1982-1984 Damon-Runyon-Walter Winchell Cancer Fund Postdoctoral Fellowship
1984-1986 National Cancer Institute Postdoctoral Fellowship
1982-1986 Research Fellow in Pathology, Harvard Medical School and Dana Farber
Cancer Institute, Boston, MA.
1986-1992 Assistant Professor, University of Chicago, Dept. of Radiation and
Cellular Oncology, Chicago, IL.
1992-2002 Medical Advisory Board, Leukemia Research Foundation, Inc., Chairman, 1995-1999, Co-Chairman, 1999-2002
1993-1998 Associate Professor, University of Chicago, Dept. of Radiation and
Cellular Oncology, Chicago, IL.
1998-2001 Associate Professor, Dept. of Human Nutrition and Dietetics, University
of Illinois at Chicago, Chicago, IL.
2001-2006 Head, Dept. of Human Nutrition,
2001-present Professor, Dept. of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, IL., Division of Nutritional Sciences, University of Illinois, Urbana, IL.
2007-present Professor, Dept. of Pathology, Co-Director of Graduate Studies, University of Illinois at Chicago, Chicago, IL
2015-present Director of Research, Department of Pathology, University of Illinois at Chicago, Chicago, IL
Research and Educational Focus
Diagnosing lethal prostate cancer and preventing death from the disease remain a major health care challenge, particularly among African American men who are at greater risk than Caucasians. Natural variations in the gene for of the SELENOF tumor suppressor are associated with increased risk of dying from prostate cancer and these variations are 10 times more frequent in the genomes of prostate cancers of African American men. SELENOF levels are dramatically reduced in prostate cancer compared to benign adjacent tissue and the degree of loss is also greater in the prostate cancers of African Americans. A SELENOF translational repressor, eIF4a3, is over-expressed in advanced prostate cancer, binds to the region of the SELENOF mRNA where the variation occurs and is targetable with an existing pharmacological inhibitor that results in enhanced SELENOF levels. Our work is intended to increase our knowledge of the mechanisms of SELENOF action and to develop a new therapeutic effective in the treatment of prostate cancer. We believe that SELENOF is a novel tumor suppressor whose loss is a risk factor for advanced prostate cancer and targeting eIF4a3 will result in elevated SELENOF and reduce prostate cancer mortality. While SELENOF genotype may serve as a marker for increased risk of dying from prostate cancer, the existence of a targetable inhibitory SELENOF mRNA binding protein presents an opportunity to develop a unique therapeutic that would be beneficial in reducing prostate cancer mortality, particular among African Americans
B.S., Biology, 1978 – Brooklyn College, Brooklyn, N.Y.
Ph.D., Biochemistry, 1982 – SUNY at Stony Brook, New York
Post-Doctoral, Molecular Biology, 1982-1986 – Harvard Medical School and Dana Farber Cancer Institute, Boston, MA.
Selected Recent Publications:
Ekoue, D.N., Ansong, A., Hong, L.K., Nonn, L., Macais, V., Deaton, R., Rupnow, R., Gann, P.H., Kajdacsy-Balla, A. and Diamond, A.M. GPX1 localizes to the nucleus in prostate epithelium and its levels are not associated with prostate cancer outcome. Antioxidants 7:doi: 10.3390/antiox7110167, 2018
Diamond A.M. Selenoproteins of the Human Prostate: Unusual properties and role in cancer etiology. Biol. Trace Elem. Res. doi: 10.1007/s12011-019-01809-0. PMID:31300958, 192:51-59, 2019.
Elhodaky, M., Hong, L.K., Kadkol, S., and Diamond A.M. Selenium-binding protein 1 alters energy metabolism in prostate cancer cells. Prostate doi: 10.11002/pros24028. PMID80:962-976, 80:962-976, 2020.
Kadkol, S., and Diamond, A,M. The interaction between dietary selenium intake and genetics in determining cancer risk and outcome. Nutrients doi: 10.3390/nu12082424. 12:E2424, 2020.
McKeever, L., Peterson, S.J., Lateef, O., Freels, S., Diamond, A.M., Braunschweig, C.A. The impact of MnSOD and GPx1 genotype at different levels of enteral nutrition exposure on oxidative stress and mortality: A post-hoc analysis from the FeDOx Trial. JPEN J Parenter. Enteral Nutr. 45:287-294, 2021.
Hong, L.K., Kadkol, S., Sverdlov, M., Kastrati, I., Ehhodaky, M., Deaton, R., Sfanos, K.S., Wang, H., Liu, L., Diamond, A.M. Loss of SELENOF induces the transformed phenotype in human immortalized prostate epithelial cells. Int. J. Mol. Sci., doi: 10.3390/ijms222112040, PMID: 34769469 222:12040, 2021.
Zigrossi, A., Hong, L.K., Ekyalongo, R.C.,Cruz-Alverez, C., Gomick, E., Diamond, A.M. and Kastrati, I. SELENOF is a new tumor suppressor in breast cancer. Oncogene 41, 1263-1268, doi: 10.1038/s41388-021-02158-wPMID: 35082382, 2022
Flowers, B., Bochnacka, Oliwa, Poles, A., Diamond, A.M. and Kastrati, I. Distinct roles of SELENOF in different human cancers. Biomolecules. 13:486. doi:10.3390/biom13030486, PMID 36979420, 2023.
Bera, S. Kadkol, S., Hong, L.K.1 Ali, W, Brockman, J.D. Sverdlov, M., Brister, E., Macais, V., Kajdacsy-Balla, A., Valyi-Nagy, K., Ziqiao Xu5, Irida Kastrati4, Li Liu5 and Alan M. Diamond. Regulation of SELENOF translation by eIF4a3: Possible role in prostate cancer progression. Molec Carcin. Doi: 10.1002/mc23616. 62:1803-1816, 2023