Evidence map›Paper›PMID 19997527›Full record

ReviewCurrent aging science2009

Aging and inflammation: etiological culprits of cancer.

Aamir Ahmad, Sanjeev Banerjee, Zhiwei Wang, Dejuan Kong, Adhip P N Majumdar, Fazlul H Sarkar

Open access · bronzeAbstract readReview
In one paragraph

Review in Current aging science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 82 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Ageing and Inflammation: What Happens in Periodontium?Bioengineering (Basel, Switzerland) · 2023
    Review
  6. Review
  7. Revisiting Epithelial Carcinogenesis.International journal of molecular sciences · 2022
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Adenosine A2A receptor (A2AR) stimulation enhances mitochondrial metabolism and mitigates reactive oxygen species-mediated mitochondrial injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  13. Cooperation of loss ofDisease models & mechanisms · 2018
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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 1 institution in 1 country.

Aamir AhmadDepartment of Pathology, Wayne State University, School of Medicine, Detroit, MI 48201, USA.
Sanjeev Banerjee
Zhiwei Wang
Dejuan Kong
Adhip P N Majumdar
Fazlul H Sarkar
Wayne State University · US

Funding

Molecular Mechanism of Genistein (Isoflavone) in Prostate CancerR01CA083695 · NCI · WAYNE STATE UNIVERSITY · PI SARKAR, FAZLUL H. · 2001 to 2011
$2.3M
RO1: A novel and targeted approach to inhibit invasion and angiogenesisR01CA131151 · NCI · WAYNE STATE UNIVERSITY · PI SARKAR, FAZLUL H. · 2008 to 2012
$1.8M
FoxM1: A molecular target in pancreatic cancerR01CA132794 · NCI · WAYNE STATE UNIVERSITY · PI SARKAR, FAZLUL H. · 2009 to 2013
$1.5M
NCI NIH HHS R01 CA083695NCI NIH HHS R01CA083695NCI NIH HHS R01 CA131151NCI NIH HHS R01CA131151NCI NIH HHS R01 CA132794NCI NIH HHS R01CA132794
6 · The paper itself

Abstract

The biochemical phenomenon of aging, as universal as it is, still remains poorly understood. A number of diseases are associated with aging either as a cause or consequence of the aging process. The incidence of human cancers increases exponentially with age and therefore cancer stands out as a disease that is intricately connected to the process of aging. Emerging evidence clearly suggests that there is a symbiotic relationship between aging, inflammation and chronic diseases such as cancer; however, it is not clear whether aging leads to the induction of inflammatory processes thereby resulting in the development and maintenance of chronic diseases or whether inflammation is the causative factor for inducing both aging and chronic diseases such as cancer. Moreover, the development of chronic diseases especially cancer could also lead to the induction of inflammatory processes and may cause premature aging, suggesting that longitudinal research strategies must be employed for dissecting the interrelationships between aging, inflammation and cancer. Here, we have described our current understanding on the importance of inflammation, activation of NF-kappaB and various cytokines and chemokines in the processes of aging and in the development of chronic diseases especially cancer. We have also reviewed the prevailing theories of aging and provided succinct evidence in support of novel theories such as those involving cancer stem cells, the molecular understanding of which would likely hold a great promise towards unraveling the complex relationships between aging, inflammation and cancer.

Indexed as

Age FactorsAgingCell HypoxiaCellular SenescenceChemokinesCytokinesHumansInflammationNeoplasmsNeoplastic Stem CellsNF-kappa BRisk FactorsSignal TransductionChemokinesCytokinesNF-kappa BAgingcancerimmunityinflammationNF-κB

Identifiers

PMID19997527
PMCPMC2789465
OpenAlexW1963653260

What OpenQuestion holds

Textmetadata
LicenceTDM
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.