Recently established by the World Health Organization classification, "nasal" and "nasal-type" NK/T-cell lymphoma arise from natural killer (NK) cells. They have distinct clinicopathologic features, specific genotype and phenotype, and a high association with Epstein-Barr virus infection. Nasal-type NK/T-cell lymphoma arise from extranasal sites including skin, soft tissue, gastrointestinal tract, liver, spleen, testes, lung, and central nervous system. Most cases are reported from Asia and South America in adults. There are very few cases reported in the pediatric age group. We report an 11-year-old child with extranodal nasal-type NK/T-cell lymphoma presenting as hemophagocytic syndrome and multiorgan system failure with fatal outcome.

A 58-yr-old male patient presented in the blastic phase of chronic myelogenous leukemia (CML). Cytogenetic studies revealed a 45 XO Ph1 chromosome pattern in bone marrow cells during a short remission and again in the blastic phase of the disease. The patient expired 8 mo following diagnosis. The blastic phase of CML can stimulate acute myelogenous leukemia (AML) clinically and hematologically; CML can be differentiated by the presence of the Ph1 chromosome and the stigmata of CML. Absence of the Y chromosome from the bone marrow in CML is a recently described finding. Previous reports indicating the prevention of the blastic phase in patients with this karyotype could not be confirmed by our or other recently reported cases.

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One of the most frequent chromosomal translocations in human beings is 11q/22q, which results in the "partial trisomy of 22q syndrome." However, the breakpoint on the long arms of chromosomes 11 and 22 is still a matter of controversy. In the present study, we have used chromosomes from lymphocytes of a neonate who happened to have this classical abnormality, and by R-banding prometaphase chromosomes with acridine orange it has been possible to establish that the translocation between chromosomes 11 and 22 resulted from 3:1 meiotic maternal nondisjunction. A detailed analysis of the chromosome regions involved in this translocation revealed that the breakpoints on chromosomes 11 and 22 were at 11q23.3 and 22q11.1, respectively.