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J Nucl Med. 2015 May;56(5):662-7. doi: 10.2967/jnumed.114.150607. Epub 2015 Mar 26.

Correlation of BRAFV600E Mutation and Glucose Metabolism in Thyroid Cancer Patients: An ¹⁸F-FDG PET Study.

Author information

1
Molecular Imaging and Therapy Service, Memorial Sloan Kettering Cancer Center and Weill Cornell Medical College, New York, New York Endocrinology Service, Memorial Sloan Kettering Cancer Center and Weill Cornell Medical College, New York, New York; and nagarajj@mskcc.org.
2
Head and Neck Oncology Service, Memorial Sloan Kettering Cancer Center and Weill Cornell Medical College, New York, New York.
3
Endocrinology Service, Memorial Sloan Kettering Cancer Center and Weill Cornell Medical College, New York, New York; and.
4
Molecular Imaging and Therapy Service, Memorial Sloan Kettering Cancer Center and Weill Cornell Medical College, New York, New York.

Abstract

There is significant interest in a better understanding of the genetic underpinnings of the increased glucose metabolic rates of cancer cells. Thyroid cancer demonstrates a broad variability of (18)F-FDG uptake as well as several well-characterized oncogenic mutations. In this study, we evaluated the differences in glucose metabolism of the BRAF(V600E) mutation versus BRAF wild-type (BRAF-WT) in patients with metastatic differentiated thyroid cancer (DTC) and poorly differentiated thyroid cancer (PDTC).

METHODS:

Forty-eight DTC and 34 PDTC patients who underwent (18)F-FDG PET/CT for tumor staging were identified from a database search. All patients were tested for the BRAF(V600E) mutation and assigned to 1 of 2 groups: BRAF(V600E) mutated and BRAF-WT. (18)F-FDG uptake of tumor tissue was quantified by maximum standardized uptake value (SUVmax) of the hottest malignant lesion in 6 prespecified body regions (thyroid bed, lymph nodes, lung, bone, soft tissue, and other). When there were multiple lesions in 1 of the prespecified body regions, only the 1 with the highest (18)F-FDG uptake was analyzed.

RESULTS:

In the DTC cohort, 24 tumors harbored a BRAF(V600E) mutation, whereas 24 tumors were BRAF-WT. (18)F-FDG uptake of BRAF(V600E)-positive lesions (median SUVmax, 6.3; n = 53) was significantly higher than that of BRAF-WT lesions (n = 39; median SUVmax, 4.7; P = 0.019). In the PDTC group, only 5 tumors were BRAF(V600E)-positive, and their (18)F-FDG uptake was not significantly different from the BRAF-WT tumors. There was also no significant difference between the SUVmax of all DTCs and PDTCs, regardless of BRAF mutational status (P = 0.90).

CONCLUSION:

These data suggest that BRAF(V600E)-mutated DTCs are significantly more (18)F-FDG-avid than BRAF-WT tumors. The effect of BRAF(V600E) on tumor glucose metabolism in PDTC needs further study in larger groups of patients.

KEYWORDS:

18F-FDG uptake; BRAFV600E-mutation; DTC; PDTC; thyroid cancer

PMID:
25814520
PMCID:
PMC4970467
DOI:
10.2967/jnumed.114.150607
[Indexed for MEDLINE]
Free PMC Article

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