To determine the demographic and systemic parameters in children with solid malignancies and to ascertain which of them affected the delay in diagnosis, a retrospective study was performed on 315 children diagnosed with a solid tumor at our hospital, including epidemiological, social, and medical issues concerning the family, the child, the medical system, and the tumor. Lag time, defined as the interval between onset of symptoms and final diagnosis, including parent delay and physician delay, was estimated for each child. Mean lag time: 15.75 weeks (w), median: 7 w, range: 0-208 w. Lowest mean values appeared in kidney tumors, highest in epithelial, brain and soft tissue sarcomas. Mean parent delay: 4.42 w, median: 1 w, range: 0-130 w. Mean physician delay: 11.17 w, median: 4 w, range: 0-206 w. Among the demographic and personal parameters, the best predictors for diagnosis delay were age of child and father's ethnic origin. Several factors influenced diagnosis delay of childhood solid tumors. Recognizing these factors could minimize the delay, thereby improving the child's chances of survival.

To determine the demographic and systemic parameters in children with solid malignancies and to ascertain which of them affected the delay in diagnosis, a retrospective study was performed on 315 children diagnosed with a solid tumor at our hospital, including epidemiological, social, and medical issues concerning the family, the child, the medical system, and the tumor. Lag time, defined as the interval between onset of symptoms and final diagnosis, including parent delay and physician delay, was estimated for each child. Mean lag time: 15.75 weeks (w), median: 7 w, range: 0-208 w. Lowest mean values appeared in kidney tumors, highest in epithelial, brain and soft tissue sarcomas. Mean parent delay: 4.42 w, median: 1 w, range: 0-130 w. Mean physician delay: 11.17 w, median: 4 w, range: 0-206 w. Among the demographic and personal parameters, the best predictors for diagnosis delay were age of child and father's ethnic origin. Several factors influenced diagnosis delay of childhood solid tumors. Recognizing these factors could minimize the delay, thereby improving the child's chances of survival.

Objectives: To summarize and analyze the experience in CNS involvement (CNSI) in children with sarcomas treated in the above-mentioned institutions. Patients and Methods: From 1990 to 2001, all medical charts were retrospectively reviewed: 19 sarcoma patients (12 boys and 7 girls) were diagnosed with CNSI (4 osteogenic sarcomas, 11 Ewing sarcomas, 2 rhabdomyosarcomas, 1 alveolar soft part sarcoma and 1 mesenchymal chondrosarcoma). Mean age of all patients at the time of initial diagnosis was 14.9 years (range: 4–24 years), mean age at the time when CNSI was diagnosed was 16.9 years (range: 5.5–27 years). Results: The frequency of CNSI among our patients was 6.17%. The following symptoms and signs (sometimes combined) presented: headache (10 patients), nausea and vomiting (6 patients), seizures (11 patients) and focal neurological signs (9 patients). The mean duration of time elapsed since diagnosis of CNSI till death or last follow-up was 5.2 months (SD: ±5.7 months). Four patients received chemotherapy (CT) alone, 8 CT and radiotherapy (RT), 2 RT alone, 3 supportive treatment only, 1 CT and surgery and 1 surgery alone. Sixteen patients died; there was no significant difference in the duration of survival between those who were treated with RT or surgery (mean ± SD: 6.77 ± 6.56 months) and those who received only CT or supportive treatment (mean ± SD: 2.60 ± 2.94 months) (p = 0.07). Brain disease was the main cause of death in all but 1 patient who died 4 days after autologous bone marrow transplantation from uncontrolled sepsis. In 16 patients, CNSI was part of a metastatic disease. Conclusions: Among children with sarcoma, CNSI is encountered in 6.17% of cases. More effective therapy has to be developed in order to improve their outcome.

Twenty-one pediatric retinoblastoma (RB) patients treated between 1976 and 1994 were evaluated for late treatment-related complications. Median age at diagnosis was 24 months; median age at follow-up was 12 years; median follow-up time was 12 years. Of the 21 patients, 14 had unilateral RB and 7 had bilateral RB. Thirteen patients had received external radiotherapy and 8 children were treated by chemotherapy. Twenty-one patients had undergone enucleation. Radiation-induced cataracts were found in 3 patients, radiation retinopathy in 1, enucleation and postradiotherapy contracted socket in 1, very low visual acuity postradiotherapy in 3, severe hypotelorism in 2, growth hormone deficiency in 2, neurocognitive disorders in 6, and orbital deformation due to radiation bone atrophy was moderate-severe in 12 patients. Azoospermia was found in 1 patient treated by cyclophosphamide and vincristine. The most frequent sequela in this group of RB-cured children were postradiotherapy orbital deformation due to bone atrophy and neurocognitive disabilities. Late radiation effects must be avoided by using modern, innovative, and more sophisticated radiotherapeutic techniques. Late treatment-related complications justify the long-term follow-up of childhood RB survivors.

Heparanase is an endoglycosidase that specifically cleaves heparan sulfate (HS) side chains of heparan sulfate proteoglycans, the major proteoglycan in the extracellular matrix (ECM) and cell surfaces. Heparanase upregulation was documented in an increasing number of primary human tumors, correlating with reduced postoperative survival rate and enhanced tumor angiogenesis. The purpose of the current study was to determine heparanase levels in blood samples collected from pediatric cancer patients using an ELISA method. Heparanase levels were elevated four-fold in the plasma of cancer patients compared with healthy controls (664 +/- 143 vs 163 +/- 18 pg/ml, respectively). Evaluating plasma samples following anticancer therapy revealed reduced heparanase levels (664 +/- 143 vs 429 +/- 82 pg/ml), differences that are statistically highly significant (P = .0048). Of the 55 patients with complete remission (CR) or very good partial remission (VGPR) at restaging, 41 (74.5%) had lower heparanase amounts, whereas 14 patients (25.5%) had similar or higher amounts of plasma heparanase. All nine patients with stable or advancing disease had similar or elevated levels of heparanase on restaging. The results show that heparanase levels are elevated in the plasma of pediatric cancer patients and closely correlate with treatment responsiveness, indicating that heparanase levels can be used to diagnose and monitor patient's response to anticancer treatment.