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Molecular Physiology

PI Sofie Mohlin


Our research group is intrigued by how we can utilize the setting of normal embryonic development to understand tumor initiation. We have a highly transdisciplinary approach, merging the worlds of developmental and tumor biology.

Children and even newborns suffer from cancer. We mainly focus on the infant tumor form neuroblastoma, originating from cells of the sympathetic nervous system (SNS) in turn derived from the transient neural crest stem cell population. We want to answer why, how and where these tumors develop during embryogenesis.

A picture that was cover image for a scientific paper.
Cover image: Developmental Biology, Volume 447, Issue 2, 15 March 2019.Mohlin et al., Maintaining multipotent trunk neural crest stem cells as self-renewing crestospheres, Dev Biol 2019

Our research

Where do the roads of normal and tumor development converge and why do we not detect childhood tumors earlier?

The sympathetic nervous system (SNS) derives from neural crest, a transient stem cell population during vertebrate embryogenesis. The neural crest is remarkable in its ability to differentiate into diverse cell types including cartilage, glia, neuronal cells of the SNS and chromaffin cells. Incorrect embryonic development can lead to neural crest derived cristopathies, including cancer. We aim to understand the function of SNS related proteins in cancer and the function of cancer related proteins in SNS development.

Image illustrating the relationship between progenitor cell specific genes and cancer cell specific genes.

Neuroblastoma is a tumor of infancy, being the most common tumor form in children less than 1 year. The majority of patients are diagnosed before the age of 5 and there are rare cases where children are born with their tumor. Tumor formation, or priming, thus occur already during embryogenesis. While the overall survival rate of neuroblastoma has steadily and impressively increased during the last decades there is a fraction of patients diagnosed with high-risk tumors presenting with dismal prognosis. Early detection is key to limit metastatic spread and reduce treatment load, but environmentally correct embryonic models with the possibility to mimic tumor initiation are lacking.

Our current projects focus on

  1. how trunk neural crest specific genes can function as oncogenes and tumor suppressor genes in neuroblastoma
  2. elucidating the role of cancer associated proteins, including HIF-2a, in neural crest development and its potential role in tumor onset
  3. develop inducible tumor models using chick embryo
Picture of PI Sofie Mohlin.

Principal Investigator

Sofie Mohlin

Phone: +46 46 222 64 39
E-mail: sofie [dot] mohlin [at] med [dot] lu [dot] se

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Team members

Niklas Engström

Elina Fredlund

Enrika Miltenyte


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