ABSTRACT
Platelet-derived growth factor [PDGF] is one of the numerous proteins that regulate cell growth and division. It is a major mitogenforfibroblasts, smooth muscle cells and other cells. Many tumors have been shown to express PDGF and its cognate receptors, and in these, an autocrine stimulation of tumor cell growth may prevail. The aim of this work was to study PDGF levels in patients with Hodgkin's disease [HD] and non Hodgkin lymphoma [NHL], both before and after 3 cycles of chemotherapy and their relation to disease progression and response to treatment. This study was conducted on 20 lymphoma patients [gpl] including 7 patients with Hodgkin s disease and 13 patients with non-Hodgkin lymphoma. 10 age and sex-matched normal healthy controls were also included in our study [gpII]. All patients were subjected to thorough history taking, clinical examination, routine laboratory investigations, lymph node biopsies to diagnose the lymphoma and staging of the lymphoma was done by radiological studies and bone marrow aspiration and trephine biopsies when needed, PDGF was measured in the serum of controls and patients before starting chemotherapy. This measurement was repeated after completion of 3 cycles of chemotherapy, together with assessment of response to chemotherapy, both clinically and radiologically. Serum PDGF levels in our lymphoma patients, both before and after 3 cycles of chemotherapy were significantly higher than the control group. No significant differences were noted between our ND and NHL patients as regards serum PDGF levels. There was a sigmfi cant positive correlation between serum PDGF levels and serum LDH levels in our patients. Patients with advanced disease [stage III, IV] at presentation had significantly higher serum PDGF levels than patients with earlier stages [stage I, II]. Also, patients who showed a response to therapy had significantly lower pretreatment values of serum PDGF than patients with no response or with progressive disease. In conclusion, serum PDGF levels were significantly higher in lymphoma patients, compared to normal controls. Significant reduction in serum PDGF levels occurred in patients who responded to 3 cycles of chemotherapy. There was no signfi cant dUiference between our HD and NHL patients as regards PDGF levels and there was a significant positive correlation between serum PDGF and serum LDH levels, both before and after treatment
Subject(s)
Humans , Male , Female , Lymphoma, Non-Hodgkin , Platelet-Derived Growth Factor , Treatment OutcomeABSTRACT
The present study was carried out in order to evaluate the effectiveness of pentoxifylline [PTX] medication in the management of both minor and major recurrent aphthous stomatitis patients. Also, to investigate the level of tumor necrosis factor-alpha in serum of these patients before [RAS] and alter treatment with pentoxifylline. A total number of forty subjects participated in this study, they were divided into two groups, the first group consisted of twenty patients with RAS. Ten patients suffered from minor RAS and ten patients suffered from major RAS. They all received PTX 400 mg three times daily for one month. The second group consisted of twenty healthy subjects who served as controls. A history about the aphthous lesion was taken from each patient regarding number, duration, location pain severity and frequency. Oral mucosa of selected patients was examined for aphthous lesions to record, size duration, frequency and number of aphthous lesions. The patients were followed up weekly during the six months period of follow up clinical examination of plaque index [P.I.] and papillary bleeding index [PB1] was performed at baseline, at the end of dose period and at the end of follow up period [6 months]. Serum tumor necrosis factor and [TNF-alpha] was estimated for both control and RAS group before and after PTX administration. Pentoxifylline led to significant clinical improvement in pain, size, duration number and frequency of aphthous lesion throughout the 6 months study period. TNF-alpha level was significantl increased in RAS patierits compared with control subjects. A significant increase was detected in major RAS patients compared with minor RAS patients. Both forms of aphthous lesion demonstrated a significant decrease in TNF- alpha after PTX treatment. No significant correlation was observed between [TNF- alpha] level PI and PBI. Also no correlation between PI and age, number, size pain and duration of aphthous lesions was observed while a negative correlation was found regarding the number of PAS lesion. A significant correlation between [TNF- alpha] level and size, duration, pain and RAS score was observed
ABSTRACT
NAD [p] H: quinone oxidoreductase NQO1 originally called DT-diaphorase is an enzyme that is able to detoxify a number of natural and synthetic compounds, including quinones and their derivatives. It is induced by synthetic antioxidants and cruciferous vegetables and protects cells against oxidative stress. The human NQO1gene is located on chromosome 16q22.1, a single nucleotide polymorphism [cytosine to thymine, [CT]] at position 609 in the NQO1 gene has been identified in a human colon cancer cell line with very low NQO1 activity. This variant produces a proline-to-serine substitution that inactivates the enzyme. People who are homozygous for the variant allele completely lack NQO1 activity, while heterozygote have low to intermediate activity compared with people with the wild type. The incidence of the polymorphism varies widely by race, and associations have been made between the presence of variant alleles and lung and urological cancers. NQO1 mutation had been identified as risk factor in AML and ALL but no avilable data in chronic myeloid leukemia. Our study included 21 chronic myeloid patients and 10 apparently healthy persons using PCR-RFLP technique to detect the NQO1 nutation. Among the cases 11[52.4%] were positive for the mutation compared to 1[10%] of control. A higher incidence of the mutation was noticed among patients in crisis stage. Conclusion from our data we noticed a high incidence of NQO1 mutation in cases of CML which may suggest an important role of this gene in the etiology and pathogenesis of chronic myeloid leukemia