18F-FDG PET Predicts Hematologic Toxicity in Patients with Locally Advanced Anal Cancer Treated With Chemoradiation.
Journal
Advances in radiation oncology
ISSN: 2452-1094
Titre abrégé: Adv Radiat Oncol
Pays: United States
ID NLM: 101677247
Informations de publication
Date de publication:
Historique:
received:
05
03
2019
revised:
10
06
2019
accepted:
19
06
2019
entrez:
5
11
2019
pubmed:
5
11
2019
medline:
5
11
2019
Statut:
epublish
Résumé
Hematologic toxicity (HT) during chemoradiation therapy (CRT) for anal cancer can lead to treatment breaks that compromise efficacy. We hypothesized that CRT-induced HT correlates with changes in active bone marrow (ABM) characterized by pre-/post-CRT positron emission tomography (PET)/computed tomography. Data from 36 patients with anal cancer who were treated with 18F-fluorodeoxyglucose PET/computed tomography scans 2 weeks before and 6 to 16 weeks after CRT were analyzed. Complete blood counts with differential within 2 weeks from, weekly during, and 2 week after treatment were obtained. HT was defined as baseline complete blood count change to nadir and posttreatment recovery. Total bone marrow was segmented into 2 subregions: lumbosacral (LS) pelvis (L5 vertebrae, sacrum, and coccyx) and lower pelvis (LP) (ilium, femoral head/neck, and greater and lesser trochanter). PET ABM was characterized as the volume having standard uptake value (SUV) greater than the mean uptake of unirradiated extrapelvic bone marrow. PET variables of pre-/post-CRT and HT predictors were analyzed by linear regression. Average pelvic ABM was significantly reduced from 52% to 41% in pre- to post-CRT PET scans for all patients ( HT was significantly associated with ΔABM in patients with anal cancer who were treated with CRT. LS-ABM was a robust surrogate for evaluating CRT-induced HT. Our results suggest implementation of ABM dosimetric constraints, V40 Gy ≤ 20-25%, may significantly reduce HT and lead to decreased treatment delays associated with clinical outcomes.
Identifiants
pubmed: 31681863
doi: 10.1016/j.adro.2019.06.005
pii: S2452-1094(19)30083-1
pmc: PMC6817719
doi:
Types de publication
Journal Article
Langues
eng
Pagination
613-622Subventions
Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States
Informations de copyright
© 2019 The Authors.
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