The primary mission of the Hematologic Malignancies Program (HEM) is to improve our understanding ofthe molecular pathogenesis, diagnosis, and treatment of leukemia and lymphoma. Examination of the differences between neoplastic cells and their normal counterparts has provided insight into the molecular and biochemical features that define the malignant phenotype. In addition, research on genetic and epigenetic alterations within premalignant and malignant lesions has provided a blueprint ofthe molecular signatures that contribute to disease development and progression. Together with research on biochemical factors that govern cell-cycle progression, cellular differentiation, response to injury, self-renewal and programmed cell death, investigators are working to identify molecular pathways and/or leukemia-associated antigens that could be targeted by antineoplastic drugs and/or immune therapy. The program is organized into four themes: identification of mutations from primary tumor samples;validation of signaling pathways using tissue culture and animal models;preclinical testing of novel therapeutic strategies, Phase l/ll clinical trials of novel therapeutics with associated correlative studies. The HEM Program has 32 members from 6 academic departments with $12.7 Million of peer review research grant funding (annual direct costs), including $2.7 Million from NCI. Members of the HEM Program published 438 programmatically aligned articles (2007-2012);16% were the result of intraprogrammatic collaborations, 14% were interprogrammatic.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
2P30CA023100-28
Application #
8695646
Study Section
Subcommittee G - Education (NCI)
Project Start
1996-07-01
Project End
2019-04-30
Budget Start
2014-07-21
Budget End
2015-04-30
Support Year
28
Fiscal Year
2014
Total Cost
$26,792
Indirect Cost
$9,335
Name
University of California San Diego
Department
Type
DUNS #
804355790
City
La Jolla
State
CA
Country
United States
Zip Code
92093
Sen, Supriya; Langiewicz, Magda; Jumaa, Hassan et al. (2015) Deletion of serine/arginine-rich splicing factor 3 in hepatocytes predisposes to hepatocellular carcinoma in mice. Hepatology 61:171-83
Hoffmann, Hanne M; Tamrazian, Anika; Xie, Huimin et al. (2014) Heterozygous deletion of ventral anterior homeobox (vax1) causes subfertility in mice. Endocrinology 155:4043-53
Hartman, Lisa L R; Crawford, John R; Makale, Milan T et al. (2014) Pediatric phase II trials of poly-ICLC in the management of newly diagnosed and recurrent brain tumors. J Pediatr Hematol Oncol 36:451-7
Williams, Richard T; Barnhill, Lisa M; Kuo, Huan-Hsien et al. (2014) Chimeras of p14ARF and p16: functional hybrids with the ability to arrest growth. PLoS One 9:e88219
Huang, Carlos P; Fofana, Mariama; Chan, Jefferson et al. (2014) Copper transporter 2 regulates intracellular copper and sensitivity to cisplatin. Metallomics 6:654-61
Paolini, Paul; Pick, Daniel; Lapira, Jennifer et al. (2014) Developmental and extracellular matrix-remodeling processes in rosiglitazone-exposed neonatal rat cardiomyocytes. Pharmacogenomics 15:759-74
Goellner, Eva M; Smith, Catherine E; Campbell, Christopher S et al. (2014) PCNA and Msh2-Msh6 activate an Mlh1-Pms1 endonuclease pathway required for Exo1-independent mismatch repair. Mol Cell 55:291-304
Glidewell-Kenney, Christine A; Trang, Crystal; Shao, Paul P et al. (2014) Neurokinin B induces c-fos transcription via protein kinase C and activation of serum response factor and Elk-1 in immortalized GnRH neurons. Endocrinology 155:3909-19
Jiang, P; Mukthavaram, R; Chao, Y et al. (2014) In vitro and in vivo anticancer effects of mevalonate pathway modulation on human cancer cells. Br J Cancer 111:1562-71
Jacques, Bonnie E; Montgomery 4th, William H; Uribe, Phillip M et al. (2014) The role of Wnt/*-catenin signaling in proliferation and regeneration of the developing basilar papilla and lateral line. Dev Neurobiol 74:438-56

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