Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten years ago, we made an incidental flow cytometric observation while immunophenotyping biopsy and marrow samples from children suspected to have leukemia/non-Hodgkin's lymphoma, but were subsequently diagnosed with neuroblastoma. The samples contained neoplastic CD45(-) cells that had an extremely bright CD56(+) (beyond the fourth decade on a four-decade scale) population distinguishable from CD45(+)CD56(usual density+) natural killer lymphocytes as well as other CD45(-)CD56(usual density+) nonhematopoietic tumors such as small cell carcinoma or melanoma. Following the "rare event" philosophy of selecting one negative and two positive antigens, we initially tried a "cocktail" of CD45(-)CD56(very bright+) neuron-specific enolase (NSE)(cytoplasmic+). We later modified the procedure to a more clinically applicable "lysed whole blood" CD45(-)CD56(very bright+) ganglioside GD2(+) cocktail to improve turnaround time (eliminating the cell permeabilization step for cytoplasmic NSE analysis), specificity, and sensitivity of the assay. A total of 123 marrow/tissue/fluid samples were analyzed by the various forms of the assay. Clearly interpretable samples had an 83% specificity and a 100% sensitivity. The three-color GD2 assay has successfully detected cells in marrow samples to a level of 0.002% (1 per 10(5) cells) using patient samples (not artificially "spiked" material). We added CD81 expression of the neuroblastoma cells as a fourth color and now use this rare event clinical test to help stage and monitor all patients with neuroblastoma.
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PMID:Flow cytometric immunophenotyping test for staging/monitoring neuroblastoma patients. 1580 71

In a retrospective cohort study of 404,106 live births in the northern region of England, 1975-1986, we investigated whether higher levels of community infections during the mother's pregnancy and in early life were risk factors for cancer, by diagnostic group (leukaemia and non-Hodgkin's lymphoma, Hodgkin's disease, brain/spinal tumours, neuroblastoma, other tumours), diagnosed 1975-2001 under age 15 years. Logistic regression was used to relate risk to measures of community infections (measles, respiratory and other infections) in 3 prenatal and 2 postnatal quarters. There was an increased risk of Hodgkin's disease among children exposed around birth to higher levels of measles (odds ratio for trend = 2.3, 95% confidence interval 1.3-4.2, p = 0.01). For other diagnostic groups, there was no consistent evidence of an association between risk and exposure to infections. Although the significant association observed for Hodgkin's disease may be a chance finding, consequent to multiple hypothesis testing or the ecologic nature of the study, it is consistent with other recent epidemiologic results suggesting that the risk of Hodgkin's disease may be associated with exposure to infections.
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PMID:Childhood cancer in relation to infections in the community during pregnancy and around the time of birth. 1264 Jun 86

The link between exposure to environmental mutagens and the development of cancer is well established. Yet there is a paucity of data on the relationship between gene-environment interactions and the mechanisms associated with the somatic mutational events involved with malignant transformation, especially in children. To gain insight into somatic mutational mechanisms in children who develop cancer, we determined the background mutant frequency (Mf) in the hypoxanthine phosphoribosyl transferase (HPRT) reporter gene of peripheral blood lymphocytes from pediatric cancer patients at the time of diagnosis and prior to therapeutic intervention. We studied 23 children with hematologic malignancies and 31 children with solid tumors prior to initial therapeutic intervention. Children with solid tumors, specifically sarcomas, and Hodgkin's disease were significantly older and had elevated HPRT Mfs (6.1 x 10(-6) and 3.7 x 10(-6), respectively) at the time of diagnosis, compared to normal controls (2.3 x 10(-6)) and other pediatric tumor groups including children with acute lymphocytic leukemia and non-Hodgkin's lymphoma (ALL/NHL, 1.7 x 10(-6)), central nervous system tumors (CNS, 3.6 x 10(-6)), and neuroblastoma (1.9 x 10(-6)). Of importance is that the significant differences observed in HPRT Mfs between these groups no longer existed after correcting for the effects of age. These data demonstrate that in children who develop cancer there appears to be no significant increase in background HPRT Mf that would indicate significant exposure to genotoxic chemicals or an underlying DNA repair defect resulting in genomic instability. In addition, these data demonstrate the importance of correcting for the effect of age when comparing the frequency of somatic mutations in children and should provide baseline data for future longitudinal biomonitoring studies on the genetic effects of chemotherapy in children treated for cancer.
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PMID:Comparative analysis of HPRT mutant frequency in children with cancer. 1287 12

Small blue cell tumors are a group of tumors that share a common histologic characteristic with H&E staining. This makes differentiation from one another difficult as they all appear small, blue and round. Even though they all appear the same, they are vastly different from each other. Several different techniques have been developed to help further delineate and classify these tumors which include: small cell lung cancer (SCLC); non-Hodgkin's lymphoma (NHL); Ewing's sarcoma; rhabdomyosarcoma; Merkel carcinoma; neuroblastoma; carcinoid tumors; and intra-abdominal desmpolastic small round cell tumor. Using immunoperoxidase staining, reverse transcriptase polymerase chain reaction and fluorescence in situ hybridization techniques, these tumors have been successfully differentiated from one another. This separation makes staging and treatment of these tumors more effective, as not all of these tumors respond to the same modality of treatment. The following review summarizes some of the recent findings in the various small blue cell tumors and with the potential of novel therapies.
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PMID:Recent advances in the molecular biology, diagnosis and novel therapies for various small blue cell tumors. 1292 79

We report an estimation of the incidence of childhood cancer among natives of French Polynesia (FP) during the 1985-1995 period. Our data were acquired from the Cancer Registry of FP and through an extensive investigation of other potential sources of information. The mean population of children between 1985 and 1995 was estimated to be 63 401 inhabitants, 32 487 of whom were boys and 30 914 girls, born and residing in FP. During the 1985-1995 period, 87 incident cases of childhood cancer were recorded among inhabitants born in FP or of an unknown place of birth (n = 2). Childhood cancer incidence had attained 125 cases/million child years and was very similar among girls (126 x 10(-6)) and boys (123 x 10(-6)), this incidence being slightly lower than among other populations of similar ethnic origin: Standardized Incidence Ratio (SIR) = 0.8 (95% CI: 0.7-1.0) when compared with New Zealand Maoris and SIR = 0.8 (95% CI: 0.6-1.0) when compared with natives from Hawaii. For both sexes considered together, the most frequent cancer type was leukaemia, followed by central nervous system (CNS) malignancies, neuroblastoma, and non-Hodgkin's lymphoma (NHL). Only one case of gonadal and germ cell tumours and one case of carcinoma were reported. Childhood cancer incidence was predominant among children living in the Windward, Leeward and Marquesas Islands and the Tuamotu-Gambier archipelago, but lower in the Austral Islands. The incidence of acute non-lymphocytic leukaemia (ANLL) decreased from 3.3 x 10(-5) between 1985 and 1989, an unexpectedly high incidence, to 0.8 x 10(-5) between 1990 and 1995.
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PMID:Childhood malignancies in French Polynesia during the 1985-1995 period. 1536 Nov 14

Improvements in the treatment of the cancers occurring among children and adolescents have resulted in a large number of patients achieving long-term survival. Treatment-related factors have been shown to have an impact on subsequent health status and quality of life, although there are limited data on survivors who are now 2 or more decades past treatment. The Childhood Cancer Survivor Study (CCSS) was established as a resource for investigating the long-term outcomes of a cohort of 5-year survivors of pediatric and adolescent cancer, who were diagnosed between 1970 and 1986. The CCSS consists of more than 14,000 active participants, including survivors of leukemia, brain tumors, Hodgkin's disease, non-Hodgkin's lymphoma, Wilms' tumor, neuroblastoma, soft-tissue sarcoma, and bone tumors, who have provided self-reported sociodemographicand health-related information. The survivor population has been found to be at increased risk of a broad spectrum of adverse outcomes, such as late mortality, second cancers, pulmonary complications, pregnancy loss, giving birth to offspring with low birth weights, and decreased educational attainment. The ongoing evaluation of large and diverse cohorts of cancer survivors, through resources such as the CCSS, will aid in further identifying high-risk individuals who should be the target of innovative intervention strategies.
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PMID:The Childhood Cancer Survivor Study: a resource for research of long-term outcomes among adult survivors of childhood cancer. 1594 96

In this study, we have aimed to characterise the survival of all 0-14 year-old New Zealand children who were diagnosed with cancer during 1990-1993. Four hundred and nine children were followed up using two largely independent sources. We calculated Kaplan-Meier survival probabilities and investigated various prognostic factors using the Cox model. Five-year survival for all cancers was 66% (95% confidence interval (CI) 62-71%) and for acute lymphoblastic leukaemia it was 70% (CI 62-79%). Cancers with particularly favourable prognoses (followed by their respective 5-year survival probabilities) included: retinoblastoma 100% (CI 74-100%), Hodgkin's disease 93% (CI 79-100%), non-Hodgkin's lymphoma 87% (CI 73-100%) and osteosarcoma 91% (CI 74-100%). Cancers with poor prognoses included: neuroblastoma 35% (CI 14-56%), rhabdomyosarcoma 42% (CI 14-70%) and central nervous system tumours 49% (CI 38-60%). Girls with any cancer had a significantly lower risk of death than boys. Generally, survival for childhood cancers in New Zealand increased greatly between 1961-1965 and 1990-1993. Nevertheless, outcomes for some cancers remained poor.
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PMID:Population-based survival of children in New Zealand diagnosed with cancer during 1990-1993. 1596 13

It has been suggested that breast milk may play a role in the prevention of certain childhood cancers. We undertook a systematic review of published studies investigating the association between breast-feeding and childhood cancers using Medline (1966 to June 2004), supplemented with auto alerts and manual searches. Analyses are based on odds ratios for specific cancers among those ever breast-fed compared with those never breast-fed, pooled using random-effects models. Forty-nine publications were potentially relevant; of these, 26 provided odds ratio estimates for at least one childhood cancer outcome and were included in metaanalyses. Overall, 92% of the studies were case-control studies, 85% relied on long-term recall of feeding history, only 8% examined breast-feeding exclusivity and control response rates were under 80% in over half. Metaanalyses suggested lower risks associated with having been breast-fed of 9% (95% CI = 2-16%) for acute lymphoblastic leukemia, 24% (3-40%) for Hodgkin's disease and 41% (22-56%) for neuroblastoma, with little between-study heterogeneity. The estimates for Hodgkin's disease and neuroblastoma, however, were driven by single studies. There was little evidence that breast-feeding was associated with acute nonlymphoblastic leukemia, non-Hodgkin's lymphoma, central nervous system cancers, malignant germ cell tumors, juvenile bone tumors, or other solid cancers. In conclusion, ever having been breast-fed is inversely associated with acute lymphoblastic leukemia, Hodgkin's disease and neuroblastoma in childhood, but noncausal explanations are possible. Even if causal, the public health importance of these associations may be small. Our estimates suggest that increasing breast-feeding from 50% to 100% would prevent at most 5% of cases of childhood acute leukemia or lymphoma. (c) 2005 Wiley-Liss, Inc.
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PMID:Breast-feeding and childhood cancer: A systematic review with metaanalysis. 1598 34

We determined risk of cancer among first-degree relatives of 5-year survivors of childhood leukemia, lymphoma, central nervous system tumors, sarcomas, Wilms' tumor, and neuroblastoma. Subjects were 13,703 participants in the Childhood Cancer Survivor Study. Family history was collected on 56,759 first-degree relatives using a self-reported questionnaire. Incidence was compared with age- and sex-specific rates using the U.S. Surveillance, Epidemiology and End Results program. Siblings of the survivors had an increased risk of cancer [standardized incidence ratio (SIR), 1.5; 95% confidence interval (95% CI), 1.35-1.7]. Risk was elevated for siblings of probands of leukemia (SIR, 1.3; 95% CI, 1.0-1.6), Hodgkin's disease (SIR, 1.5; 95% CI, 1.2-1.9), non-Hodgkin's lymphoma (SIR, 1.8; 95% CI, 1.3-2.5), Wilms' tumor (SIR, 1.9; 95% CI, 1.2-3.2), soft tissue sarcoma (SIR, 1.5; 95% CI, 1.0-2.2), and bone tumors (SIR, 1.6; 95% CI, 1.2-2.2). Cancer risk was elevated in siblings (SIR, 2.4; 95% CI, 1.5-3.7) and offspring (SIR, 15.0; 95% CI, 5.3-42.9) of probands with second malignant neoplasms (SMN) compared with relatives of probands without SMNs. Siblings of probands with leukemia, Hodgkin's disease, neuroblastoma, and Wilms' tumor had elevated risks for the same malignancies. Parents had no increased risk (fathers' SIR, 0.7; 95% CI, 0.7-0.8; mothers' SIR, 0.9; 95% CI, 0.9-1.0). Seventy percent of siblings' cancers developed in adulthood. These findings suggest that familial cancer syndromes may be revealed as this cohort and family members age and with accrual of more offspring and subjects with SMNs.
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PMID:Increased risk of cancer among siblings of long-term childhood cancer survivors: a report from the childhood cancer survivor study. 1610 38

The oncogenic transcription factor PAX5 is an important developmental regulator and is implicated in the pathogenesis of several malignancies. The PAX5 gene is involved in medulloblastoma, non-Hodgkin's lymphoma, transitional cell carcinoma of the bladder, neuroblastoma, breast cancer and SCC. In the current study, to determine the potential involvement of PAX5 in oral squamous-cell carcinoma (OSCC) and leukoplakias, we evaluated the status of PAX5 mRNA and protein expression in OSCC cell lines, human primary OSCCs, and leukoplakias by real-time quantitative reverse transcriptase-polymerase chain reaction, Western blot analysis, and immunohistochemistry. A significant increase in PAX5 expression was observed in all OSCC-derived cell lines examined compared to human normal oral keratinocytes (HNOKs). In immunohistochemistry, 78% of tumors and 42% of leukoplakias examined were positive for PAX5, while no immunoreaction was observed in corresponding normal tissues. The results suggest that PAX5 plays an important role during oral carcinogenesis, especially in the early stage, and that the gene may have potential as a biomarker and therapeutic target for OSCC.
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PMID:Overexpression of PAX5 in oral carcinogenesis. 1701 84


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