Ola Landgren

This study shows that durable CAR-T therapy in lymphoma requires cooperation with endogenous CD8 T cells, and tumors lacking MHC class I or CD58 resist treatment.

This study uses SCID-rab PDX models to analyze genomic and transcriptomic features of multiple myeloma, revealing selection of pre-existing high-risk clones.

The paper identifies genomic and transcriptional changes in multiple myeloma cells that drive resistance to anti-BCMA therapies, termed 'plasma cell identity escape'.

Fate-AI improves cancer detection sensitivity and generalization by integrating fragmentomic and methylation features from cfDNA sequencing.

This study analyzes whole-genome sequencing data from multiple myeloma patients to show that the timing of genetic events, not just their presence, affects clinical outcomes.

This study identifies biallelic CD38 loss as a mechanism of resistance to anti-CD38 antibodies in multiple myeloma, with specific mutations affecting antibody efficacy.

The paper investigates the mutagenic impact of radiotherapy in hematologic malignancies and finds that RT contributes to the ID8 mutational signature, which is associated with treatment resistance and relapse.

The paper shows that genomic antigen escape mechanisms in multiple myeloma occur during CAR-T/TCE treatment, not pre-existing, and emerge after one year of therapy.

This study identifies genomic and immune factors associated with resistance to anti-CD38 therapy in multiple myeloma patients.

This study shows copy number signatures predict chromothripsis in multiple myeloma and link to poor clinical outcomes using whole genome and exome sequencing data.

This study identifies 100 SV hotspots and 31 new candidate driver genes in multiple myeloma, revealing that 63% of SVs remain unexplained and are associated with outlier gene expression.