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)

Endobronchial metastasis (EM) from nonpulmonary tumors is uncommon. A 9-year retrospective study at the University Hospital Vall d'Hebron (Barcelona, Spain) identified 32 patients with EM. All but four cases were diagnosed by fiberoptic bronchoscopy with bronchial biopsy. Primary tumors included the following types: breast cancer (20), colorectal cancer (3), melanoma (2), gastric cancer (1), neuroblastoma of the olfactory nerve (1), abdominal leiomyosarcoma (1), hypernephroma (1), endometrial carcinoma (1), papillary thyroid cancer (1), and hepatocarcinoma (1). Median age at diagnosis of EM was 58.7 years and median interval from the diagnosis of the primary tumor to the diagnosis of EM was 50.4 months. Seventeen patients (53%) had evidence of other metastatic sites at endobronchial relapse. The more common clinical manifestations included cough (37.5%), haemoptysis (28%), dyspnea (18.7%), and recurrent pulmonary infections (6.2%). Eight patients (25%) had no symptoms. There appears to be a predilection for metastatic involvement of the right and left upper lobe bronchus. Treatment was instituted in 20 patients, and their median survival was 11 months, in comparison with the 3 months found in 12 patients who received only palliative therapy because of advanced disseminated disease. Breast cancer is the most common tumor causing EM. The prognosis of patients with EM depends on the type of the primary tumor and the presence of other metastatic sites. Treatment must be individualized.
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PMID:Endobronchial metastatic disease: analysis of 32 cases. 869 37

Blood group-related antigens have been attractive targets for immunotherapy of cancer since their initial identification as cancer-related antigens. However, available information on the relative expression of most of these antigens on human malignant and normal tissues has been insufficient for selecting optimal antigens and tumors for immune attack. In this study, the distribution of the blood group-related antigens TF, Tn, sTn, Le(a), sialyl Le(a), Le(b), Le(x), sialyl Le(x), polyfucosyl Le(x) and Le(y) on 13 types of cancer and 16 normal tissues was compared. Our results show that sTn is strongly expressed on cancers of breast, colon, stomach, ovary, prostate and uterus; Tn on prostate cancer; TF on cancers of breast, colon, ovary, prostate and uterus; Le(y) on the cancers of colon, lung, pancreas and ovary; Le(a) and Le(x) on gastric cancer; and sialyl Le(a) and sialyl Le(x) on colon cancer. The complete absence of these antigens on cancers of neuroectodermal or mesodermal origin including melanoma, sarcoma, neuroblastoma and B cell lymphoma is as striking as their widespread presence on tumors of epithelial origin. Normal tissues were also tested. Tn and Le(b) were only detected on gastric and ovarian epithelia; sTn on Leydig cells of testis in addition to gastric and ovarian epithelia; Le(x) and sialyl Le(x) on polymorphonuclear leukocytes; and TF, Le(a), sialyl Le(a), Le(x), sialyl Le(x), polyfucosyl Le(x) and Le(y) on epithelia from a variety of tissues.
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PMID:Selection of tumor antigens as targets for immune attack using immunohistochemistry: II. Blood group-related antigens. 933 9

Mononitrosocaffeidine (MNC) and dinitrosocaffeidine (DNC) are new N-nitroso compounds obtained from in vitro nitrosation of caffeidine, a hydrolysis product of caffeine present in a typically made and widely consumed tea from Kashmir (India), a high incidence area of esophageal and stomach cancer. The chemical synthesis, in vitro metabolic studies and mutagenicity of the compounds has been previously reported. DNC, a nitrosamide is highly mutagenic both with and without metabolic activation whereas MNC, like several other aromatic asymmetric nitrosamines, does not exhibit genotoxic or mutagenic properties. We now report the results of the first carcinogenicity experiments on chronic oral administration of these compounds in BD-IX rats. The acute LD50 of MNC and DNC were about 1300 and 230 mg/kg b.w., respectively. Lung oedema and gastrointestinal haemorrhages were the first symptoms of intoxication observed after 2 days for both the compounds. All three dose groups of MNC treated rats showed localization of tumours in nasal cavity (93.9-100% of all malignant tumours). The tumours were histologically diagnosed as neuroepitheliomas of the olfactory epithelium (neuroblastoma of the bulbus olfactorii) and squamous cell carcinoma of the nasal cavity in the ratio of 3:1. No tumours of the nasal cavity were observed in the untreated controls. DNC, in contrast, induced squamous cell carcinoma of forestomach in 100% animals at low and high doses, of which nearly half the tumours metastasized predominantly into the peritoneum. No forestomach tumours were seen in the untreated controls. The data presented here clearly show the potential for induction of malignant tumours and distinct organ-specificity by MNC and DNC in rats, and support the postulate that a chronic exposure to these compounds may provide a carcinogenic risk for high incidence of gastrointestinal cancers in Kashmir.
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PMID:Caffeine-derived N-nitroso compounds. V. Carcinogenicity of mononitrosocaffeidine and dinitrosocaffeidine in bd-ix rats. 963 85

In this paper the use of arsenic compounds as anticancer agents in clinical trials and in in vitro investigations is reviewed, including the experience at our institute. Treatment of newly diagnosed and relapsed patients with acute promyelocytic leukemia (APL) with arsenic trioxide (As2O3) has been found to result in complete remission (CR) rates of 85-93% when given by intravenous infusion for 2-3 h at a dose of 10 mg/day diluted in 5% glucose saline solution. Patients exhibit a response in 28-42 days. CR rates after administration of Composite Indigo Naturalis tablets containing arsenic sulfide and of pure tetraarsenic tetrasulfide reached 98% and 84.9%, respectively. At higher concentrations (1-2 microM), arsenic induced apoptosis, while at lower concentrations (0.1-0.5 microM), it triggered cell differentiation in vitro. As2O3-induced apoptosis has been observed in many cancer cell lines, including esophageal carcinoma, gastric cancer, neuroblastoma, lymphoid malignancies, and multiple myeloma. Its effectiveness was confirmed in the treatment of multiple myeloma. Arsenic compounds are effective agents in the treatment of APL and their activity against other types of cancer requires further investigation.
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PMID:Arsenic compounds as anticancer agents. 1158 71

A review of reports on metastatic orbital tumors published from 1903 to 1998 in Japan revealed 128 patients, 74 males, 52 females and 2 whose sex was not recorded. The average age was 44.8 years, but varied depending on the primary tumor. Since 1980, metastatic orbital tumors have increased in Japan, especially those from the lung, liver and adrenal gland, while metastasis from the stomach has decreased slightly. Metastasis from the breast is still common. Most metastatic orbital tumors were from the lung, followed, in order, by breast, liver, adrenal gland and stomach. Males had four times as many metastatic orbital tumors from lung cancer than did females; only females had metastases from breast cancer; almost 90% of metastases from hepatoma were in males; metastasis from renal carcinoma was 2-3 times more common in males than in females. Metastasis from the liver and stomach is seen more frequently in Japan than in the United States and Europe. Ocular signs due to orbital metastases from hepatoma, neuroblastoma and gastric cancer were apt to appear earlier than the signs of the primary lesion. Metastases to the orbit were frequently bilateral in patients with neuroblastoma and malignant lymphoma. Specific ocular signs such as ecchymosis and conjunctival hemorrhages were seen in orbital metastasis from neuroblastoma and seminoma, while ocular pain was characteristic of malignant lymphoma. Orbital metastasis was very rare in patients with carcinoma of the uterus, ovaries, bladder, pancreas, colon or rectum in both Japan, the United States and Europe.
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PMID:Metastatic orbital tumors in Japan: a review of the literature. 1181 94

Gangliosides such as GD3, GM2, and GD2 are abundantly expressed on the cell surfaces of various malignant cells, suggesting the potential for anti-ganglioside antibody therapy for tumors. Anti-ganglioside GD2 antibody treatment is currently undergoing clinical trials for melanoma and neuroblastoma. We previously reported high in vivo antitumor effects of anti-GM2 ganglioside antibody against lung cancer. To determine whether anti-GM2 antibody may be clinically indicated for gastrointestinal cancers, we evaluated the mRNA expression of alpha2,8 sialyltransferase, a GD3 synthase, and beta1,4 N-acetylgalactosaminyltransferase (beta1,4 GalNAc-T), a GM2/GD2 synthase, in gastrointestinal cancers. We performed modified semi-quantitative RT-PCR, which reduces complexity incidental to radiolabeling on samples taken from small surgically removed clinical specimens. Stomach (19/22) and colorectal (21/30) cancers showed decreased expression of alpha2,8 sialyltransferase as compared with respective normal tissues (P < 0.05). In contrast, increased expression of beta1,4 GalNAc-T was detected in both types of tumors. Clinicopathological analysis revealed significantly higher expression level of alpha2,8 sialyltransferase in the poorly differentiated than in the well-differentiated stomach cancer group (P < 0.05). Furthermore, the expression level of alpha2,8 sialyltransferase was significantly decreased in male as compared with female colorectal cancer patients (P < 0.05). These results suggest that expression level of GM2 ganglioside is elevated in gastrointestinal cancer, and that anti-GM2 antibody may be applicable to its treatment.
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PMID:Decreased expression of alpha2,8 sialyltransferase and increased expression of beta1,4 N-acetylgalactosaminyltransferase in gastrointestinal cancers. 1185 18

Several tumor suppressor genes are located within human chromosome 11q23 region. We have cloned and characterized MFRP and RNF26 genes at 11q23.3. We also identified and characterized KIAA1735/MTHDIX gene at 11q23.1 and CLDN24 gene at 11q23.2 by using bioinformatics. Here, a novel human gene corresponding to a 5'-truncated FLJ20535 cDNA was identified. FLJ20535 corresponded to nucleotide position 55-2255 of FLJ13859, and nucleotide position 52-2169 of FLJ13859 was the coding region. Because of tetratricopeptide repeat (TPR) and armadillo repeat (ARM) domains within its gene product, the novel human gene was designated TPARM. Mouse E330017O07Rik cDNA was derived from mouse Tparm gene. Human TPARM (705 aa) and mouse Tparm (704 aa), showing 75.4% total-amino-acid identity, consist of TPR domain and three ARM domains. TPR domain of TPARM was most homologous to that of SMAP1, while ARM1-ARM3 domains of TPARM were most homologous to ARM7-ARM9 domains of CTNNB1 (also known as beta-catenin). TPARM might be implicated in the WNT-beta-catenin signaling pathway. TPARM mRNA was expressed in testis, prostate, lung, germinal center B-cells, and also in neuroblastoma, teratocarcinoma, colon cancer, and gastric cancer. Human TPARM gene was found to consist of 22 exons. TPARM gene, located between NCAM1 and DRD2 genes, was mapped to human chromosome 11q23.2. TPARM as well as NCAM1 and DRD2 were predicted to be candidate tumor suppressor genes within the commonly deleted region of malignant melanoma on 11q23.1-q23.2 (between microsatellite markers D11S1347 and D11S4122).
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PMID:Identification and characterization of TPARM gene in silico. 1296 6

Immunoglobulin superfamily members are implicated in immune responses, growth factor signaling, and cell adhesion. IGSF4 (IGSF4A), homologous to IGSF4B, IGSF4C, IGSF4D, PVR, PVRL1, PVRL2, PVRL3 and PVRL4, is down-regulated in lung cancer. IGSF11, homologous to CXADR (CAR), ESAM and ASAM, is up-regulated in the intestinal-type gastric cancer. Here, we identified and characterized a novel member of the immunoglobulin superfamily, TMEM25, by using bioinformatics. BC042896 and AY358919 cDNAs were derived from human TMEM25 gene, while AK002841 cDNA was derived from mouse Tmem25 gene. TMEM25 isoform 1 (BC042896), consisting of exons 1-9, encoded a 366-aa transmembrane protein. TMEM25 isoform 2 (AY358919), consisting of exons 1-4 and 6-9, encoded a 322-aa secreted protein. Human TMEM25 gene was found to encode transmembrane-type as well as secreted-type proteins due to alternative splicing of exon-skipping type. TMEM25 mRNA was expressed in brain, including cerebellar cortex and hippocampus, as well as in neuroblastoma, brain tumors, and gastric cancer. Human TMEM25 isoform 1 showed 91.0% total-amino-acid identity with mouse Tmem25. TMEM25 was identified as a member of immunoglobulin superfamily, because codon 42-112 of TMEM25 was the C-2 type immunoglobulin domain homologous to Hemicentin (Fibulin-6, FIBL6), Titin (TTN), Sialoadhesin (SN) and Nephrin (NEPHS1). Human TMEM25 gene was located at the 11q23.3 oncogenomic recombination hotspot around the MLL amplicon and the neuroblastoma deleted region. TMEM25 is a target of pharmacogenomics in the field of oncology and regenerative medicine.
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PMID:Identification and characterization of human TMEM25 and mouse Tmem25 genes in silico. 1525 12

Cancer epigenetics is rapidly moving into a translational phase, and knowledge on how aberrant DNA methylation is induced is becoming important. Aging, chronic inflammation, and viral infections are known to promote methylation of non-core regions of promoter CpG islands (CGI). The non-core methylation and 'seeds of methylation', scattered methylation in a CGI, are considered to serve as triggers for dense methylation of a promoter CGI, which permanently represses expression of its downstream gene. Decreased gene transcription is an important factor that promotes induction of dense methylation. The presence of the CGI methylator phenotype (CIMP), in which methylation of multiple CGI was observed, is under dispute. Some gastric cancer cell lines have increased rates of de novo methylation, and neuroblastoma cases with CIMP show qualitatively different prognosis from those without. This strongly supports the presence of CIMP, but it seems to contain multiple entities. Limited knowledge is available for epimutagens, the chemicals that induce DNA demethylation or methylation. We have developed an assay system to detect demethylating agents, and an assay system for methylating agents is necessary. Efforts in the field on how aberrant methylation is induced will lead to new cancer prevention, diagnostics, and therapeutics.
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PMID:Aberrant methylations in cancer cells: where do they come from? 1581 17

SNAI1, SNAI2, and SNAI3 genes, encoding transcriptional repressors implicated in epithelial mesenchymal transition (EMT), are human homologs of Drosophila snail (sna) and slug genes. SNAI1 represses transcription of CDH1 (E-cadherin) gene. SNAI2 induces the first phase of EMT, including desmosome dissociation, cell spreading, and initiation of cell separation. Because SNAI family proteins are implicated in EMT during embryogenesis and carcinogenesis, SNAI family genes are potent targets of pharmacogenomics. Here, comparative genomics analyses and comparative proteomics analyses on SNAI family orthologs were performed. Rat Snai3 gene, consisting of three exons, was identified within rat genome sequence AC111791.4. Zebrafish snai1a (NM_131066.1) was identified as SNAI1 ortholog. Chicken ChEST362l17 (CR407272.1), Xenopus slug (AF368041.1), and zebrafish zgc92564 (NM_001008581.1) were identified as SNAI2 orthologs. Chicken snail (NM_ 205142.1), Xenopus snail (BC056857.1), and zebrafish snai1b (NM_130989.1) were identified as SNAI3 orthologs. SNAI1 orthologs consisted of SNAG domain and four zinc finger (ZNF) domains, while SNAI2 and SNAI3 orthologs consisted of SNAG domain and five ZNF domains. Based on the integromics analyses, SNAI2 orthologs were found to be more conserved than SNAI1 and SNAI3 orthologs. SNAI1 mRNA was expressed in placenta, neuroblastoma, and diffuse type gastric cancer. SNAI2 mRNA was expressed in placenta, melanocyte, embryonic stem (ES) cells, leiomyosarcoma, neuroblastoma, and glioblastoma. SNAI3 mRNA was expressed in B cells. Expression of SNAI3 mRNA was repressed due to the existence of anti-sense single-exon transcript. SNAI1, functioning as E-cadherin repressor, is implicated in the malignant infiltrating phenotype of diffuse type gastric cancer through the induction of EMT or fibroblastoid transformation.
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PMID:Comparative genomics on SNAI1, SNAI2, and SNAI3 orthologs. 1614 76


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