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)

All known tumor types have been reported in the neonate. A numerical listing and discussion are beyond the scope of this review. Wells and Fraumeni give some insight into common congenital malignant neoplasms. Table 2 lists the percentage of neonatal deaths caused by type-specific cancers. Retinoblastoma is probably the most common malignant tumor in the neonate. About seven per cent of these tumors have been apparent at birth. This tumor is not discussed in either article because it is not lethal until muypes in neonatal and pediatric patients. Some congenital malformations in the in the neonate are recognized as being frankly benign (cysts), potentially malignant (teratomas), and frankly malignant (neuroblastoma). A high percentage of teratomas are benign in the newborn period. Leukemia in the newborn appears to be more aggressive yet neuroblastoma has a better prognosis. More studies are needed to help us define why the neonate does better with some tumors and worse with others. Surface cell markers on neonatal leukemia, B and T cell function studies, and other immunologic surveillance studies are needed. Study of neonatal oncology may add to our knowledge of carcinogenesis and oncogenesis in the future.
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PMID:Neonatal oncology. 19 75

Malignant mesenchymoma developed in an 18-year-old patient with phenytoin-associated cleft lip and palate. Although these conditions may be related by chance, the possibility of transplacental carcinogenesis by phenytoin should be considered, especially since neuroblastoma was reported recently in two children with phenytoin-induced malformations. Following combination chemotherapy for metastases, the patient experienced a 7-year disease-free interval, which is consistent with recent improvement in the treatment of soft-tissue sarcomas.
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PMID:Malignant mesenchymoma and birth defects. Prenatal exposure to phenytoin. 57 39

A case-control study was conducted 1) to determine whether maternal prenatal drug consumption increases the risk of neuroblastoma in the child and, if so, 2) to see if the size of the risk depends on whether the case is inherited or sporadic. Mothers of children with newly diagnosed neuroblastoma (n = 101) were compared with mothers of children newly diagnosed with other forms of childhood cancer (n = 690). Cases and controls were selected from the population of childhood cancer patients at St. Jude Children's Research Hospital, Memphis, Tennessee, between 1979 and 1986. The patients' mothers were interviewed to ascertain their prenatal medication, alcohol, and tobacco consumption patterns. Unconditional logistic regression models were used to adjust for maternal age at birth, patient age at diagnosis, race, social class, exposure to x-ray, miscarriage, and other confounding variables. Adjusted odds ratios were estimated for the total sample and for subgroups that had a higher probability of containing inherited cases. Drugs associated with neuroblastoma case status include diuretics for hypertension (odds ratio (OR) = 4.1, 95 percent confidence interval (CI) 1.0-16.9), tranquilizers (OR = 2.1, 95 percent CI 1.1-4.3), nonprescription pain relievers (OR = 1.9, 95 percent CI 1.1-3.1), and cigarettes (OR = 1.9, 95 percent CI 1.1-3.2). The odds ratios for maternal prenatal drug consumption for the group with inherited cases and the total sample were approximately the same. This equality is inconsistent with predictors based on Knudson's two-stage model of carcinogenesis.
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PMID:Influence of the mother's prenatal drug consumption on risk of neuroblastoma in the child. 151 82

We developed a new approach for detecting the gene amplification of cancer DNAs with restriction landmark genomic scanning (RLGS). In cancer research, much effort has been made to find the amplified loci of cancer DNAs, because many lines of evidence indicate association between oncogene amplification and carcinogenesis. Conventionally, such gene amplification has been detected by using Southern hybridization with DNA probes. However, only the information of one locus can be obtained by one hybridization procedure, and analysis of many loci throughout the genome is too laborious and time consuming, even if only several candidate genes are investigated. On the other hand, the "in-gel renaturation method" was reported as another alternative for detection of amplified regions. However, even though this method is much improved, it is difficult to detect less than 7-fold amplification, which is often higher than the amplification of many cancer cases. To overcome these limitations and, in addition, to locate the amplified DNA two dimensionally, we applied RLGS for analysis of DNA amplification in cancer tissues, such as breast cancer (infiltrative tubuloadenocarcinoma), neuroblastoma, meningioma (endotheliomatous meningioma), and thyroid cancer (papillary adenocarcinoma). In some cases of breast cancer, several amplified spots located on the same amplicon were detected. In thyroid cancer, in which no amplification has yet been reported, low-grade amplification was also detected. In this report, we demonstrated that RLGS allows us to screen 2000-3000 restriction landmarks distributed on the genome simultaneously, and even low-grade amplification could be detected effectively. Thus, RLGS has proven to be a very useful method in detecting DNA amplification.
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PMID:New approach for detection of amplification in cancer DNA using restriction landmark genomic scanning. 161 37

The common malignancies apparently develop by a stepwise accumulation of gene alterations including oncogenes and suppressor genes. Point mutation or deletion might be an early event for carcinogenesis and tumor progression, while amplification of several oncogenes occur as a late event. Amplification of some oncogenes apparently relate with patient prognosis, i.e. erbB2 for breast, ovarian and gastric carcinomas, HST-1/INT-2 for esophageal and breast carcinomas, and N-myc for neuroblastoma. Although amplification of erbB1 is less common, its expression indicate poorer prognosis in patients with esophageal, gastric and bladder carcinomas. Combination analysis of the gene amplification and other gene alterations, such as p53 gene might provide more useful clinical informations for the postoperative management and prognosis of cancer patients.
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PMID:[Oncogene and patient prognosis]. 205 66

N-Nitrosomorpholine (NMOR) is a potent liver carcinogen in rats when administered orally. NMOR was found in the atmosphere at working places in the rubber industry in concentrations up to several hundred micrograms/m3. It can be assumed that NMOR inhalation may play a role in human carcinogenesis. Therefore an inhalation study was carried out to evaluate the carcinogenic potency of NMOR vapors in rats and hamsters. The concentration of volatile NMOR in the inhalation chamber was continuously determined with a Thermal Energy Analyzer. The rats received 29 administrations (4th/day, 5 days/week; mean inhaled daily dose: 130 micrograms/animal; total dose: 15 mg/kg bodyweight). The hamsters inhaled a total of 38 mg/kg of NMOR (21 applications, daily dose 260 micrograms/animal). In rats 4 carcinomas and 5 neoplastic nodules of the liver, 1 neuroblastoma and 1 mucoepidermoidal carcinoma of the nose, and 1 carcinoma of the thyroid gland were induced. In treated hamsters 4 carcinomas of the liver, 2 neurogenic sarcomas of the nasal region, and 5 papillomas of the trachea were found. None of these tumors were observed in control rats and control hamsters.
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PMID:Inhalation carcinogenesis of N-nitrosomorpholine (NMOR) in rats and hamsters. 210 36

Endogenous opioids and opioid receptors (i.e. endogenous opioid systems) are involved in carcinogenesis. Using homogenates of S20Y neuroblastoma (NB) cells grown in culture, the binding of a growth-selective ligand, [Met5]enkephalin, was examined to ascertain the zeta (zeta) opioid receptor. Specific and saturable binding of [3H]-[Met5]enkephalin was detected in NB cells; the data were consistent with a single binding site. Scatchard analysis yielded a Kd of 1.6 nM and a binding capacity (Bmax) of 48.1 fmol/mg protein; 14,000 receptors per cell were estimated. Binding was dependent on protein concentration, time, temperature, and pH, and was sensitive to 100 nM, but not 5 nM, Na+, Ca2+, and Mg2+; GppNHp at concentrations of 100-500 mM had little effect on binding. Optimal binding required protease inhibitors, and pretreatment of the tumor cell homogenates with trypsin markedly reduced [3H]-[Met5]enkephalin binding, suggesting that the binding site was proteinaceous in character. Displacement experiments indicated that [Met5]enkephalin was the most potent displacer of [3H]-[Met5]enkephalin. Cell density (log, confluence, postconfluence) did not alter the Kd or Bmax. This study serves as the first demonstration and characterization of the zeta (zeta) opioid receptor in tissue culture cells. The homogeneous nature of NB cell cultures, along with the enrichment in receptor number, provides an excellent model system to isolate and purify the zeta receptor.
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PMID:Demonstration and characterization of zeta (zeta), a growth-related opioid receptor, in a neuroblastoma cell line. 215 55

Natural carotene sample obtained from palm oil was proved to suppress the promoting stage of two-stage carcinogenesis of mouse skin, and also inhibit the proliferation of human malignant tumor cells, such as neuroblastoma GOTO cells, stomach cancer HGC-27 cells, and pancreatic cancer PANC-I cells. Among the major constituents of palm carotene, alpha-carotene showed stronger anti-proliferative effect than beta-carotene. The present results indicate that further investigation for not only beta-carotene but also other kinds of natural carotenes, such as alpha-carotene, should be carried out.
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PMID:[Anticarcinogenesis activity of natural carotenes]. 252 99

The rapid progress in molecular biology has allowed investigators to define some of the basic mechanisms of carcinogenesis. At the molecular level, cellular transformation results from the occurrence of two or three distinct genetic events that uncouple the cell from its normal regulatory mechanisms. One family of genes, the oncogenes, may be particularly important in the process. The aberrant expression of oncogenes, either by mutation or simply by increased transcription, may result in cellular transformation. The genes usually code for growth factors, growth factor receptors or for proteins involved in the transduction of growth signals into the nucleus. Genetic activation causes the cell to continuously sense a message to undergo mitosis, and the cell no longer responds to its normal regulatory signals. The concepts are rapidly moving into the clinical realm as the genetic mechanisms of particular neoplasms have been investigated. The neuroblastoma is the first tumor system in which the biologic characteristics of the tumor were found to be related to a known oncogene; the amplification of the myc gene is an independent marker of the aggressiveness of the tumor. In addition, much progress has been made in defining the specific genetic lesions responsible for retinoblastomas, Wilms' tumors and carcinomas of the colon that arise in patients with familial polyposis coli. As more knowledge accumulates regarding the exact mechanisms through which the proteins encoded by oncogenes affect these carcinomas and others, it may become possible to design pharmacologic agents rationally to hinder their growth selectively.
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PMID:The emerging genetics of cancer. 264 25

Based on the two mutation hypothesis in the development of retinoblastoma, loss of heterozygosity (LOH) of specific chromosome has been implicated in the presence of tumor suppressor gene. Studies on the LOH in different types of tumors revealed that LOH of each chromosome might play a different role in the multistep process of carcinogenesis: LOH of some chromosomes may play an etiological role in the development of some tumors, while that of other chromosomes or the same chromosome in other tumors, may play a role in the progression of tumors. LOH of chromosome 13 is an example for the former cases, and the latter cases involve LOH of chromosome 17 in colorectal carcinoma and osteosarcoma, chromosome 10 in glioblastoma, chromosome 1 in neuroblastoma and malignant melanoma, and chromosome 11 in breast carcinoma. These studies indicates that the progressive or concerted LOH could be a measure of the highly malignant or metastatic potentiality. However, it should be borne in mind that, especially in polyploid tumors, LOH also occurs as a random event following the polyploidization-segregation process.
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PMID:[Loss of heterozygosity in the progression of tumors]. 267 92


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