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Relevancia Evaluación Nuevo primero Antiguo primero

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

- 29/11/22 - 5 formularios, 1 itemgroup, 5 items, 1 idioma
Itemgroup: 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 itemgroup 1 item

pht003386.v1.p1

1 itemgroup 5 items

pht003387.v1.p1

1 itemgroup 8 items

pht003385.v1.p1

1 itemgroup 4 items

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

- 25/11/22 - 5 formularios, 1 itemgroup, 5 items, 1 idioma
Itemgroup: 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 itemgroup 1 item

pht003830.v1.p1

1 itemgroup 3 items

pht003831.v1.p1

1 itemgroup 14 items

pht003832.v1.p1

1 itemgroup 4 items

dbGaP phs000299 Genentech Lung Cancer Sequencing - pht001553.v2.p1

- 12/10/22 - 6 formularios, 1 itemgroup, 5 items, 1 idioma
Itemgroup: pht001553
Principal Investigator: Zemin Zhang, PhD, Genentech Inc., South San Francisco, CA, USA MeSH: Lung Neoplasms,Carcinoma, Non-Small-Cell Lung https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000299 Version 1 Whole genome sequencing was applied to tumor and adjacent normal lung tissue in an individual non-small-cell lung cancer patient. We present an analysis of somatic changes identified throughout the tumor genome, including single-nucleotide variants, copy number variants, and large-scale chromosomal rearrangements. Over 50,000 high-confidence single-nucleotide variants were identified, revealing evidence of substantial smoking-related DNA damage as well as distinct mutational pressures within the tumor resulting in uneven distribution of somatic mutations across the genome. Version 2 Lung cancer is a highly heterogeneous disease in terms of both underlying genetic lesions and response to therapeutic treatments. We performed deep whole genome sequencing and transcriptome sequencing on 19 lung cancer cell lines and 3 lung tumor/normal pairs. Overall, our data show that cell line models exhibit similar mutation spectra to human tumor samples. Smoker and never-smoker cancer samples exhibit distinguishable patterns of mutations. A number of epigenetic regulators are frequently altered by mutations or copy number changes. A systematic survey of splice-site mutations identified over 100 splice site mutations associated with cancer specific aberrant splicing, including mutations in several known cancer-related genes. Differential usages of splice isoforms were also studied. Taken together, these data present a comprehensive genomic landscape of a large number of lung cancer samples and further demonstrate that cancer specific alternative splicing is a widespread phenomenon that has potential utility as therapeutic biomarkers.

pht001881.v2.p1

1 itemgroup 2 items

pht001882.v2.p1

1 itemgroup 7 items

pht001551.v2.p1

1 itemgroup 5 items

pht001552.v2.p1

1 itemgroup 5 items

Eligibility

1 itemgroup 4 items

dbGaP phs000336 DCEG Lung Cancer Study - pht002218.v1.p1

- 12/10/22 - 4 formularios, 1 itemgroup, 3 items, 1 idioma
Itemgroup: pht002218
Principal Investigator: Maria Teresa Landi, Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA MeSH: Lung Neoplasms,Smoking https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000336 Three genetic loci for lung cancer risk have been identified by genome-wide association studies (GWAS), but inherited susceptibility to specific histologic types of lung cancer is not well established. We conducted a GWAS of lung cancer and its major histologic types genotyping 515,922 single nucleotide polymorphisms (SNPs) in 5,739 incident lung cancer cases and 5,848 controls from one population-based case-control study and three cohort studies. Results were combined with summary data from 10 additional studies for a total of 13,300 cases and 19,666 controls of European descent. Four studies also provided histology data for replication resulting in 3,333 adenocarcinomas (AD), 2,589 squamous cell carcinomas (SQ), and 1,418 small cell carcinomas (SC). In analyses by histology, rs2736100 (*TERT*) on chromosome 5p15.33, was associated with risk of adenocarcinoma (OR=1.23, 95%CI=1.13-1.33, P=3.02x10sup-7/sup), but not other histologic types (OR=1.01, P=0.84, and OR=1.00, P=0.93, for SQ and SC, respectively). This finding was confirmed in each replication study and overall meta-analysis (OR=1.24, 95%CI=1.17-1.31, P=3.74x10sup-14/sup for AD and OR=0.99, P=0.69 and OR=0.97, P=0.48, for SQ and SC, respectively). Other previously reported association signals on 15q25 and 6p21 were also refined, but no additional loci reached genome-wide significance. In conclusion, a lung cancer GWAS identified a distinct hereditary contribution to adenocarcinoma. *Note: The lung study dataset to be released to dbGaP and caBIG excludes 47 individuals from the PLCO cohort who consented to participate only in cancer research projects and 22 individuals because of updated QC. Thus, the released dataset is derived from 11517 subjects, 5699 cases and 5818 controls. After the updated QC, the dataset to be released to dbGaP and caBIG includes 506062 SNPs.*

pht002219.v1.p1

1 itemgroup 2 items

pht002220.v1.p1

1 itemgroup 9 items

Eligibility

1 itemgroup 5 items

Eligibility Lung Cancer NCT02225405

- 18/11/21 - 1 formulario, 2 itemgroups, 27 items, 1 idioma
Itemgroups: Inclusion Criteria, Exclusion Criteria
Induction Study of Cisplatin, Docetaxel, and Nintedanib Stage IB-IIIA Non-Small Cell Lung Cancer (NCLC); ODM derived from: https://clinicaltrials.gov/show/NCT02225405

Eligibility Carcinoma, Non-Small-Cell Lung NCT00001499

- 17/11/21 - 1 formulario, 1 itemgroup, 20 items, 1 idioma
Itemgroup: Criteria
Phase II Neoadjuvant Trial of a Continuous Infusion of Paclitaxel Plus Cisplatin Followed by Chest Radiotherapy for Patients With Stage III Non-Small Cell Lung Cancer; ODM derived from: https://clinicaltrials.gov/show/NCT00001499

Follow-Up - Phase II Lung Cancer - Advanced Disease Follow-Up Form - 2399268v1.0 - Phase II Lung Cancer - Advanced Disease Follow-Up Form

- 27/9/21 - 1 formulario, 9 itemgroups, 36 items, 1 idioma
Itemgroups: CRF Header, Form Administration, Lung: Vital Status, Lung: Disease Follow-Up Status, Lung: Notice of Progression/Site, Lung: Subsequent Non-Protocol Therapy, Lung: Notice of New Primary, Lung: Long-Term Toxicity, Comments
Phase II Consortium Phase II Lung Cancer - Advanced Disease Follow-Up Form Source Form: NCI FormBuilder: https://formbuilder.nci.nih.gov/FormBuilder/formDetailsAction.do?method=getFormDetails&formIdSeq=FF8E0C9E-44F2-3242-E034-0003BA3F9857

Follow-Up - Phase II Lung Cancer - Localized Disease Follow-Up Form - 2402852v1.0 - Phase II Lung Cancer - Localized Disease Follow-Up Form

- 27/9/21 - 1 formulario, 9 itemgroups, 38 items, 1 idioma
Itemgroups: CRF Header, Form Administration, Lung: Vital Status, Lung: Disease Follow-Up Status, Lung: Notice of Progression/Site, Lung: Subsequent Non-Protocol Therapy, Lung: Notice of New Primary, Lung: Long-Term Toxicity, Comments
Phase II Consortium Phase II Lung Cancer - Localized Disease Follow-Up Form Source Form: NCI FormBuilder: https://formbuilder.nci.nih.gov/FormBuilder/formDetailsAction.do?method=getFormDetails&formIdSeq=00212490-27A3-4F0A-E044-0003BA3F9857

Lung Cancer NCT00096265 Quality of Life - PQ RTOG Phase III Multiple Brain Metastases Fact Subscale - 2277326v3.0 - PQ RTOG Phase III Multiple Brain Metastases Fact Subscale

- 27/9/21 - 1 formulario, 3 itemgroups, 43 items, 1 idioma
Itemgroups: Header, Physical Well-Being, Additional Concerns
PQ RTOG Phase III Multiple Brain Metastases Fact Subscale Radiation Therapy and Stereotactic Radiosurgery With or Without Temozolomide or Erlotinib in Treating Patients With Brain Metastases Secondary to Non-Small Cell Lung Cancer Source Form: NCI FormBuilder: https://formbuilder.nci.nih.gov/FormBuilder/formDetailsAction.do?method=getFormDetails&formIdSeq=D7FA7BFE-292F-6626-E034-0003BA12F5E7

Lung Cancer NCT00113386 On-Study - RTOG-0412 I1: Initial Evaluation Form - 2288131v3.0 - RTOG-0412 I1: Initial Evaluation Form

- 27/9/21 - 1 formulario, 3 itemgroups, 23 items, 1 idioma
Itemgroups: MODULE 1, PRE-TREATMENT CHACTERISTICS, LYMPH NODE ASSESSMENT
RTOG-0412 I1: Initial Evaluation Form Cisplatin and Docetaxel With or Without Radiation Therapy in Treating Patients Who Are Undergoing Surgery for Newly Diagnosed Stage III Non-Small Cell Lung Cancer Source Form: NCI FormBuilder: https://formbuilder.nci.nih.gov/FormBuilder/formDetailsAction.do?method=getFormDetails&formIdSeq=E489FECB-49D8-0477-E034-0003BA3F9857

Eligibility Lung Cancer NCT00955942

- 27/9/21 - 1 formulario, 1 itemgroup, 17 items, 1 idioma
Itemgroup: Criteria
Flaxseed Supplement in Treating Patients With Locally Advanced or Metastatic Non-Small Cell Lung Cancer Undergoing Chemotherapy and Radiation Therapy; ODM derived from: https://clinicaltrials.gov/show/NCT00955942

Treatment Summary NSCLC Stage III RTOG NCT00533949

- 20/9/21 - 1 formulario, 3 itemgroups, 36 items, 1 idioma
Itemgroups: RTOG clinical trial administrative data, Assessment of Chemotherapy, REPORT ALL CONTINUING OR NEW ADVERSE EVENTS
NCT00533949 TF: Radiation Therapy Oncology Group Phase III High-dose Vs Standard-dose Conformal XRT with Chemotherapy Treatment Summary Form High-Dose or Standard-Dose Radiation Therapy and Chemotherapy With or Without Cetuximab in Treating Patients With Newly Diagnosed Stage III Non-Small Cell Lung Cancer That Cannot Be Removed by Surgery Source Form: NCI FormBuilder: https://formbuilder.nci.nih.gov/FormBuilder/formDetailsAction.do?method=getFormDetails&formIdSeq=24FB4F78-9A8F-669C-E044-0003BA3F9857

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