PubMed Health⌕ Search

Biomedical subjects

Zita Borbényi

Publications and source records attributed to Zita Borbényi.

6 recordsLinked to original sources
PubMed2005

[Disorders with eosinophilia, treatment of hypereosinophilic syndrome].

Eosinophilia may be associated with reactive conditions and with clonal disorders of the hematopoietic cells. The hypereosinophilic syndrome takes an intermedier place in this group. In this disease a sustained eosinophilia with end organ damage can occur. The author summarized the diagnostic procedures and differential diagnosis in the group of these diseases focusing on characteristics and treatment of hypereosinophilic syndrome. The treatment has been varied and included steroids, hydroxyurea, interferon-alpha, and in some cases chemotherapy. On the basis of FIP1L1-PDGFRa fusion gene hypereosinophilic syndrome would be classified as a clonal disease and in the FIP1L1-PDGFRa positive cases the tyrosine kinase inhibitor imatinib mesylate (Glivec) would be effective.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2005

Clinical importance of transforming growth factor-beta but not of tumor necrosis factor-alpha gene polymorphisms in patients with the myelodysplastic syndrome belonging to the refractory anemia subtype.

OBJECTIVES: Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta (TGF-beta) are cytokines that play key roles in the myelodysplastic syndrome (MDS). There have been several reports on the presence of genetic polymorphisms in the DNA sequence encoding the leader sequence of the TGF-beta1 protein, located in codon 10 in exon 1 and in the -308 promoter region of TNF-alpha. The objective of this study was to investigate the association between TNF-alpha and TGF-beta1 gene polymorphisms and the susceptibility to MDS and the progression of the disease among patients with MDS belonging to the refractory anemia (RA) subtype. METHODS: The diagnosis of MDS (n = 50) was based on the FAB criteria. The TNF-alpha genotypes were analyzed by PCR-RFLP and the TGF-beta genotypes were analyzed using an amplification refractory mutation system. RESULTS AND CONCLUSIONS: Compared with healthy control subjects, patients with RA showed no significant deviations in genotype or allele frequencies of TNF-alpha. The TT homozygosity at codon 10 of TGF-beta1 was significantly higher among patients with bi- or pancytopenia (severe group) than in the patients with anemia only (mild group; odds ratio = 6.99, p = 0.003). These findings suggest that the TGF-beta1 gene polymorphism in codon 10 and the -308 TNF-alpha gene polymorphism do not predispose to the development of RA, but the TGF-beta1 gene polymorphism may affect disease progression.

Adult↗
PubMed2005

Genetic polymorphisms in patients with myelodysplastic syndrome.

Myelodysplastic syndrome (MDS) is a family of clonal disorders characterized by dyshematopoiesis and susceptibility to acute myelogenous leukemia. Tumor necrosis factor-a (TNF-alpha) and transforming growth factor-beta (TGF-beta) are cytokines that play key roles in the pathogenesis of MDS. There have been several reports on the presence of genetic polymorphisms in the DNA sequence encoding the leader sequence of the TGF-beta protein, and in the -308 promoter region of TNF-alpha. The association between TNF-alpha and TGF-beta1 gene polymorphism and the susceptibility to MDS and the progression of the disease was investigated. As compared with healthy control subjects (n = 74), patients with MDS (n = 55) showed no significant deviations in genotype or allele frequencies of TNF-alpha. Similarly, there were no differences in the distribution of TNF-alpha genotypes between the MDS patients with only anemia (mild group) and those with bi- or pancytopenia (severe group). On the other hand the TT homozygosity at codon 10 in exon 1 of TGF-beta1 gene was associated with a severe degree of cytopenia [95% CI OR = 4.889, p = 0.0071]. These findings suggest that the investigated genetic polymorphisms do not predispose to the development of MDS, but that TGF-beta1 gene polymorphism may affect the disease progression.

Adult↗
PubMed2003

[Follicular lymphoma].

Follicular lymphoma is one of the most common indolent nodal non-Hodgkin's lymphomas. The follicular lymphoma should be differentiated from other nodal non-germinal centre derived lymphomas. Since bcl-2 gene translocation can be detected in 80-90% of the cases, it could be used for the confirmation of the diagnosis, measure of the treatment efficacy as well as for the evaluation of the prognosis and follow-up of the disease. There is no uniform therapy employed for follicular lymphoma patients. The treatment depends on the histological grade, stage, age and condition of the patients. Since disease cannot be cured by conventional dosage therapy in the vast majority of the cases, a treatment--adjusted to the condition of the patients as well as the stage and grade of the disease--ensuring the longest period and best quality of life should be selected. The authors review the questions of diagnosis and treatment, including the results of radiotherapy and chemotherapy and discuss the role of the interferon-alpha, purine analogues, monoclonal antibodies and high-dose therapy.

Antibodies, Monoclonal↗
PubMed2002

[Treatment of acute leukemia in older patients].

The median age of patients with acute leukemia is more than 60 years, and the incidence of the disease increases with age. There are several unfavorable biologic and clinical factors in older patients with acute leukemia, the remission rate and their survival are much worse than in younger adults. The poor performance score and any other concomitant disease and the poor reserve capacity of their bone marrow represent significant difficulties to deliver the proper remission induction and postremission therapy. The poor biologic factors like acute leukemia following myelodysplasia, unfavorable cytogenetic abnormalities and multidrug resistance among elderly patients are more common comparing to younger patients. The authors summarize the international data and attempt to define the proper therapy namely who are candidates for induction and intensive postremission therapy, what is the role of palliative cytostatic treatment or supportive care for these patients.

Acute Disease↗