Evidence map›Paper›PMID 31127191›Full record

ReviewNature reviews. Clinical oncology2019

Genetic alterations and their clinical implications in DLBCL.

Yi Miao, L Jeffrey Medeiros, Yong Li, Jianyong Li, Ken H Young

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Clinical oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
131citing papers in PubMed, 1 pooled it
18.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

131 citing papers in PubMed, 1 synthesis or guideline pooled it, 220 citations in OpenAlex.

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  12. A proof of concept study ofScientific reports · 2025
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  16. PAX Family, Master Regulator in Cancer.Diagnostics (Basel, Switzerland) · 2025
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71 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 4 institutions in 2 countries.

Yi MiaoDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
L Jeffrey MedeirosDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Yong LiDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Jianyong LiDepartment of Hematology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Ken H YoungDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. khyoung@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USCleveland Clinic Lerner College of Medicine · USNanjing Medical University · CNThe University of Texas Health Science Center at Houston · US

Funding

Convergence of MicroRNAs and p53 Signaling in Multiple Myeloma: Environmental CoR01CA138688 · NCI · UNIVERSITY OF LOUISVILLE · PI LI, YONG · 2009 to 2017
$2.9M
MYC as a Biomarker in Aggressive Non-Hodgkin LymphomaR01CA187415 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI LI, YONG · 2015 to 2019
$2.2M
Deep Sequencing of Small Regulatory RNAs in Diffuse Large B cell LymphomaRC1CA146299 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI XIAO, CHANGCHUN · 2009 to 2010
$1000k
NCI NIH HHS R01 CA138688NCI NIH HHS R01 CA187415NCI NIH HHS RC1 CA146299
6 · The paper itself

Abstract

Diffuse large B cell lymphoma (DLBCL) is a highly heterogeneous lymphoid neoplasm with variations in gene expression profiles and genetic alterations, which lead to substantial variations in clinical course and response to therapy. The advent of high-throughput genome sequencing platforms, and especially whole-exome sequencing, has helped to define the genetic landscape of DLBCL. In the past 10 years, these studies have identified many genetic alterations in DLBCL, some of which are specific to B cell lymphomas, whereas others can also be observed in other types of cancer. These aberrations result in altered activation of a wide range of signalling pathways and other cellular processes, including those involved in B cell differentiation, B cell receptor signalling, activation of the NF-κB pathway, apoptosis and epigenetic regulation. Further elaboration of the genetics of DLBCL will not only improve our understanding of disease pathogenesis but also provide further insight into disease classification, prognostication and therapeutic targets. In this Review, we describe the current understanding of the prevalence and causes of specific genetic alterations in DLBCL and their role in disease development and progression. We also summarize the available clinical data on therapies designed to target the aberrant pathways driven by these alterations.

Indexed as

HumansLymphoma, Large B-Cell, Diffuse

Identifiers

PMID31127191
OpenAlexW2945525000

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.