Evidence map›Paper›PMID 10852857›Full record

ReviewEnvironmental health perspectives2000

Critical windows of exposure for children's health: cancer in human epidemiological studies and neoplasms in experimental animal models.

L M Anderson, B A Diwan, N T Fear, E Roman

Open access · diamondAbstract readReview
In one paragraph

Review in Environmental health perspectives, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed, 4 pooled it
4.0field-weighted citation impact, top 6% 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

127 citing papers in PubMed, 4 syntheses or guidelines pooled it, 364 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  4. Pooled it
  5. Trial
  6. Article
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  11. Article
  12. Maternal Prenatal Use of Alcohol, Tobacco, and Illicit Drugs and Associations with Childhood Cancer Subtypes.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2024
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Toxicology reports · 2022
    Article
  18. Lymphoblastic Lymphoma: a Concise Review.Current oncology reports · 2022
    Review
  19. Article
  20. Article

67 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

4 authors at 1 institution in 1 country.

L M AndersonLaboratory of Comparative Carcinogenesis, National Cancer Institute, FCRDC, Frederick, Maryland, USA. andersol@mail.ncifcrf.gov
B A Diwan
N T Fear
E Roman
National Cancer Institute · US

Funding

Mechanisms in Perinatal CarcinogenesisZIABC005352 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI ANDERSON, LUCY M · 2009 to 2010
$1.4M
METABOLIC AND PHARMACOLOGICAL DETERMINANTS IN PERINATAL CARCINOGENESISZ01BC005352 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI ANDERSON, LUCY M · 1996 to 2008
$1.2M
BIOLOGY AND PATHOLOGY OF NATURALLY OCCURRING AND EXPERIMENTALLY INDUCED TUMORSZ01BC005301 · BC · BASIC SCIENCES · PI ANDERSON, LUCY M · 1996 to 1999
–
6 · The paper itself

Abstract

In humans, cancer may be caused by genetics and environmental exposures; however, in the majority of instances the identification of the critical time window of exposure is problematic. The evidence for exposures occurring during the preconceptional period that have an association with childhood or adulthood cancers is equivocal. Agents definitely related to cancer in children, and adulthood if exposure occurs in utero, include: maternal exposure to ionizing radiation during pregnancy and childhood leukemia and certain other cancers, and maternal use of diethylstilbestrol during pregnancy and clear-cell adenocarcinoma of the vagina of their daughters. The list of environmental exposures that occur during the perinatal/postnatal period with potential to increase the risk of cancer is lengthening, but evidence available to date is inconsistent and inconclusive. In animal models, preconceptional carcinogenesis has been demonstrated for a variety of types of radiation and chemicals, with demonstrated sensitivity for all stages from fetal gonocytes to postmeiotic germ cells. Transplacental and neonatal carcinogenesis show marked ontogenetic stage specificity in some cases. Mechanistic factors include the number of cells at risk, the rate of cell division, the development of differentiated characteristics including the ability to activate and detoxify carcinogens, the presence of stem cells, and possibly others. Usefulness for human risk estimation would be strengthened by the study of these factors in more than one species, and by a focus on specific human risk issues.

Indexed as

Cell Transformation, NeoplasticAdultAnimalsChildDisease Models, AnimalEnvironmental ExposureEpidemiologic StudiesFemaleGonadsHumansNeoplasmsNeoplasms, ExperimentalPregnancyRadiation, IonizingRisk AssessmentXenobioticsXenobiotics

Identifiers

PMID10852857
PMCPMC1637809
OpenAlexW2031052102

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.