Evidence map›Paper›PMID 28476195›Full record

ArticleArchives of medical research2016

Tobacco Smoke and Ras Mutations Among Latino and Non-Latino Children with Acute Lymphoblastic Leukemia.

Maneet Kaur, Adam J de Smith, Steve Selvin, Luoping Zhang, Marc Cunningham, Michelle W Kang, Helen M Hansen, Robert M Cooper, Roberta McKean-Cowdin, Joseph L Wiemels and 1 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Archives of medical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.9field-weighted citation impact, top 18% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Is There Etiologic Heterogeneity between Subtypes of Childhood Acute Lymphoblastic Leukemia? A Review of Variation in Risk by Subtype.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2019
    Review
  2. Childhood Leukemia and Primary Prevention.Current problems in pediatric and adolescent health care · 2016
    Article
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

11 authors at 6 institutions in 1 country.

Maneet KaurDivision of Epidemiology, School of Public Health, University of California Berkeley, Berkeley, California.
Adam J de SmithDepartment of Epidemiology and Biostatistics, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California.
Steve SelvinDivison of Biostatistics, School of Public Health, University of California Berkeley, Berkeley, California.
Luoping ZhangDivision of Environmental Health Sciences, School of Public Health, University of California Berkeley, Berkeley, California.
Marc CunninghamDepartment of Epidemiology and Biostatistics, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California.
Michelle W KangDepartment of Epidemiology and Biostatistics, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California.
Helen M HansenDepartment of Neurological Surgery, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California.
Robert M CooperDepartment of Pediatric Hematology/Oncology, Kaiser Permanente Los Angeles Medical Center, Los Angeles, California.
Roberta McKean-CowdinDepartment of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California.
Joseph L WiemelsDepartment of Epidemiology and Biostatistics, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California; Department of Neurological Surgery, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California.
Catherine MetayerDivision of Epidemiology, School of Public Health, University of California Berkeley, Berkeley, California. Electronic address: cmetayer@berkeley.edu.
UCSF Helen Diller Family Comprehensive Cancer Center · USUniversity of California, Berkeley · USBerkeley Public Health Division · USKaiser Permanente · USUniversity of California, San Francisco · USUniversity of Southern California · US

Funding

Training CoreP42ES004705 · NIEHS · UNIVERSITY OF CALIFORNIA BERKELEY · PI SEDLAK, DAVID L. · 1987 to 2025
$74.6M
Environmental and Molecular Epidemiology of Childhood LeukemiaR01ES009137 · NIEHS · UNIVERSITY OF CALIFORNIA BERKELEY · PI METAYER, CATHERINE · 1999 to 2013
$21.1M
Project 3 - Prenatal Exposures, Constitutive Genetics, DNA Methylation & Childhood LeukemiaP50ES018172 · NIEHS · UNIVERSITY OF CALIFORNIA BERKELEY · PI METAYER, CATHERINE · 2015 to 2019
$3.8M
Project 3: Prenatal Exposure, DNA Methylation & Childhood LeukemiaP01ES018172 · NIEHS · UNIVERSITY OF CALIFORNIA BERKELEY · PI METAYER, CATHERINE · 2009 to 2013
$3.7M
NIEHS NIH HHS P01 ES018172NIEHS NIH HHS P42 ES004705NIEHS NIH HHS P50 ES018172NIEHS NIH HHS R01 ES009137
6 · The paper itself

Abstract

BACKGROUND AND

aimsChildhood acute lymphoblastic leukemia (ALL) is a biologically heterogeneous disease, and mutations in the KRAS and NRAS oncogenes are present at diagnosis in about one-fifth of cases. Ras mutations were previously associated with environmental exposures in leukemias as well as in many other cancer types. This study examined whether Ras mutation could define a unique etiologic group of childhood ALL associated with tobacco smoke, a well-established mutagen and carcinogen.

methodsWe included 670 children with ALL enrolled in a case-control study in California (1995-2013), including 50.6% Latinos. Parental and child exposure to tobacco smoke was obtained from interviews. Sanger sequencing was used to detect the common KRAS and NRAS hotspot mutations in diagnostic bone marrow DNA. ALL cases were also characterized for common chromosome abnormalities. In case-case analyses, logistic regression analyses were used to estimate odds ratios to describe the association between tobacco smoke exposure and childhood ALL with Ras mutations.

resultsKRAS or NRAS mutations were detected in ∼18% of children diagnosed with ALL. Ras mutations were more common among Latino cases compared with non-Latino whites and in high-hyperdiploid ALL. No associations were observed between parental smoking or child's passive exposure to smoke and Ras positive ALL.

conclusionsThe apparent lack of association between tobacco smoke and Ras mutation in childhood ALL suggests that Ras mutations do not specifically define a tobacco-related etiologic pathway. Reasons for racial and ethnic differences in ALL are not well understood and could reflect differences in etiology that warrant further examination.

Indexed as

CaliforniaCase-Control StudiesChildChild, PreschoolFemaleGenetic Association StudiesGTP PhosphohydrolasesHispanic or LatinoHumansInfantMaleMembrane ProteinsMutationNicotianaOdds RatioPrecursor Cell Lymphoblastic Leukemia-LymphomaGTP PhosphohydrolasesKRAS protein, humanMembrane ProteinsNRAS protein, humanProto-Oncogene Proteins p21(ras)Tobacco Smoke PollutionChildhood acute lymphoblastic leukemiaHispanicLatinoRas mutationTobacco smoke

Identifiers

PMID28476195
PMCPMC5424620
OpenAlexW2610874951

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.