Evidence map›Paper›PMID 26405224›Full record

ReviewBlood2015

Familial predisposition and genetic risk factors for lymphoma.

James R Cerhan, Susan L Slager

Open access · bronzeAbstract readReview
In one paragraph

Review in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 2 pooled it
9.1field-weighted citation impact, top 2% 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

78 citing papers in PubMed, 2 syntheses or guidelines pooled it, 177 citations in OpenAlex.

  1. Guideline
  2. Pooled it
  3. Trial
  4. Article
  5. Review
  6. Article
  7. Article
  8. Familial risk of placental abruption.European journal of obstetrics, gynecology, and reproductive biology · 2026
    Article
  9. Article
  10. Genetic Predisposition to Hematologic Malignancies.Cold Spring Harbor perspectives in medicine · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Exploring G Protein-Coupled Receptors in Hematological Cancers.ACS pharmacology & translational science · 2024
    Article
  17. Association of Genetic Variants at theInternational journal of molecular sciences · 2024
    Article
  18. Article
  19. Article
  20. Article

18 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

2 authors at 2 institutions in 2 countries.

James R CerhanDivision of Epidemiology, Department of Health Sciences Research, Genetic Epidemiology and Risk Assessment Program, Mayo Clinic Comprehensive Cancer Center, and.ORCID http://orcid.org/0000-0002-7482-178X
Susan L SlagerGenetic Epidemiology and Risk Assessment Program, Mayo Clinic Comprehensive Cancer Center, and Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN.ORCID http://orcid.org/0000-0002-5173-4712
Department of Medical Sciences · BYMayo Clinic in Florida · US

Funding

The Role of Monocytes in non-Hodgkin LymphomaP50CA097274 · NCI · UNIVERSITY OF IOWA · PI WEINER, GEORGE J. · 2002 to 2021
$45.7M
Genetic Epidemiology of Chronic Lymphocytic LeukemiaU01CA118444 · NCI · MAYO CLINIC ROCHESTER · PI SLAGER, SUSAN L · 2006 to 2015
$7.1M
Molecular Epidemiology of NHL and CLLR01CA092153 · NCI · MAYO CLINIC ROCHESTER · PI CERHAN, JAMES R · 2003 to 2012
$6.7M
NCI NIH HHS P50 CA097274NCI NIH HHS P50 CA97274NCI NIH HHS R01 CA092153NCI NIH HHS R01 CA92153NCI NIH HHS U01 CA118444
6 · The paper itself

Abstract

Our understanding of familial predisposition to lymphoma (collectively defined as non-Hodgkin lymphoma [NHL], Hodgkin lymphoma [HL], and chronic lymphocytic leukemia [CLL]) outside of rare hereditary syndromes has progressed rapidly during the last decade. First-degree relatives of NHL, HL, and CLL patients have an ∼1.7-fold, 3.1-fold, and 8.5-fold elevated risk of developing NHL, HL, and CLL, respectively. These familial risks are elevated for multiple lymphoma subtypes and do not appear to be confounded by nongenetic risk factors, suggesting at least some shared genetic etiology across the lymphoma subtypes. However, a family history of a specific subtype is most strongly associated with risk for that subtype, supporting subtype-specific genetic factors. Although candidate gene studies have had limited success in identifying susceptibility loci, genome-wide association studies (GWAS) have successfully identified 67 single nucleotide polymorphisms from 41 loci, predominately associated with specific subtypes. In general, these GWAS-discovered loci are common (minor allele frequency >5%), have small effect sizes (odds ratios, 0.60-2.0), and are of largely unknown function. The relatively low incidence of lymphoma, modest familial risk, and the lack of a screening test and associated intervention, all argue against active clinical surveillance for lymphoma in affected families at this time.

Indexed as

Gene FrequencyGenetic LociGenetic Predisposition to DiseasePolymorphism, Single NucleotideAllelesAnimalsFamilyGenome-Wide Association StudyHumansLymphoma

Identifiers

PMID26405224
PMCPMC4643002
OpenAlexW2190030883

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.