A positron emission tomography–computed tomography (PET-CT) maximum standardized uptake value (SUVmax) of 10 or greater is not sufficient for determining whether patients with chronic lymphocytic leukemia (CLL) who fail kinase inhibitor (KI) treatment are undergoing Richter transformation (RT).1
Previous studies showed that a PET-CT SUVmax of 10 or greater among KI-naive patients with CLL can distinguish between progression and RT, and may therefore predict for survival. For this prospective phase 2 study, researchers investigated whether PET-CT SUV has clinical utility among patients with CLL receiving venetoclax who failed therapy with ibrutinib or idelalisib.
Of the 57 patients who met the criteria for biopsy at screening, only 35 underwent biopsy, of which 8 patients had RT, 2 had other malignancies, and 25 had a biopsy that revealed CLL.
A logistic regression analysis of these 35 patients showed that PET SUVmax of 10 or greater did not detect RT effectively in post-KI patients vs CLL (odds ratio [OR], 1.79; 95% CI, 0.4-9; P = .5); sensitivity was 26%, specificity was 82%, positive predictive value was 63%, and negative predictive value was 50%. The receiver operator characteristic (ROC) area for SUVmax of 10 or greater was 56%.
Fifty-six patients discontinued venetoclax because of CLL progression (28) or biopsy-confirmed RT (6). PET SUV of at least 10 did not predict for patient outcomes among those treated with venetoclax.
Median time to CLL progression and to RT was 8.4 months and 11.5 months, respectively. Among patients who discontinued venetoclax because of RT, the median number of FDG-avid nodes before venetoclax treatment at screening was 3, and SUVmax was 5.5.
The authors concluded that “PET SUV [of at least] 10 alone lacks both sensitivity and specificity to distinguish CLL progression vs RT…Analysis to identify clinical factors distinguishing KI-treated pts with likely RT is ongoing.”
- Mato AR, Wierda WG, Davids MS, et al. Analysis of PET-CT to identify Richter’s transformation in 167 patients with disease progression following kinase inhibitor therapy. Oral presentation at: American Society of Hematology 59th Annual Meeting & Exposition; December 9-12, 2017; Atlanta, GA.
This article originally appeared on Cancer Therapy Advisor