Abstract #0769

Hypoxia alters normal fibroblast metabolism towards a cancer associated fibroblast phenotype

Jesus Pacheco-Torres¹, Tariq Shah¹, W. Nathaniel Brennen², Flonne Wildes¹, and Zaver M Bhujwalla^1,3,4

¹Division of Cancer Imaging Research, The Russell H. Morgan Department of Radiology and Radiological Science, The Johns Hopkins University School of Medicine, Baltimore, MD, United States, ²Department of Oncology, The Johns Hopkins University School of Medicine, Baltimore, MD, United States, ³Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, United States, ⁴Radiation Oncology and Molecular Radiation Sciences, The Johns Hopkins University School of Medicine, Baltimore, MD, United States

Fibroblasts play a pivotal role in cancer progression. In prostate cancer, fibroblasts have been shown to induce growth and increase metastatic potential. To further understand how fibroblasts respond to hypoxic tumor microenvironments that are frequently observed in prostate cancer, we have characterized the effects of hypoxia on normal and cancer associated prostate fibroblast (PCAF) metabolomics and invasion using ¹H MRS/I. We found that hypoxia increased matrix degradation by normal fibroblasts. Furthermore, hypoxia metabolically reprogrammed normal prostate fibroblasts to mimic the metabolic pattern of PCAFs, highlighting the potential role of hypoxia in the transition of normal fibroblasts to CAFs.

How to access this content:

For one year after publication, abstracts and videos are only open to registrants of this annual meeting. Registrants should use their existing login information. Non-registrant access can be purchased via the ISMRM E-Library.

After one year, current ISMRM & ISMRT members get free access to both the abstracts and videos. Non-members and non-registrants must purchase access via the ISMRM E-Library.

After two years, the meeting proceedings (abstracts) are opened to the public and require no login information. Videos remain behind password for access by members, registrants and E-Library customers.

Click here for more information on becoming a member.