About

Cory Abate-Shen, PhD, is a Professor of Molecular Pharmacology and Therapeutics, as well as Urologic Sciences, and holds the Robert Sonneborn Professor of Medicine title at Columbia University Vagelos College of Physicians and Surgeons. Her research focuses on the molecular mechanisms of cancer development, with a longstanding commitment to generating mouse models of cancer for translational research. She has developed novel models of prostate and bladder cancer, which are utilized for investigating the molecular basis of these diseases and for evaluating new therapies. Dr. Abate-Shen is an internationally-recognized leader in genitourinary malignancies, with her studies leading to the discovery of new biomarkers for early detection and advances in cancer prevention and treatment. Her career began at Rutgers Medical School in 1991, where she quickly rose through the ranks to become Professor and Chief of the Division of Research in the Department of Medicine, as well as co-leader of the Prostate Program for The Cancer Institute of New Jersey. In 2007, she joined Columbia University, where she has held multiple leadership roles, including Associate Director and Interim Director of the Herbert Irving Comprehensive Cancer Center, before being appointed Chair of the Department of Pharmacology in 2019. Dr. Abate-Shen has received numerous awards, including a Sinsheimer Scholar Award, an NSF Young Investigator Award, and an American Cancer Society Research Professorship. She has served on the Board of Scientific Counselors of the National Cancer Institute, participated in the Cancer Moonshot Initiative, and held leadership roles in the American Association for Cancer Research. Recently, she was elected as a fellow of the American Association for the Advancement of Science.

Selected publications

• Extracellular-vesicles from the peri-prostatic adipose tissue of obese, but not lean, men promote prostate cancer aggressivity

  Endocrine Abstracts · 2025-02-19

  article
  PublisherDOI

• Supplementary Figure S1 from ATAD2 Drives Prostate Cancer Progression to Metastasis

  2025-05-02

  preprintOpen access

  <p>Additional analysis of ATAD2 expression in prostate cancer.</p>

  PublisherOA PDFDOI

• Supplementary Table S2 from ATAD2 Drives Prostate Cancer Progression to Metastasis

  2025-05-02

  supplementary-materialsOpen access

  <p>Oligonucleotides used in this Study</p>

  PublisherDOI

• Table S1 from OncoLoop: A Network-Based Precision Cancer Medicine Framework

  2025-12-11

  articleOpen accessSenior author

  <p>Supplementary Table 1: Phenotypic analysis of the GEMMs</p>

  PublisherDOI

• Table S7 from OncoLoop: A Network-Based Precision Cancer Medicine Framework

  2025-12-11

  articleOpen accessSenior author

  <p>Supplementary Table 7. Transcriptomic analyses of the PDX models A. PDX interactome B. OncoTreat for drugs to PDX using DU145 cell perturbation data</p>

  PublisherDOI

• Supplementary Figure S2 from ATAD2 Drives Prostate Cancer Progression to Metastasis

  2025-05-02

  preprintOpen access

  <p>Additional analyses of MYC regulation of ATAD2.</p>

  PublisherOA PDFDOI

• ATAD2 Drives Prostate Cancer Progression to Metastasis

  Molecular Cancer Research · 2025-02-05 · 3 citations

  articleOpen access

  Metastasis accounts for the overwhelming majority of cancer deaths. In prostate cancer and many other solid tumors, progression to metastasis is associated with drastically reduced survival outcomes, yet the mechanisms behind this progression remain largely unknown. ATPase family AAA domain containing 2 (ATAD2) is an epigenetic reader of acetylated histones that is overexpressed in multiple cancer types and usually associated with poor patient outcomes. However, the functional role of ATAD2 in cancer progression and metastasis has been relatively understudied. Here, we employ genetically engineered mouse models of prostate cancer bone metastasis, as well as multiple independent human cohorts, to show that ATAD2 is highly enriched in bone metastasis compared with primary tumors and significantly associated with the development of metastasis. We show that ATAD2 expression is associated with MYC pathway activation in patient datasets and that, at least in a subset of tumors, MYC and ATAD2 can regulate each other's expression. Using functional studies on mouse bone metastatic cell lines and innovative organ-on-a-chip bone invasion assays, we establish a functional role for ATAD2 inhibition in reducing prostate cancer metastasis and growth in bone. Implications: Our study highlights ATAD2 as a driver of prostate cancer progression and metastasis and suggests it may constitute a promising novel therapeutic target.

  PublisherOA PDFDOI

• Table S3 from OncoLoop: A Network-Based Precision Cancer Medicine Framework

  2025-12-11

  articleOpen accessSenior author

  <p>Supplementary Table 3: Transcriptomic analyses of the human patient samples A. TCGA Interactome B. SU2C Interactome C. Protein activity TCGA D. Protein Activity SU2C</p>

  PublisherDOI

• Data from ATAD2 Drives Prostate Cancer Progression to Metastasis

  2025-05-02

  preprintOpen access

  <div>Abstract<p>Metastasis accounts for the overwhelming majority of cancer deaths. In prostate cancer and many other solid tumors, progression to metastasis is associated with drastically reduced survival outcomes, yet the mechanisms behind this progression remain largely unknown. ATPase family AAA domain containing 2 (ATAD2) is an epigenetic reader of acetylated histones that is overexpressed in multiple cancer types and usually associated with poor patient outcomes. However, the functional role of ATAD2 in cancer progression and metastasis has been relatively understudied. Here, we employ genetically engineered mouse models of prostate cancer bone metastasis, as well as multiple independent human cohorts, to show that ATAD2 is highly enriched in bone metastasis compared with primary tumors and significantly associated with the development of metastasis. We show that ATAD2 expression is associated with MYC pathway activation in patient datasets and that, at least in a subset of tumors, MYC and ATAD2 can regulate each other’s expression. Using functional studies on mouse bone metastatic cell lines and innovative organ-on-a-chip bone invasion assays, we establish a functional role for ATAD2 inhibition in reducing prostate cancer metastasis and growth in bone.</p><p><b>Implications:</b> Our study highlights ATAD2 as a driver of prostate cancer progression and metastasis and suggests it may constitute a promising novel therapeutic target.</p></div>

  PublisherDOI

• Combination regimen of intravesical docetaxel, gemcitabine, and cisplatin in patients with BCG-unresponsive bladder cancer: clinical outcomes and genomic correlations

  Urologic Oncology Seminars and Original Investigations · 2025-06-07

  article
  PublisherDOI

Awards & honors

• Sinsheimer Scholar Award
• NSF Young Investigator Award
• American Cancer Society Research Professorship
• Fellow of the American Association for the Advancement of Sc…