Andrew Bradford, PhD

Assistant Dean, Essentials Curriculum
Divisions of Reproductive Sciences
Department of Obstetrics and Gynecology

PhD (1987) University of Newcastle upon Tyne

Research Complex 2
12700 East 19th Avenue
Room 3007, MS 8309
Aurora, CO 80045

Phone: (303) 724-3507
Fax: (303) 724-3512

Research Interests
My research interests focus on hormone/growth factor signaling and cancer. Specifically, our laboratory is studying the role of selective protein kinase C (PKC) isoforms in the modulation of cell growth and death in endometrial cancer. Endometrial cancer is the most common invasive gynecological malignancy in the United States. Although the annual incidence of endometrial cancer has remained relatively constant over the past decade, statistics indicate a dramatic increase in mortality, suggesting a higher prevalence of tumors, which are refractory to treatment. Thus, there is an urgent need to identify prognostic markers in endometrial cancer and to develop agents that have greater efficacy and biological specificity in the treatment of gynecological malignancies.

Recent studies from our laboratory and others suggest that members of the protein kinase C (PKC) family play critical roles in the pathogenesis of endometrial tumors, regulating both proliferation and programmed cell death (apoptosis), Moreover, PKC isozyme expression patterns may reflect the invasive or metastatic potential of endometrial cancers. Using endometrial cancer cell lines and specific adenoviral constructs, we have investigated the role of specific PKCs in etoposide-induced cell cycle arrest and apoptosis. Our results suggest that PKCα and δ exert opposing influences on proliferation and apoptosis in endometrial tumors. PKCα appears to promote proliferation and survival of endometrial cancer cells, whereas PKCδ is pro-apoptotic. Thus, PKCs are clearly important factors in the formation and progression of endometrial tumors. However, little is known regarding the molecular mechanisms underlying PKC modulation of proliferation and apoptosis in the endometrium, particularly with respect to the possible differential role of specific PKC isoforms. We postulate that specific transcriptional, mitogenic and/or apoptotic responses to PKC and isoforms may result in a more aggressive, chemotherapy-resistant endometrial tumor phenotype. Further study of PKCs in the endometrium may identify novel diagnostic/ prognostic indicators and provide new potential targets for therapeutic intervention.

We are also investigating the role of growth factor signaling and Ets transcription factors in the pathogenesis of uterine fibroids or leiomyomata.

Full List of Publications

Recent Publications

  1. Jones K, Ryan S, Carlson NE, Chosich J, Bradford AP, Santoro N, Polotsky AJ. Aromatase Inhibition Ameliorates Decreased LH Output Found in Obese Women. Reprod Sci. 2020 Apr; 27(4):1018-1023. PMID: 32046430.
  2. Adams CL, Dimitrova I, Post MD, Gibson L, Spillman MA, Behbakht K, Bradford AP. Identification of a novel diagnostic gene expression signature to discriminate uterine leiomyoma from leiomyosarcoma. Exp Mol Pathol. 2019 10; 110:104284. PMID: 31301306.
  3. Bauer JL, Kuhn K, Bradford AP, Al-Safi ZA, Harris MA, Eckel RH, Robledo CY, Malkhasyan A, Johnson J, Gee NR, Polotsky AJ. Reduction in FSH Throughout the Menstrual Cycle After Omega-3 Fatty Acid Supplementation in Young Normal Weight but not Obese Women. Reprod Sci. 2019 08; 26(8):1025-1033. PMID: 30773100.
  4. Komori H, Goto Y, Kurayoshi K, Ozono E, Iwanaga R, Bradford AP, Araki K, Ohtani K. Differential requirement for dimerization partner DP between E2F-dependent activation of tumor suppressor and growth-related genes. Sci Rep. 2018 05 31; 8(1):8438. PMID: 29855511.
  5. Al-Safi ZA, Polotsky A, Chosich J, Roth L, Allshouse AA, Bradford AP, Santoro N. Evidence for disruption of normal circadian cortisol rhythm in women with obesity. Gynecol Endocrinol. 2018 Apr; 34(4):336-340. PMID: 29068243.
  6. Chosich J, Bradford AP, Allshouse AA, Reusch JE, Santoro N, Schauer IE. Acute recapitulation of the hyperinsulinemia and hyperlipidemia characteristic of metabolic syndrome suppresses gonadotropins. Obesity (Silver Spring). 2017 03; 25(3):553-560. PMID: 28158916.
  7. Kurayoshi K, Shiromoto A, Ozono E, Iwanaga R, Bradford AP, Araki K, Ohtani K. Ectopic expression of the CDK inhibitor p21Cip1 enhances deregulated E2F activity and increases cancer cell-specific cytotoxic gene expression mediated by the ARF tumor suppressor promoter. Biochem Biophys Res Commun. 2017 01 29; 483(1):107-114. PMID: 28042030.
  8. Kurayoshi K, Okuno J, Ozono E, Iwanaga R, Bradford AP, Kugawa K, Araki K, Ohtani K. The phosphatidyl inositol 3 kinase pathway does not suppress activation of the ARF and BIM genes by deregulated E2F1 activity. Biochem Biophys Res Commun. 2017 Jan 22; 482(4):784-790. PMID: 27888102.
  9. Kuokkanen S, Polotsky AJ, Chosich J, Bradford AP, Jasinska A, Phang T, Santoro N, Appt SE. Corpus luteum as a novel target of weight changes that contribute to impaired female reproductive physiology and function. Syst Biol Reprod Med. 2016 Aug; 62(4):227-42. PMID: 27187064.
  10. Al-Safi ZA, Liu H, Carlson NE, Chosich J, Harris M, Bradford AP, Robledo C, Eckel RH, Polotsky AJ. Omega-3 Fatty Acid Supplementation Lowers Serum FSH in Normal Weight But Not Obese Women. J Clin Endocrinol Metab. 2016 Jan; 101(1):324-33. PMID: 26523525.


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