Glucose metabolism of breast cancer assessed by F-18-FDG PET: Histologic and immunohistochemical tissue analysis

Citation
N. Avril et al., Glucose metabolism of breast cancer assessed by F-18-FDG PET: Histologic and immunohistochemical tissue analysis, J NUCL MED, 42(1), 2001, pp. 9-16
Citations number
40
Categorie Soggetti
Radiology ,Nuclear Medicine & Imaging","Medical Research Diagnosis & Treatment
Journal title
JOURNAL OF NUCLEAR MEDICINE
ISSN journal
01615505 → ACNP
Volume
42
Issue
1
Year of publication
2001
Pages
9 - 16
Database
ISI
SICI code
0161-5505(200101)42:1<9:GMOBCA>2.0.ZU;2-0
Abstract
Breast cancer is characterized by elevated glucose consumption resulting in increased uptake of F-18-FDG. However, tracer uptake Varies considerably a mong tumors imaged with PET. This study compared histologic and immunohisto chemical tissue analysis of breast carcinomas with preoperative FDG uptake assessed by PET to identify tumor characteristics that define the degree of tracer accumulation Methods: FDG uptake in breast tumors was quantified by calculating standardized uptake values (SUVs) corrected for partial-volume effect and normalized to blood glucose level at the time of tracer injecti on. The histologic sections of 50 invasive and 6 noninvasive breast carcino mas were analyzed for histologic type, microscopic tumor growth pattern, pe rcentage of tumor cells, presence of inflammatory cells, density of blood v essels, histopathologic grading, tumor cell proliferation (mitotic rate and antibody binding of MIB-1), expression of estrogen and progesterone recept ors, and expression of the glucose transporter protein Glut-1. Results: A p ositive correlation was found between FDG uptake and histologic tumor type (ductal vs. lobular; P = 0.003), microscopic tumor growth pattern (nodular vs. diffuse; P = 0.007), and tumor cell proliferation (MIB-1; P = 0.009). T umors with diffuse growth patterns had significantly lower SUVs compared wi th clearly defined tumors. A weak relationship was found between FDG uptake and the percentage of tumor cells (P = 0.06). Lower densities of brood ves sels corresponded to higher FDG uptakes (P = 0.08). However, even significa nt correlations showed poor correlation coefficients. No relationship was f ound between FDG uptake and the following: tumor size; axillary lymph node status; percentage of necrotic, fibrotic, and cystic compounds; presence of inflammatory cells; steroid receptor status; and expression of Glut-1. Con clusion: Histologic and immunohistochemical tissue analysis was unable to s ufficiently explain the variation of FDG uptake in breast cancer. The degre e of metabolic changes after malignant transformation is most likely explai ned by a complex interaction between cellular energy demand and tumoral mic roenvironment. Therefore, FDG PET imaging may not be used to estimate tumor biologic behavior of breast cancer such as differentiation, histopathologi c grading, cell proliferation, or axillary lymph node status.