The DF/HCC Leukemia Program continues to focus on advancing the understanding of molecular pathogenesis as a means to define novel pathways and protein targets that can be inhibited to improve the outcome of patients with acute leukemias, myelodysplastic syndromes and myeloproliferative neoplasms. The long-range goal of the Program is to accelerate the translation of novel discoveries from the laboratory to the clinic, first into preclinical testing in animal models and then into innovative, investigator-initiated Phase I or 11 clinical trials. The Program's Specific Aims are: 1) to identify novel cellular and molecular mechanisms that contribute to the pathogenesis of leukemia and related diseases;2) to generate accurate animal models of leukemia to improve the understanding of pathogenesis and to develop targeted anti-leukemic agents;and 3) to design and implement clinical trials to translate laboratory research discoveries made within the Leukemia Program and the Cancer Center as a whole. The Leukemia Program has been CCSG funded since 2000. The Program received an outstanding merit score at the time of the last competitive review in 2005. The 60 Program members represent four departments of HMS, one department of HSPH and six DF/HCC member institutions. The Program continues to be well-funded with $35.6 million in peer-reviewed funding, of which $16 million was from the NCI and $19.6 million was other peer reviewed funding (2009, total costs). Program members had 879 in Program-relevant publications from 2006 through 2010. Of these 16% were intra-programmatic interactions, 43% were inter-programmatic and 27% were inter-institutional.
Acute leukemias, myelodysplastic syndromes and myeloproliferative neoplasms represent major causes of cancer deaths each year in the United States. The Program seeks to understand how leukemia cells are disrupted to initiate and maintain the cancer phenotype and to translate these important discoveries into clinical trials to improve patient outcomes.
|Agoston, Agoston T; Pham, Thai H; Odze, Robert D et al. (2018) Columnar-Lined Esophagus Develops via Wound Repair in a Surgical Model of Reflux Esophagitis. Cell Mol Gastroenterol Hepatol 6:389-404|
|Barber, Lauren; Gerke, Travis; Markt, Sarah C et al. (2018) Family History of Breast or Prostate Cancer and Prostate Cancer Risk. Clin Cancer Res 24:5910-5917|
|Kwee, Brian J; Budina, Erica; Najibi, Alexander J et al. (2018) CD4 T-cells regulate angiogenesis and myogenesis. Biomaterials 178:109-121|
|Madsen, Thomas; Braun, Danielle; Peng, Gang et al. (2018) Efficient computation of the joint probability of multiple inherited risk alleles from pedigree data. Genet Epidemiol 42:528-538|
|Chen, Jingjing; Guccini, Ilaria; Di Mitri, Diletta et al. (2018) Compartmentalized activities of the pyruvate dehydrogenase complex sustain lipogenesis in prostate cancer. Nat Genet 50:219-228|
|Li, Andrew G; Murphy, Elizabeth C; Culhane, Aedin C et al. (2018) BRCA1-IRIS promotes human tumor progression through PTEN blockade and HIF-1? activation. Proc Natl Acad Sci U S A 115:E9600-E9609|
|McBrayer, Samuel K; Mayers, Jared R; DiNatale, Gabriel J et al. (2018) Transaminase Inhibition by 2-Hydroxyglutarate Impairs Glutamate Biosynthesis and Redox Homeostasis in Glioma. Cell 175:101-116.e25|
|Stopsack, Konrad H; Gonzalez-Feliciano, Amparo G; Peisch, Samuel F et al. (2018) A Prospective Study of Aspirin Use and Prostate Cancer Risk by TMPRSS2:ERG Status. Cancer Epidemiol Biomarkers Prev 27:1231-1233|
|Kamareddine, Layla; Wong, Adam C N; Vanhove, Audrey S et al. (2018) Activation of Vibrio cholerae quorum sensing promotes survival of an arthropod host. Nat Microbiol 3:243-252|
|Schilit, Samantha L P; Morton, Cynthia C (2018) 3C-PCR: a novel proximity ligation-based approach to phase chromosomal rearrangement breakpoints with distal allelic variants. Hum Genet 137:55-62|
Showing the most recent 10 out of 411 publications