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Articles by Anders Valind
Early evolutionary branching across spatial domains predisposes to clonal replacement under chemotherapy in neuroblastoma - Nature Communications
Abstract Neuroblastoma (NB) is one of the most lethal childhood cancers due to its propensity to become treatment resistant.
A dynamic mutational landscape associated to an inter‐regionally diverse immune response in malignant rhabdoid tumour
Brief Definitive Report Hiroaki Yasui Corresponding Author E-mail address: hiroaki.yasui.2850@med.lu.se https://orcid.org/0000-0002-2607-5233 Division of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden Department of Obstetrics and Gynaecology, Nagoya University Graduate School of Medicine, Nagoya, Japan Correspondence to: Hiroaki Yasui, Lund University, BMC C13, 22184, Lund, Sweden.
Extensive clonal branching shapes the evolutionary history of high-risk pediatric cancers
Research Article Natalie Andersson, Bjorn Bakker, Jenny Karlsson, Anders Valind, Linda Holmquist Mengelbier, Diana C.J. Spierings, Floris Foijer and David Gisselsson DOI: 10.1158/0008-5472.CAN-19-3468 Abstract Darwinian evolution of tumor cells remains underexplored in childhood cancer. We here reconstruct the evolutionary histories of 56 pediatric primary tumors, including 24 neuroblastomas, 24 Wilms tumors and 8 rhabdomyosarcomas.
Neuroblastoma with flat genomic profile: a question of representativity?
Neuroblastoma is one of the most common paediatric malignancies. Detection of somatic genetic alterations in this tumour is instrumental for its risk stratification and treatment. On the other hand, an absence of detected chromosomal imbalances in neuroblastoma biopsies is difficult to interpret because it is unclear whether this situation truly reflects the tumour genome or if it is due to suboptimal sampling. We here present a neuroblastoma in the left adrenal of a newborn.
Four evolutionary trajectories underlie genetic intratumoral variation in childhood cancer
A major challenge to personalized oncology is that driver mutations vary among cancer cells inhabiting the same tumor. Whether this reflects principally disparate patterns of Darwinian evolution in different tumor regions has remained unexplored1,2,3,4,5. We mapped the prevalence of genetically distinct clones over 250 regions in 54 childhood cancers. This showed that primary tumors can simultaneously follow up to four evolutionary trajectories over different anatomic areas.
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