The main objective of this core Is the enrollment of every patient AML and MDS referred to Washington University into the Tissue Acquisition and Clinical Database protocol of the GAML program project. Skin, oral mucosa, bone marrow, peripheral blood leukocytes and serum specimens collected from patients will be banked and processed by Core B, the Specimen Acquisition, Genomic, Transcriptomic, and Epigenetic Profiling Core, whereupon they will serve as the basis for genomic analyses outlined In Core C, to be utilized in Projects 1-4. This Clinical Core will also maintain and expand a comprehensive database that captures essential clinical, pathological, karyotypic, molecular, therapeutic, and outcomes data of enrolled AML and MDS patients, anonymously linked with the corresponding tissue specimens. The Clinical Core database will provide key clinical annotation that, in conjunction with gene expression data generated by Core B and DNA sequence data generated by Core C, which will be utilized by Projects 1-4. A.1.
Specific Aim 1 : We will prospectively collect and bank tissue for analysis at diagnosis, in remission, and at relapse from every patient referred to the Washington University Siteman Cancer Center with AML and MDS. A.2.
Specific Aim2 : We will maintain a comprehensive clinical leukemia database that will capture epidemiological data, disease-related characteristics, prognostic factors, therapeutic information, and outcomes data from all enrolled AML and MDS patients, with de-identified linkage to corresponding banked tissue specimens.

Public Health Relevance

The specimens collected and the database maintained by Core A are essential to the success of Projects 1- 4 outlined in this proposal. These have served as a unique and invaluable resource both for this Program Project since Its inception, and for extramural projects (TCGA) as well.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
5P01CA101937-11
Application #
8696963
Study Section
Special Emphasis Panel (ZCA1-RPRB-J)
Project Start
Project End
Budget Start
2014-04-01
Budget End
2015-03-31
Support Year
11
Fiscal Year
2014
Total Cost
$258,926
Indirect Cost
$101,870
Name
Washington University
Department
Type
DUNS #
068552207
City
Saint Louis
State
MO
Country
United States
Zip Code
63130
Jacoby, Meagan A; Duncavage, Eric J; Chang, Gue Su et al. (2018) Subclones dominate at MDS progression following allogeneic hematopoietic cell transplant. JCI Insight 3:
Warner, Wayne A; Spencer, David H; Trissal, Maria et al. (2018) Expression profiling of snoRNAs in normal hematopoiesis and AML. Blood Adv 2:151-163
Bansal, Dhruv; Vij, Kiran; Chang, Gue Su et al. (2018) Lenalidomide results in a durable complete remission in acute myeloid leukemia accompanied by persistence of somatic mutations and a T-cell infiltrate in the bone marrow. Haematologica 103:e270-e273
Xia, Jun; Miller, Christopher A; Baty, Jack et al. (2018) Somatic mutations and clonal hematopoiesis in congenital neutropenia. Blood 131:408-416
Duncavage, Eric J; Jacoby, Meagan A; Chang, Gue Su et al. (2018) Mutation Clearance after Transplantation for Myelodysplastic Syndrome. N Engl J Med 379:1028-1041
Schroeder, Mark A; Choi, Jaebok; Staser, Karl et al. (2018) The Role of Janus Kinase Signaling in Graft-Versus-Host Disease and Graft Versus Leukemia. Biol Blood Marrow Transplant 24:1125-1134
Christopher, Matthew J; Petti, Allegra A; Rettig, Michael P et al. (2018) Immune Escape of Relapsed AML Cells after Allogeneic Transplantation. N Engl J Med 379:2330-2341
Trissal, Maria C; Wong, Terrence N; Yao, Juo-Chin et al. (2018) MIR142 Loss-of-Function Mutations Derepress ASH1L to Increase HOXA Gene Expression and Promote Leukemogenesis. Cancer Res 78:3510-3521
Fisher, D A C; Malkova, O; Engle, E K et al. (2017) Mass cytometry analysis reveals hyperactive NF Kappa B signaling in myelofibrosis and secondary acute myeloid leukemia. Leukemia 31:1962-1974
Shirai, Cara Lunn; White, Brian S; Tripathi, Manorama et al. (2017) Mutant U2AF1-expressing cells are sensitive to pharmacological modulation of the spliceosome. Nat Commun 8:14060

Showing the most recent 10 out of 122 publications