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)

A butenolide compound (1E,3E,5E,7E)-5-hydroxy-4-(8-phenyl-1,3,5,7- octatetraenyl)-2(5H)-furanone (KNK-41), was shown to have strong anti-tumor activity. KNK-41 inhibited the proliferation of various kinds of human malignant tumor cells, such as HeLa (cervical carcinoma), HGC-27 (gastric cancer), PANC-1 (pancreatic cancer) and GOTO (neuroblastoma). Flow cytometric analysis indicated that KNK-41 caused an arrest in G0/G1 phase of the cell cycle. However, it scarcely affected DNA synthesis and the level of c-myc mRNA. These results suggest that the growth-inhibitory effect of KNK-41 is the result of G0/G1 arrest and not of the suppression of DNA synthesis and/or c-myc expression.
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PMID:Inhibitory effects of (1E,3E,5E,7E)-5-hydroxy-4-(8-phenyl-1,3,5,7- octatetraenyl)-2(5H)-furanone on proliferation of human malignant tumor cells. 157 90

Restriction-fragment-length polymorphism analysis was performed on several different types of human cancers, including carcinoma of the uterine cervix, neuroblastoma, hepatocellular carcinoma, pheochromocytoma, stomach cancer, and small-cell lung carcinoma (SCLC), to determine the chromosomal loci of putative tumor-suppressor genes in each type of tumor because less of heterozygosity (LOH) is supposed to unmask the recessive mutation of tumor-suppressor gene in the remaining allele. Chromosomal loci showing frequent LOH differed among these tumors, suggesting that there are several tumor-suppressor genes in the human genome and that critical genes for the development of each type of tumor are different. In some cases LOH was observed in the early stage of tumor such as chromosome 3p loss in carcinoma of the uterine cervix, and in other cases it was observed only in the advanced stage of tumor such as chromosomes 4 and 16q loss in hepatocellular carcinoma. These results suggest that there are two different types of tumor-suppressor genes: one is the gene whose inactivation is responsible for malignant transformation of a normal cell and the other is the gene whose inactivation is responsible for the progression of a tumor cell. In SCLC, LOH at three different chromosomal loci, 3p, 13q, and 17p, was simultaneously observed in nearly 100% of tumors. It was observed even in stage I tumors and an untreated tumor, and it occurred prior to N-myc amplification. These results may imply that at least six genetic alterations are necessary to convert a normal cell into a fully malignant cancer cell in SCLC.
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PMID:Chromosomal localization of putative tumor-suppressor genes in several human cancers. 168 40

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

By restriction fragment length polymorphism (RFLP) analysis, it was found that loss of heterozygosity (LOH) at three different chromosomal loci, 3p, 13q, and 17p, occurs simultaneously in nearly 100% of small-cell lung carcinomas (SCLC). This was observed even in stage I tumors and an untreated tumor, and it occurred prior to NMYC amplification. The common region of LOH on chromosome 3p was 3p14-24.1, and this region was also frequently lost in carcinoma of the uterine cervix (100% at D3S2 on 3p14-21) as well as renal cell carcinoma (56% at ERBA beta on 3p22-24.1), suggesting the presence of tumor suppressor gene(s) for these cancers in this region. On chromosome 13, LOH was observed commonly in the region between 13q12 and 13q22, including the RB locus on 13q14, and normal RB protein was not detected in any of 9 SCLC cell lines by immunoprecipitation analysis. The common region of LOH on chromosome 17 was 17p13 and is the same as that in colon carcinoma and osteogenic sarcoma. Since LOH is supposed to unmask the recessive mutation of tumor suppressor gene in the remaining allele, these results may imply that at least six genetic alterations are necessary to convert a normal cell into a fully malignant cancer cell in SCLC. RFLP analysis was performed on several other types of human cancers, including carcinoma of the uterine cervix, neuroblastoma, hepatocellular carcinoma, pheochromocytoma, and stomach cancer to determine the chromosomal loci of putative tumor suppressor genes in each tumor. Chromosomal loci showing frequent LOH were different among these tumors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Multiple genetic alterations in small-cell lung carcinoma. 257 37

The most important activity of SSM is stimulation of collagenation from cancer-infiltrated stromal tissue which confines the cancer. In order to elucidate the proliferative responses of collagen in cancer, single and double xenografts were prepared by transplantation of human gastric cancer (HGC), human lung cancer (HLC), and NB41A3 (mouse neuroblastoma) into nude mice. The collagen responses were dependent on the type of cancer cell used, particularly the cell membranes. SSM distinctly stimulated the proliferation of collagen fibers which showed a response to these cancer cells. When examined by CD, stromal collagenation was found to be dependent upon changes in the molecular structure of the cancer cell membrane. One of the glycoproteins, fibronectin, was presumed to be the most important of the substances involved.
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PMID:Antitumor effects of polysaccharides of human-type Mycobacterium tuberculosis on collagenation in human cancer xenografts. 312 16

Neuroblastoma (NB) arises from primitive sympathetic neuroblasts in the adrenal gland or the sympathetic ganglion. NB in situ, sometimes observed in the adrenal glands of autopsied infants, is considered to be a premalignant lesion that may develop into NB. Little is understood about the morphological and biochemical changes that accompany this malignant progression. In this study, a unique monoclonal antibody, KP-NAC8, raised against a human NB cell line is described. This binds to NB cells but not to fetal neuroblasts. The antibody recognizes a Mr 200,000 surface protein on NB cells. KP-NAC8 binds to 15 of 17 human NB cell lines and all 26 fresh NB samples either from tumor tissues or from marrow aspirates involved with tumor. The antibody was found to cross-react with some other tumor cell lines, namely, Ewing's sarcoma (1 of 2), melanoma (1 of 4), lung cancer (3 of 3), and leukemia (2 of 14) cell lines. However, KP-NAC8 did not bind to any rhabdomyosarcoma (0 of 4), Wilms' tumor (0 of 4), retinoblastoma (0 of 2), glioma (0 of 4), and gastric cancer (0 of 2) cell lines examined. Among fetal tissues, KP-NAC8 did not react with normal neuroblasts in the adrenal glands of 5 fetuses. In a further study, the membrane phenotype of fetal adrenal neuroblasts was analyzed by a panel of 12 monoclonal antibodies including KP-NAC8. A comparison of the binding of the same panel of antibodies to fresh NB revealed that antibodies UJ13A, UJ127:11, PI153/3, anti-Thy-1, A2B5, BA-1, BA-2, HSAN1.2, and Leu-7 bound to both fetal adrenal neuroblasts and NB cells. Monoclonal antibodies OKIa-1 and J5 did not bind to either tissues. The only antibody that could distinguish fetal adrenal neuroblasts from NB cells was KP-NAC8. KP-NAC8 may, therefore, define a differentiation-related antigen that may prove helpful in understanding the biological nature of NB and NB in situ.
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PMID:Cell surface membrane antigen present on neuroblastoma cells but not fetal neuroblasts recognized by a monoclonal antibody (KP-NAC8). 356 10

Eleven patients with spinal cord compression due to metastatic epidural tumors were analyzed. Primary tumors were Hodgkin's disease, non-Hodgkin's lymphoma, multiple myeloma (two patients each), cervical cancer, malignant melanoma, gastric cancer, lung cancer, and neuroblastoma (one patient each). It was felt that myelography is the most important diagnostic test, although CT scan and bone scan may give further diagnostic information in some patients. Six patients were treated with decompressive laminectomy and postoperative radiotherapy, and five with radiotherapy alone. Regardless of the pretreatment neurological status and the type of treatment given, the functional prognosis in our small series of patients appeared to be favorable for radiosensitive tumors such as malignant lymphoma and multiple myeloma.
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PMID:[Clinical study of spinal cord compression due to metastatic epidural tumors]. 395 Nov 27

3'-methyl-3-hydroxy-chalcone (3'Me-3-C), a derivative of chalcone, inhibited the proliferation of various kinds of human malignant tumor cells, such as HGC-27 (gastric cancer), HeLa (cervical carcinoma), PANC-1 (pancreatic cancer) and GOTO (neuroblastoma). Flow-cytometric analysis of HGC-27 cells revealed that 3'Me-3-C perturbed the cell cycle, i.e., it delayed passage through the S phase, and/or caused arrest in the G0/G1 phase. 3'Me-3-C inhibited the binding of [6,7-3H]estradiol to type-II estrogen-binding sites dose-dependently, and altered the pattern of protein synthesis and phosphorylation, which may explain 3'Me-3-C-induced inhibition of cell proliferation. In addition, 3'Me-3-C also suppressed the promoting activity of 12-0-tetradecanoylphorbol-13-acetate on skin carcinogenesis in 7,12-dimethylbenz[a]anthracene-initiated mice.
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PMID:Inhibitory effects of 3'-methyl-3-hydroxy-chalcone on proliferation of human malignant tumor cells and on skin carcinogenesis. 837 34

A two-site enzyme immunoassay for gliostatin (GLS)/platelet-derived endothelial cell growth factor (PD-ECGF) has been developed. The detection limit of gliostatin/PD-ECGF was 30 pg/well, and the optimal assay range was 0.1 to ng/well. This assay system enabled us to confirm the immunochemical identity of both factors and to detect immunoreactive gliostatin/PD-ECGF (IR-GLS/PD-ECGF) in human biological body fluids. The age-related analysis from newborn to 69 years revealed that the serum IR-GLS/PD-ECGF level was high in infants younger than 1 year old (1.8 ng/ml) and in the 20-year-old age group (1.8 ng/ml), and highest in the umbilical cord blood (2.1 ng/ml). Curiously high concentrations were detected in saliva with a significant sex difference (11.3 ng/ml for males and 48.7 ng/ml for females), and in synovial fluids (3.7 ng/ml). A number of human tumor cells, gastric cancer cells, MKN-74, neuroblastoma cells, GOTO, as well as epidermoid carcinoma cells, A431, were found to produce a significant amount of IR-GLS/PD-ECGF (0.2 to 21.8 ng/mg protein), and some of them secreted the IR-GLS/PD-ECGF in the conditioned medium (approximately 0.5 ng/ml). The enzyme immunoassay system is sufficiently sensitive for the basic and clinical study of gliostatin/PD-ECGF in human body fluids, tissues and organs.
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PMID:Establishment of an enzyme immunoassay system for gliostatin/platelet-derived endothelial cell growth factor (PD-ECGF). 847 30

A group of structurally related drugs representing diverse therapeutic classes share, among a number of pharmacological properties, enhancement of tumor growth in several rodent models of malignancy. One common action, the inhibition of histamine binding to and catalytic activity of cytochrome P450 monooxygenases, is highly correlated with potency to enhance tumor growth. Among members of this drug ensemble, the antiestrogen tamoxifen has been shown in controlled clinical studies to increase the incidence of uterine and gastrointestinal cancer and to accelerate the course of gastric cancer, and the tamoxifen analogue clomiphene has been linked to neuroblastoma and the tricyclic group of antidepressants to ovarian cancer. The determination of drug affinities for protein modulators of cell growth, proliferation, and transformation suggests a strategy for identifying at least some classes of chemicals that impart oncologic risks to humans.
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PMID:Enhancement of tumor growth by drugs with some common molecular actions. 864 28


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