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Medulloblastoma 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.

Medulloblastoma 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.

Tumor 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.

Tumor 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.

Despite 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.

Despite 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.

Despite 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.

Despite 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.

Despite 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.