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PubMed1996

Loss of adipocyte-type fatty acid binding protein and other protein biomarkers is associated with progression of human bladder transitional cell carcinomas.

Multifocal recurrent papillary tumors provide a unique model system to study the molecular mechanisms underlying the steps involved in transitional cell carcinoma progression and offer a valuable source of material to search for biomarkers that may form the basis for diagnosis, prognosis, and treatment. We have examined the protein expression profiles of normal bladder urothelium and of 63 transitional cell carcinomas of various histopathological grades and T stages using high-resolution, two-dimensional gel electrophoresis, microsequencing, mass spectrometry, and a two-dimensional gel protein database approach for polypeptide identification (http://biobase.dk/cgi-bin/celis). In general, the results revealed a striking similarity between the overall qualitative expression patterns of papillary tumors of all grades, as well as of papillary and solid tumors of grade III. With few exceptions, tumors of grades I-III expressed, albeit at different levels, all of the keratins (7, 8, 13, 17, 18, 19, and 20) found in the normal urothelium. Grade IV tumors lacked or expressed reduced levels of keratin 13 but most resembled low-grade tumors. One invasive grade IV tumor, however, expressed a fibroblast-like protein phenotype. Four proteins that were expressed by normal urothelium and were lost at various stages of progression were identified as glutathione S-transferase mu, prostaglandin dehydrogenase (PGDH), a fatty acid binding protein with homology to the adipocyte isoform (A-FABP), and keratin 13. The percentage of tumors expressing A-FABP was very high in low-grade lesions but decreased drastically (P = 0.0006) in grade III and IV neoplasms. In addition, low-grade tumors contained more A-FABP than their high-grade counterparts. The stage of the disease was also statistically (P = 0.0269) related to the presence or absence of A-FABP in grade III tumors. Similar analysis of glutathione S-transferase mu and PGDH showed a statistically significant decrease of these proteins in high-grade (grades III and IV) tumors (P = 0.0026 and P = 0.0044, respectively). Only PGDH showed a suggestive correlation (P = 0.0775) with the stage of the disease in grade III tumors. Keratin 13 showed a drastic decrease in grade IV tumors. In addition to identifying biomarkers that may have prognostic value, our studies have suggested that A-FABP is an important component of the pathway(s) leading to bladder cancer development.

Biomarkers, Tumor↗
PubMed2003

Dietary supplementation of conjugated linoleic acid reduces colon tumor incidence in DMH-treated rats by increasing apoptosis with modulation of biomarkers.

OBJECTIVES: We investigated the effects of conjugated linoleic acid (CLA) on tumor incidence, apoptosis, eicosanoid formation, 1,2-diacylglycerol (DAG), and fatty acid profiles of colonic mucosa in 1,2-dimethylhydrazine-treated rats fed different types of dietary fats. METHODS: One hundred twenty male 7-wk-old Sprague-Dawley rats were assigned to a beef tallow (BT) diet or a fish oil (FO) diet; each group was further divided into two groups, one with CLA supplementation (BTC and FOC) and the other without (BT and FO). All groups were fed for 30 wk on experimental diets that contained 12% (w/w) dietary fat (including 1% CLA for the BTC and FOC groups) and were intramuscularly injected with 1,2-dimethylhydrazine for 6 wk, for a total dose of 180 mg/kg of body weight. RESULTS: Rats fed the FOC, BTC, or FO (omega-3 fatty acids, mainly docosahexaenoic acid) showed a reduced incidence of tumors, increased apoptotic index values (P < 0.05), and lower levels of eicosanoids (prostaglandin E(2) and thromboxane B(2)) and DAG in colonic mucosa (P < 0.05). CLA and docosahexaenoic acid were incorporated into membrane phospholipids and significantly reduced the distribution of arachidonic acid in colonic mucosal phospholipids. Because CLA and omega-3 fatty acids reduced tumor incidence and levels of cell response regulators (prostaglandin E(2), thromboxane B(2), and DAG), they may share at least one common path of action in promoting the apoptotic process of colon carcinogenesis. CONCLUSIONS: These results suggested that increased apoptosis by dietary CLA may be attributed, at least in part, to changes in arachidonic acid metabolism in rats. Therefore, CLA may have anticarcinogenic effects by inducing apoptosis through modification of signal transduction in colonic mucosal cells.

1,2-Dimethylhydrazine↗
PubMed2002

A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men.

Very low-carbohydrate (ketogenic) diets are popular yet little is known regarding the effects on serum biomarkers for cardiovascular disease (CVD). This study examined the effects of a 6-wk ketogenic diet on fasting and postprandial serum biomarkers in 20 normal-weight, normolipidemic men. Twelve men switched from their habitual diet (17% protein, 47% carbohydrate and 32% fat) to a ketogenic diet (30% protein, 8% carbohydrate and 61% fat) and eight control subjects consumed their habitual diet for 6 wk. Fasting blood lipids, insulin, LDL particle size, oxidized LDL and postprandial triacylglycerol (TAG) and insulin responses to a fat-rich meal were determined before and after treatment. There were significant decreases in fasting serum TAG (-33%), postprandial lipemia after a fat-rich meal (-29%), and fasting serum insulin concentrations (-34%) after men consumed the ketogenic diet. Fasting serum total and LDL cholesterol and oxidized LDL were unaffected and HDL cholesterol tended to increase with the ketogenic diet (+11.5%; P = 0.066). In subjects with a predominance of small LDL particles pattern B, there were significant increases in mean and peak LDL particle diameter and the percentage of LDL-1 after the ketogenic diet. There were no significant changes in blood lipids in the control group. To our knowledge this is the first study to document the effects of a ketogenic diet on fasting and postprandial CVD biomarkers independent of weight loss. The results suggest that a short-term ketogenic diet does not have a deleterious effect on CVD risk profile and may improve the lipid disorders characteristic of atherogenic dyslipidemia.

Adult↗
PubMed2005

Constructing support vector machine ensembles for cancer classification based on proteomic profiling.

In this study, we present a constructive algorithm for training cooperative support vector machine ensembles (CSVMEs). CSVME combines ensemble architecture design with cooperative training for individual SVMs in ensembles. Unlike most previous studies on training ensembles, CSVME puts emphasis on both accuracy and collaboration among individual SVMs in an ensemble. A group of SVMs selected on the basis of recursive classifier elimination is used in CSVME, and the number of the individual SVMs selected to construct CSVME is determined by 10-fold cross-validation. This kind of SVME has been tested on two ovarian cancer datasets previously obtained by proteomic mass spectrometry. By combining several individual SVMs, the proposed method achieves better performance than the SVME of all base SVMs.

Algorithms↗
PubMed2005

Development of oncology drug response markers using transcription profiling.

Transcriptional profiling of a tumor's entire genomic complement has become a key tool in the analysis of human cancers and identification of novel markers to predict disease state, outcome, and response to therapy. At present, this technology provides the most comprehensive approach for the analysis of somatic changes altering critical pathways during transformation of stable diploid cells into unstable tumor cells. Such analyses are impacting the development of novel anti-cancer drugs through the early detection of cancer, development of targeted therapies, identification of optimal dose and regimens for new drugs, and segmentation of patients to enrich response rates and reduce risk of adverse events.

Antineoplastic Agents↗
PubMed2001

Gene expression in papillary thyroid carcinoma reveals highly consistent profiles.

Papillary thyroid carcinoma (PTC) is clinically heterogeneous. Apart from an association with ionizing radiation, the etiology and molecular biology of PTC is poorly understood. We used oligo-based DNA arrays to study the expression profiles of eight matched pairs of normal thyroid and PTC tissues. Additional PTC tumors and other tissues were studied by reverse transcriptase-PCR and immunohistochemistry. The PTCs showed concordant expression of many genes and distinct clustered profiles. Genes with increased expression in PTC included many encoding adhesion and extracellular matrix proteins. Expression was increased in 8/8 tumors for 24 genes and in 7/8 tumors for 22 genes. Among these genes were several previously known to be overexpressed in PTC, such as MET, LGALS3, KRT19, DPP4, MDK, TIMP1, and FN1. The numerous additional genes include CITED1, CHI3L1, ODZ1, N33, SFTPB, and SCEL. Reverse transcriptase-PCR showed high expression of CITED1, CHI3L1, ODZ1, and SCEL in 6/6 additional PTCs. Immunohistochemical analysis detected CITED1 and SFTPB in 49/52 and 39/52 PTCs, respectively, but not in follicular thyroid carcinoma and normal thyroid tissue. Genes underexpressed in PTC included tumor suppressors, thyroid function-related proteins, and fatty acid binding proteins. Expression was decreased in 7/8 tumors for eight genes and decreased in 6/8 tumors for 19 genes. We conclude that, despite its clinical heterogeneity, PTC is characterized by consistent and specific molecular changes. These findings reveal clues to the molecular pathways involved in PTC and may provide biomarkers for clinical use.

Biomarkers, Tumor↗
PubMed2025

Methylation Signatures Identify Two Distinct Clusters of Uterine Leiomyosarcoma With Unique Histologic and Clinical Behaviors.

Uterine leiomyosarcoma (uLMS) is a rare and deadly gynecologic malignancy. uLMS is histologically heterogeneous and presents with a wide spectrum of tumor differentiation, with a broad range of genomic DNA instability, which can make the diagnosis and prognosis of uLMS challenging. Methylation has emerged as a useful molecular tool in tumor classification and diagnosis in certain neoplasms. We initiated this study to investigate the role of global methylation in the differential diagnosis of uLMS from its mimics in correlation with pathologic characteristics and clinical outcomes. In this study, we performed array-based global methylation profiling analysis in a total of 71 uLMS and compared the methylation signatures of uLMS with several other uterine mesenchymal tumors and soft tissue leiomyosarcoma. We found that uLMS demonstrated distinct methylation patterns differing from all other tumor types. Notably, methylation profiling defines 2 distinct subgroups of uLMS with differing copy number alterations, resulting in unique histologic and clinical behaviors, further emphasized by differences in methylation pathway analysis. This study is the first to report methylation profiling as a useful diagnostic tool in differentiating uLMS from mimics and defines 2 subtypes of uLMS based on methylation signatures.

Humans↗
PubMed2006

Profiling activities of transcription factors in breast cancer cell lines.

Transcription factors (TFs) are critical regulators of cell growth and differentiation, whose dysfunction is associated with many human diseases, including cancer. To facilitate the discovery of functionally altered TFs among the approximately 2,000 human TFs, we (Panomics, Inc., Fremont, CA) developed a Protein/DNA array technology that can be used to profile the activities of multiple TFs simultaneously. In this study, we applied this technology to examine the TF activities in three different breast cancer cell lines: MCF7 (estrogen receptor [ER] +, tamoxifen-sensitive), T47D (ER+, tamoxifen-resistant), and HCC1806 (ER-, tamoxifen-resistant). We compared the differences in TF activity in these cells lines following treatment with estradiol or tamoxifen. We found a number of TF activities unique to each of these cell lines. In addition to verifying previous findings, the novel findings of this study provide a more comprehensive view of the differences in the response of these cancer lines to estrogen and tamoxifen.

Animals↗
PubMed2006

DNA damage responses after exposure to DNA-based products.

BACKGROUND: The development of DNA-based therapies holds great promise for the treatment of diseases that remain difficult to manage using conventional pharmaceuticals. Whilst there are considerable data regarding chemical-induced DNA damage, there are limited reports published studying the potential of exogenous DNA to damage genomic DNA. METHODS: To investigate this problem, the differential gene expression (DGE) of DNA repair genes was examined to identify biomarkers, based on the hypothesis that DNA damage, including double-strand breaks (DSBs) and insertional mutagenesis, would be expected to induce biological pathways associated with repair. Human HepG2 cells were exposed to the chemical genotoxins, etoposide (ETOP) and methylmethanesulphonate (MMS), as positive controls, or biological agents (i.e. exogenous DNA with and without the use of transfection complexes or via various viral vectors). Following transfection (6-72 h) the cells were harvested for RNA and DGE was determined by quantitative real-time polymerase chain reaction (qRT-PCR). RESULTS: The expression of genes involved in the repair of DSBs were significantly increased after treatment with ETOP (>4-fold) or MMS (>5-fold). Transfection using Effectene and ExGen 500 resulted in no significant changes; however, transfection with ExGen 500 resulted in an increase in the expression levels of GADD45 mRNA, consistent with global cellular stress. Viral vectors increased (3-6-fold) expression of genes associated with DSBs and cellular stress responses and, as expected, the effect was the most marked with the retroviral vector. CONCLUSIONS: The DGE profiles observed in HepG2 cells following transduction/transfection suggest that a subset of DNA repair genes may provide novel biomarkers to rapidly detect DNA damage induced by DNA products at the level of the genome, rather than at selected genes.

Cell Line↗
PubMed2006

Sex-related differences in immune development and the expression of atopy in early childhood.

BACKGROUND: Sex and age are known to influence the clinical expression of asthma and allergic diseases. OBJECTIVE: We sought to evaluate whether immune response profiles also vary by sex and age. METHODS: We performed a prospective birth cohort study (Childhood Origins of Asthma) designed to evaluate interactions among age, sex, immune responses, and virus infections on the development of asthma and allergic diseases. Two hundred eighty-nine subjects were enrolled at birth, and 275 maintained prospective follow-up for 3 years. Cytokine response profiles at birth, 1, and 3 years of age; rates of wheezing, atopic dermatitis, and viral illnesses; and biomarkers of atopy, including total and specific IgE levels and peripheral eosinophil counts, were evaluated. RESULTS: PHA-induced IFN-gamma responses were higher in boys at 1 year of age (median, 35 vs 19 pg/mL; P < .001) and at 3 years of age (median, 282 vs 181 pg/mL; P = .07). Among children who wheezed during the third year of life, boys had increased IFN-gamma, IL-5, and IL-13 responses at age 3 years (P < .001, P = .008, and P = .01, respectively). Boys also demonstrated increased rates of sensitization (P = .05 at year 1), total IgE levels (P = .03 at year 1 and P = .006 at year 3), and peripheral eosinophil counts (2.62 vs 1.85; P = .05 at year 3). CONCLUSION: Sex-specific differences in immune responses develop during early childhood; some of these differences developmentally proceed, whereas others occur in parallel to the clinical expression of various atopic phenotypes. CLINICAL IMPLICATIONS: The differential expression of atopic diseases between boys and girls in early childhood is accompanied by sex-specific differences in immune response profiles.

Cells, Cultured↗
PubMed2005

Direct profiling of lipid distribution in brain tissue using MALDI-TOFMS.

Recent developments in mass spectrometry have permitted direct analysis of biomolecules in tissue. However, most studies have focused on proteins with emphasis on biomarker discovery. In the present work, matrix-assisted laser desorption/ionization mass spectrometry was used for the direct analysis of lipids in rat cerebellum. The lipid bilayer role as a storage depot for small organic molecules such as therapeutic drugs and pollutants such as DDT, as well as the ability to compare lipid profiles in healthy and diseased animal models, are a few of the many reasons why the direct probing of tissue to determine the qualitative and possibly quantitative lipid content could be a very useful tool. Molecular ions corresponding to cholesterol, phosphatidylcholines, sphingomyelins, and phosphatidylethanolamines were recorded in positive ion mode, while ones corresponding to phosphatidylinositols, sulfatides, and gangliosides were recorded in negative ion mode. Overall, representatives from all major categories of brain lipids including cholesterol, 15 phospholipid species (9 phosphatidylcholines, 1 sphingomyelin, 3 phosphatidylethanolamines, 2 phosphatidylinositols), 10 sulfatides (5 hydroxylated species and 5 nonhydroxylated species), and 7 species of gangliosides were detected.

Animals↗
PubMed2006

Optimization and evaluation of surface-enhanced laser-desorption/ionization time-of-flight mass spectrometry for protein profiling of cerebrospinal fluid.

Cerebrospinal fluid (CSF) potentially carries an archive of peptides and small proteins relevant to pathological processes in the central nervous system (CNS) and surrounding brain tissue. Proteomics is especially well suited for the discovery of biomarkers of diagnostic potential in CSF for early diagnosis and discrimination of several neurodegenerative diseases. ProteinChip surface-enhanced laser-desorption/ionization time-of-flight mass spectrometry (SELDI-TOF-MS) is one such approach which offers a unique platform for high throughput profiling of peptides and small proteins in CSF. In this study, we evaluated methodologies for the retention of CSF proteins < 20 kDa in size, and identify a strategy for screening small proteins and peptides in CSF. ProteinChip array types, along with sample and binding buffer conditions, and matrices were investigated. By coupling the processing of arrays to a liquid handler reproducible and reliable profiles, with mean peak coefficients of variation < 20%, were achieved for intra- and inter-assays under selected conditions. Based on peak m/z we found a high degree of overlap between the tested array surfaces. The combination of CM10 and IMAC30 arrays was sufficient to represent between 80-90% of all assigned peaks when using either sinapinic acid or alpha-Cyano-4-hydroxycinnamic acid as the energy absorbing matrices. Moreover, arrays processed with SPA consistently showed better peak resolution and higher peak number across all surfaces within the measured mass range. We intend to use CM10 and IMAC30 arrays prepared in sinapinic acid as a fast and cost-effective approach to drive decisions on sample selection prior to more in-depth discovery of diagnostic biomarkers in CSF using alternative but complementary proteomic strategies.

Journal Article↗
PubMed2002

Application of a multigene reverse transcription-PCR assay for detection of mammaglobin and complementary transcribed genes in breast cancer lymph nodes.

BACKGROUND: Mammaglobin mRNA expression is found in 70-80% of primary and metastatic breast tumor biopsies. The potential breast tumor markers B305D, B726P, and gamma-aminobutyrate type A receptor pi subunit (GABApi) complement the expression of mammaglobin. Collectively the expression profile of these four genes could be used as a diagnostic and prognostic indicator for breast cancer. METHODS: A multigene reverse transcription-PCR (RT-PCR) assay was established to detect the expression of mammaglobin, GABApi, B305D, and B726P simultaneously. Specific primers and TaqMan probes were used to analyze combined mRNA expression profiles in primary breast tumors and metastatic lymph node specimens. RESULTS: The multigene RT-PCR assay detected substantial expression signals in 27 of 27 primary tumor and 50 of 50 metastatic breast lymph node samples. Specificity studies demonstrated no significant expression signal in 27 non-breast cancer lymph nodes, in 22 various healthy tissue samples, or in 14 colon tumor samples. CONCLUSION: The novel RT-PCR-based assay described here provides a sensitive detection system for disseminated breast tumor cells in lymph nodes. In addition, this multigene assay could also be used to test peripheral blood and bone marrow samples.

Amino Acid Substitution↗
PubMed2005

Overexpression of G protein-coupled receptors in cancer cells: involvement in tumor progression.

G protein-coupled receptors (GPCRs) play important roles in a variety of biological and pathological processes. They are considered among the most desirable targets for drug development. Recent studies have demonstrated that many GPCRs, such as endothelin receptors, chemokine receptors and lysophosphatidic acid receptors have been implicated in the tumorigenesis and metastasis of multiple human cancers. In this study, we conducted an in silico analysis of GPCR gene expression in primary human tumors by analyzing some publicly available gene expression profiling data. Statistical analysis was performed on eight microarray data sets of non-small cell lung cancer, breast cancer, prostate cancer, melanoma, gastric cancer and diffused large B cell lymphoma to identify GPCRs that are up-regulated in primary or metastatic cancer cells. Our analysis has demonstrated overexpression of several GPCRs in primary tumor cells, including chemokine receptors and protease-activated receptors that were shown to be important for tumorigenesis by previous studies. In addition, we have uncovered several GPCRs, such as neuropeptide receptors, adenosine A2B receptor, P2Y purinoceptor, calcium-sensing receptor and metabotropic glutamate receptors, that are expressed at a significantly higher level in some cancer tissue and may play a role in cancer progression. Analysis of cancer samples in different disease stages also suggests that some GPCRs, such as endothelin receptor A, may be involved in early tumor progression and others, such as CXCR4, may play a critical role in tumor invasion and metastasis. The present study demonstrates the value of publicly available microarray data as a resource to gain more understanding of cancer biology, to validate previous findings from in vitro experiments, and to identify potential novel anticancer targets and biomarkers.

Biomarkers, Tumor↗
PubMed1990

HbA1 in assessment of metabolic control in diabetic BB/E rats.

Estimations of HbA1 levels have been used to assess long-term glycaemic control in spontaneously diabetic BB/E rats. The degree of metabolic control achieved by once daily insulin injections and continuous insulin infusion by osmotic minipump was compared. Citrate gel electrophoresis of lysed erythrocytes, previously washed and incubated in 0.9% NaCl, gave accurate HbA1 values without interference from either abnormal Hb variants or labile glycosylation products. Over a 12 week period there was no significant difference in the mean random weekly plasma glucose concentrations between diabetic rats maintained on insulin injections or continuous infusion therapy. The HbA1 values in the injection-treated animals remained unchanged throughout the study period (mean +/- SEM = 5.1 +/- 0.1%). Diabetic rats treated by osmotic minipump showed a steady decline in values over the same period (4.1 +/- 0.1%; p less than 0.001 vs injected rats) but levels remained higher than those recorded in non-diabetic control rats (2.9 +/- 0.01%; p less than 0.001 vs pump-treated rats). These differences in HbA1 were reflected in the plasma glucose values obtained during a 30 h glucose profile performed after six weeks of insulin therapy. Diabetic rats on injection therapy showed considerable diurnal variation in plasma glucose concentration (5.5-11.2 mmol/l; mean 8.9 +/- 0.5) but continuous insulin infusion eliminated the fluctuations giving a significantly lower mean glucose level over the 30 h period (7.3 +/- 0.1 mmol/l; p less than 0.005). HbA1 levels show a poor correlation with random plasma glucose estimations (r = 0.43) but provide a simple and accurate assessment of long-term glycaemic control without the need for multiple 24 h glucose profiles.

Animals↗
PubMed2006

[Epithelioid hemangioendothelioma of the lung (IVBAT)--clinicopathological and immunohistochemical analysis of 11 cases].

Epithelioid hemangioendothelioma (EHE) of the lungs (syn.: intravascular bronchioloalveolar tumor/IVBAT) is a neoplasm with a vascular line of differentiation. This study provides a clinicopathological analysis of 11 cases of this tumor. There were 7 female and 4 male patients. Patients' age ranged from 33 to 83 years (mean: 49.8, median: 48 years) showing 2 peaks (third/fourth and sixth/eighth decades). The typical radiological appearance revealed multiple bilateral lung nodules from 0.5 to 2 cm. In 2 cases, a striking perivascular and intravascular growth pattern associated to pulmonary veins was evident. All tumors were characterized by epithelioid tumor cells with nests, cords and strands embedded in a sclerosing, hyaline matrix with alveolar, bronchiolar and vascular extension. Necrosis was identified in 8 tumors and ossification in 2 tumors. The mitotic index was below one mitosis in 10 HPF. By immunohistochemistry, all tumors were positive for CD 31, CD 34, and vimentin, 60% positive for factor VIII, and negative for pancytokeratin and calretinin. Follow-up was available for 8 patients with a range of 6 to 105 months (mean: 51.5 months, median: 52 months): 3 patients died (2 certainly from their tumors), 4 are alive disease-free, and one is alive with metastases. EHE of the lungs (IVBAT) represents an intermediate-grade, malignant, mesenchymal neoplasm with a characteristic histological appearance and immunohistochemical profile.

Adult↗
PubMed2003

New frontiers in the treatment of malignant glioma.

Despite many technologic advances in neuroimaging, neurosurgery, and radiation therapy, there has been little improvement in survival for patients with malignant glioma. Given the failure of traditional treatment approaches to significantly improve survival in patients with malignant gliomas, research in this field has focused on gaining a better understanding of the molecular pathogenesis of gliomas with the goal of identifying novel drug targets and therapeutic strategies. The influence of molecular genetics on response and survival has been best shown in oligodendrogliomas. The hallmarks of low-grade and anaplastic oligodendrogliomas are their exquisite sensitivity to chemotherapy and favorable prognosis, which are correlated with loss of heterozygosity of chromosomes 1p and 19q. Together, loss of heterozygosity of 1p and 19q appears to confer responsiveness to chemotherapy and to correlate with improved survival. In contrast, deletion of the CDKN2A gene is correlated with poor response to chemotherapy and poor survival, and loss of heterozygosity of chromosome 10q is associated with shorter progression-free and overall survival compared with intact 10q. A variety of other molecular genetic abnormalities have been recognized in gliomas, and these genetic changes are not only important prognostic factors, but also offer new therapeutic targets. With the increased use of improved surgical and radiotherapy techniques and targeted biologic therapy over the next 20 years, many patients with malignant gliomas may be cured or their disease may be controlled for the long term. Molecular profiling of patients using gene chip technology will likely become commonplace, and many patients will receive a tailored treatment regimen based on the unique genetic profile of their tumor.

Antineoplastic Agents↗
PubMedDate not supplied

[Value of determining fructosamine levels in serum of pregnant patients with diabetes to evaluate the level of compensation for glycemia].

The results in 16 pregnant women with diabetes mellitus are analysed. All patients were treated with an intensive insulin-therapy at the Voivodeship Clinic for Diabetic Patients in Zabrze. Multipoint glycaemia profiles made by the treated patients as a self control were compared with serum fructosamine and HbAlC concentrations. A significant correlation of fructosamine levels with glycaemia and HbAlC levels was noted. No significant dependence of fructosamine and glycaemia fasting levels, incidence of hyperglycaemia and Schlichtkrull's Mw index was noted. Results suggest, that the fructosamine serum concentration is a useful marker of metabolic compensation in pregnant women with diabetes mellitus. It enables less frequent performance of the daily profiles of glycaemia by the patients.

Adult↗