About

Brittany L. Allen-Petersen, Ph.D., is an Assistant Professor in the Department of Biological Sciences at Purdue University and a Co-leader of the Indiana University Pancreatic Cancer Working Group. She completed her Ph.D. in Cell and Developmental Biology at the University of Colorado Anschutz Medical Campus and her B.S. in Molecular, Cellular, and Developmental Biology at the University of Michigan. Prior to her current position, she was a Postdoctoral Fellow at Oregon Health & Science University. Her professional biography highlights her academic background and leadership roles within cancer research, particularly pancreatic cancer, at Purdue University and Indiana University.

Research topics

• Biology
• Genetics
• Medicine
• Cancer research
• Cell biology
• Internal medicine
• Biochemistry

Selected publications

• Supplementary Figure S2 from The Prolyl Isomerase PIN1 Affects Fibroblast Differentiation States and Cross-talk in Pancreatic Cancer

  2025-12-15

  articleOpen access

  <p>PIN1 inhibition slows PSC growth and prevents TGFβ-driven activation</p>

  PublisherOA PDFDOI

• The Prolyl Isomerase PIN1 Affects Fibroblast Differentiation States and Cross-talk in Pancreatic Cancer

  Cancer Research · 2025-09-18 · 1 citations

  articleOpen access

  The prolyl isomerase PIN1 is overexpressed in cancer and contributes to cancer cell-intrinsic phenotypes, including proliferation and migration. However, PIN1 may also function in stromal cells within the tumor microenvironment. In this study, we showed that PIN1 is a critical regulator of pancreatic stellate cell (PSC) state at baseline and in response to the myofibroblast-activating factor TGFβ. Loss or inhibition of PIN1 altered the epigenetic and transcriptional responses of PSCs to TGFβ, preventing PSC differentiation to a myofibroblast state and altering expression of secreted matrix proteins and signaling molecules. Consistent with inhibition of the TGFβ response, low fibroblast PIN1 expression in mouse and human pancreatic ductal adenocarcinoma correlated with low expression of αSMA, a marker of myofibroblast activation. Decreased PIN1 expression at baseline also altered paracrine hepatocyte growth factor (HGF) signaling from fibroblasts to tumor cells. PSCs with low PIN1 expression displayed reduced expression and secretion of HGF, resulting in an attenuation of c-MET receptor phosphorylation and signaling in nearby cancer cells. In allograft models, host PIN1 was critical for normal growth of a subset of pancreatic cancer cell lines that are responsive to HGF signaling. Through the identification of changes to fibroblast activation state and cross-talk following PIN1 loss or inhibition, these data suggest that systemic targeting of PIN1 will suppress the protumorigenic pancreatic ductal adenocarcinoma microenvironment and may differentially affect heterogeneous patient populations. SIGNIFICANCE: PIN1 plays a critical role in the response of pancreatic stellate cells to TGFβ and can be targeted to attenuate myofibroblast activation and protumor cross-talk to suppress pancreatic cancer progression.

  PublisherOA PDFDOI

• Supplementary Figure S4 from The Prolyl Isomerase PIN1 Affects Fibroblast Differentiation States and Cross-talk in Pancreatic Cancer

  2025-12-15

  articleOpen access

  <p>PIN1 knockdown or inhibition impacts the transcriptional response to TGFβ</p>

  PublisherOA PDFDOI

• Supplementary Dataset 3 from The Prolyl Isomerase PIN1 Affects Fibroblast Differentiation States and Cross-talk in Pancreatic Cancer

  2025-12-15

  articleOpen access

  <p>FPKMs of 1220 DEGs across knockdown samples</p>

  PublisherDOI

• Supplementary Figure S7 from The Prolyl Isomerase PIN1 Affects Fibroblast Differentiation States and Cross-talk in Pancreatic Cancer

  2025-12-15

  articleOpen access

  <p>Loss of PIN1 in host cells slows tumor growth and alters trichrome staining in orthotopic allografts of two KPC cell lines</p>

  PublisherOA PDFDOI

• Supplementary Dataset 5 from The Prolyl Isomerase PIN1 Affects Fibroblast Differentiation States and Cross-talk in Pancreatic Cancer

  2025-12-15

  articleOpen access

  <p>RNA-seq on inhibitor samples, FPKMs all protein coding genes</p>

  PublisherDOI

• Supplementary Dataset 12 from The Prolyl Isomerase PIN1 Affects Fibroblast Differentiation States and Cross-talk in Pancreatic Cancer

  2025-12-15

  articleOpen access

  <p>Motif analysis from sciATAC-seq</p>

  PublisherDOI

• Supplementary Figure S6 from The Prolyl Isomerase PIN1 Affects Fibroblast Differentiation States and Cross-talk in Pancreatic Cancer

  2025-12-15

  articleOpen access

  <p>PIN1 knockdown in PSCs impacts signaling to tumor cells via altered HGF secretion</p>

  PublisherOA PDFDOI

• Supplementary Dataset 8 from The Prolyl Isomerase PIN1 Affects Fibroblast Differentiation States and Cross-talk in Pancreatic Cancer

  2025-12-15

  articleOpen access

  <p>CAF marker FPKMs in inhibitor samples</p>

  PublisherDOI

• Supplementary Dataset 1 from The Prolyl Isomerase PIN1 Affects Fibroblast Differentiation States and Cross-talk in Pancreatic Cancer

  2025-12-15

  articleOpen access

  <p>RNA-seq on shSCR and shPIN1 samples, FPKMs all protein coding genes</p>

  PublisherDOI

Recent grants

• MYC is a critical downstream effector in KRAS-driven pancreatic cancer

  NIH · $176k · 2015–2018

Frequent coauthors

• Rosalie C. Sears

  Oregon Health & Science University

  53 shared

• Brett C. Sheppard

  University of Portland

  24 shared

• Jennifer P. Morton

  Cancer Research UK

  21 shared

• Dale J. Christensen

  21 shared

• Mary C. Thoma

  Oregon Health & Science University

  21 shared

• Goutham Narla

  University of Michigan–Ann Arbor

  18 shared

• Charles D. Lopez

  University of Portland

  16 shared

• Colin J. Daniel

  University of Portland

  16 shared

Labs

• Allen-Petersen LabPI

  Not provided