LeukemiaCCLSNCT00015587
Molecular Epidemiology of Childhood Leukemia (Aka The California Childhood Leukemia Study)
An observational study of Leukemia and Acute Myelocytic Leukemia, run by National Institute of Environmental Health Sciences (NIEHS) at 1 site in United States.
Trial summary
This study is a case-control study investigating the causes of childhood leukemia in Northern California. The overall purpose of this epidemiologic study is to find specific genetic or environmental factors that may increase the risk of leukemia in children. Read more about this study
- Who is it for?
- Ages 1 day to 14 years
- Conditions the study is for
- Leukemia, Acute Myelocytic Leukemia, Acute Lymphoblastic Leukemia
- How many people
- 3,523 participants
- Where
- 1 siteUnited States
- Study dates
- Apr 1995to Jul 2016
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 1 day to 14 years
- All sexes
- No healthy volunteers
- Child
Study population: Children diagnosed with leukemia and matched controls
Cases must be children ages 0-14 newly diagnosed with leukemia (any type) at one of participating hospitals. They must live in the state of California at diagnosis, never have been diagnosed with a prior cancer and have a parent or guardian that speaks English or Spanish.
Controls are matched on the case child's DOB, gender, mother's race, parent's Hispanicity. In order to be eligible, they must have no history of cancer, have a parent or guardian that speaks English or Spanish and they must live in the state of California.
Trial locations and contacts
1 site in 1 country.
United States1 site
University of California, School of Public Health, Childhood Leukemia Study
Berkeley, California, 94720-7392
About this study
Official title: Chemical Exposures and Leukemia Risks and Childhood Leukemia and Environmental Exposure
This study is a case-control study investigating the causes of childhood leukemia in Northern California. The overall purpose of this epidemiologic study is to find specific genetic or environmental factors that may increase the risk of leukemia in children. The study is being conducted by Patricia Buffler, PhD at the School of Public Health - University of California Berkeley in collaboration with the California Department of Health Services and 16 hospitals located throughout the state of California. The study began in 1995 and will continue to 2014.
Read the detailed description
This study is a case-control study of incident childhood leukemia (all subtypes) diagnosed since mid-1995. Children newly diagnosed with leukemia are enrolled in the study. Criteria for inclusion in the study are: under 15 years of age, no prior cancer diagnosis, residency in the state of California at the time of diagnosis, and availability of an English or Spanish speaking parent or guardian. Pre-treatment biological specimens, including bone marrow and peripheral blood, are obtained for analysis in the UCB lab of Dr M. Smith. The lab will use Fluorescence In Situ Hybridization (FISH) to detect chromosome specific aneuploidy and translocations. A number of chromosomal translocations, including t(9;22) and t(8;21), are known to be centrally involved in the development of childhood leukemia. Molecular characterization of the cases with translocations may provide insight into the timing of critical exposures and the nature of the etiological agent involved.
One comparison subject (control) is recruited for each consenting case. For each case, four potential controls are randomly selected from California birth certificate files and matched on date of birth, gender, mother's race, parental Hispanicity, and county of residence. One of the four birth certificate controls is randomly selected to be recruited to participate in the study.
An in-depth personal interview asks a variety of questions, including: residential history; occupational and household exposure histories; mothers' reproductive history; events during index pregnancy and delivery; family history of illness; child's health and vaccination history, contact with other children; maternal and child exposure to cigarette smoke during pregnancy and since birth; maternal and child history of x-rays.
Saliva specimens are obtained from both cases and controls and their biological mothers. The saliva samples are sent to the study office and processed in the Genetic Epidemiology lab at UC Berkeley. DNA from cases and controls will be analyzed by polymerase chain reaction for genetic polymorphisms. Genetic polymorphisms will be examined in two glutathione transferase genes, M1 and Tl. Case samples of peripheral blood, bone marrow, and archived newborn blood will be also used to detect N-ras mutation.
Three tiers of an exposure assessment are being implemented. Tier 1 enrolls and interviews cases and controls seeking to identify risk factors, including residential and occupational chemical exposures. In Tier 2, cases and birth certificate controls that have not changed residence based on specific criteria are part of a reliability study, which seeks to determine if self-reported chemicals used at the time of interview are found in the home during a visual survey several months after interview. Tier 3 aims to document the potential for household exposures by sampling dust on the floor surfaces. The objective is to identify if there are differences in concentrations of pesticides, metals, polyaromatic hydrocarbons, cotinine, polychorinated biphenyls, and ethylenethiourea in the homes of cases and controls. Further, a case-case analysis will identify if cases with chromosomal translocations of interest live in homes with higher concentrations of target compounds than cases that do not have such translocations. These analyses will determine whether leukemic children with common genetic changes experience common exposures and whether these genetic changes have approximately the same temporal occurrence. Finally, we will evaluate whether children with and without leukemia differ with respect to susceptibility.
- Conditions
- Leukemia, Acute Myelocytic Leukemia, Acute Lymphoblastic Leukemia, Acute Myelogenous Leukemia
- Keywords
- Molecular Epidemiology, Case Control
- Medical subject headings
- Leukemia, Leukemia, Myeloid, Acute, Precursor Cell Lymphoblastic Leukemia-Lymphoma
What is being measured
The primary outcome is the main question the study is designed to answer.
Outcome of study
Using a case-control study design, we are studying the role of environmental and genetic factors in the etiology of a rare cancer in a vulnerable and ethnically diverse population, using an integrated multi-disciplinary approach to improve disease classification and exposure assessment.
Measured: duration of study
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted25 Apr 2001 (estimated)
- Study startApr 1995
- Primary completionJul 2016
- Study completionJul 2016
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (86)Papers the sponsor has linked to this study.
- Other trials for LeukemiaStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Case-control
- Time perspective
- Prospective
- Enrolment
- 3,523 participants (actual)
Sponsor and investigators
- Lead sponsor
- National Institute of Environmental Health Sciences (NIEHS)
- Sponsor type
- US National Institutes of Health
- Collaborators
- National Cancer Institute (NCI)
- Responsible party
- Sponsor
- Investigators
- Catherine Metayer, MD, PhD, Principal investigator, University of California Berkeley, School of Public Health
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT00015587
- Sponsor's protocol ID
- 9137-CP-001
- Acronym
- CCLS
- Status last verified
- Oct 2016
- First submitted
- 23 Apr 2001
- Last updated
- 12 Oct 2016
- Results posted
- No
- Data monitoring committee
- No
Publications
Xiao Z, Greaves MF, Buffler P, Smith MT, Segal MR, Dicks BM, Wiencke JK, Wiemels JL. Molecular characterization of genomic AML1-ETO fusions in childhood leukemia. Leukemia. 2001 Dec;15(12):1906-13. doi: 10.1038/sj.leu.2402318.
PubMed 11753612Zheng S, Ma X, Buffler PA, Smith MT, Wiencke JK. Whole genome amplification increases the efficiency and validity of buccal cell genotyping in pediatric populations. Cancer Epidemiol Biomarkers Prev. 2001 Jun;10(6):697-700.
PubMed 11401921Ma X, Buffler PA, Gunier RB, Dahl G, Smith MT, Reinier K, Reynolds P. Critical windows of exposure to household pesticides and risk of childhood leukemia. Environ Health Perspect. 2002 Sep;110(9):955-60. doi: 10.1289/ehp.02110955.
PubMed 12204832Ma X, Buffler PA, Selvin S, Matthay KK, Wiencke JK, Wiemels JL, Reynolds P. Daycare attendance and risk of childhood acute lymphoblastic leukaemia. Br J Cancer. 2002 May 6;86(9):1419-24. doi: 10.1038/sj.bjc.6600274.
PubMed 11986774Reynolds P, Von Behren J, Gunier RB, Goldberg DE, Hertz A, Harnly ME. Childhood cancer and agricultural pesticide use: an ecologic study in California. Environ Health Perspect. 2002 Mar;110(3):319-24. doi: 10.1289/ehp.02110319.
PubMed 11882484Reynolds P, Von Behren J, Gunier RB, Goldberg DE, Hertz A, Smith D. Traffic patterns and childhood cancer incidence rates in California, United States. Cancer Causes Control. 2002 Sep;13(7):665-73. doi: 10.1023/a:1019579430978.
PubMed 12296514Wiemels JL, Leonard BC, Wang Y, Segal MR, Hunger SP, Smith MT, Crouse V, Ma X, Buffler PA, Pine SR. Site-specific translocation and evidence of postnatal origin of the t(1;19) E2A-PBX1 fusion in childhood acute lymphoblastic leukemia. Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):15101-6. doi: 10.1073/pnas.222481199. Epub 2002 Nov 1.
PubMed 12415113Wiemels JL, Xiao Z, Buffler PA, Maia AT, Ma X, Dicks BM, Smith MT, Zhang L, Feusner J, Wiencke J, Pritchard-Jones K, Kempski H, Greaves M. In utero origin of t(8;21) AML1-ETO translocations in childhood acute myeloid leukemia. Blood. 2002 May 15;99(10):3801-5. doi: 10.1182/blood.v99.10.3801.
PubMed 11986239Greaves MF, Wiemels J. Origins of chromosome translocations in childhood leukaemia. Nat Rev Cancer. 2003 Sep;3(9):639-49. doi: 10.1038/nrc1164.
PubMed 12951583McHale CM, Wiemels JL, Zhang L, Ma X, Buffler PA, Feusner J, Matthay K, Dahl G, Smith MT. Prenatal origin of childhood acute myeloid leukemias harboring chromosomal rearrangements t(15;17) and inv(16). Blood. 2003 Jun 1;101(11):4640-1. doi: 10.1182/blood-2003-01-0313. No abstract available.
PubMed 12756163McHale CM, Wiemels JL, Zhang L, Ma X, Buffler PA, Guo W, Loh ML, Smith MT. Prenatal origin of TEL-AML1-positive acute lymphoblastic leukemia in children born in California. Genes Chromosomes Cancer. 2003 May;37(1):36-43. doi: 10.1002/gcc.10199.
PubMed 12661004Pine SR, Moy FH, Wiemels JL, Gill RK, Levendoglu-Tugal O, Ozkaynak MF, Sandoval C, Jayabose S. Real-time quantitative PCR: standardized detection of minimal residual disease in pediatric acute lymphoblastic leukemia. Polymerase chain reaction. J Pediatr Hematol Oncol. 2003 Feb;25(2):103-8. doi: 10.1097/00043426-200302000-00004.
PubMed 12571459Pine SR, Wiemels JL, Jayabose S, Sandoval C. TEL-AML1 fusion precedes differentiation to pre-B cells in childhood acute lymphoblastic leukemia. Leuk Res. 2003 Feb;27(2):155-64. doi: 10.1016/s0145-2126(02)00183-2.
PubMed 12526921Reiter A, Saussele S, Grimwade D, Wiemels JL, Segal MR, Lafage-Pochitaloff M, Walz C, Weisser A, Hochhaus A, Willer A, Reichert A, Buchner T, Lengfelder E, Hehlmann R, Cross NC. Genomic anatomy of the specific reciprocal translocation t(15;17) in acute promyelocytic leukemia. Genes Chromosomes Cancer. 2003 Feb;36(2):175-88. doi: 10.1002/gcc.10154.
PubMed 12508246Jensen CD, Block G, Buffler P, Ma X, Selvin S, Month S. Maternal dietary risk factors in childhood acute lymphoblastic leukemia (United States). Cancer Causes Control. 2004 Aug;15(6):559-70. doi: 10.1023/B:CACO.0000036161.98734.17.
PubMed 15280635
Study at a glance
From the registry record, last updated by the sponsor on 12 Oct 2016. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Chemical Exposures and Leukemia Risks and Childhood Leukemia and Environmental Exposure
- ClinicalTrials.gov ID
- NCT00015587
- Acronym / sponsor ID
- CCLS / 9137-CP-001
- Conditions
- Leukemia, Acute Myelocytic Leukemia, Acute Lymphoblastic Leukemia, Acute Myelogenous Leukemia
- Keywords
- Molecular Epidemiology, Case Control
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 3,523 participants (actual)
- Lead sponsor
- National Institute of Environmental Health Sciences (NIEHS)US National Institutes of Health
- Collaborators
- National Cancer Institute (NCI)
- Study start
- Apr 1995
- Primary completion
- Jul 2016 (actual)
- Study completion
- Jul 2016 (actual)
- First posted
- 25 Apr 2001 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
This study is a case-control study investigating the causes of childhood leukemia in Northern California. The overall purpose of this epidemiologic study is to find specific genetic or environmental factors that may increase the risk of leukemia in children. The study is being conducted by Patricia Buffler, PhD at the School of Public Health - University of California Berkeley in collaboration with the California Department of Health Services and 16 hospitals located throughout the state of California. The study began in 1995 and will continue to 2014.
Detailed description
This study is a case-control study of incident childhood leukemia (all subtypes) diagnosed since mid-1995. Children newly diagnosed with leukemia are enrolled in the study. Criteria for inclusion in the study are: under 15 years of age, no prior cancer diagnosis, residency in the state of California at the time of diagnosis, and availability of an English or Spanish speaking parent or guardian. Pre-treatment biological specimens, including bone marrow and peripheral blood, are obtained for analysis in the UCB lab of Dr M. Smith. The lab will use Fluorescence In Situ Hybridization (FISH) to detect chromosome specific aneuploidy and translocations. A number of chromosomal translocations, including t(9;22) and t(8;21), are known to be centrally involved in the development of childhood leukemia. Molecular characterization of the cases with translocations may provide insight into the timing of critical exposures and the nature of the etiological agent involved.
One comparison subject (control) is recruited for each consenting case. For each case, four potential controls are randomly selected from California birth certificate files and matched on date of birth, gender, mother's race, parental Hispanicity, and county of residence. One of the four birth certificate controls is randomly selected to be recruited to participate in the study.
An in-depth personal interview asks a variety of questions, including: residential history; occupational and household exposure histories; mothers' reproductive history; events during index pregnancy and delivery; family history of illness; child's health and vaccination history, contact with other children; maternal and child exposure to cigarette smoke during pregnancy and since birth; maternal and child history of x-rays.
Saliva specimens are obtained from both cases and controls and their biological mothers. The saliva samples are sent to the study office and processed in the Genetic Epidemiology lab at UC Berkeley. DNA from cases and controls will be analyzed by polymerase chain reaction for genetic polymorphisms. Genetic polymorphisms will be examined in two glutathione transferase genes, M1 and Tl. Case samples of peripheral blood, bone marrow, and archived newborn blood will be also used to detect N-ras mutation.
Three tiers of an exposure assessment are being implemented. Tier 1 enrolls and interviews cases and controls seeking to identify risk factors, including residential and occupational chemical exposures. In Tier 2, cases and birth certificate controls that have not changed residence based on specific criteria are part of a reliability study, which seeks to determine if self-reported chemicals used at the time of interview are found in the home during a visual survey several months after interview. Tier 3 aims to document the potential for household exposures by sampling dust on the floor surfaces. The objective is to identify if there are differences in concentrations of pesticides, metals, polyaromatic hydrocarbons, cotinine, polychorinated biphenyls, and ethylenethiourea in the homes of cases and controls. Further, a case-case analysis will identify if cases with chromosomal translocations of interest live in homes with higher concentrations of target compounds than cases that do not have such translocations. These analyses will determine whether leukemic children with common genetic changes experience common exposures and whether these genetic changes have approximately the same temporal occurrence. Finally, we will evaluate whether children with and without leukemia differ with respect to susceptibility.
Study design
- Observational model
- Case-control
- Time perspective
- Prospective
Who may qualify
- Ages
- 1 day to 14 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Child
- Study population
- Children diagnosed with leukemia and matched controls
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Outcome of study
Time frame: duration of study
Using a case-control study design, we are studying the role of environmental and genetic factors in the etiology of a rare cancer in a vulnerable and ethnically diverse population, using an integrated multi-disciplinary approach to improve disease classification and exposure assessment.
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 12 Oct 2016.
- Results publication: PubMed 11753612Xiao Z, Greaves MF, Buffler P, Smith MT, Segal MR, Dicks BM, Wiencke JK, Wiemels JL. Molecular characterization of genomic AML1-ETO fusions in childhood leukemia. Leukemia. 2001 Dec;15(12):1906-13. doi: 10.1038/sj.leu.2402318.
- Results publication: PubMed 11401921Zheng S, Ma X, Buffler PA, Smith MT, Wiencke JK. Whole genome amplification increases the efficiency and validity of buccal cell genotyping in pediatric populations. Cancer Epidemiol Biomarkers Prev. 2001 Jun;10(6):697-700.
- Results publication: PubMed 12204832Ma X, Buffler PA, Gunier RB, Dahl G, Smith MT, Reinier K, Reynolds P. Critical windows of exposure to household pesticides and risk of childhood leukemia. Environ Health Perspect. 2002 Sep;110(9):955-60. doi: 10.1289/ehp.02110955.
- Results publication: PubMed 11986774Ma X, Buffler PA, Selvin S, Matthay KK, Wiencke JK, Wiemels JL, Reynolds P. Daycare attendance and risk of childhood acute lymphoblastic leukaemia. Br J Cancer. 2002 May 6;86(9):1419-24. doi: 10.1038/sj.bjc.6600274.
- Results publication: PubMed 11882484Reynolds P, Von Behren J, Gunier RB, Goldberg DE, Hertz A, Harnly ME. Childhood cancer and agricultural pesticide use: an ecologic study in California. Environ Health Perspect. 2002 Mar;110(3):319-24. doi: 10.1289/ehp.02110319.
- Results publication: PubMed 12296514Reynolds P, Von Behren J, Gunier RB, Goldberg DE, Hertz A, Smith D. Traffic patterns and childhood cancer incidence rates in California, United States. Cancer Causes Control. 2002 Sep;13(7):665-73. doi: 10.1023/a:1019579430978.
- Results publication: PubMed 12415113Wiemels JL, Leonard BC, Wang Y, Segal MR, Hunger SP, Smith MT, Crouse V, Ma X, Buffler PA, Pine SR. Site-specific translocation and evidence of postnatal origin of the t(1;19) E2A-PBX1 fusion in childhood acute lymphoblastic leukemia. Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):15101-6. doi: 10.1073/pnas.222481199. Epub 2002 Nov 1.
- Results publication: PubMed 11986239Wiemels JL, Xiao Z, Buffler PA, Maia AT, Ma X, Dicks BM, Smith MT, Zhang L, Feusner J, Wiencke J, Pritchard-Jones K, Kempski H, Greaves M. In utero origin of t(8;21) AML1-ETO translocations in childhood acute myeloid leukemia. Blood. 2002 May 15;99(10):3801-5. doi: 10.1182/blood.v99.10.3801.
- Results publication: PubMed 12951583Greaves MF, Wiemels J. Origins of chromosome translocations in childhood leukaemia. Nat Rev Cancer. 2003 Sep;3(9):639-49. doi: 10.1038/nrc1164.
- Results publication: PubMed 12756163McHale CM, Wiemels JL, Zhang L, Ma X, Buffler PA, Feusner J, Matthay K, Dahl G, Smith MT. Prenatal origin of childhood acute myeloid leukemias harboring chromosomal rearrangements t(15;17) and inv(16). Blood. 2003 Jun 1;101(11):4640-1. doi: 10.1182/blood-2003-01-0313. No abstract available.
- Results publication: PubMed 12661004McHale CM, Wiemels JL, Zhang L, Ma X, Buffler PA, Guo W, Loh ML, Smith MT. Prenatal origin of TEL-AML1-positive acute lymphoblastic leukemia in children born in California. Genes Chromosomes Cancer. 2003 May;37(1):36-43. doi: 10.1002/gcc.10199.
- Results publication: PubMed 12571459Pine SR, Moy FH, Wiemels JL, Gill RK, Levendoglu-Tugal O, Ozkaynak MF, Sandoval C, Jayabose S. Real-time quantitative PCR: standardized detection of minimal residual disease in pediatric acute lymphoblastic leukemia. Polymerase chain reaction. J Pediatr Hematol Oncol. 2003 Feb;25(2):103-8. doi: 10.1097/00043426-200302000-00004.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Catherine Metayer, MD, PhD principal investigator
University of California Berkeley, School of Public Health
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Leukemia and Acute Myelocytic Leukemia, run by National Institute of Environmental Health Sciences (NIEHS) at 1 site in United States.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 12 Oct 2016. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Outcome of study (time frame: duration of study). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT00015587, which also lists 86 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 12 Oct 2016.