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.
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.
|Al-Hussaini, Muneera; Rettig, Michael P; Ritchey, Julie K et al. (2016) Targeting CD123 in acute myeloid leukemia using a T-cell-directed dual-affinity retargeting platform. Blood 127:122-31|
|Welch, John S; Petti, Allegra A; Miller, Christopher A et al. (2016) TP53 and Decitabine in Acute Myeloid Leukemia and Myelodysplastic Syndromes. N Engl J Med 375:2023-2036|
|Wong, Terrence N; Miller, Christopher A; Klco, Jeffery M et al. (2016) Rapid expansion of preexisting nonleukemic hematopoietic clones frequently follows induction therapy for de novo AML. Blood 127:893-7|
|Griffith, Malachi; Griffith, Obi L; Krysiak, Kilannin et al. (2016) Comprehensive genomic analysis reveals FLT3 activation and a therapeutic strategy for a patient with relapsed adult B-lymphoblastic leukemia. Exp Hematol 44:603-13|
|Cole, Christopher B; Verdoni, Angela M; Ketkar, Shamika et al. (2016) PML-RARA requires DNA methyltransferase 3A to initiate acute promyelocytic leukemia. J Clin Invest 126:85-98|
|Churpek, Jane E; Pyrtel, Khateriaa; Kanchi, Krishna-Latha et al. (2015) Genomic analysis of germ line and somatic variants in familial myelodysplasia/acute myeloid leukemia. Blood 126:2484-90|
|Wong, Terrence N; Ramsingh, Giridharan; Young, Andrew L et al. (2015) Role of TP53 mutations in the origin and evolution of therapy-related acute myeloid leukaemia. Nature 518:552-5|
|Engle, E K; Fisher, D A C; Miller, C A et al. (2015) Clonal evolution revealed by whole genome sequencing in a case of primary myelofibrosis transformed to secondary acute myeloid leukemia. Leukemia 29:869-76|
|Griffith, Malachi; Miller, Christopher A; Griffith, Obi L et al. (2015) Optimizing cancer genome sequencing and analysis. Cell Syst 1:210-223|
|Lu, Charles; Xie, Mingchao; Wendl, Michael C et al. (2015) Patterns and functional implications of rare germline variants across 12 cancer types. Nat Commun 6:10086|
Showing the most recent 10 out of 98 publications