ReviewThe oncologist2012
Are we ready to stratify treatment for diffuse large B-cell lymphoma using molecular hallmarks?
Review in The oncologist, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 42 citations in OpenAlex.
- HOXA13 overexpression is associated with poor prognosis in colorectal liver metastasesSurgical oncology insight · 2025Article
- microRNA sequencing for biomarker detection in the diagnosis, classification and prognosis of Diffuse Large B Cell Lymphoma.Scientific reports · 2023Article
- Value of total lesion glycolysis and cell-of-origin subtypes for prognostic stratification of diffuse large B-cell lymphoma patients.Quantitative imaging in medicine and surgery · 2021Article
- Genomics of diffuse large B cell lymphoma.Blood research · 2021Review
- Expression patterns of the activator protein-1 (AP-1) family members in lymphoid neoplasms.Clinical and experimental medicine · 2017Review
- Cell-of-origin of diffuse large B-cell lymphomas determined by the Lymph2Cx assay: better prognostic indicator than Hans algorithm.Oncotarget · 2017Article
- Role of Rituximab and Rituximab Biosimilars in Diffuse Large B-Cell Lymphoma.Clinical lymphoma, myeloma & leukemia · 2016Review
- Cross-platform assessment of genomic imbalance confirms the clinical relevance of genomic complexity and reveals loci with potential pathogenic roles in diffuse large B-cell lymphoma.Leukemia & lymphoma · 2016Article
- Whole-exome analysis reveals novel somatic genomic alterations associated with outcome in immunochemotherapy-treated diffuse large B-cell lymphoma.Blood cancer journal · 2015Article
- Precision medicine in diffuse large B-cell lymphoma: hitting the target.Haematologica · 2015Article
- Constitutive NF- κ B Activation Underlines Major Mechanism of Drug Resistance in Relapsed Refractory Diffuse Large B Cell Lymphoma.BioMed research international · 2015Review
- Diffuse large B cell lymphoma: using pathologic and molecular biomarkers to define subgroups for novel therapy.Annals of hematology · 2014Review
- Moving forward in HIV-associated cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2014Article
- Translating cancer genomes and transcriptomes for precision oncology.CA: a cancer journal for cliniciansReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The division of the heterogeneous entity of diffuse large B-cell lymphoma (DLBCL) into the ontogenic phenotypes of germinal center B-cell-like (GCB) and activated B-cell-like (ABC) is optimally determined by gene expression profiling (GEP), although simpler immunohistochemistry (IHC) algorithms are alternatively being used. The cell-of-origin (COO) classification assists in prognostication and may be predictive of response to therapy. Mounting data suggests that IHC methods of classifying COO may be inaccurate. GEP categorization of COO is superior in defining prognostically and biologically distinct DLBCL subtypes, but current barriers to its widescale use include inaccessibility, cost, and lack of methodological standardization and prospective validation. The poorer prognosis of ABC-DLBCL is frequently associated with constitutive activity in the NF-κB pathway and aberrations in upstream or downstream regulators of this pathway. The molecular mechanisms underlying lymphomagenesis in GCB-DLBCL are arguably less well defined, but C-REL amplification and mutations in BCL-2 and EZH2 are common. New technologies, such as next-generation sequencing, are rapidly revealing novel pathogenic genetic aberrations, and DLBCL treatment strategies are increasingly being designed focusing on distinctive pathogenic drivers within ontogenic phenotypes. This review examines emerging molecular targets and novel therapeutic agents in DLBCL, and discusses whether stratifying therapy for DLBCL using molecular features is merited by current preclinical and clinical evidence.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.