About

Dr. Demaretta S. Rush is a Professor of Pathology at the University of Arizona College of Medicine, serving on the Clinical Scholar Track. She is board certified in Anatomic and Clinical Pathology and Cytopathology, with fellowship training in gynecologic and perinatal pathology as well as in cytopathology. Her clinical responsibilities include providing surgical pathology diagnostic interpretations in gynecologic, gastrointestinal, and cardiovascular pathology, along with cytopathology interpretations. Dr. Rush also contributes to medical education by teaching in the preclinical years of the College of Medicine curriculum, focusing on gynecologic and cardiovascular pathology, and supervising medical students on elective in surgical pathology. Her scholarly work primarily concentrates on diseases of the lower female genital tract, with additional contributions to research involving diseases of the endometrium, ovary, fallopian tube, and placenta. She has a particular interest in medical education within pathology. Dr. Rush has served as residency program director and is actively involved in mentoring and training future pathologists. Her professional background includes training at New York Presbyterian Hospital, Weill Cornell Center, and the University of Florida College of Medicine, with numerous awards and recognitions for her contributions to pathology.

Research topics

• Medicine
• Radiology
• Pathology
• Gynecology
• Oncology
• Biology
• Pedagogy
• Internal medicine
• Obstetrics
• Cancer research
• Psychology
• Medical education
• Andrology

Selected publications

• 967 Use of p53 Immunohistochemistry Can Improve Diagnostic Agreement for Differentiated Vulvar Intraepithelial Neoplasia (dVIN): An International Reproducibility Study

  Laboratory Investigation · 2025-03-01

  article
  PublisherDOI

• Use of p53 immunohistochemistry can improve diagnostic agreement for differentiated vulvar intraepithelial neoplasia ( <scp>dVIN</scp> ): an international reproducibility study

  Histopathology · 2025-08-05 · 1 citations

  articleOpen access

  AIMS: Differentiated or HPV-independent vulvar intraepithelial neoplasia (dVIN) can progress rapidly to invasive cancer and accurate pathological diagnosis is essential to facilitate appropriate interventions. Histological similarities of dVIN with non-neoplastic lesions, however, often make the diagnosis less reproducible. We investigated among a diverse group of pathologists whether the diagnostic agreement improves with the use of p53 immunohistochemistry (IHC) interpreted using the pattern-based schema. METHODS AND RESULTS: Fifty haematoxylin-eosin (HE) stained archival slides (30 dVIN and 20 non-dysplastic vulvar lesions) were selected and p53-IHC was performed. Twenty-four board-certified pathologists from eight countries first assessed the HE slides alone, and after a washout period, re-evaluated them alongside the p53-IHC slides. During both rounds, slides were diagnosed as dVIN, favour dVIN, favour no-VIN or no-VIN. p53-IHC was scored as wild-type or mutant (diffuse, basal, cytoplasmic or null). Kappa (κ) statistics and McNemar's test were used for statistical analyses. Overall diagnostic agreement for dVIN saw a significant increase in the Kappa value (κ = 0.6 vs. κ = 0.4, P = 0.002) when HE and p53-IHC slides were assessed together compared with histology assessment alone, although the level of agreement remained moderate. For p53-IHC assessment, overall agreement was substantial (κ = 0.7). Diagnoses changing from no-VIN/favour no-VIN to dVIN correlated significantly with the identification of a p53-mutant pattern (P < 0.001). CONCLUSIONS: Our findings indicate that p53-IHC is a robust ancillary tool that can be reproducibly interpreted by pathologists with varying experience levels and supports the routine use of p53-IHC in cases where dVIN is considered in the differential diagnosis.

  PublisherOA PDFDOI

• Zebras in a snowstorm: ultrasound guidance for differentiating placental mesenchymal dysplasia from hydatidiform mole

  American Journal of Obstetrics and Gynecology · 2024 · 2 citations

  • Medicine
  • Obstetrics
  • Andrology
  PublisherDOI

• S5132 When Nivolumab Turns Nasty: A Rare Case of Hemorrhagic Gastritis

  The American Journal of Gastroenterology · 2024-10-01 · 2 citations

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  PublisherDOI

• Antiandrogen Flutamide-Induced Restoration of miR-449 Expression Mitigates Functional Biomarkers Associated with Ovarian Cancer Risk

  medRxiv (Cold Spring Harbor Laboratory) · 2024

  • Oncology
  • Cancer research
  • Medicine

  Background: The involvement of the androgen and androgen receptor (AR) pathway in the development of epithelial ovarian cancer is increasingly recognized. However, the specific mechanisms by which anti-androgen agents, such as flutamide, may prevent ovarian cancer and their efficacy remain unknown. We examined the effects of flutamide on the miRNA expression profile found in women at high risk (HR) for ovarian cancer. Methods: Ovarian and tubal tissues, free from ovarian, tubal, peritoneal cancers, and serous tubal intraepithelial carcinoma (STIC), were collected from untreated and flutamide-treated HR women. Low-risk (LR) women served as controls. Transcriptomic miRNA sequencing was performed on these 3 sample cohorts. The miRNAs that showed the most notable differential expression were subjected to functional assays in primary ovarian epithelial cells and ovarian cancer cells. Results: ), both of which are known contributors to ovarian cancer progression, with emerging evidence also supporting their roles in ovarian cancer initiation. These findings were experimentally validated in primary ovarian epithelial cells and ovarian cancer cell lines (SKOV3 and Hey): flutamide treatment resulted in elevated levels of miR-449a and miR-449b-5p, and introducing mimics of these miRNAs reduced the mRNA and protein levels of CSF1R and AR. Furthermore, introducing miR-449a and miR-449b-5p mimics showed inhibitory effects on the migration and proliferation of ovarian cancer cells. Conclusion: Flutamide treatment restored the reduced expression of miR-449a and miR-449b-5p in HR tissues, thereby decreasing the expression of CSF1R and AR, functional biomarkers associated with an increased risk of ovarian cancer. In addition to the known direct binding of flutamide to the AR, we found that flutamide also suppresses AR expression via miR-449a and miR-449b-5p upregulation, revealing a novel dual-inhibitory mechanism on the AR pathway. Taken together, our study highlights mechanisms supporting the chemopreventive potential of flutamide in ovarian cancer, particularly in HR patients with reduced miR-449 expression.

  PublisherOA PDFDOI

• miR-449, identified through antiandrogen exposure, mitigates functional biomarkers associated with ovarian cancer risk

  Scientific Reports · 2024-12-02 · 4 citations

  articleOpen access

  The involvement of the androgen receptor (AR) pathway in developing epithelial ovarian cancer is increasingly acknowledged. However, the specific mechanisms by which anti-androgen agents, such as flutamide, may prevent ovarian cancer and their efficacy remain unknown. This study was initiated by investigating the impact of flutamide on miRNA expression in women at high risk (HR) for ovarian cancer. Ovarian and tubal tissues, free from ovarian, tubal, peritoneal cancers, and serous tubal intraepithelial carcinoma (STIC), were collected from untreated and flutamide-treated HR women as well as low-risk (LR) women controls. We performed miRNA sequencing on these 3 sample cohorts and observed that flutamide normalized miRNA levels in HR tissues, notably upregulating the miR-449 family to levels seen in LR tissues. In subsequent tests in primary ovarian epithelial cells and ovarian cancer cell lines (SKOV3 and Hey), flutamide also increased miR-449a and miR-449b-5p levels. Introducing mimics of these miRNAs reduced the mRNA and protein levels of AR and colony-stimulating factor 1 receptor (CSF1R, also known as c-fms), both of which are known contributors to ovarian cancer progression, with emerging evidence also supporting their roles in ovarian cancer initiation. Ovarian cancer cell migration was inhibited upon introducing miR-449a and miR-449b-5p mimics. Together, our study suggests a novel dual-inhibitory mechanism of flutamide on the AR pathway (AR expression suppression in addition to direct androgen antagonism) and supports its chemopreventive potential in ovarian cancer, especially for HR patients with low miR-449 expression.

  PublisherOA PDFDOI

• National pilot of entrustable professional activities in pathology residency training

  Academic Pathology · 2024 · 7 citations

  • Medical education
  • Medicine
  • Psychology

  Entrustable professional activities (EPAs) are observable clinical skills and/or procedures that have been introduced into medical education at the student and resident levels in most specialties to determine readiness to advance into residency or independent practice, respectively. This publication describes the process and outcomes of a pilot study looking at the feasibility of using two anatomic pathology and two clinical pathology EPAs in pathology residency in 6 pathology residency programs that volunteered for the study. Faculty development on EPAs and their assessment was provided to pilot program faculty, and EPA assessment tools were developed and used by the pilot programs. Pre- and post-study surveys were given to participating residents, faculty, and program directors to gauge baseline practices and to gather feedback on the EPA implementation experience. Results demonstrated overall good feasibility in implementing EPAs. Faculty acceptance of EPAs varied and was less than that of program directors. Residents reported a significant increase in the frequency with which faculty provided formative assessments that included specific examples of performance and specific ways to improve, as well as increased frequency with which faculty provided summative assessments that included specific ways to improve. EPAs offered the most benefit in setting clear expectations for performance of each task, for providing more specific feedback to residents, and in increasing Program director's understanding of resident strengths abilities and weaknesses.

  PublisherDOI

• Occult Synchronous Bilateral Fallopian Tube Cancers: Hysterectomy and Bilateral Salpingectomy for a Benign Indication

  Journal of Gynecologic Surgery · 2021-11-01

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  PublisherDOI

• Benign Diseases of the Vulva

  2019-01-01

  book-chapter1st author
  PublisherDOI

• Precursor Lesions and Malignant Tumors of the Vulva

  2019-01-01 · 1 citations

  book-chapterSenior author
  PublisherDOI

Frequent coauthors

• Robert A. Soslow

  Cleveland Clinic

  25 shared

• Rebecca N. Baergen

  Gynecologic Oncology Group

  21 shared

• Edward J. Wilkinson

  Duke University

  20 shared

• Edyta C. Pirog

  Cornell University

  19 shared

• Lora H. Ellenson

  19 shared

• Elizabeth Hyjek

  16 shared

• Andrew J. Dannenberg

  BioVentures (United States)

  12 shared

• Nash S. Moawad

  University of Florida

  7 shared

Awards & honors

• Fellow, International Society for the Study of Vulvovaginal…
• Fellow, American College of Pathologists (2005)
• Fred S. Mandelbaum Award for Excellence in Pathology and All…
• Janet M. Glasgow Memorial Achievement Citation (1998)