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  1. 1. Essai clinique
  2. 2. Routinedokumentation
  3. 3. Études de registres/cohortes
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Modèles de données sélectionnés

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329 Résultats de recherche.
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Radiation Therapy Oncology Group Initial Follow-up Form Phase III Lung Prophylactic Cranial RT NCT00048997

- 20/09/2021 - 1 Formulaire, 3 Groupes Item, 46 Eléments de données, 1 Langue
Groupes Item: Header Module, Medical history, Comments
Radiation Therapy Oncology Group Initial Follow-up Form Phase III Lung Prophylactic Cranial RT Radiation Therapy in Preventing CNS Metastases in Patients With Non-Small Cell Lung Cancer NCT00048997 Source Form: NCI FormBuilder: https://formbuilder.nci.nih.gov/FormBuilder/formDetailsAction.do?method=getFormDetails&formIdSeq=9EC372A6-7094-05D5-E034-080020C9C0E0

Southwest Oncology Group Registration Form

- 20/09/2021 - 1 Formulaire, 4 Groupes Item, 30 Eléments de données, 1 Langue
Groupes Item: SWOG clinical trial administrative data, patient demographics, Notes, CCRR MODULE
Southwest Oncology Group Registration Form Source Form: NCI FormBuilder: https://formbuilder.nci.nih.gov/FormBuilder/formDetailsAction.do?method=getFormDetails&formIdSeq=A4CF746B-17EF-3705-E034-080020C9C0E0

ECOG 4599 Toxicity Form

- 28/05/2015 - 1 Formulaire, 1 Groupe Item, 27 Eléments de données, 1 Langue
Groupe Item: ECOG clinical trial administrative data
ECOG 4599 Toxicity Form Source Form: NCI FormBuilder: https://formbuilder.nci.nih.gov/FormBuilder/formDetailsAction.do?method=getFormDetails&formIdSeq=A16E9046-8508-5FB4-E034-080020C9C0E0

ECOG 4599 Treatment Form

- 28/05/2015 - 1 Formulaire, 1 Groupe Item, 30 Eléments de données, 1 Langue
Groupe Item: ECOG treatment data
ECOG 4599 Toxicity Form Source Form: NCI FormBuilder: https://formbuilder.nci.nih.gov/FormBuilder/formDetailsAction.do?method=getFormDetails&formIdSeq=A16E9DCC-CE6C-6087-E034-080020C9C0E0

dbGaP phs001192 Thoracic Patient-Derived Xenografts - pht005690.v1.p1

- 01/06/2023 - 3 Formulaires, 1 Groupe Item, 5 Eléments de données, 1 Langue
Groupe Item: pht005690
Principal Investigator: John Thomas Poirier, PhD, Memorial Sloan Kettering Cancer Center, New York, NY, USA MeSH: Lung Neoplasms https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001192 Targeted capture sequencing of 341 cancer associated genes in thoracic patient-derived xenografts.

pht005691.v1.p1

1 Groupe Item 5 Eléments de données

pht005692.v1.p1

1 Groupe Item 9 Eléments de données

dbGaP phs001210 NCI Lung Cancer and Smoking Phenotypes in African-American Subjects - pht005961.v1.p1

- 17/05/2023 - 5 Formulaires, 1 Groupe Item, 3 Eléments de données, 1 Langue
Groupe Item: pht005961
Principal Investigator: Curtis C. Harris, National Institutes of Health, Bethesda, MD, USA MeSH: Lung Neoplasms https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001210 This is a two-stage case-control study designed to evaluate the association between common genetic variants and the risk of lung cancer. The stage 1 studies included 1737 cases and 3602 controls from the following studies: MD Anderson Lung Cancer Epidemiology Study, The Multiethnic Cohort Study (MEC), NCI-MD Lung Cancer-Case Control Study, Northern California Lung Cancer Study, Project CHURCH (Creating a Higher Understanding of Cancer Research δ Community Health), Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO), Southern Community Cohort Study (SCCS), and the Karmanos Cancer Institute at Wayne State University (KCI/WSU). The stage 2 studies included an independent set of 866 cases and 796 controls from the following studies: The Black Women's Health Study (BWHS), The Harvard-MGH Lung Cancer Susceptibility Study (HLCS), MD Anderson Lung Cancer Epidemiology Study, MD Anderson/LBJ Hospital Biorepository, NCI-MD Lung Cancer Case-Control Study, Northern California Lung Cancer Study, Philadelphia Lung Cancer Study on Gene Environment Interactions (Plus-Gene), Southern Community Cohort Study (SCCS), and KCI/WSU.

pht005962.v1.p1

1 Groupe Item 3 Eléments de données

pht005963.v1.p1

1 Groupe Item 9 Eléments de données

Eligibility

1 Groupe Item 1 Élément de données

pht005964.v1.p1

1 Groupe Item 5 Eléments de données

dbGaP phs001249 Chemosensitive Relapse in Small Cell Lung Cancer Patient-Derived Xenografts - pht006175.v1.p1

- 23/03/2023 - 3 Formulaires, 1 Groupe Item, 5 Eléments de données, 1 Langue
Groupe Item: pht006175
Principal Investigator: John Thomas Poirier, PhD, Memorial Sloan Kettering Cancer Center, New York, NY, USA MeSH: Lung Neoplasms https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001249 Genetic and epigenetic analysis of patient-derived xenograft models of acquired chemoresistance in small cell lung cancer.

pht006176.v1.p1

1 Groupe Item 5 Eléments de données

pht006177.v1.p1

1 Groupe Item 11 Eléments de données

Radiation Therapy Oncology Group Follow-up Form Phase III Lung Prophylactic Cranial RT 10363 NCT00048997

- 20/09/2021 - 1 Formulaire, 3 Groupes Item, 44 Eléments de données, 1 Langue
Groupes Item: Header Module, Patient medical history, Comments
Radiation Therapy Oncology Group Follow-up Form Phase III Lung Prophylactic Cranial RT 10363 Radiation Therapy in Preventing CNS Metastases in Patients With Non-Small Cell Lung Cancer NCT00048997 Source Form: NCI FormBuilder: https://formbuilder.nci.nih.gov/FormBuilder/formDetailsAction.do?method=getFormDetails&formIdSeq=9EC372A6-6F06-05D5-E034-080020C9C0E0

dbGaP phs000728 Lung Cancer Susceptibility in Smokers - pht003768.v1.p1

- 13/12/2022 - 3 Formulaires, 1 Groupe Item, 4 Eléments de données, 1 Langue
Groupe Item: pht003768
Principal Investigator: Susan K. Dutcher, PhD, Washington University School of Medicine, St. Louis, MO, USA MeSH: Lung Neoplasms https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000728 Over 85% of all patients diagnosed with lung cancer report a history of tobacco use, though only 10% of tobacco smokers eventually develop lung cancer. Epidemiologic studies have shown that family members of patients with lung cancer have a higher risk of developing lung cancer than controls. In an effort to identify variants associated with tobacco induced lung cancer, we have sequenced germline DNA from affected and unaffected members of families with strong histories of tobacco related lung cancer.

pht003766.v1.p1

1 Groupe Item 2 Eléments de données

pht003767.v1.p1

1 Groupe Item 3 Eléments de données

dbGaP phs000753 High Density SNP Association Analysis of Lung Cancer - Eligibility

- 07/12/2022 - 5 Formulaires, 1 Groupe Item, 4 Eléments de données, 1 Langue
Groupe Item: IG.elig
Principal Investigator: Chris Amos, PhD, Geisel School of Medicine, Dartmouth College, Lebanon, NH, USA MeSH: Lung Neoplasms https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000753 This research builds upon an extensive resource of a case-control study that has been ongoing at the UT MD Anderson Cancer Center since 1991. To identify risk variants for lung cancer, we conducted a genome-wide association study. Cases are newly diagnosed, histologically-confirmed patients presenting at MD Anderson Cancer and who had not previously received treatment other than surgery. Controls are healthy individuals seen for routine care at Kelsey-Seybold Clinics, the largest physician group-practice plan in the Houston Metropolitan area. This lung GWAS led to the identification of a susceptibility locus for lung cancer at 15q25.1. We used data from 315,450 tagging SNPs in 1,154 current and former (ever) smoking cases of European ancestry and 1,137 frequency-matched, ever-smoking controls from Houston, Texas in the discovery followed by the replication of the ten SNPs most significantly associated with lung cancer in an additional 711 cases and 632 controls from Texas and 2,013 cases and 3,062 controls from the UK. Two SNPs, rs1051730 and rs8034191, were significantly associated with risk of lung cancer with combined analysis yielded odds ratios of 1.32 (P 1X10-17) for both SNPs. These two SNPs mapped to a region of strong linkage disequilibrium within 15q25.1 containing PSMA4 and the nicotinic acetylcholine receptor subunit genes CHRNA3 and CHRNA5. (Nat Genet. 2008 May;40(5):616-22. PMID:18385676)

pht003874.v1.p1

1 Groupe Item 5 Eléments de données

pht003875.v1.p1

1 Groupe Item 5 Eléments de données

pht003876.v1.p1

1 Groupe Item 6 Eléments de données

pht003877.v1.p1

1 Groupe Item 4 Eléments de données

dbGaP phs000629 GWAS of Familial Lung Cancer - pht003388.v1.p1

- 29/11/2022 - 5 Formulaires, 1 Groupe Item, 5 Eléments de données, 1 Langue
Groupe Item: pht003388
Principal Investigator: Ann G. Schwartz, PhD, MPH, Karmanos Cancer Institute, Wayne State University, Detroit, MI, USA MeSH: Lung Neoplasms https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000629 Familial lung cancer cases were collected by the Genetic Epidemiology of Lung Cancer Consortium (GELCC) recruitment sites: University of Cincinnati, Karmanos Cancer Institute at Wayne State University, Louisiana State University Health Sciences Center-New Orleans, Mayo Clinic, and Medical College of Ohio. Familial cases for this study came from three sources: 1) one case each from families (at least 3 affected lung cancer cases in the family) included in the linkage analysis; 2) one case from linkage-eligible families (at least 3 affected lung cancer cases in the family) but where there were insufficient biospecimens available to make them informative for linkage analysis; and 3) one case from families not eligible for the linkage study with a family history of at least one first or second degree relative affected with lung cancer. Unrelated controls were selected from 1) among the spouses of family members, thus matching on socio-economic status (SES) and ethnicity (typically) of the cases or 2) from case-control studies of lung cancer conducted in the same location in which the linkage families were collected and matched on age, sex, and race. All cases and controls self-reported as European American. Biospecimens used for normal DNA extraction included blood, saliva or mouthwash. Some samples underwent whole genome amplication.

Eligibility

1 Groupe Item 1 Élément de données

pht003386.v1.p1

1 Groupe Item 5 Eléments de données

pht003387.v1.p1

1 Groupe Item 8 Eléments de données

pht003385.v1.p1

1 Groupe Item 4 Eléments de données

dbGaP phs000634 NCI GWAS of Lung Cancer in Never Smokers - pht003829.v1.p1

- 25/11/2022 - 5 Formulaires, 1 Groupe Item, 5 Eléments de données, 1 Langue
Groupe Item: pht003829
Principal Investigator: Olga Gorlova, PhD, UT MD Anderson Cancer Center, Houston, TX MeSH: Lung Neoplasms https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000634 *A genomewide study of lung cancer in never smokers* *Abstract and specific aims* In the United States, lung cancer incidence and mortality rates have been steadily declining over the past decade, following decline in the prevalence of tobacco smoking. However, lung cancer remains the leading cause of cancer death, killing more patients than breast, colon, and prostate cancers combined. Although tobacco smoke is the predominant risk factor for development of lung cancer, some patients develop the disease without a history of tobacco smoking. About 10 - 15% of all lung cancers occur in lilfetime never smokers. This figure will increase as the proportion of never smokers increases in the population. Even at present rates, lung cancer in never smokers, if considered a separate disease, is 6th to 8th top cause of cancer death. The growing number of never smokers in the USA and other countries emphasizes the importance of understanding the epidemiology and biology underlying lung cancer in this group. Genetic polymorphisms associated with the risk of lung cancer in never smokers are expected to overlap with those associated with the risk of lung cancer in ever smokers only partially. Epidemiological, molecular and clinical data suggest that molecular mechanisms of LC may differ in smokers and non-smokers, implying that lung cancer in never smokers is a different disease compared to the lung cancer in smokers. One can expect that there should be stronger genetic component in the control lung cancer in never smokers because effects of the genetic factors in never smokers are unmasked by the lack of tobacco smoke exposure. The genetic epidemiology of lung cancer in never smokers has not been well explored, largely because of difficulties in accruing the needed sample size for association studies. We propose a multicenter (total 14 sites from the US and Europe) genomewide association study of lung cancer in never smokers with the following specific aims: *Aim 1: To identify candidate SNPs influencing risk for lung cancer in never smokers using Discovery sample.* In the Discovery phase we will genotype 1256 Caucasian cases and 1365 age- and gender-matched never smoker controls using the Illumina Human660W-Quad platform. In addition, we will include in the analysis 284 cases and 175 matched controls already genotyped on the 610Quad platform. In this phase we will only include the study sites that have collected blood specimens (MDACC, Mayo Clinic, Karmanos Cancer Institute, The University of Liverpool Cancer research Centre, Institute of Cancer Research in Sutton, and Lunenfeld Research Institute in Toronto, Canada). All the samples will be sent to the independent lab for genotyping, to reduce site-specific technical artifacts. The final sample will consist of 1540 cases and 1540 controls matched by study site. *Aim 2: To perform the second phase (validation) analysis of significant SNPs identified in aim 1 using an independent set of cases and controls.* SNPs associated with risk at the significance level of 0.01 or below in the discovery set will be included in the replication phase. The proposed threshold guarantees an adequate power to retain SNPs with the typical effect size of 1.3. We plan to carry 6000-7000 SNPs for validation. The independent replication set will include 800 cases and 800 controls, mostly from sites that collected tissue (Mayo Clinic, Karmanos Cancer Institute, UT Southwestern) or buccal specimens (UCLA), but also blood samples (Imperial College London, University of Pennsylvana, German Cancer Research Center, Heidelberg, National Research Center for Environment and Health, Neuherberg, Carmel Medical Center, Haifa). We will then perform a joint analysis to test the significance of the SNPs identified in the first stage using a stringent critical p-value of 10-7. There will be 2340 cases and 2340 controls in the joint set. Based on our experience with GWAS in smokers and assuming that genetic component in lung cancer risk in never smokers can be higher than genetic component in smokers, we expect to identify about 5-10 candidate regions associated with lung cancer risk in never smokers. *Aim 3: To identify and explore pathways associated with the risk of lung cancer in never smokers.* Results of the number of studies on the molecular mechanisms and drug response suggest that lung cancer in never smokers is a different disease and different pathways will be associated with lung cancer risk in non-smokers and smokers. To identify pathways and molecular functions associated with lung cancer risk in never smokers we will apply Ingenuity and DAVID bioinformatics tools. We will use at least 300 top candidate genes identified in joint and discovery analysis. The reason why we select rather large number of candidate genes for functional annotation is two-fold: 1. Both algorithms are looking for enrichment of pathways and function by most significant genes and they produce statistically robust results only when number of genes is relatively high. 2. Despite the fact that this study will be largest possible for never smokers we still are underpowered to detect SNPs with relatively small effect size. But though those SNPs will not reach genome wide level of significance they will tend to be on the top of the list. In other words genes from the gray zone (significant on individual level and non-significant for genome wide level) are expected to be enriched by true discoveries. True discoveries are likely to be associated with limited number of pathways / functions while false positives are expected to be uniformly distributed across functions and pathways. Therefore significant clustering of the gene to a given function will suggest that that those genes are true discoveries. This is the first GWAS aiming at identifying the genetic control of susceptibility to lung cancer in Caucasian never smokers. We will combine the available resources from the multiple sites to achieve the sample size sufficient for this study. The study will identify genetic architecture of the predisposition to the lung cancer in never smokers.

Eligibility

1 Groupe Item 1 Élément de données

pht003830.v1.p1

1 Groupe Item 3 Eléments de données

pht003831.v1.p1

1 Groupe Item 14 Eléments de données

pht003832.v1.p1

1 Groupe Item 4 Eléments de données

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