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[Preprint]. 2023 Jun 10:2023.06.07.23290748. [Version 1] doi: 10.1101/2023.06.07.23290748

Multiomic Analysis Identifies a High-Risk Metabolic and TME Depleted Signature that Predicts Early Clinical Failure in DLBCL

Kerstin Wenzl, Matt Stokes, Joseph P Novak, Allison M Bock, Sana Khan, Melissa A Hopper, Jordan E Krull, Abigail R Dropik, Janek S Walker, Vivekananda Sarangi, Raphael Mwangi, Maria Ortiz, Nicholas Stong, C Chris Huang, Matthew J Maurer, Lisa Rimsza, Brian K Link, Susan L Slager, Yan Asmann, Patrizia Mondello, Ryan Morin, Stephen M Ansell, Thomas M Habermann, Andrew L Feldman, Rebecca L King, Grzegorz Nowakowski, James R Cerhan, Anita K Gandhi, Anne J Novak
PMCID: PMC10274962  PMID: 37333387

ABSTRACT

PURPOSE

60-70% of newly diagnosed diffuse large B-cell lymphoma (DLBCL) patients avoid events within 24 months of diagnosis (EFS24) and the remainder have poor outcomes. Recent genetic and molecular classification of DLBCL has advanced our knowledge of disease biology, yet were not designed to predict early events and guide anticipatory selection of novel therapies. To address this unmet need, we used an integrative multiomic approach to identify a signature at diagnosis that will identify DLBCL at high risk of early clinical failure.

PATIENTS AND METHODS

Tumor biopsies from 444 newly diagnosed DLBCL were analyzed by WES and RNAseq. A combination of weighted gene correlation network analysis and differential gene expression analysis followed by integration with clinical and genomic data was used to identify a multiomic signature associated with high risk of early clinical failure.

RESULTS

Current DLBCL classifiers are unable to discriminate cases who fail EFS24. We identified a high risk RNA signature that had a hazard ratio (HR, 18.46 [95% CI 6.51-52.31] P < .001) in a univariate model, which did not attenuate after adjustment for age, IPI and COO (HR, 20.8 [95% CI, 7.14-61.09] P < .001). Further analysis revealed the signature was associated with metabolic reprogramming and a depleted immune microenvironment. Finally, WES data was integrated into the signature and we found that inclusion of ARID1A mutations resulted in identification of 45% of cases with an early clinical failure which was validated in external DLBCL cohorts.

CONCLUSION

This novel and integrative approach is the first to identify a signature at diagnosis that will identify DLBCL at high risk for early clinical failure and may have significant implications for design of therapeutic options.

Full Text Availability

The license terms selected by the author(s) for this preprint version do not permit archiving in PMC. The full text is available from the preprint server.


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