F18-fluorodeoxyglucose positron emission tomography in the context of other imaging techniques and prognostic factors in multiple myeloma.

Publication Type:

Journal Article

Source:

Blood, Volume 114, Issue 10, p.2068-76 (2009)

Keywords:

2009, Aged, Aged, 80 and over, beta 2-Microglobulin, Bone Neoplasms, C-Reactive Protein, Cell Proliferation, Center-Authored Paper, Disease-Free Survival, Female, Fluorodeoxyglucose F18, Humans, L-Lactate Dehydrogenase, Male, Multiple Myeloma, Neoplasm Metastasis, Positron-Emission Tomography, Public Health Sciences Division, Radiopharmaceuticals, Risk Factors, Survival Rate

Abstract:

F18-fluorodeoxyglucose positron emission tomography (FDG-PET) is a powerful tool to investigate the role of tumor metabolic activity and its suppression by therapy for cancer survival. As part of Total Therapy 3 for newly diagnosed multiple myeloma, metastatic bone survey, magnetic resonance imaging, and FDG-PET scanning were evaluated in 239 untreated patients. All 3 imaging techniques showed correlations with prognostically relevant baseline parameters: the number of focal lesions (FLs), especially when FDG-avid by PET-computed tomography, was positively linked to high levels of beta-2-microglobulin, C-reactive protein, and lactate dehydrogenase; among gene expression profiling parameters, high-risk and proliferation-related parameters were positively and low-bone-disease molecular subtype inversely correlated with FL. The presence of more than 3 FDG-avid FLs, related to fundamental features of myeloma biology and genomics, was the leading independent parameter associated with inferior overall and event-free survival. Complete FDG suppression in FL before first transplantation conferred significantly better outcomes and was only opposed by gene expression profiling-defined high-risk status, which together accounted for approximately 50% of survival variability (R(2) test). Our results provide a rationale for testing the hypothesis that myeloma survival can be improved by altering treatment in patients in whom FDG suppression cannot be achieved after induction therapy.