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)

Total sialic acid (TSA) and "lipid-bound" sialic acid (LSA) were evaluated in comparison to carcinoembryonic antigen (CEA) and ferritin and neuron specific enolase (NSE) in 152 untreated patients with primary lung cancer, 107 benign pulmonary disease patients and 207 notmal controls. The mean concentrations of TSA, LSA and CEA in lung cancer patients, were significantly higher than in benign and normal controls (p less than 0.001), while the mean ferritin and NSE levels were significantly higher than in normal controls only (p less than 0.001). At the designated cut-off serum levels, sensitivities of the five markers for lung cancer were in decreasing order: TSA 86.5% (greater than 80 mg/dL), LSA 77% (greater than 20 mg/dL), CEA 46.4% (greater than 5 ng/mL), ferritin 36% (greater than 300 ng/mL) and NSE 34.5% (greater than 12.5 ng/mL). Using the benign pulmonary values as negative controls the specificity of each marker was as follows: CEA 88%, ferritin 72%, NSE 58%, TSA 44% and LSA 44%. In small cell lung cancer (SCLC) patients, NSE mean concentrations and sensitivity were significantly higher than in non-small lung cancer (NSCLC) patients (9.63 +/- 4.4 versus 23.54 +/- 16.9, p less than 0.001 and 74% versus 21.4% respectively). While in NSCLC patients only CEA levels correlated well with the stage of the disease, in SCLC patients concentrations of TSA, LSA and ferritin were significantly higher in extensive than in limited disease stages. These preliminary data suggest that, although TSA and LSA are highly sensitive markers in lung cancer, their specificity is low.
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PMID:Five tumor markers in lung cancer: significance of total and "lipid"-bound sialic acid. 166 20

The relative usefulness of a combination of some tumor markers, such as CEA, AFP, ferritin and NSE for the diagnosis of lung cancer was assessed by multiple logistic analysis. Serum concentration of these markers was determined in 68 patients with lung cancer (50 with NSCLC and 18 with SCLC, in 68 patients with benign lung disease and 75 normal control subjects. Ferritin proved to be the most useful in diagnosing both NSCLC and SCLC, while NSE was found to be of some help in diagnosing SCLC only. The multiple marker panel proved to be more sensitive and specific than any single marker in discriminating lung cancer from normal control tissue, but it was of limited value in discriminating malignant from benign lung disease. The results of the present study would suggest that the panel of investigated tumor markers is not of great help for the early diagnosis of lung cancer.
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PMID:Clinical significance of a multiple biomarker assay in patients with lung cancer. A study with logistic regression analysis. 168 30

The value of serum ferritin assays in the diagnosis and staging of non-microcytoma bronchial cancer is assessed. It is pointed out that the marker is only minimally specific and sensitive in the diagnostic phase as well as being only slightly indicative in the staging of NSCLC.
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PMID:[Usefulness of measuring serum ferritin in the diagnosis and staging of non-microcytoma bronchial carcinoma]. 380 80

Within the past few years, the measurement of serum and tissue markers has had an increasing influence on clinical decisions about initial treatment and follow-up. Lung cancer illustrates the types and importance of these various markers. This review presents data concerning the most studied and interesting markers in non-small cell (NSCLC) and small cell lung cancer (SCLC). CEA, TPA, SCC-Ag, CYFRA 21-1, ferritin, CA19-9, CA50, CA242, H-K-N-ras mutations and p53 mutation seem to be the most prolific in NSCLC, while NSE, BN/GRP, CK-BB, NCAM, IL-2R, IGF-I, transferrin, ANP, mAb (cluster 5), Le-y and c-N-L-myc mutation are markers in SCLC patients. Some of these serum markers might be useful adjuncts for monitoring response to therapy, including early detection of tumour reactivation to allow curative therapy and rapid detection of treatment failure to allow change of the regimen. The study of these markers also may lead to a better understanding of the biological characteristics of lung cancer. The information derived from these biological studies represents the most promising avenue towards new treatment strategies, as well as attempts at secondary prevention.
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PMID:Clinical tumour markers in lung cancer. 753 17

To define the toxicity profile of recombinant human interleukin-6 (rhIL-6) and to study its effect on hematopoiesis, biochemical parameters and other cytokines, rhIL-6 was administered in a phase I-II study to 20 patients with breast carcinoma or nonsmall cell lung cancer. RhIL-6 doses were 0.5, 1.0, 2.5, 5.0, 10, and 20 micrograms/kg/d, with at least three patients per dose level. RhIL-6 was administered 24 hours by continuous intravenous infusion followed by subcutaneous (SC) administration for 6 days, partly on an outpatient basis. RhIL-6-related side effects were fever, headache, myalgia, and local erythema. Starting at 2.5 micrograms/kg/d, these side effects were compounded by nausea, reversible increase in liver enzymes, and anemia. Flu-like symptoms were controllable up to and including 10 micrograms rhIL-6/kg/d with acetaminophen. RhIL-6 increased platelet counts with a decrease in mean platelet volume and increased leukocytes caused by neutrophil, monocyte, and lymphocyte increase, with an increase in T cells and natural killer cells at 1.0 and 2.5 micrograms rhIL-6/kg/d. The reversible anemia was characterized by a decrease in serum iron, and an increase in ferritin and erythropoietin without reticulocytosis. RhIL-6 reduced total cholesterol levels and a dose-related increase of C-reactive protein and serum amyloid A plasma levels was observed. Serum IL-6 levels were increased, especially at 10 and 20 micrograms/kg/d, whereas no change in IL-1 beta and tumor necrosis factor alpha levels was observed. RhIL-6 can be administered with controllable side effects in this setting, up to and including a SC dose of 10 micrograms/kg/d on an outpatient basis, and has a promising stimulating effect on leukopoiesis and thrombopoiesis.
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PMID:Effects of recombinant human interleukin-6 in cancer patients: a phase I-II study. 806 39

The prognostic significance of serum ferritin on survival in lung cancer was evaluated. One hundred and ninety-seven patients were referred for evaluation of pulmonary lesions; 115 patients (85 men) had primary lung cancer. Their median age was 57 years. Seventy-four patients (43 men) with benign lung disease were enrolled as controls. Their median age was 53 years. Serum ferritin was measured at diagnosis. Non-small cell lung cancer (NSCLC) (n=90) was graded according to the TNM-system and small cell lung cancer (SCLC) (n=25) in limited and extensive disease. Follow-up was median 30 months (range 23-36). Patients with lung cancer had higher median ferritin than controls (245 vs. 145 microg/l, p<0.00001): the prevalence of ferritin >300 microg/l was 37% in patients with lung cancer and 14% in controls (p<0.001). There was no significant difference in ferritin between patients with different stages either in NSCLC or in SCLC. Patients with SCLC had higher median ferritin than patients with NSCLC (344 vs. 233 microg/l, p<0.05). No significant differences in ferritin could be demonstrated among the other histological tumour types. The overall survival rate in patients with lung cancer was 52% after 1 year, 33% after 2 years, and 13% after 3 years. Survival rate was lower in patients with ferritin >300 microg/l than in those with ferritin < or =300 microg/l (p<0.0001). The probability of survival 1, 2 and 3 years after diagnosis in patients with ferritin >300 microg/l was 36, 20 and 4%, respectively, and in patients with ferritin < or =300 it was 63, 42 and 18%, respectively (p<0.0001). An elevated ferritin was a significant prognostic factor (p<0.01) even after adjustment for performance status, age, sex, TNM stage, and histological tumour type. TNM stage and performance status were likewise predictors of survival (p<0.01 and p<0.001, respectively). There exists a clinically relevant relationship between serum ferritin concentration and the prognosis of survival in patients with primary lung cancer. The routine use of serum ferritin should be considered in the evaluation and follow-up of pulmonary malignancies.
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PMID:The serum ferritin concentration is a significant prognostic indicator of survival in primary lung cancer. 1174 82

Leptin is an anorexia inductor peptide produced by adipocytes and related to fat mass. Leptin is also produced by fat under proinflammatory cytokine action. Our objective is to study serum leptin levels in relation to nutritional status and acute phase response in advanced-stage non-small cell lung cancer.Seventy-six patients newly diagnosed of non surgical non-small cell lung cancer before chemotherapy treatment and 30 healthy controls were included. BMI, serum leptin and cholesterol levels and lymphocyte count were decreased in lung cancer patients. Cytokine IL-6, TNF-alpha, sTNF-RII, sIL-2R, IL-12, IL-10 and IFN-gamma, and other acute phase reactants as alpha1 antitrypsin, ferritin, CRP and platelets were all raised in patients, whereas the IL-2 was decreased. We found a direct relationship between leptin and other indicators of the status of nutrition, especially total fat mass. We also found a close relationship between the status of nutrition and the performance status (Karnofsky index). However, serum leptin and nutritional status were inversely correlated with acute phase proteins and proinflammatory cytokines, suggesting a stress-type malnutrition. Although serum leptin levels, nutritional status and Karnofsky index are related to survival, at multivariate analysis they all were displaced by the acute phase reaction markers. These results suggest that cancer anorexia and cachexia are not due to a dysregulation of leptin production. Circulating leptin concentrations are not elevated in weight-losing cancer patients and are inversely related to the intensity of the inflammatory response. In advanced lung cancer patients serum leptin concentrations only depend on the total amount of fat.
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PMID:Leptin role in advanced lung cancer. A mediator of the acute phase response or a marker of the status of nutrition? 1220 Jan 9

The aim of the study was to assess the role of serum tumour markers (NSE, Cyfra 21-1, CEA, LDH, ferritin) as a prognostic and predictive factors in 79 patients with advanced NSCLC treated with chemotherapy. Objective response to treatment was significantly more frequent in the patient with serum NSE > 12.5 ng/ml. Progression of disease was observed more often in patients with serum Cyfra 21-1 >10 ng/ml or LDH >480 U/L. CEA >3 ng/ml, LDH >480 U/L, for coefficient >1, NSE >20 ng/ml and Cyfra 21-1 >10 ng/ml had a negative impact on survival in univariate analysis. Independent negative prognostic significance of fer coefficient >1 was confirmed by multivariate analysis.
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PMID:[The significance of the serum tumour markers as a prognostic and predictor factors in nonsmall cell lung cancer patients]. 1698 65

Pemetrexed is a multitargeted antifolate approved for the second-line treatment of locally advanced or metastatic non-small cell lung cancer. The combination of pemetrexed with gemcitabine has been studied in several clinical trials showing a promising antitumor activity with a mild toxicity profile. We present the case of a patient who experienced fever, arthralgia, skin rash and high serum ferritin levels after first cycle of this chemotherapy combination, compatible with an adult onset Still's disease. This adverse event has not been previously reported.
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PMID:Adult onset Still's disease after first cycle of pemetrexed and gemcitabine for non-small cell lung cancer. 1900 12

Ferritin is a nanocage protein composed by the variable assembly of 24 heavy and light subunits. As major intracellular iron storage protein, ferritin has been studied for many years in the context of iron metabolism. However, recent evidences have highlighted its role, in particular that of the heavy subunit (FHC), in pathways related to cancer development and progression, such as cell proliferation, growth suppressor evasion, cell death inhibition, and angiogenesis. At least partly, the involvement in these pathways is due to the ability of FHC to control the expression of a repertoire of oncogenes and oncomiRNAs. Moreover, the existence of a feedback loop between FHC and the tumor suppressor p53 has been demonstrated in different cell types. Here, we show that ectopic over-expression of FHC induces the promoter hypermethylation and the down-regulation of miR-125b that, in turn, enhances p53 protein expression in non-small cell lung cancer (NSCLC) cell lines. Notably, analysis by absolute quantitative RT-PCR of FHC, miR-125b, and p53 strongly suggests that this axis might be active in human NSCLC tissue specimens. In vitro, FHC over-expression attenuates survival of NSCLC cells by inducing p53-mediated intrinsic apoptosis that is partially abrogated upon miR-125b re-expression. Overall, our findings demonstrate that FHC acts as a tumor suppressor gene, thus providing a potential molecular strategy for induction of NSCLC apoptotic cell death.
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PMID:Ferritin heavy subunit enhances apoptosis of non-small cell lung cancer cells through modulation of miR-125b/p53 axis. 3051 22


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