Your browser has javascript turned off or blocked. This will lead to some parts of our website to not work properly or at all. Turn on javascript for best performance.

The browser you are using is not supported by this website. All versions of Internet Explorer are no longer supported, either by us or Microsoft (read more here:

Please use a modern browser to fully experience our website, such as the newest versions of Edge, Chrome, Firefox or Safari etc.

Complex Genomes in Cancer


Karolin 2

Fig. 1. The highly complex genome of an osteosarcoma.

Many high-grade cancers harbor extensively rearranged genomes and concomitant loss-of-function mutations in the tumor suppressor gene TP53. Disruption of the TP53 pathway is a well-known prerequisite for continued proliferation of cells with massively damaged DNA. However, the competitive advantage conferred by such a damaged genome is largely unknown. We study this phenomenon in osteosarcoma, a high-grade childhood malignancy that harbors one of the most rearranged genomes in cancer. Our aim is to develop new treatment strategies for patients with osteosarcoma and other high-grade malignancies. To this end, we screen primary tumor material for pathogenic aberrations using deep sequencing technology and we manipulate genes of interest in cancer model systems using the CRISPR/Cas9 gene editing system.


Selected publications

Loss of NF2 defines a genetic subgroup of non-FOS-rearranged osteoblastoma. Saba KH, Cornmark L, Hofvander J, Magnusson L, Nilsson J, van den Bos H, Spierings DC, Foijer F, Staaf J, Brosjö O, Sumathi VP, Lam SW, Szuhai K, Bovée JVMG, Kovac M, Baumhoer D, Styring E, Nord KH. The Journal of Pathology Clinical Research 2020;6:231-237.

NTRK fusions in osteosarcoma are rare and non-functional events. Ameline B, Saba KH, KovacM, Magnusson L, Witt O, Bielack S, Nathrath M, Nord KH, Baumhoer D. The Journal of Pathology Clinical Research 2020;6:107-112. 

Loss of the tumor suppressor gene AIP mediates the browning of human brown fat tumors. Magnusson L, Hansen N, Saba KH, Nilsson J, Fioretos T, Rissler P, Nord KH. The Journal of Pathology 2017;243:160-4.

GRM1 is upregulated through gene fusion and promoter swapping in chondromyxoid fibroma. Nord KH, Lilljebjörn H, Vezzi F, Nilsson J, Magnusson L, Tayebwa J, de Jong D, Bovée JVMG, Hogendoorn PCW, Szuhai K. Nature Genetics 2014;46:474-7.

Concomitant deletions of tumor suppressor genes MEN1 and AIP are essential for the pathogenesis of the brown fat tumor hibernoma. Nord KH, Magnusson L, Isaksson M, Nilsson J, Lilljebjörn H, Domanski HA, Kindblom LG, Mandahl N,Mertens F. Proceedings of the National Academy of Sciences U S A 2010;107:21122-7.


Oncogenes hijack a constitutively active TP53 promoter in osteosarcoma. Saba KH, Cornmark L, Kovac M, Magnusson L, Nilsson J, van den Bos H, Spierings DCJ, Bidgoli M, Jonson T, Sumathi VP, Brosjö O, Staaf J, Foijer F, Styring E, Nathrath M, Baumhoer D, Nord KH. Unpublished preprint at bioRxiv doi:

Complete list of publications

ORCID: 0000-0002-2397-2254
My profile at the Lund University Research Portal




Karolin 2

Karolin Hansén Nord, PhD
Associate Professor
Senior Lecturer

Department of Laboratory Medicin
Division of Clinical Genetics

Lund University
SE-221 84 Lund, Sweden

Phone: +46 70 283 18 37
Karolin [dot] Hansen_Nord [at] med [dot] lu [dot] se
Twitter @Karolin_H_Nord


Research group members

Linda 3

linda [dot] magnusson [at] med [dot] lu [dot] se (Linda Magnusson), Laboratory engineer

Jenny 1

jenny [dot] nilsson [at] med [dot] lu [dot] se (Jenny Nilsson), Laboratory engineer

Foto. Karim Saba.

karim [dot] saba [at] med [dot] lu [dot] se (Karim Saba), Postdoc

Valeria 1

valeria [dot] difilippo [at] med [dot] lu [dot] se (Valeria Difilippo), PhD student