TY - JOUR
T1 - PET tumor metabolism in locally advanced breast cancer patients undergoing neoadjuvant chemotherapy
T2 - Value of static versus kinetic measures of fluorodeoxyglucose uptake
AU - Dunnwald, Lisa K.
AU - Doot, Robert K.
AU - Specht, Jennifer M.
AU - Gralow, Julie R.
AU - Ellis, Georgiana K.
AU - Livingston, Robert B.
AU - Linden, Hannah M.
AU - Gadi, Vijayakrishna K.
AU - Kurland, Brenda F.
AU - Schubert, Erin K.
AU - Muzi, Mark
AU - Mankoff, David A.
PY - 2011/4/15
Y1 - 2011/4/15
N2 - Purpose: Changes in tumor metabolism from positron emission tomography (PET) in locally advanced breast cancer (LABC) patients treated with neoadjuvant chemotherapy (NC) are predictive of pathologic response. Serial dynamic [ 18F]-FDG (fluorodeoxyglucose) PET scans were used to compare kinetic parameters with the standardized uptake value (SUV) as predictors of pathologic response, disease-free survival (DFS), and overall survival (OS). Experimental Design: Seventy-five LABC patients underwent FDG PET prior to and at midpoint of NC. FDG delivery (K1), FDG flux (Ki), and SUV measures were calculated and compared by clinical and pathologic tumor characteristics using regression methods and area under the receiver operating characteristic curve (AUC). Associations between K1, Ki, and SUV and DFS and OS were evaluated using the Cox proportional hazards model. Results: Tumors that were hormone receptor negative, high grade, highly proliferative, or of ductal histology had higher FDG Ki and SUV values; on an average, FDG K1 did not differ systematically by tumor features. Predicting pathologic response in conjunction with estrogen receptor (ER) and axillary lymph node positivity, kinetic measures (AUC-0.97) were more robust predictors than SUV (AUC - 0.84, P = 0.005). Changes in K1 and Ki predicted both DFS and OS, whereas changes in SUV predicted OS only. In multivariate modeling, only changes in K1 remained an independent prognosticator of DFS and OS. Conclusion: Kinetic measures of FDG PET for LABC patients treated with NC accurately measured treatment response and predicted outcome compared with static SUV measures, suggesting that kinetic analysis may hold advantage of static uptake measures for response assessment.
AB - Purpose: Changes in tumor metabolism from positron emission tomography (PET) in locally advanced breast cancer (LABC) patients treated with neoadjuvant chemotherapy (NC) are predictive of pathologic response. Serial dynamic [ 18F]-FDG (fluorodeoxyglucose) PET scans were used to compare kinetic parameters with the standardized uptake value (SUV) as predictors of pathologic response, disease-free survival (DFS), and overall survival (OS). Experimental Design: Seventy-five LABC patients underwent FDG PET prior to and at midpoint of NC. FDG delivery (K1), FDG flux (Ki), and SUV measures were calculated and compared by clinical and pathologic tumor characteristics using regression methods and area under the receiver operating characteristic curve (AUC). Associations between K1, Ki, and SUV and DFS and OS were evaluated using the Cox proportional hazards model. Results: Tumors that were hormone receptor negative, high grade, highly proliferative, or of ductal histology had higher FDG Ki and SUV values; on an average, FDG K1 did not differ systematically by tumor features. Predicting pathologic response in conjunction with estrogen receptor (ER) and axillary lymph node positivity, kinetic measures (AUC-0.97) were more robust predictors than SUV (AUC - 0.84, P = 0.005). Changes in K1 and Ki predicted both DFS and OS, whereas changes in SUV predicted OS only. In multivariate modeling, only changes in K1 remained an independent prognosticator of DFS and OS. Conclusion: Kinetic measures of FDG PET for LABC patients treated with NC accurately measured treatment response and predicted outcome compared with static SUV measures, suggesting that kinetic analysis may hold advantage of static uptake measures for response assessment.
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U2 - 10.1158/1078-0432.CCR-10-2649
DO - 10.1158/1078-0432.CCR-10-2649
M3 - Article
C2 - 21364034
AN - SCOPUS:79954611821
SN - 1078-0432
VL - 17
SP - 2400
EP - 2409
JO - Clinical Cancer Research
JF - Clinical Cancer Research
IS - 8
ER -