Benita S. Katzenellenbogen

About

Benita S. Katzenellenbogen is a Swanlund Professor of Molecular & Integrative Physiology and Cell & Developmental Biology at the University of Illinois. Her research focuses on the regulation of gene expression, signal transduction, and cell proliferation and phenotypic properties by hormones and growth factors. She conducts functional analyses of nuclear hormone receptors, particularly estrogen and progesterone receptors, and their genome-wide activities. Her work involves understanding the mechanisms of hormone and antihormone action in normal and cancer cells, especially in breast cancer, and identifying biomarkers related to therapeutic resistance. Her studies include detailed biochemical and structure-function analyses of receptors and coregulators, genome-wide analyses of receptor and transcription factor cistromes and transcriptomes, and examining the cross-talk between nuclear hormone receptors and cell signaling pathways. She investigates how these receptors regulate gene expression and cell growth, with a particular emphasis on breast cancer, reproductive biology, and fertility. Katzenellenbogen's contributions have advanced understanding of hormone receptor biochemistry, receptor mutations in therapy resistance, and the development of targeted therapies, including selective estrogen receptor degraders and antiestrogens. Her work has significant implications for cancer treatment, endocrine sensitivity, and reproductive health.

Research topics

• Biology
• Cancer research
• Medicine
• Internal medicine
• Endocrinology
• Cell biology
• Genetics
• Oncology
• Immunology
• Biochemistry

Selected publications

• Targeting the oncogenic transcription factor FOXM1 to improve outcomes in all subtypes of breast cancer

  Breast Cancer Research · 2023 · 84 citations

  1st authorCorresponding

  FOXM1 (Forkhead box M1) is an oncogenic transcription factor that is greatly upregulated in breast cancer and many other cancers where it promotes tumorigenesis, and cancer growth and progression. It is expressed in all subtypes of breast cancer and is the factor most associated with risk of poor patient survival, especially so in triple negative breast cancer (TNBC). Thus, new approaches to inhibiting FOXM1 and its activities, and combination therapies utilizing FOXM1 inhibitors in conjunction…

  PublisherOA PDFDOI

• FOXM1 regulates glycolysis and energy production in multiple myeloma

  Oncogene · 2022 · 56 citations

  The transcription factor, forkhead box M1 (FOXM1), has been implicated in the natural history and outcome of newly diagnosed high-risk myeloma (HRMM) and relapsed/refractory myeloma (RRMM), but the mechanism with which FOXM1 promotes the growth of neoplastic plasma cells is poorly understood. Here we show that FOXM1 is a positive regulator of myeloma metabolism that greatly impacts the bioenergetic pathways of glycolysis and oxidative phosphorylation (OxPhos). Using FOXM1-deficient myeloma cells…

  DOI

• Suppression of Tumor Growth, Metastasis, and Signaling Pathways by Reducing FOXM1 Activity in Triple Negative Breast Cancer

  Cancers · 2020 · 41 citations

  Senior authorCorresponding

  Metastasis-related complications account for the overwhelming majority of breast cancer mortalities. Triple negative breast cancer (TNBC), the most aggressive breast cancer subtype, has a high propensity to metastasize to distant organs, leading to poor patient survival. The forkhead transcription factor, FOXM1, is especially upregulated and overexpressed in TNBC and is known to regulate multiple signaling pathways that control many key cancer properties, including proliferation, invasiveness, s…

  DOI

• Contrasting activities of estrogen receptor beta isoforms in triple negative breast cancer

  Breast Cancer Research and Treatment · 2020 · 33 citations

  Senior authorCorresponding
  DOI

• Endothelial ERα promotes glucose tolerance by enhancing endothelial insulin transport to skeletal muscle

  Nature Communications · 2023-08-17 · 22 citations

  articleOpen access

  The estrogen receptor (ER) designated ERα has actions in many cell and tissue types that impact glucose homeostasis. It is unknown if these include mechanisms in endothelial cells, which have the potential to influence relative obesity, and processes in adipose tissue and skeletal muscle that impact glucose control. Here we show that independent of impact on events in adipose tissue, endothelial ERα promotes glucose tolerance by enhancing endothelial insulin transport to skeletal muscle. Endothe…

  PublisherOA PDFDOI

Recent grants

• NIH Grant R01CA060514

  NIH · $2.5M · 2004

• NIH Grant R37CA018119

  NIH · $1.9M · 1999

• NIH Grant R01CA018119

  NIH · $4.0M · 2010

Frequent coauthors

• John A. Katzenellenbogen

  University of Illinois Urbana-Champaign

  353 shared

• Kathryn E. Carlson

  University of Illinois Urbana-Champaign

  116 shared

• Geoffrey L. Greene

  University of Chicago

  94 shared

• Zeynep Madak‐Erdogan

  71 shared

• K.W. Nettles

  Scripps Research Institute

  63 shared

• Yvonne Ziegler

  University of Illinois Urbana-Champaign

  62 shared

• Sung Hoon Kim

  University of Illinois Urbana-Champaign

  57 shared

• Shubin Sheng

  55 shared

Education

• Postdoctoral Research Scientist, Physiology and Biophysics

  University of Illinois Urbana-Champaign

  1971

• PhD, Biology

  Harvard University

  1970

Awards & honors

• Ernst Oppenheimer Memorial Award of The Endocrine Society fo…
• Thomas A. Murphy University Scholar (1987-1990)
• MERIT Award from National Institutes of Health, National Can…
• Faculty Member of the Year Award, University of Illinois Col…
• American Academy of Arts and Sciences, elected Fellow (1993)

Similar researchers at University of Illinois Urbana-Champaign

• Martha U. Gilletteh-61
• Milan K. Bagchih-51
• Erik R. Nelsonh-44