide greater biological understanding and can also lead to better tools for diagnosis and treatment methods for cancer patients.
- Mechanisms controlled by p73 isoforms during tumor developmentSwedish Cancer Society1 January 2017Despite improvements in cancer treatment, there are still many who cannot be cured. Therefore, a greater understanding of the molecular mechanisms underlying the formation of tumors is required. My research group wants to understand how the p73 gene controls tumor emergence. The special feature of the p73 gene is that it encodes two different types of protein, TAp73 and DNp73. TAp73 prevents the onset of tumors, while DNp73 instead accelerates tumor growth. In tumors, the balance between TAp73 and DNp73 shifts, and high levels of DNp73 lead to inability to respond to chemotherapy, poorer prognosis and survival in patients. To clarify the function of the various p73 variants in tumor development, we have produced genetic models that lack either TAp73 or DNp73. We now want to investigate in more detail how the balance between TAp73 and DNp73 affects normal cells during the actual initiation to become a cancer cell and how they affect the energy levels of tumors, blood supply and the spread of established tumors. By studying p73 we hope to gain a better insight into basic mechanisms that prevent or increase tumor development. The importance of this is reflected in the fact that overexpression of DNp73 in tumors has been correlated with inability to respond to chemotherapy with reduced survival in cancer patients. Our discoveries will provide greater biological understanding and can also lead to better tools for diagnosis and treatment methods for cancer patients.
- Swedish Research Council1 January 2017 - 31 December 2019
- Mechanisms controlled by p73 isoforms during tumor developmentSwedish Cancer Society1 January 2016Despite improvements in cancer treatment, there are still many who cannot be cured. Therefore, a greater understanding of the molecular mechanisms underlying the formation of tumors is required. My research group wants to understand how the p73 gene controls tumor emergence. The special feature of the p73 gene is that it encodes two different types of protein, TAp73 and DNp73. TAp73 prevents the onset of tumors, while DNp73 instead accelerates tumor growth. In tumors, the balance between TAp73 and DNp73 shifts, and high levels of DNp73 lead to inability to respond to chemotherapy, poorer prognosis and survival in patients. To clarify the function of the various p73 variants in tumor development, we have produced genetic models that lack either TAp73 or DNp73. We now want to investigate in more detail how the balance between TAp73 and DNp73 affects normal cells during the actual initiation to become a cancer cell and how they affect the energy levels of tumors, blood supply and the spread of established tumors. By studying p73 we hope to gain a better insight into basic mechanisms that prevent or increase tumor development. The importance of this is reflected in the fact that overexpression of DNp73 in tumors has been correlated with inability to respond to chemotherapy with reduced survival in cancer patients. Our discoveries will provide greater biological understanding and can also lead to better tools for diagnosis and treatment methods for cancer patients.
- Study on how two different p73 protein variants control tumor development.Swedish Cancer Society1 January 2015Despite improvements in cancer treatment, there are still many who cannot be cured. Therefore, a greater understanding of the molecular mechanisms underlying the formation of tumors is required. My research group wants to understand how the p73 gene controls tumor emergence. The special feature of the p73 gene is that it encodes two different types of protein, TAp73 and DNp73. TAp73 prevents the onset of tumors, while DNp73 instead accelerates tumor growth. In tumors, the balance between TAp73 and DNp73 shifts, and high levels of DNp73 lead to inability to respond to chemotherapy, poorer prognosis and survival in patients. To clarify the function of the various p73 variants in tumor development, we have produced genetic models that lack either TAp73 or DNp73. We now want to investigate in more detail how the balance between TAp73 and DNp73 affects normal cells during the actual initiation to become a cancer cell and how they affect the blood supply and the spread of established tumors to tumors. By studying p73 we hope to gain a better insight into basic mechanisms that prevent or increase tumor development. The importance of this is reflected in the fact that overexpression of DNp73 in tumors has been correlated with inability to respond to chemotherapy with reduced survival in cancer patients. Our discoveries will provide greater biological understanding and can also lead to better tools for diagnosis and treatment methods for cancer patients.
- Study on how two different p73 protein variants control tumor development.Swedish Cancer Society1 January 2014Despite improvements in cancer treatment, there are still many who cannot be cured. Therefore, a greater understanding of the molecular mechanisms underlying the formation of tumors is required. My research group wants to understand how the p73 gene controls tumor emergence. The special feature of the p73 gene is that it encodes two different types of protein, TAp73 and DNp73. TAp73 prevents the onset of tumors, while DNp73 instead accelerates tumor growth. In tumors, the balance between TAp73 and DNp73 shifts, and high levels of DNp73 lead to inability to respond to chemotherapy, poorer prognosis and survival in patients. To clarify the function of the various p73 variants in tumor development, we have produced genetic models that lack either TAp73 or DNp73. We now want to investigate in more detail how the balance between TAp73 and DNp73 affects normal cells during the actual initiation to become a cancer cell and how they affect the blood supply and the spread of established tumors to tumors. By studying p73 we hope to gain a better insight into basic mechanisms that prevent or increase tumor development. The importance of this is reflected in the fact that overexpression of DNp73 in tumors has been correlated with inability to respond to chemotherapy with reduced survival in cancer patients. Our discoveries will provide greater biological understanding and can also lead to better tools for diagnosis and treatment methods for cancer patients.
- Swedish Research Council1 January 2013 - 31 December 2015
- Knut and Alice Wallenberg Foundation1 January 2013 - 1 January 2018
- Swedish Research Council1 January 2011 - 31 December 2014
- Swedish Research Council1 January 2011 - 31 December 2013
- Swedish Research Council1 January 2009 - 31 December 2012
Employments
- Principal Researcher, Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 2022-
Degrees and Education
- Docent, Karolinska Institutet, 2016
- Doctor Of Philosophy, Department of Oncology-Pathology, Karolinska Institutet, 2003
Leadership and responsibility assignments
- Responsible for a section, Division Tumor Biology, Microbiology, Tumor and Cell biology (MTC), Karolinska Institutet, 2024-