Correlation Between the Intensity of Breast FDG Uptake and Menstrual Cycle

Lin, Chun Yi; Ding, Hueisch‐Jy; Liu, Chiu Shoung; Chen, Yen Kung; Lin, Cheng Chieh; Kao, Chia Hung

doi:10.1016/j.acra.2007.03.010

Cited by 26 publications

(18 citation statements)

References 17 publications

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“…Our data support and provide the molecular basis for the proposal that circulating estrogens influence 18 F-FDG uptake in responsive normal and malignant breast tissues (9,33). This finding does not imply that breast tumors with high 18 F-FDG uptake likely have estrogen-stimulated ER.…”

Section: Figuresupporting

confidence: 71%

17β-Estradiol Augments ¹⁸F-FDG Uptake and Glycolysis of T47D Breast Cancer Cells via Membrane-Initiated Rapid PI3K–Akt Activation

Ko¹,

Paik²,

Jung³

et al. 2010

J Nucl Med

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Use of 18 F-FDG uptake as a surrogate marker of therapeutic response requires the recognition of biologic factors that influence cancer cell glucose metabolism. Estrogen is a potent stimulator of breast cancer proliferation, a process that requires sufficient energy, which is likely met by increased glycolysis. We thus explored the effect of estrogen on 18 F-FDG uptake in responsive breast cancer cells and investigated the mediating molecular mechanisms. Methods: T47D breast cancer cells were stimulated with 17b-estradiol (E 2 ) or bovine serum albumin (BSA)-E 2 and measured for 18 F-FDG uptake, lactate release, and mitochondrial hexokinase activity. The effects of antiestrogens, cycloheximide, and major protein kinase inhibitors were investigated. Immunoblots were performed for membrane glucose transporter type 1, phosphorylated phosphatidylinositol 3-kinase (PI3K), and Akt. Results: E 2 augmented T47D cell 18 F-FDG uptake in a dose-and time-dependent manner that preceded and surpassed its proliferative effect. With exposure to 10 nM E 2 , protein content-corrected 18 F-FDG uptake reached 172.7% 6 6.6% and 294.4% 6 9.5% of controls by 24 and 48 h, respectively. Lactate release reached 110.9% 6 7.3% and 145.2% 6 10.5% of controls at 24 and 48 h, and mitochondrial hexokinase activity increased to 187.1% 6 31.6% at 24 h. Membrane glucose transporter type 1 expression was unaltered. The effect was absent in estrogen receptor (ER)-negative breast cancer cells and was abrogated by ICI182780, indicating ER dependence. The E 2 effect was not blocked by tamoxifen and was mimicked by membrane-impermeable BSA-E 2 , consistent with nongenomic membrane-initiated E 2 action. Inhibition by cycloheximide demonstrated the requirement of a new protein synthesis. Immunoblots displayed rapid phosphorylation of PI3K and Akt within minutes of E 2 treatment, and the specific PI3K inhibitors wortmannin and LY294002 abolished the ability of E 2 to elevate 18 F-FDG uptake. Conclusion: Estrogen augments breast cancer cell 18 F-FDG uptake by stimulating glycolysis and hexokinase activity via membrane-initiated E 2 action that activates the PI3K-Akt pathway. These findings yield important insight into our understanding of the biology of breast cancer metabolism and may have potential implications for 18 F-FDG uptake as a surrogate marker of therapeutic response.

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Section: Figuresupporting

confidence: 71%

17β-Estradiol Augments ¹⁸F-FDG Uptake and Glycolysis of T47D Breast Cancer Cells via Membrane-Initiated Rapid PI3K–Akt Activation

Ko¹,

Paik²,

Jung³

et al. 2010

J Nucl Med

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“…During the menstrual cycle, five phases, varying in the vascularity and histologic features of the epithelial and stromal components, have been described (proliferative, follicular, BREAST IMAGING: Diffusion-Tensor MR Imaging of the Breast Nissan et al it appears from our results that it was not sufficiently robust to change significantly the diffusion coefficients. Because of its clinical relevance, there is a rising interest in the effects of the menstrual cycle on different breast imaging modalities (36)(37)(38) and in DCE MR imaging in particular, where the cyclic vasodilatation phenomenon may be interpreted as a false-positive finding, creating a diagnostic challenge (39). More recently, findings of studies on background parenchymal enhancement during the menstrual cycle (40-42) have supported the current recommendation of edema in interlobular stroma (35).…”

Section: Discussionmentioning

confidence: 98%

Diffusion-Tensor MR Imaging of the Breast: Hormonal Regulation

Nissan¹,

Furman‐Haran²,

Shapiro-Feinberg³

et al. 2014

Radiology

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“…In addition, although the breast tissue typically has a homogeneous uptake of both tracers, they can accumulate in normal glandular tissue resulting in a diffuse heterogeneous uptake pattern, especially in pre-menopausal women who are in the luteal phase of their menstrual cycle (Lin et al, 2007). This is not surprising as it reflects the heterogeneous nature of the breast tissue and the impact of blood hormone levels on the breast parenchyma.…”

Section: Comparison Of Bsgi/mbi and Pem Radiotracersmentioning

confidence: 95%

The Role of Molecular Imaging Technologies in Breast Cancer Diagnosis and Management

Rosenberg¹,

Kieper²,

Williams³

et al. 2012

Imaging of the Breast - Technical Aspects and Clinical Implication

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Correlation Between the Intensity of Breast FDG Uptake and Menstrual Cycle

Cited by 26 publications

References 17 publications

17β-Estradiol Augments ¹⁸F-FDG Uptake and Glycolysis of T47D Breast Cancer Cells via Membrane-Initiated Rapid PI3K–Akt Activation

17β-Estradiol Augments ¹⁸F-FDG Uptake and Glycolysis of T47D Breast Cancer Cells via Membrane-Initiated Rapid PI3K–Akt Activation

Diffusion-Tensor MR Imaging of the Breast: Hormonal Regulation

The Role of Molecular Imaging Technologies in Breast Cancer Diagnosis and Management

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Correlation Between the Intensity of Breast FDG Uptake and Menstrual Cycle

Cited by 26 publications

References 17 publications

17β-Estradiol Augments 18F-FDG Uptake and Glycolysis of T47D Breast Cancer Cells via Membrane-Initiated Rapid PI3K–Akt Activation

17β-Estradiol Augments 18F-FDG Uptake and Glycolysis of T47D Breast Cancer Cells via Membrane-Initiated Rapid PI3K–Akt Activation

Diffusion-Tensor MR Imaging of the Breast: Hormonal Regulation

The Role of Molecular Imaging Technologies in Breast Cancer Diagnosis and Management

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Resources

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17β-Estradiol Augments ¹⁸F-FDG Uptake and Glycolysis of T47D Breast Cancer Cells via Membrane-Initiated Rapid PI3K–Akt Activation

17β-Estradiol Augments ¹⁸F-FDG Uptake and Glycolysis of T47D Breast Cancer Cells via Membrane-Initiated Rapid PI3K–Akt Activation