Prenatally diagnosed neuroblastomas are predominantly adrenal in origin and frequently cystic. The liver is the most common site of dissemination and bone involvement is notably absent. The vast majority of these infants have a favorable stage of disease (I, II, and IV-S) and favorable biologic features, and consequently have an excellent prognosis. Although surgery alone is curative for most patients, a period of observation may avoid surgery in some individuals who may achieve spontaneous regression.

Telomerase activity and telomere length in mononuclear cells proliferation of lymphoid or myeloid precursors with arrested (MNCs) and granulocytes from peripheral blood (PB) and bone maturation. 1 In this disorder, the leukemic clone expands in marrow (BM) specimens were studied in pediatric acute leukethe bone marrow (BM), interferes with normal hematopoiesis mia (ALL, n = 15; AML, n = 1) and pediatric solid tumor (ST) and eventually, non-hematopoietic tissues are infiltrated. patients (n = 9) at diagnosis, during and after chemotherapy. In Acute lymphocytic leukemia (ALL) was one of the first maligfour ST patients, tumor tissue was also available. For comparative analysis, MNCs from healthy donors (n = 53) were ananancies reported to respond to chemotherapy and is curable that can synthesize telomeric repeats onto chromosomes. [3][4][5][6] telomere loss in granulocytes as compared to MNCs was more Recently, borderline telomerase activity has been detected in pronounced with 1.8 vs 1 kbp, respectively (P = 0.014). Our results demonstrate that at diagnosis, telomerase was consisthuman primitive hematopoietic cells and in stimulated lymently and highly upregulated in BM and PB specimens in leukephocytes which increased significantly with cytokine-induced mia, decreased after induction therapy, and correlated with ex vivo expansion. 7-10 However, in most other normal remission. BM specimens in leukemia had higher telomerase somatic cells, telomerase has not been detected, and conseactivity, probably due to the greater leukemic burden than in quently telomere shortening may be anticipated after a limited PB. Telomeres were significantly longer in children than in number of population doublings. [11][12][13] In contrast, spon- progressive telomere length shortening in the absence of telo-

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Trichodynia is a commonly encountered symptom in patients with diffuse alopecia, and depression and somatoform dissociation disorders may play an important role in its aetiology. Our data provide no evidence that serum levels of zinc, folate or vitamin B(12) are involved in the pathogenesis of trichodynia.

Telomeres of hematopoietic cells shorten with age, possibly contributing to the aging-associated hematopoietic pathology (immunosenescence, malignant transformation). Accelerated telomere shortening is seen with replicative stress, such as during administration of serial chemotherapy cycles for the treatment of childhood cancer. To define the long-term consequences of pediatric cancer treatment on hematopoietic cell telomere length, we undertook a prospective 4-year follow-up study of a 61-patient cohort of pediatric malignancies in a community-based setting. We found that mononuclear cells (MNC) and granulocytes of children with standard-risk acute lymphoblastic leukemia (ALL) suffered minimal telomere shortening throughout therapy (less than 1 kbp; average follow-up, 20 months), while those of children with solid tumors showed greater and more heterogenous telomere attrition (0.5-2.8 kbp, average follow-up, 9 months). In addition, we evaluated the role of telomerase, the enzyme commonly up-regulated in pediatric leukemic and solid tumor cells for telomere length maintenance, as a disease marker. Serial determinations of telomerase in MNC were useful to confirm disease remission in leukemia, but play no role in the follow-up of children with solid tumors.