Cytogenetics can inform risk stratification in pediatric acute myeloid leukemia (AML). We describe the first case of a newborn with leukemia cutis found to have AML harboring a cryptic insertional t(8;16)(p11.2;p13.3) with associated KAT6A/CREBBP fusion identified exclusively by fluorescence in situ hybridization (FISH). Expectant management resulted in spontaneous leukemia resolution. The identification of t(8;16)(p11.2;p13.3) may serve as a biomarker for spontaneous remission in congenital AML. FISH for this translocation is warranted in congenital AML with a normal karyotype, and patients with KAT6A/CREBBP fusion should be conservatively managed. While 50% of spontaneously remitting congenital AML with t(8;16)(p11.2;p13.3) may recur, high salvage rates are attained with standard therapy.

In vitro conditions affecting synthesis of sulfated proteoglycans by cell suspensions derived from monolayer cell cultures of normal and rheumatoid synovial tissue were examined. The capacity of cells to synthesize proteoglycans was estimated by the incorporation of 35sSulfate into cetylpyridinium chloride-precipitable material. Synthesis of sulfated proteoglycans was maximal during log phase, and after 2-3 hours of recovery from disaggregation. Normal synovial cells appeared to be more sensitive to changes in serum concentration than were rheumatoid synovial cells, but rheumatoid synovial cells were more sensitive to changes in cell density. The proportion of newly synthesized extracellular proteoglycans increased with the duration of incubation in 3 5~u~f a t e . Synthesis of sulfated proteoglycans by human synovial cells has recently been demonstrated by several techniques, including the incorporation of "Ssulfate into cetylpyridinium chloride (CPC)-precipitable material (1-5). Synthesis of sulfated proteoglycans by normal and rheumatoid synovial cell lines in longterm culture was influenced by repeated passage of the

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