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Folkert H.M. Morsink on Muck Rack

Folkert H.M. Morsink

As seen in: Nature, BioRxiv
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Articles

Emergence of oncofetal plasticity is ubiquitous in early colorectal cancers

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By Joris H. Hageman, Sascha R. Brunner, Maria C. Puschhof, Arne Van Hoeck, Sjors Middelkamp, Lisa van der Schee, Folkert H.M. Morsink, Robin Geene, Sander Mertens, Ingrid Verlaan-Klink, Lianne Kraaier, Onno Kranenburg, Miangela M Lacle, Hugo J. G. Snippert, Suzanne E. M. van der Horst, Inge van Lierop, Sven van Kempen, David S. Cavigelli, Jorieke Salij, Renate Bezemer, Leon M. G. Moons
| Nature Verified
Abstract Metastasis formation is classically considered a late-stage event in colorectal cancer evolution. Yet the time and spatial patterning by which metastatic competence is acquired remain poorly understood1,2. Here we show that metastasis-associated oncofetal cell states already emerge at the earliest stages of colorectal cancer, concurrent with invasive front formation.
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Intestinal LKB1 loss drives a pre-malignant program along the serrated cancer pathway

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By Susanna F. Plugge, Huiying Ma, Joep Sprangers, Folkert H.M. Morsink
| BioRxiv
Abstract Background & Aims: Heterozygous inactivating mutations of Liver Kinase B1 (LKB1) are causative to the Peutz-Jeghers syndrome (PJS), a hereditary disease characterized by gastrointestinal polyposis and increased cancer susceptibility. While LKB1 loss-induced polyp formation has been ascribed to non-epithelial tissues, how LKB1 deficiency increases cancer risk of patients by altering the phenotypical landscape and hierarchical organization of epithelial tissues remains poorly understood.
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Intestinal LKB1 loss drives a pre-malignant program along the serrated cancer pathway

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By Susanna F. Plugge, Huiying Ma, Joep Sprangers, Folkert H.M. Morsink
| BioRxiv
Abstract Peutz-Jeghers syndrome (PJS) is a familial disorder caused by heterozygous inactivating Liver Kinase B1 (LKB1/STK11) mutations that induce hamartomatous polyp formation in the gastrointestinal tract. Additionally, PJS patients carry an elevated risk of developing malignancies in multiple tissues, including the intestine. How LKB1 deficiency alters the hierarchical organization and phenotypical landscape of epithelial tissues to mediate an increased cancer risk remains poorly understood.
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