Rare monosomy 7 and deletion 7p at diagnosis of chronic myeloid leukemia in accelerated phase.

Clonal cytogenic evolution with the development of additional chromosomal abnormalities (ACAs) in chronic myelogenous leukemia (CML) is a marker for disease progression and is known to impact therapy and survival. The presence of ACAs has been shown to affect the responses to tyrosine kinase inhibitors (TKI) in patients with newly diagnosed CML in accelerated phase (CML-AP). We report a rare case of a CML patient who presented in CML-AP and was found to have multiple ACAs including monosomy 7, deletion 7p, trisomy 8, and an extra Philadelphia chromosome (Ph) in separate Ph-positive cell line, respectively. Six months after combined chemotherapy with TKI, the patient achieved a major cytogenetic response with disappearance of monosomy 7/deletion 7p with no major molecular response.

Clinicopathologic features of histiocytic lesions following ALL, with a review of the literature.

We describe the clinicopathologic features of 15 patients who had histiocytic lesions that followed acute lymphoblastic leukemia (ALL). Twenty-one separate histiocytic lesions were evaluated that covered a wide spectrum, some conforming to the usual categories of juvenile xanthogranulomas (5), Langerhans' cell histiocytosis (1), Langerhans' cell sarcoma (4), Rosai-Dorfman disease (1), and histiocytic sarcoma (4). Most were atypical for the category by histology, phenotype, or abnormally high turnover rate. Seven low-grade lesions defied easy categorization and were characterized only as "atypical histiocytic lesion" following ALL. For those evaluated, the molecular signature of the prior leukemia was present in the histiocytic lesion. In 3 of 15 patients, the leukemia and histiocytic lesion shared immunoglobulin H or monoclonal TCR gene rearrangements and, in 4 of 15 patients, clonal identity was documented by fluorescence in situ hybridization. Four patients died of progressive disease, 3 of whom had histiocytic sarcoma and 1 who had an atypical lesion. One patient died of recurrent ALL. The other 10 patients are alive, 7 after recurrences and treatment with surgery and/or chemotherapy. The post-ALL lesions are more aggressive than their native counterparts, but despite the demonstration of the presence of the leukemia signature in 7 of 15 patients, the prognosis is generally favorable, except for patients with histiocytic sarcoma. It remains unclear whether the histiocytic lesions arise as a line from the original ALL or whether transdifferentiation is involved.

Issues in neonatal cellular analysis.

Hematologic values in neonates differ significantly from those in older children and adults. Quantitative and qualitative differences are present as a reflection of the developmental changes during fetal hematopoiesis and, so, correlate with gestational age. At birth, the hemoglobin, mean corpuscular volume, and WBC counts of term newborns are significantly higher than those of older children and adults, and in preterm neonates the differences are even more pronounced. This review explores these differences and the major factors that account for them from the hematology laboratory standpoint. After a discussion of the developmental hematopoiesis and normal hematologic values in term and preterm neonates, important preanalytic factors, such as limited blood availability, effect of sampling site, and violent crying, and analytic interferences are examined. Finally, the review addresses resulting challenges in interpretation of hematologic test results in term and preterm neonates, especially issues surrounding neonatal reference intervals and critical value reporting, and suggests possible solutions.