Abstract #0702

Metabolic and imaging phenotypes associated with RB1 loss in castrate resistant prostate cancer

Fahim Ahmad¹, Margaret White², Kazutoshi Yamamoto³, Daniel R. Crooks⁴, Supreet Agarwal², Ye Yang⁴, Brian Capaldo², Sonam Raj², Aian Neil Alilin², Anita Ton³, Stephen Adler⁵, Jurgen Seidel³, Colleen Olkowski³, Murali Krishna Cherukuri⁶, Peter L Choyke³, Kathleen Kelly², and Jeffrey R Brender⁶

¹3. Laboratory of Genitourinary Cancer Pathogenesis, NCI/NIH, Bethesda, MD, United States, ²Laboratory of Genitourinary Cancer Pathogenesis, NCI/NIH, Bethesda, MD, United States, ³Molecular Imaging Branch, NCI/NIH, Bethesda, MD, United States, ⁴Urologic Oncology Branch, NCI/NIH, Bethesda, MD, United States, ⁵6. Clinical Research Directorate, Frederick National Laboratory for Cancer Research, NCI/NIH, Frederick, MD, United States, ⁶Radiation Biology Branch, NCI/NIH, Bethesda, MD, United States

Synopsis

Keywords: Biology, Models, Methods, Cancer, prostate, metabolomics

Motivation: The progression of prostate cancer is marked by both RB1 and T53 inactivation and higher ¹⁸FDG-PET uptake, but it's unclear whether RB1 or TP53 inactivation drives increased glucose import.

Goal(s): Can metabolic changes be used as a biomarker for RB1 and TP53 loss?

Approach: Metabolomic analysis by NMR and IC-MS for a comprehensive measure of metabolic changes ex vivo and and hyperpolarized MRI to measure the Warburg effect in vivo.

Results: ¹⁸FDG uptake was unaffected by loss of either RB1 or TP53. RB1 and TP53 did induce a series of other metabolic changes which could be detected in vivo by hyperpolarized MRI

Impact: Neuroendrocrine prostate cancer is a life-threatening progression of prostate cancer that is characterized by mutations in two key genes. Hyperpolarized MRI may enhance early diagnosis of NEPC without biopsy.

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