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Research Article

Standardized uptake value (SUVmax) in 18F-FDG PET/CT is correlated with the total number of main oncogenic anomalies in cancer patients

ORCID Icon, , ORCID Icon &
Pages 1067-1071 | Received 21 Oct 2019, Accepted 24 Sep 2020, Published online: 01 Nov 2020
 

ABSTRACT

Cancer diagnosis and therapy is quickly moving from the traditional histology-based approaches to genomic stratification, providing a huge opportunity for radiogenomics, associating imaging features with genomic data. Genome sequencing is time consuming, expensive and invasive whereas 18F-FDG PET/CT is readily available, fast and noninvasive. The aim of this study was to determine the relationship between the maximum standardized uptake value (SUVmax) and the frequency of 11 common oncogenic anomalies determined by specific common genomic alterations in tissue biopsies from patients with cancer. We retrospectively studied 102 consecutive untreated patients with gastrointestinal, lung, and breast cancer who underwent 18F-FDG PET/CT imaging, shortly prior to molecular testing by a biopsy for genomic profiling that consisted of 11 common DNA alterations: (1) TP53, (2) DNA repair, (3) EGFR, (4) PI3K/AKT/MTOR (PAM) pathway including PTEN, PIK3CA, AKT, TSC, CCNB1, MTOR, FBXW2, and NF2, (5) MEK, (6) CYCLIN including CCND,CDK, CDKN, and RB, (7) WNT, (8) ALK, (9) MYC, (10) MET, and (11) FGF/FGFR. Higher SUVmax was associated with the presence of TP53 and PAM genomic anomalies (p < .05), but not the other 9 gene groups (p > .05). More importantly, SUVmax was positively correlated with total number of oncogenic anomalies (r = 0.27, p = .005). We propose higher SUVmax as an indicator for total number of common oncogenic anomalies. This finding is a step forward in noninvasive stratification of cancer patients, in terms of the overall load of oncogenic anomalies, based on their SUVmax.

Ethical approval and consent to participate

This study was performed in accordance with the guidelines of the UCSD Internal Review Board (PREDICT [Profile Related Evidence Determining Individualized Cancer Therapy], protocol; NCT02478931).

Disclosure of potential conflicts of interest

Razelle Kurzrock receives research funding from Genentech, Incyte, Merck Serono, Pfizer, Sequenom, Foundation Medicine, Grifols, Konica Minolta, Omniseq and Guardant, as well as consultant fees from Loxo, X Biotech, NeoMed, and Actuate Therapeutics, speaker fees from Roche, and an equity interest in IDby DNA and Curematch Inc.

Additional information

Funding

Amin Haghighat Jahromi is supported by [NIH T32-4T32EB005970] grant. This work was also supported in part by the Joan and Irwin Jacobs Fund philanthropic fund; and by National Cancer Institute at the National Institutes of Health grant [P30 CA023100].