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Clinical survey Micafungin Phase NIT

- 5/8/16 - 1 Formulaire, 29 Groupes Item, 267 Eléments de données, 1 Langue

Groupes Item: Medical History (PGID 272) , Diseases, conditions , Treatment, Indication for treatment, Treatment target, Involved sites, Risk Factors, APACHE Score, Immunosuppressants, Types of isolation, Other Antifungals BEFORE initiation, Other Antifungals AFTER initiation, Temperature, Diagnostic procedures, Sites of Mycosis, CT finding, Sites of Mycosis, MRT finding, Sites of Mycosis, Sonography finding, Sites of Mycosis, Fundoscopy finding, Sites of Mycosis, microbiological culture finding, Sites of Mycosis, Tissue specimen finding, Method of biopsy, Micafungin Treatment (PGID 280), CYP450 inductors DURING treatment, Breakthrough Infections (PGID 281), Adverse Events, Laboratory Parameters (PGID 283) , Outcome Micafungin (PGID 284) , Other Antifungal, Outcome Final Antifungal Treatment (PGID 286), Follow Up (PGID 287)

Clinical survey Micafungin Phase NIT Principal Investigator PD Dr. Jörg Janne Vehreschild, Universitätsklinikum Köln Licence:CC-BY

dbGaP phs000913 Genomic Analysis of Mycosis Fungoides and Sézary Syndrome - Eligibility

- 14/4/24 - 5 Formulaires, 1 Groupe Item, 1 Élément de données, 1 Langue

Groupe Item: IG.elig

Principal Investigator: Paul A. Khavari, MD, PhD, Stanford University, Stanford, CA USA MeSH: Mycosis Fungoides,Sezary Syndrome https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000913 Mycosis Fungoides (MF) and Sézary Syndrome (Sz) comprise the majority of Cutaneous T-Cell Lymphoma (CTCL) cases and are characterized by clinical heterogeneity. This array of symptoms includes skin patches, plaques and tumors as well as blood involvement and erythroderma. Because the genetic basis of CTCL is still poorly understood, we performed whole-exome sequencing on 11 MF/Sz samples and their matched, normal control DNA. Upon analyzing this data, we distilled a list of an additional 494 genes to be sequenced at depth. The majority of these 494 genes were sequenced in the exons alone, however, for a small subset of these genes we sequenced the entire genomic locus in search of structural variation events. This 494 gene targeted resequencing effort was performed upon 72 patients with MF/Sz and their matched, normal control DNA. An additional 5 MF/Sz and matched, normal DNA samples underwent whole genome amplification (WGA) prior to library preparation, which appears to have introduced mutations into these samples, however we also include them here. We additionally include 10 MF/Sz samples without a matched, normal control samples, 1 of which underwent WGA. In addition to primary disease samples, we also performed targeted resequencing on 4 CTCL cell lines (HH, MyLa, SeAx and Hut78) as well as on H9 cells (a subclone of Hut78 cells) and Jurkat cells, a T-ALL derived cell line that was used as an experimental system for our work. In sum, this data deposition includes exome and/or targeted resequencing from 92 individuals with 192 samples submitted.

pht004893.v1.p1

1 Groupe Item 2 Eléments de données

pht004894.v1.p1

1 Groupe Item 5 Eléments de données

pht004895.v1.p1

1 Groupe Item 4 Eléments de données

pht004896.v1.p1

1 Groupe Item 6 Eléments de données

dbGaP phs000994 The Mutational Landscape of CTCL and Sezary Syndrome. - pht005062.v1.p1

- 13/11/23 - 4 Formulaires, 1 Groupe Item, 5 Eléments de données, 1 Langue

Groupe Item: pht005062

Principal Investigator: Teresa Palomero, Columbia University, New York, NY, USA MeSH: Sezary Syndrome,Mycosis Fungoides https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000994 Sezary syndrome is a leukemic and aggressive form of cutaneous T-cell lymphoma (CTCL) resulting from the malignant transformation of skin-homing central memory CD4+ T cells. To identify new genetic alterations involved in Sezary syndrome and CTCL transformation we performed whole-exome sequencing of tumor-normal sample pairs from 26 Sezary syndrome and 16 CTCL patients. These analyses revealed a distinctive pattern of somatic copy number alterations in Sezary syndrome including highly prevalent recurrent chromosomal deletions involving the TP53, RB1, PTEN, DNMT3A, and CDKN1B tumor suppressor genes. Mutation analysis identified a broad spectrum of somatic mutations involving key genes involved in epigenetic regulation (TET2, CREBBP, MLL3, BRD9, SMARCA4 and CHD3) and signaling, including mutations in MAPK1, BRAF, CARD11 and PRKG1 driving increased MAPK, NFKB and NFAT activity upon T-cell receptor stimulation. Collectively, our findings provide new insights into the genetics of Sezary syndrome and CTCL and support the development of personalized therapies targeting key oncogenically activated signaling pathways for the treatment of these diseases.

pht005063.v1.p1

1 Groupe Item 5 Eléments de données

pht005064.v1.p1

1 Groupe Item 3 Eléments de données

pht005065.v1.p1

1 Groupe Item 8 Eléments de données

Baseline-Imaging Stem-Cell Transplantation CASLAMB NCT00148148

- 26/11/15 - 1 Formulaire, 5 Groupes Item, 15 Eléments de données, 2 Langues

Groupes Item: Chest X-ray, High Resolution Computed Tomography (HRCT) of the Lung, Other methods, Other examinations, Detection of infection status

A Study of Caspofungin, Liposomal Amphotericin B or the Combination of Both for Patients After Stem-Cell Transplantation NCT00148148

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