Lack of early bevacizumab‐related skeletal radiographic changes in children with neuroblastoma—response

Smith, Angela R.; Hennessy, Jane M.; Nelson, Stephen C.

doi:10.1002/pbc.21771

Cited by 1 publication

(1 citation statement)

References 4 publications

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“…Likewise, in a non-COG phase 1 study of the TKI sorafenib no increases in growth plate volume were observed; although one patient had delayed longitudinal growth, possibly related to concurrent anorexia and 9% weight loss, rather than physeal toxicity per se [33]. Smith et al have suggested that the patient's age at the time of drug administration may dictate the degree of skeletal toxicity more than simply the presence of open physes [34]. Despite the small number of patients in whom physeal abnormalities were detected in the six studies described herein, our results do not indicate a specific association between young age and the effect of anti-angiogenic agents on the developing skeleton.…”

Section: Discussionmentioning

confidence: 99%

Growth plate abnormalities in pediatric cancer patients undergoing phase 1 anti‐angiogenic therapy: A report from the children's oncology group phase I consortium

Voss

Bender

Spunt

et al. 2014

Pediatric Blood & Cancer

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Purpose Pre-clinical studies suggest that anti-angiogenic agents may be toxic to the developing growth plate. The purpose of this study was to evaluate the incidence of growth plate abnormalities in children with refractory cancer undergoing anti-angiogenic therapy. Materials and methods Targeted radiographic studies from 53 subjects enrolled on six separate Children’s Oncology Group Phase 1 and Pilot Consortium clinical trials evaluating new anti-cancer agents agents interfering with angiogenesis were reviewed. Subjects received tyrosine kinase inhibitors with anti-angiogenic effects (n=35), monoclonal antibodies targeting VEGF (n=13), or angiopoietin (n=5). Radiographs of their distal femur/proximal tibia were obtained at baseline. Follow-up radiographs were obtained after odd-numbered treatment cycles in patients with open growth plates who did not experience disease progression prior to cycle 3. Results Baseline and follow-up growth plate radiographs were acquired in 48/53 (90%) of patients. Five patients (9.4%), all of whom received a specific VEGF/VEGFR blocking agent [sunitinib (n=1) or pazopanib (n=4)], had growth plate abnormalities. Four patients had growth plate widening that was apparent on at least two successive radiographs, but was not confirmed by MRI. The fifth patient had progressive growth plate widening and evidence of physeal cartilage hypertrophy on MRI. Subsequent off treatment radiographs showed that the growth plate changes were reversible. Conclusion Growth plate abnormalities occur in a small, but relevant number of patients undergoing anti-angiogenic therapy. These results support the need for growth plate monitoring in children with open growth plates who are receiving anti-angiogenic therapy, and for improved methods to assess toxicity of anti-angiogenic agents to the developing skeleton.

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Section: Discussionmentioning

confidence: 99%