Group Mattias Andersson

Research summary

We are studying the role of the MYB oncogene in acute leukemias in children and adults. MYB is a master transcription factor that regulates cell cycle progression, differentiation, apoptosis, and chromatin condensation. It is overexpressed in the majority of human leukemias.

We have recently identified several new small molecule MYB inhibitors that cause growth arrest, differentiation, and cell death in leukemia cells. We have also shown that MYB expression is a potential biomarker for relapse in childhood acute lymphoblastic leukemia. We are currently developing new MYB-targeted therapy and further investigating the biological and clinical relevance of MYB in acute leukemias.

Research tools and resources

We use a wide range of cell and molecular biological assays and bioinformatics to study MYB function in cultured leukemic cells. We are validating our findings in primary patient material and in mouse models. The group works together with international and national collaboration partners.

Current group members

Mattias Andersson, Associate professor
Peter Larsson, Postdoc
Elisabeth Vidblom, Graduate student
 

Selected publications

1. MYB alternative promoter activity is increased in adenoid cystic carcinoma metastases and is associated with a specific gene expression signature.
   Huang J, Fehr A, Jäwert F, Nilsson JA, Morris LGT, Stenman G, Andersson MK. Oral Oncol. 2024;151:106763. doi: 10.1016/j.oraloncology.2024.106763.
    
2. Increased MYB alternative promoter usage is associated with relapse in acute lymphoblastic leukemia.
   Fehr A, Arvidsson G, Nordlund J, Lönnerholm G, Stenman G, Andersson MK. Genes Chromosomes Cancer. 2023. doi: 10.1002/gcc.23151.
    
3. Synthetic oleanane triterpenoids suppress MYB oncogene activity and sensitize T-cell acute lymphoblastic leukemia cells to chemotherapy.
   Tejera Nevado P, Tešan Tomić T, Atefyekta A, Fehr A, Stenman G, Andersson MK. Front Oncol. 2023;13:1126354. doi: 10.3389/fonc.2023.1126354.
    
4. Targeting the oncogenic transcriptional regulator MYB in adenoid cystic carcinoma by inhibition of IGF1R/AKT signaling.
   Andersson MK, Afshari MK, Andrén Y, Wick MJ, Stenman G. J Natl Cancer Inst. 2017;109:djx017. doi: 10.1093/jnci/djx017.
    
5. ATR is a MYB regulated gene and potential therapeutic target in adenoid cystic carcinoma.
   Andersson MK*, Mangiapane G*, Nevado PT, Tsakaneli A, Carlsson T, Corda G, Nieddu V, Abrahamian C, Chayka O, Rai L, Wick M, Kedaigle A, Stenman G, Sala A. Oncogenesis. 2020;9:5. doi: 10.1038/s41389-020-0194-3. *equal contribution
    
6. Rearrangements, expression, and clinical significance of MYB and MYBL1 in adenoid cystic carcinoma: A multi-institutional study.
   Persson M*, Andersson MK*, Mitani Y, Brandwein-Weber MS, Frierson HF Jr, Moskaluk C, Fonseca I, Ferrarotto R, Boecker W, Loening T, El-Naggar AK, Stenman G. Cancers (Basel). 2022;14:3691. doi: 10.3390/cancers14153691. *equal contribution
    
7. Bcr-TMP, a novel nanomolar-active compound that exhibits both MYB- and microtubule-inhibitory activity.
   Yusenko MV, Biyanee A, Frank D, Köhler LHF, Andersson MK, Khandanpour C, Schobert R, Stenman G, Biersack B, Klempnauer KH. Cancers (Basel). 2021;14:43. doi: 10.3390/cancers14010043.
    
8. Proteasome inhibitors suppress MYB oncogenic activity in a p300-dependent manner
   Yusenko MV, Biyanee A, Andersson MK, Radetzki S, von Kries JP, Stenman G, Klempnauer KH. Cancer Lett. 2021;520:132-142. doi: 10.1016/j.canlet.2021.07.010.
    
9. Monensin, a novel potent MYB inhibitor, suppresses proliferation of acute myeloid leukemia and adenoid cystic carcinoma cells.
   Yusenko MV, Trentmann A, Andersson MK, Ghani LA, Jakobs A, Arteaga Paz MF, Mikesch JH, Peter von Kries J, Stenman G, Klempnauer KH. Cancer Lett. 2020;479:61-70. doi: 10.1016/j.canlet.2020.01.039.
10. Clinical and genomic features of adult and paediatric acute leukaemias with ophthalmic manifestations.
    Skarsgård LS, Andersson MK, Persson M, Larsen AC, Coupland SE, Stenman G, Heegaard S. BMJ Open Ophthalmol. 2019;4:e000362. doi: 10.1136/bmjophth-2019-00036

More group Mattias Andersson publications on PubMed