Evidence map›Paper›PMID 33748835›Full record

SynthesisInternational journal of epidemiology2021

Common genetic polymorphisms contribute to the association between chronic lymphocytic leukaemia and non-melanoma skin cancer.

Caroline Besson, Amy Moore, Wenting Wu, Claire M Vajdic, Silvia de Sanjose, Nicola J Camp, Karin E Smedby, Tait D Shanafelt, Lindsay M Morton, Jerry D Brewer and 7 more

Open access · bronzeAbstract readMeta-Analysis
In one paragraph

Synthesis in International journal of epidemiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
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

17 authors at 11 institutions in 5 countries.

Caroline BessonService d'hématologie et Oncologie, Centre Hospitalier de Versailles, Le Chesnay; Université Paris-Saclay, UVSQ, Inserm, Équipe "Exposome et Hérédité", CESP, 94805, Villejuif, France.ORCID 0000-0003-4364-7173
Amy MooreDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA.
Wenting WuDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, USA.
Claire M VajdicCentre for Big Data Research in Health, University of New South Wales, Sydney, New South Wales, Australia.
Silvia de SanjoseCIBER de Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain.
Nicola J CampDepartment of Internal Medicine and Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, UT, USA.
Karin E SmedbyDepartment of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
Tait D ShanafeltDepartment of Internal Medicine, Mayo Clinic, Rochester, MN, USA.
Lindsay M MortonDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA.
Jerry D BrewerDepartment of Dermatology, Mayo Clinic, Rochester, MN, USA.
Lydia ZablotskaDepartment of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA, USA.
Eric A EngelsDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA.
James R CerhanService d'hématologie et Oncologie, Centre Hospitalier de Versailles, Le Chesnay; Université Paris-Saclay, UVSQ, Inserm, Équipe "Exposome et Hérédité", CESP, 94805, Villejuif, France.ORCID 0000-0002-7482-178X
Susan L SlagerDepartment of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.
Jiali HanChanning Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-8309-7092
Sonja I BerndtDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA.
InterLymph Consortium. Full authors list is given at the end of the manuscript
National Cancer Institute · USInserm · FRMayo Clinic in Arizona · USBrigham and Women's Hospital · USCentro de Investigación Biomédica en Red de Epidemiología y Salud Pública · ESIndiana University School of MedicineKarolinska Institutet · SEMayo Clinic in Florida · USUniversity of California, San Francisco · USUniversity of Utah · USUNSW Sydney · AU

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

backgroundEpidemiological studies have demonstrated a positive association between chronic lymphocytic leukaemia (CLL) and non-melanoma skin cancer (NMSC). We hypothesized that shared genetic risk factors between CLL and NMSC could contribute to the association observed between these diseases.

methodsWe examined the association between (i) established NMSC susceptibility loci and CLL risk in a meta-analysis including 3100 CLL cases and 7667 controls and (ii) established CLL loci and NMSC risk in a study of 4242 basal cell carcinoma (BCC) cases, 825 squamous cell carcinoma (SCC) cases and 12802 controls. Polygenic risk scores (PRS) for CLL, BCC and SCC were constructed using established loci. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs).

resultsHigher CLL-PRS was associated with increased BCC risk (OR4th-quartile-vs-1st-quartile = 1.13, 95% CI: 1.02-1.24, Ptrend = 0.009), even after removing the shared 6p25.3 locus. No association was observed with BCC-PRS and CLL risk (Ptrend = 0.68). These findings support a contributory role for CLL in BCC risk, but not for BCC in CLL risk. Increased CLL risk was observed with higher SCC-PRS (OR4th-quartile-vs-1st-quartile = 1.22, 95% CI: 1.08-1.38, Ptrend = 1.36 × 10-5), which was driven by shared genetic susceptibility at the 6p25.3 locus.

conclusionThese findings highlight the role of pleiotropy regarding the pathogenesis of CLL and NMSC and shows that a single pleiotropic locus, 6p25.3, drives the observed association between genetic susceptibility to SCC and increased CLL risk. The study also provides evidence that genetic susceptibility for CLL increases BCC risk.

Indexed as

Basal Cell CarcinomaCarcinoma, Squamous CellLeukemia, Lymphocytic, Chronic, B-CellSkin NeoplasmsHumansPolymorphism, Single NucleotideRisk FactorsCLLNMSCpleiotropypolygenic risk score

Identifiers

PMID33748835
PMCPMC8521875
OpenAlexW3138511144

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.