Evidence map›Paper›PMID 27465553›Full record

ReviewTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

Mechanisms underlying the association between obesity and Hodgkin lymphoma.

Andreia Matos, Joana Marinho-Dias, Sofia Ramalheira, Maria José Oliveira, Manuel Bicho, Ricardo Ribeiro

Abstract readReview
PubMed Publisher
In one paragraph

Review in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 34% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Obesity and Risk for Lymphoma: Possible Role of Leptin.International journal of molecular sciences · 2022
    Review
  6. 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

6 authors at 4 institutions in 2 countries.

Andreia MatosGenetics Laboratory and Environmental Health Institute, Faculdade de Medicina, Universidade de Lisboa, Lisbon, 1649-028, Portugal. andreiamatos@medicina.ulisboa.pt.
Joana Marinho-DiasMolecular Oncology Group, Portuguese Institute of Oncology Porto Centre, Porto, 4200-072, Portugal.
Sofia RamalheiraOncohematology Department, Portuguese Institute of Oncology Porto Centre, Porto, 4200-072, Portugal.
Maria José Oliveirai3S-Instituto de Investigação e Inovação em Saúde/INEB-Institute of Biomedical Engineering, University of Porto, Porto, 4200-135, Portugal.
Manuel BichoGenetics Laboratory and Environmental Health Institute, Faculdade de Medicina, Universidade de Lisboa, Lisbon, 1649-028, Portugal.
Ricardo RibeiroGenetics Laboratory and Environmental Health Institute, Faculdade de Medicina, Universidade de Lisboa, Lisbon, 1649-028, Portugal. oriebir.r@gmail.com.
Instituto de Investigação Científica Tropical · PTInstituto Português de Oncologia Francisco Gentil · PTUniversidade do Porto · PTUniversity of Lisbon · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A solid body of knowledge indicates that overweight and obese subjects are prone to develop cancer, aggressive disease, and death more than their lean counterparts. While obesity has been causally associated with various cancers, only a limited number of studies beheld the link with classical Hodgkin lymphoma (HL). Contemporary meta-analysis and prospective studies confirmed the association of body mass index with HL. Besides epidemiological evidence, excess adiposity is known to influence tumor behavior through adipokines, adipose-derived stem cell migration, and metabolism regulation, and by modulating immunoinflammatory response. Nevertheless, the obesity paradox has been described in few cancers. Considering that adipose tissue is an immunomodulatory organ, and that inflammation is the cornerstone of HL pathophysiology, the rationale for being causally related due to endocrine/paracrine interactions cannot be negligible. In this hypothesis-generating review, we explore the biologically plausible links between excess adiposity and HL in light of recent basic and clinical data, in order to create a basis for understanding the underlying mechanisms and foster applied research. The establishment of an association of excess adiposity with HL will determine public health preventive measures to fight obesity and eventually novel therapeutic approaches in HL patients.

Indexed as

Hodgkin DiseaseHumansObesityBone marrow adipocytesHodgkin lymphomaObesityTumor microenvironment

Identifiers

PMID27465553
OpenAlexW2486861505

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.