About

Aysenur Keske is an Assistant Professor in the Department of Pathology and Laboratory Medicine at the University of Wisconsin School of Medicine and Public Health. She holds an MD degree from Uludag Universitesi Tip Fakultesi in Bursa, Turkey, and completed her residency training in Anatomic and Clinical Pathology at the University of Wisconsin Hospital and Clinics in Madison, Wisconsin. She also completed a fellowship in Breast Pathology at Memorial Sloan Kettering Cancer Center. Her clinical interests include hereditary breast cancer. Her research contributions include immunohistochemical analysis of GATA2 expression in endometrium and its relationship with hormone receptor expression in benign and premalignant endometrial disorders, as well as studies on the clinicopathological features of breast cancers in monoallelic MUTYH germline mutation carriers, and the identification of a subset of low positive ER carcinomas through immunoprofile analysis. She has also contributed to research on Betapapillomaviruses in vulvar intraepithelial lesions associated with squamous cell carcinoma.

Research topics

• Biology
• Cancer research
• Internal medicine
• Artificial Intelligence
• Computer Science
• Medicine
• Biochemistry
• Immunology
• Endocrinology
• Pathology

Selected publications

• 174 Germline Genetic Alterations in Homologous Recombination Deficiency/DNA Damage Response Genes in Breast Cancer

  Laboratory Investigation · 2025-03-01

  articleOpen access1st authorCorresponding
  PublisherOA PDFDOI

• Interleukin-1α release during necrotic-like cell death generates myeloid-driven immunosuppression that restricts anti-tumor immunity

  Cancer Cell · 2024-11-21 · 52 citations

  articleOpen access
  PublisherOA PDFDOI

• Immunohistochemical Analysis of GATA2 Expression in Endometrium and its Relationship with Hormone Receptor Expression in Benign and Premalignant Endometrial Disorders

  Reproductive Sciences · 2024-10-23 · 4 citations

  articleOpen access1st authorCorresponding

  The GATA gene family encodes highly conserved zinc-finger transcription factors that facilitate the development and function of multiple organ systems including the uterus. In the endometrium, GATA2 functions in a positive autoregulatory loop with the progesterone receptor (PGR) and colocalizes with PGR on chromatin to promote PGR transcriptional programs. GATA2 also has PGR-independent functions that maintain endometrial cell identity, and GATA2 transcripts reportedly are down-regulated in endometrial disorders including endometriosis. This event is accompanied by a reciprocal increase in GATA6. Here, we applied custom anti-GATA2 monoclonal antibodies and performed GATA2 immunohistochemistry (IHC) on patient endometrial tissues corresponding to proliferative, secretory, inactive, and hormone-treated endometrium, as well as endometriosis and endometrial atypical hyperplasia/endometrioid intraepithelial neoplasia (EAH/EIN). We also performed IHC for the estrogen receptor, PGR, and GATA6 in relevant groups. The results reveal a tight correlation between GATA2 and PGR expression in the glandular and stromal cells of benign endometrium. GATA2 expression is markedly reduced in stromal but not glandular cells in endometriosis and EAH/EIN. This reduction in GATA2 expression does not lead to a detectable increase in GATA6 expression in endometriosis. Although average glandular GATA2 expression was preserved in endometriosis and EAH/EIN cases, its expression was decoupled from PGR, implying that alternative pathways regulate GATA2 levels in these disorders. Our findings indicate that GATA2 dysregulation is a feature of endometriosis and EAH/EIN, and support a model whereby loss of stromal GATA2 in these disorders contributes to their progesterone insensitivity.

  PublisherOA PDFDOI

• Grading of lung adenocarcinomas with simultaneous segmentation by artificial intelligence (GLASS-AI)

  npj Precision Oncology · 2023 · 11 citations

  • Artificial Intelligence
  • Computer Science
  • Artificial Intelligence

  Preclinical genetically engineered mouse models (GEMMs) of lung adenocarcinoma are invaluable for investigating molecular drivers of tumor formation, progression, and therapeutic resistance. However, histological analysis of these GEMMs requires significant time and training to ensure accuracy and consistency. To achieve a more objective and standardized analysis, we used machine learning to create GLASS-AI, a histological image analysis tool that the broader cancer research community can utilize to grade, segment, and analyze tumors in preclinical models of lung adenocarcinoma. GLASS-AI demonstrates strong agreement with expert human raters while uncovering a significant degree of unreported intratumor heterogeneity. Integrating immunohistochemical staining with high-resolution grade analysis by GLASS-AI identified dysregulation of Mapk/Erk signaling in high-grade lung adenocarcinomas and locally advanced tumor regions. Our work demonstrates the benefit of employing GLASS-AI in preclinical lung adenocarcinoma models and the power of integrating machine learning and molecular biology techniques for studying the molecular pathways that underlie cancer progression.

  PublisherOA PDFDOI

• Data from Macrophage-Derived Cholesterol Contributes to Therapeutic Resistance in Prostate Cancer

  2023-03-31

  preprintOpen access

  <div>Abstract<p>Castration-resistant prostate cancer (CRPC) is a lethal stage of disease in which androgen receptor (AR) signaling is persistent despite androgen deprivation therapy (ADT). Most studies have focused on investigating cell-autonomous alterations in CRPC, while the contributions of the tumor microenvironment are less well understood. Here we sought to determine the role of tumor-associated macrophages in CRPC, based upon their role in cancer progression and therapeutic resistance. In a syngeneic model that reflected the mutational landscape of CRPC, macrophage depletion resulted in a reduced transcriptional signature for steroid and bile acid synthesis, indicating potential perturbation of cholesterol metabolism. As cholesterol is the precursor of the five major types of steroid hormones, we hypothesized that macrophages were regulating androgen biosynthesis within the prostate tumor microenvironment. Macrophage depletion reduced androgen levels within prostate tumors and restricted AR nuclear localization <i>in vitro</i> and <i>in vivo</i>. Macrophages were also cholesterol-rich and were able to transfer cholesterol to tumor cells <i>in vitro</i>. AR nuclear translocation was inhibited by activation of liver X receptor (LXR)-β, the master regulator of cholesterol homeostasis. Consistent with these data, macrophage depletion extended survival during ADT and the presence of macrophages correlated with therapeutic resistance in patient-derived explants. Taken together, these findings support the therapeutic targeting of macrophages in CRPC.</p>Significance:<p>These results suggest that macrophage-targeted therapies can be combined with androgen deprivation therapy to treat patients with prostate cancer by limiting cholesterol bioavailability and the production of intratumoral androgens.</p><p><i>See related commentary by Al-Janabi and Lewis, p. 5399</i></p></div>

  PublisherDOI

• Adenosquamous carcinoma in situ of the anus: a case series

  Archiv für Pathologische Anatomie und Physiologie und für Klinische Medicin · 2023-04-01 · 3 citations

  article1st author
  PublisherDOI

• Supplementary Figure from Stress Keratin 17 Expression in Head and Neck Cancer Contributes to Immune Evasion and Resistance to Immune-Checkpoint Blockade

  2023-03-31

  preprintOpen access

  Supplementary Figure from Stress Keratin 17 Expression in Head and Neck Cancer Contributes to Immune Evasion and Resistance to Immune-Checkpoint Blockade

  PublisherDOI

• Supplementary Figure from Stress Keratin 17 Expression in Head and Neck Cancer Contributes to Immune Evasion and Resistance to Immune-Checkpoint Blockade

  2023-03-31

  preprintOpen access

  Supplementary Figure from Stress Keratin 17 Expression in Head and Neck Cancer Contributes to Immune Evasion and Resistance to Immune-Checkpoint Blockade

  PublisherOA PDFDOI

• Betapapillomaviruses in p16-Negative Vulvar Intraepithelial Lesions Associated with Squamous Cell Carcinoma

  Viruses · 2023-09-19 · 3 citations

  articleOpen access

  Approximately 40% of vulvar squamous cell carcinoma (vSCC) cases are etiologically associated with high-risk human papillomaviruses (HPVs) of the alpha genera (α-HPV) that cause other anogenital cancers; however, the etiology of α-HPV-negative vSCC is poorly understood. HPVs of the beta genera (β-HPV) are risk factors for cutaneous squamous cell carcinoma (cSCC) and may be related to carcinomas originating in other cutaneous sites such as the vulva. In this study, we investigate the presence of β-HPVs, with an emphasis on p16-negative squamous lesions adjacent to vSCC. We subjected 28 vulvar squamous intraepithelial lesions adjacent to vSCC for comprehensive HPV genotyping, p16 and p53 immunohistochemistry, and consensus morphology review. Selected cases were subjected to qPCR and RNA in situ hybridization. Clinical data were obtained from medical records. β-HPV DNA was detected in eight of ten p16-negative lesions and three of fourteen p16-positive high-grade squamous intraepithelial lesions. The HPV DNA loads in vulvar squamous intraepithelial lesions ranged between less than 1 HPV DNA copy per cell to more than 100 HPV DNA copies per cell. This is, to the best of our knowledge, the first report of the association of p16-negative vulvar intraepithelial squamous lesions with detection of β-HPVs. These findings expand possible etiologic mechanisms that may contribute to p16-negative lesions of the vulva.

  PublisherOA PDFDOI

• Supplementary Figure from Stress Keratin 17 Expression in Head and Neck Cancer Contributes to Immune Evasion and Resistance to Immune-Checkpoint Blockade

  2023-03-31

  preprintOpen access

  Supplementary Figure from Stress Keratin 17 Expression in Head and Neck Cancer Contributes to Immune Evasion and Resistance to Immune-Checkpoint Blockade

  PublisherDOI

Frequent coauthors

• Taja Ložar

  University of Wisconsin–Madison

  36 shared

• Paul F. Lambert

  University of Leicester

  34 shared

• Huy Q. Dinh

  33 shared

• Paul M. Harari

  University of Wisconsin Carbone Cancer Center

  33 shared

• Megan B. Fitzpatrick

  University of Wisconsin–Madison

  33 shared

• Justine Y. Bruce

  University of Wisconsin–Madison

  32 shared

• Paul M. Sondel

  University of Wisconsin–Madison

  31 shared

• Athena E. Golfinos

  31 shared