Purpose: To describe the timing of chemotherapy initiation after surgery for Wilms tumor (WT) and neuroblastoma within a dedicated children’s cancer center. Methods: A single-institution retrospective cohort study identified patients that underwent resection of unilateral WT or high-risk neuroblastoma and received adjuvant chemotherapy treatment. Adjuvant chemotherapy initiation and postoperative complications were recorded. Results: Among 47 WT patients, the median time to chemotherapy initiation was 11 days [interquartile range IQR 7-14]. 3 WT patients had post-operative complications, but all preceded chemotherapy. Among 83 patients treated for high-risk neuroblastoma, the median time to chemotherapy was 11 days [IQR 9-14]. High-risk neuroblastoma patients with 30-day postoperative complications had a significantly longer time to initiation of adjuvant chemotherapy (odds ratio 1.13; p=0.008). Many of these complications preceded and delayed the initiation of post-operative chemotherapy. No complications occurred in the group of 12 (25%) WT patients or 16 (19.3%) neuroblastoma patients who started chemotherapy ≤7 days after surgery. Conclusion: There is no association between early initiation of adjuvant chemotherapy and post-operative complications including wound healing. Early initiation of chemotherapy (≤7 days) is feasible in unilateral WT or high-risk neuroblastoma patients who are otherwise doing well without resulting in a preponderance of wound healing complications.

32GABA type-A (GABA-A) receptors containing the α2 subunit (Gabra2) are expressed in most brain regions and are 33 critical in modulating inhibitory synaptic function. Genetic variation at the GABRA2 locus has been implicated in epilepsy, 34 affective and psychiatric disorders, alcoholism and drug abuse. Gabra2 expression varies as a function of genotype and is 35 modulated by sequence variants in several brain structures and populations, including F2 crosses originating from 36 C57BL/6J (B6J) and the BXD recombinant inbred family derived from B6J and DBA/2J. Here we demonstrate a global 37 reduction of Gabra2 brain mRNA and protein in the B6J strain relative to other inbred strains, and identify and validate 38 the causal mutation in B6J. The mutation is a single base pair intronic deletion located adjacent to a splice acceptor site 39 that only occurs in the B6J reference genome. The deletion became fixed in B6J between 1976 and 1991 and is now 40 pervasive in many engineered lines, BXD strains generated after 1991, the Collaborative Cross, and the majority of 41 consomic lines. Repair of the deletion using CRISPR-Cas9 mediated gene editing on a B6J genetic background completely 42 restored brain levels of Gabra2 mRNA and protein. Comparison of transcript expression in hippocampus, cortex, and 43 striatum between B6J and repaired genotypes revealed alterations in GABA-A receptor subunit expression, especially in 44 striatum. These results suggest that naturally occurring variation in GABRA2 levels between B6J and other substrains or 45 inbred strains may also explain strain differences in anxiety-like or alcohol and drug response traits related to striatal 46 function. Characterization of the B6J private mutation in the Gabra2 gene is of critical importance to molecular genetic 47 studies in neurobiological research as this strain is widely used to generate genetically engineered mice and murine genetic 48 populations, and is the most widely utilized strain for evaluation of anxiety-like, depression-like, pain, epilepsy, and drug 49