Evidence map›Paper›PMID 31548407›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

Cell division rates decrease with age, providing a potential explanation for the age-dependent deceleration in cancer incidence.

Cristian Tomasetti, Justin Poling, Nicholas J Roberts, Nyall R London, Meredith E Pittman, Michael C Haffner, Anthony Rizzo, Alex Baras, Baktiar Karim, Antonio Kim and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.3field-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

53 citing papers in PubMed, 106 citations in OpenAlex.

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  18. Effect of Vitamin E on Transcriptomic Alterations in Alzheimer's Disease.International journal of molecular sciences · 2023
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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

15 authors at 6 institutions in 1 country.

Cristian TomasettiDivision of Biostatistics and Bioinformatics, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21205; bertvog@gmail.com ctomasetti@jhu.edu.
Justin PolingPathology, Williamson Medical Center, Brentwood, TN 37207.
Nicholas J RobertsSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD 21205.ORCID 0000-0002-8709-0664
Nyall R LondonDepartment of Otolaryngology, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Meredith E PittmanDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY 10065.
Michael C HaffnerSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD 21205.
Anthony RizzoDepartment of Pathology, The Johns Hopkins University, Baltimore, MD 21231.
Alex BarasDepartment of Pathology, The Johns Hopkins University, Baltimore, MD 21231.
Baktiar KarimPathology & Histotechnology Laboratory, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD 21702.
Antonio KimSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD 21205.
Christopher M HeaphySidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD 21205.ORCID 0000-0003-4264-1810
Alan K MeekerSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD 21205.
Ralph H HrubanSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD 21205.
Christine A Iacobuzio-DonahueDepartment of Pathology, Rubenstein Center for Pancreatic Cancer Research, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065.
Bert VogelsteinSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD 21205; bertvog@gmail.com ctomasetti@jhu.edu.
Johns Hopkins University · USHoward Hughes Medical Institute · USCornell University · USLeidos (United States) · USMemorial Sloan Kettering Cancer Center · USWilliamson College · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
Tumor Antigens for Individual Signatures and TherapyP50CA062924 · NCI · JOHNS HOPKINS UNIVERSITY · PI LENNON, ANNE MARIE · 1993 to 2022
$54.6M
MOLECULAR GENETIC ANALYSIS OF COLORECTAL CANCERR37CA043460 · NCI · JOHNS HOPKINS UNIVERSITY · PI VOGELSTEIN, BERT · 1997 to 2016
$7.4M
(PQB6) Genetics of Subclonal Evolution in Pancreatic CancerR01CA179991 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI IACOBUZIO-DONAHUE, CHRISTINE A · 2013 to 2016
$1.3M
Integrative Analyses to Identify Pancreatic Cancer Susceptibility GenesR00CA190889 · NCI · JOHNS HOPKINS UNIVERSITY · PI ROBERTS, NICHOLAS JASON · 2017 to 2019
$747k
GENES FROM THE FAP LOCUSR01CA057345 · NCI · JOHNS HOPKINS UNIVERSITY · PI KINZLER, KENNETH W. · 1992 to 2001
$734k
NCI NIH HHS P30 CA006973NCI NIH HHS P30 CA008748NCI NIH HHS P50 CA062924NCI NIH HHS R00 CA190889NCI NIH HHS R01 CA057345NCI NIH HHS R01 CA179991NCI NIH HHS R37 CA043460
6 · The paper itself

Abstract

A new evaluation of previously published data suggested to us that the accumulation of mutations might slow, rather than increase, as individuals age. To explain this unexpected finding, we hypothesized that normal stem cell division rates might decrease as we age. To test this hypothesis, we evaluated cell division rates in the epithelium of human colonic, duodenal, esophageal, and posterior ethmoid sinonasal tissues. In all 4 tissues, there was a significant decrease in cell division rates with age. In contrast, cell division rates did not decrease in the colon of aged mice, and only small decreases were observed in their small intestine or esophagus. These results have important implications for understanding the relationship between normal stem cells, aging, and cancer. Moreover, they provide a plausible explanation for the enigmatic age-dependent deceleration in cancer incidence in very old humans but not in mice.

Indexed as

AgingCell DivisionDecelerationMutationAdultAgedAged, 80 and overAnimalsColonDuodenumEsophagusHumansIncidenceKi-67 AntigenMaleMiceKi-67 Antigenagingcancercell divisionmutation rate

Identifiers

PMID31548407
PMCPMC6789572
OpenAlexW2975814872

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.