Molecular Subtyping in Diffuse Large B Cell Lymphoma: Closer to an Approach of Precision Therapy

Reem Karmali*, Leo I. Gordon

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

16 Scopus citations

Abstract

It has become clear that there is immense biological heterogeneity in diffuse large B cell lymphoma (DLBCL). Developing technology has allowed better characterization of patient subsets at a molecular level, allowing for a link of phenotype and clinical outcomes to oncogenic mechanisms and biologic signatures. Cell of origin and double hit status are able to identify aggressive subsets, with molecular profiling allowing for a clearer understanding of biologic pathways that contribute to cellular resistance to conventional treatment in these subsets. Although the standard treatment for DLBCL remains R-CHOP or R-CHOP-like therapy at present, rational drug targets have been established with novel classes of drugs under investigation. In germinal center (GC) DLBCL, mechanisms of therapeutic interest include anti-apoptosis mediated by BCL-2, PI3K/AKT/mTOR, and EZH2, whereas drug interventions are directed at BCR, NF-κB, and/or JAK-STAT pathways in activated B cell (ABC) DLBCL. There is also evidence for cooperation of various oncogenic pathways in these subsets. As such, we are arguably on the verge of shifting to a more tailored approach using single and combinatorial strategies—this, however, relies on prioritizing the exploration of biomarkers for patient selection for validating novel treatment strategies.

Original languageEnglish (US)
Article number11
JournalCurrent treatment options in oncology
Volume18
Issue number2
DOIs
StatePublished - Feb 1 2017

Keywords

  • Apoptosis
  • CART
  • Checkpoint inhibition
  • DLBCL
  • Epigenetics
  • Immunotherapy

ASJC Scopus subject areas

  • Oncology
  • Pharmacology (medical)

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