Pam Kreeger · University of Wisconsin-Madison · PhdFit
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Pam Kreeger
· Vilas Distinguished Achievement ProfessorVerified
University of Wisconsin-Madison · Pathology and Laboratory Medicine
Pamela Kreeger is a Vilas Distinguished Achievement Professor in the Department of Pathology and Laboratory Medicine at the University of Wisconsin-Madison. She is the principal investigator of the Kreeger Lab, where her research focuses on understanding cellular and molecular mechanisms, likely related to pathology and laboratory medicine. Her work involves leading research efforts, mentoring students and staff, and contributing to the scientific community through her role at the university.
bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-29
article
Summary High-grade serous ovarian cancer (HGSOC) represents 75% of ovarian cancer cases and 80% of deaths, with most patients relapsing despite initial treatment response. The limited effectiveness of immunotherapies in HGSOC indicates urgent need for novel therapeutic approaches. HGSOC patients produce tumor-binding autoantibodies (TBAs) with high tumor selectivity. Since effective antibody-mediated tumor cell killing requires Fc domain interactions with immune cells, we hypothesized that, although TBAs recognize tumor cells, they might still poorly elicit cell killing responses. Using a systems serology approach, we profiled TBA subclass and biophysical interactions with Fc receptors in HGSOC, comparing them to antiviral antibody responses. TBAs were consistently identified within ascites and serum and were heterogeneous in subclass composition. However, TBAs consistently lacked the capacity to bind FcγRIIIa despite abundant interaction with FcγRIIa and poorly elicited antibody-dependent cellular cytotoxicity, suggesting their Fc features prevent cell killing responses. Restoring FcγRIIIa interaction may be a promising therapeutic approach in HGSOC. Highlights TBAs in ovarian carcinoma patients consistently lack interaction with FcγRIIIa Ascites- and serum-derived TBAs have heterogeneous subclass composition Systems analysis shows complex serologic differences between TBAs and antiviral responses Patient-expressed TBAs demonstrate little antibody-dependent cellular cytotoxicity
bioRxiv (Cold Spring Harbor Laboratory) · 2025-05-16 · 2 citations
preprintOpen accessSenior authorCorresponding
HGSOC). The levels of both proteins were significantly elevated and collagen I fibers were significantly thicker in HGSOC metastases. Moreover, the ECM cross-linking enzyme transglutaminase 2 (TG2) was increased in omental metastases, where it is enzymatically active in the extracellular environment. This information was used to develop ECM constructs recapitulating these key changes, alone and in combination, to investigate their impact on HGSOC cell adhesion. To our knowledge, this is the first report using TG2 as a cross-linking agent to generate constructs from multiple ECM components. Low levels of HGSOC cell adhesion were observed on colIagen-only (coll) gels, while inclusion of cFN or plasma fibronection (pFN) increased cell adhesion. TG2-mediated cross-linking of colI/cFN hydrogels promoted HGSOC cell adhesion, while cross-linking of coll/pFN had no effect. Cell adhesion was dependent on ligand identity and fiber diameter. When fiber thickness was held constant, the inclusion of cFN led to greater HGSOC cell adhesion relative to pFN or coll, due to interactions of β1 integrins with the EDA and RGD domains of cFN. Meanwhile, when gel composition was held constant, HGSOC cell adhesion increased as fiber thickness was increased through modifications to gelation temperature. Combined, our results demonstrate how ECM changes associated with omental metastasis can support tumor progression and provide insights into methods to tailor biomaterials to support cell adhesion.
bioRxiv (Cold Spring Harbor Laboratory) · 2025-07-31 · 1 citations
preprintOpen access
Due to its limited symptoms, high-grade serous ovarian cancer (HGSOC) has frequently metastasized extensively throughout the peritoneal cavity prior to its diagnosis, resulting in an overall five-year survival rate of less than 50%. The greater omentum and the small bowel mesentery are two of the most common metastatic sites in advanced HGSOC. However, the mechanisms underlying HGSOC metastatic tropism remain unknown. The extracellular matrix is a complex and dynamic meshwork of proteins that provides biochemical and mechanical signals to surrounding cells and has been shown to drive the dissemination of several cancer types to preferential distant sites. Here, using histological assessment and proteomics, we examined the composition of the extracellular matrix of paired omentum and mesentery samples from disease-free adult females. We found that the fibrillar collagen content of the mesothelial layer of the omentum was significantly higher than that of the mesentery. Using ECM-focused proteomics, we further defined the ECM composition - or matrisome - of these two tissues. We found that over 90% of the proteins detected were shared between the omentum and mesentery. Our analysis also revealed small subsets of tissue-specific ECM proteins. Future work will aim to test the possible functional contributions of these ECM proteins to HGSOC metastatic tropism. To facilitate the reuse of our dataset, we have deposited the raw mass spectrometry data and accompanying metadata files to the ProteomeXchange Consortium with the dataset identifier PXD061586.
Abstract Background: Piezo1 is a mechanosensitive ion channel that couples extracellular matrix (ECM) properties to intracellular signaling cascades that can modulate cell phenotypes. Piezo1 was recently shown to regulate metastasis in high-grade ovarian serous carcinoma (HGSOC) by promoting tumor budding in an ECM stiffness-dependent manner. Uterine serous carcinoma (USC) is an aggressive gynecologic malignancy that is increasing in incidence and responsible for 40% of uterine cancer deaths. USC rapidly invades and metastasizes via mechanisms that remain incompletely understood. Whether Piezo1 may have a similar function in USC, which shares many molecular and clinical features of HGSOC, is not known. We recently showed that expression of the transcription factor GATA2 is lost in USCs that locally invade into the wall of the uterus versus non-invasive USCs. However, the transcriptional targets of GATA2 that mediate this activity are not known. Methods: We performed RNAseq in patient-derived USC cells lines after GATA2 depletion to identify differentially expressed genes. We performed anti-GATA2 ChIPseq in patient derived USC cells to identify genome wide sites of GATA2 occupancy. Western blots were performed for GATA2, Piezo1, and Tubulin after GATA2 depletion in patient-derived USC cells modified to express doxycycline-inducible anti-GATA2 shRNAs or shScramble control. In vitro models of ECM with different stiffnesses (3.7 and 14 kPa) were generated using an interpenetrating network of collagen I and methacrylated gelatin (GelMA), crosslinked within transwell inserts. USC cells were seeded on top of the gels and monitored over 24 hours for invasion in response to GATA2 depletion. Results: GATA2 depletion led to an increase in Piezo1 transcripts in patient-derived USC cells (log2fold change = 0.28, FDR<0.005), while western blot revealed a significant increase in Piezo1 protein expression after GATA2 depletion in two unique patient-derived USC cell lines. Anti-GATA2 ChIPseq identified two significant peaks of GATA2 occupancy within intron 1 of the Piezo1 gene, each harboring conserved canonical GATA motifs. Depletion of GATA2 in patient-derived USC cells led to increased tumor cell invasion, but only on the stiffer substrates. Conclusions: GATA2 binds two putative GATA enhancers within intron 1 of the Piezo1 gene in USC. GATA2 depletion leads to increased Piezo1 RNA and protein expression, which is accompanied by increased tumor cell invasion in a stiffness-dependent manner. Our findings support a model where loss of GATA2-mediated Piezo1 suppression facilitates increased Piezo1 expression, and Piezo1-driven ECM stiffness-dependent USC tumor invasion. They justify further studies to evaluate whether a GATA2-Piezo1 axis is a critical driver of USC invasion in vivo. Citation Format: Brittany Baikie, Mayuri Dutta, Pamela K. Kreeger, Daniel R. Matson. GATA2 loss promotes Piezo1 expression and stiffness-dependent invasion in uterine serous carcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 2658.
Due to its limited symptoms, high-grade serous ovarian cancer (HGSOC) has frequently metastasized extensively throughout the peritoneal cavity prior to its diagnosis, resulting in an overall five-year survival rate of less than 50%. The omentum and mesentery are two of the most common metastatic sites in HGSOC. However, the mechanisms underlying HGSOC metastatic tropism remain unknown. The extracellular matrix (ECM) is a meshwork of proteins that provides biochemical and mechanical signals to cells and has been shown to drive the dissemination of several cancer types to preferential distant sites. Here, combining histological assessment and proteomics, we defined the architectural features and composition of the ECM of paired omentum and mesentery samples from disease-free adult women. We found that over 90% of the proteins detected were shared between the omentum and mesentery, but also identified tissue-specific ECM proteins, including collagen XII and tenascin-C.
Proceedings on CD-ROM - International Society for Magnetic Resonance in Medicine. Scientific Meeting and Exhibition/Proceedings of the International Society for Magnetic Resonance in Medicine, Scientific Meeting and Exhibition · 2024-11-26
article
Motivation: High-grade serous ovarian cancer (HGSOC) is hypothesized to initiate at fallopian tubes and ovaries, and then spreads by detaching and floating through the peritoneal fluid to the upper abdomen. Goal(s): Create a framework that could potentially assess HGSOC cell movement and deposition in the peritoneal cavity using MRI-based computational fluid dynamics. Approach: Under the assumption that ovarian cancer cells are already prevalent in peritoneal fluid, ovarian cancer cell displacement can be analyzed using MRI-based CFD. Results: Velocity maps and streamlines and WSS maps were created using CFD simulation results to predict cells transport to the lower peritoneum and diaphragm. Impact: MRI-based CFD allows temporal and volumetric analysis of the peritoneal cavity and provides insight in ovarian cancer cell spread due to peritoneal fluid flow. Velocities and wall shear stress analysis can be used to identify stagnation points for cell deposition.
