Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 211 patients with neuroblastoma, serum vanillylmandelic acid (VMA) and homovanillic acid (HVA) levels were determined and correlated to stage, histological differentiation, ferritin, neuron-specific enolase, lactate dehydrogenase (LDH) and outcome. Elevated serum VMA and/or HVA levels were found 16% less frequently than elevated urine levels. The incidence of the elevated serum levels increased with stage (stages I-III 58%, IV 78%, IVS 100%). Increased VMA/HVA ratios were not associated with a higher grade of tumour differentiation. Serum ferritin and neuron-specific enolase showed no correlation, and LDH a borderline non-random correlation with the serum catecholamine metabolites. Using age-related reference values a quotient of serum VMA/HVA (P = 0.061) < 0.7 indicated a poorer event-free survival (48 +/- 10%) than ratios > or = 0.7 (event-free survival 81 +/- 6%) for children with localised neuroblastoma (P = 0.0004). No correlation with prognosis was detected for patients with stage IV and stage IVS disease. We conclude that serum VMA and HVA determinations may be useful as tumour markers for 71% of neuroblastoma patients, and aid in estimating the prognosis in children with localised disease.
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PMID:Serum vanillylmandelic acid/homovanillic acid contributes to prognosis estimation in patients with localised but not with metastatic neuroblastoma. 141 87

Tumour samples from 38 patients with neuroblastoma were analysed for the presence of N-myc amplification. N-myc gene copy number in tumour DNA was determined by Southern blotting, and by dilution analysis where appropriate. Available clinical data, obtained at tissue collection and by subsequent questionnaire included patient age at diagnosis, catecholamine, ferritin and neuron-specific enolase levels, treatment and disease status. This study was designed to investigate the use of N-myc amplification data as an additional indicator for determination of prognosis. Patients with amplified N-myc had more rapid disease progression than those without amplification (P less than 0.005). Stratification of Stage III and IV patients using N-myc amplification permitted identification of a subgroup with poorer prognosis. The results demonstrate that determination of N-myc amplification is important in assessment of prognosis and subsequent treatment in patients with neuroblastoma.
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PMID:Association of N-myc amplification with neuroblastoma: the Australian and New Zealand experience. 155 17

A direct two-site binding assay on the basis of antibodies from sheep for the quantification of human gamma-gamma enolase is described. The antibody was produced by immunization with human NSE coupled to horse spleen ferritin. The assay shows two feature: a decreased reactivity with NSE from rat and NSE from human serum in spite of 100% recovery of purified human brain NSE. The sheep antibody seems to react with epitopes less accessible on the rat NSE and on the NSE of human serum. The assay is characterized by gamma-gamma enolase specificity, a high sensitivity (2 pg) and a precision of CV = 3-7%.
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PMID:[Enzyme immunoassays for the quantification of human gamma-gamma-enolase (NSE)]. 212 65

Chromogranin A is an acidic protein costored and coreleased with catecholamines from storage vesicles. Its serum concentration is elevated in patients with peptide-producing endocrine neoplasia. We measured serum chromogranin A at the time of diagnosis in 34 children with all stages of neuroblastoma. With a sensitivity of 91% and specificity of 100%, serum chromogranin A emerged as a useful diagnostic tool for neuroblastoma, comparable to or better than other measurements such as neuron-specific enolase, ferritin, or dopamine-beta-hydroxylase. Mean serum chromogranin A correlated with disease stage (r = 0.76, P less than 0.01). The relationship of prognosis (progression-free survival) to baseline serum chromogranin A, age, and disease stage was determined in 34 patients at risk for relapse, with a median followup period of 18 mo (range, 1-48 mo). The survival rate for patients with lower serum chromogranin A levels (less than 190 ng/ml at the time of diagnosis) was 69%, whereas it was 30% for those with higher chromogranin A levels (P less than 0.05). Furthermore, when subjects were additionally stratified by either age or stage, chromogranin A was an effective prognostic tool in patients who either were older than 1 yr (P less than 0.005) or had more advanced disease (stage III or IV; P less than 0.05). We conclude that serum chromogranin A in neuroblastoma is (a) a valuable (sensitive and specific) diagnostic tool, (b) a correlate of tumor burden, and (c) a useful predictor of survival.
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PMID:Chromogranin A in children with neuroblastoma. Serum concentration parallels disease stage and predicts survival. 233 6

As neuroblastoma, the most common solid tumour in childhood, may contain all the constituents of the catecholamine biosynthesis cascade, some of these constituents may be produced in excess in a varying mixture reflecting the wide variability in expression of differentiated features of the tumour. We have measured plasma levels of norepinephrine (NE), epinephrine (E), dopamine (DA) and 3,4-dihydroxyphenylalanine (DOPA), and plasma activities of dopamine beta-hydroxylase (DBH) and aromatic L-amino acid decarboxylase (ALAAD) in 18 patients with neuroblastoma, in 13 at various times during the course of their disease. Activities of serum lactic dehydrogenase (LDH), serum levels of ferritin (FER) and neuron-specific enolase (NSE), and urinary vanilmandelic acid (VMA) were also determined. NE, E and DBH were found not to reflect tumour activity. In untreated active neuroblastoma DOPA or ALAAD (10 out of 10) or both (six out of 10) were clearly elevated. In all 13 patients where samples were obtained during chemotherapy, ALAAD activities fell within the normal range, while DOPA decreased more slowly. During relapse, DOPA and, especially, ALAAD, rapidly increased; in all six patients who had a relapse both DOPA and ALAAD were elevated. In complete remission (eight patients), ALAAD was normal in all patients, but DOPA remained elevated in the one patient who later experienced a relapse. Our preliminary conclusion is that combined measurements of plasma ALAAD and DOPA may be useful markers for neuroblastoma activity at diagnosis, but even more so in indicating residual disease (DOPA) and in the early detection of relapse (ALAAD).
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PMID:Combined measurements of plasma aromatic L-amino acid decarboxylase and DOPA as tumour markers in diagnosis and follow-up of neuroblastoma. 250 83

Spontaneous maturation of Stage IVS neuroblastoma has been postulated as a mechanism for its favorable prognosis, but this has rarely been documented pathologically. We report on a patient with congenital Stage IVS neuroblastoma who had extensive subcutaneous and bone-marrow involvement. Serial photographs, biopsies, and vanillomandelic acid determinations documented the tumor's initial progression which was followed by spontaneous maturation and involution of the patient's disease over a 6-year period. No cytotoxic therapy was administered. Favorable biologic prognostic factors were documented, including tumor DNA and protein analyses for N-myc amplification or overexpression and analysis for serum neuron-specific enolase and ferritin. Implications for management and therapy of Stage IVS neuroblastoma are discussed with reference to this case and the recent literature.
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PMID:Complete pathologic maturation and regression of stage IVS neuroblastoma without treatment. 329 64

The significance of neuron-specific enolase (NSE) in the diagnosis and treatment monitoring of lung cancer was investigated in comparison with such established tumour markers as carcinoembryonic antigen (CEA), tissue polypeptide antigen (TPA), ferritin and calcitonin. We determined the serum concentrations of these tumour markers in 25 patients with small cell lung cancer (SCLC), 30 patients with non small cell lung cancer (NSCLC), and 38 patients with benign pulmonary diseases (BPD). In 14 patients with lung cancer, it was possible to follow up the behaviour of the tumour markers under treatment for up to 16 months. Calcitonin proved to have a surprisingly low sensitivity for SCLC. The utility of TPA and of ferritin was restricted, although the sensitivity was comparably high, by the high rate of false positive results. For NSCLC, CEA proved to be the best tumour marker. At present, NSE appears to be the tumour marker with the greatest specificity and sensitivity for SCLC. Its determination in the diagnosis, treatment and follow-up of SCLC makes good sense.
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PMID:Neuron-specific enolase in the diagnosis and therapy monitoring of lung cancer: a comparison with CEA, TPA, ferritin and calcitonin. 342 47

Known prognostic factors in neuroblastoma were analyzed in 124 children to determine which were independent and which were most useful in predicting outcome. The following factors were analyzed: age, sex, stage of disease, serum neuron-specific enolase (NSE), serum ferritin, E-rosette inhibition, urinary catecholamines, and histologic type according to the criteria of Shimada. Estimates of survival were calculated using the method of Kaplan and Meier. The overall survival for 124 patients was 60% at 2 years. There were significant differences in survival by pathology, age, NSE, ferritin, vanilmandelic acid (VMA): homovanillic acid (HVA) ratio, and stage. There was a strong association among NSE, age, stage, and ferritin. Using the recursive partitioning approach, it was possible to subdivide patients into three groups (based on diagnostic values of ferritin, age, and stage) with a good, intermediate, and poor prognosis and estimated 2-year survival of 100%, 62%, and 19%, respectively. Further analysis could not be done because of small numbers in the subgroups, but the results suggest that combinations of age, stage, serum ferritin, and histologic type may be able to define two populations: favorable with 80% + 2-year survival and unfavorable with less than 20%.
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PMID:Prognostic factor in neuroblastoma. 356 48

Twenty-six studies by meta-(131I)-iodobenzylguanidine scintigraphy (131I-MIBG), 26 studies by 67Ga-citrate and 33 99mTc-hydorxymethylene diphosphate (99mTc-HMDP) scintigraphic studies were performed for 10 patients with abdominal neuroblastoma. Comparing the 131I-MIBG images obtained at 24, 48 and 72 h, the 48-h image was the most distinctive for the tumor. Intrabdominal primary lesions, which ranged from bean to fist-size, were visualized in 7/7 cases (100%) by 131I-MIBG, 4/7 cases (57%) by 67Ga-citrate and 4/8 cases (50%) by 99mTc-HMDP before surgery and at diagnosis. In serial follow-up of these patients after starting chemotherapy, 131I-MIGB detected 100% of regressing primary tumors. Studies of 5 postoperative patients showed negative images for the primary tumor in all 3 scintigraphies except one in whom 131I-MIBG was positive, but not 67Ga-citrate or 99mTc-HMDP, for an unresectable residual tumor. 131I-MIBG also detected metastatic lesions not predicted by 67Ga-citrate or 99mTc-HMDP and reflected tumor progression more sensitively than known tumor markers such as urinary vanillylmandelic acid (VMA), homovanillic acid (HVA), serum neuron-specific enolase (NSE) and ferritin. These findings indicate that the 48 hr 131I-MIBG scintigraphy is superior to 67Ga-citrate or 99mTc-HMDP images and to other biochemical markers in monitoring the effect of treatment on neuroblastoma.
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PMID:131I-meta-iodobenzylguanidine scintigraphy in patients with neuroblastoma. 360 63

Recently accumulated data on the biology of the tumors of neuroblastoma group are reviewed. Histopathological classification system developed by Shimada et al, elevated levels of serum neuron-specific enolase and ferritin, and gene abnormalities including partial deletion of the short arm of chromosome #1 and N-myc gene amplification are discussed as well as their prognostic significance. Also, the current activities of CCSG (Childrens Cancer Study Group) neuroblastoma studies are briefly reported.
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PMID:[Neuroblastoma; biology and prognostic factors]. 380 Apr 8


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