Effects of enhancer of zeste homolog 2 and mucin 1 expressions on treatment response in breast cancer.

OBJECTIVE: Breast cancer is the most common malignancy in women. In the treatment of these patients, pathological complete response is defined as the absence of invasive cancer in breast or lymph node tissue after the completion of neoadjuvant chemotherapy. In this study, we aimed to investigate the relationship of enhancer of zeste homolog 2 and mucin 1 expressions with pathological complete response in patients with breast cancer receiving neoadjuvant chemotherapy. METHODS: A total of 151 patients were included in the study. Enhancer of zeste homolog 2 and mucin 1 expressions were evaluated in the biopsy materials pre-neoadjuvant chemotherapy and post-neoadjuvant chemotherapy surgical material, and their relationship with pathological complete response was investigated. RESULTS: The pathological complete response rates were significantly higher among the hormone receptor-negative patients, those with a high Ki-67 score, and patients with HER2-positive. Higher pathological complete response rates were obtained from patients with enhancer of zeste homolog 2 expression positivity pre-neoadjuvant chemotherapy. In addition, after neoadjuvant chemotherapy, enhancer of zeste homolog 2 expression was found to be completely negative in materials with pathological complete response; that is, in breast tissues considered to be tumor-free. While there was no significant relationship between mucin 1 expression and pathological complete response pre-neoadjuvant chemotherapy, mucin 1 expression was determined to significantly differ between the tissues with and without pathological complete response among the surgical materials examined. CONCLUSION: In our study investigating the relationship between enhancer of zeste homolog 2 and mucin 1 expression and pathological complete response in patients who received neoadjuvant chemotherapy, we found that enhancer of zeste homolog 2 expression could be used as a predictive marker for pathological complete response. However, mucin 1 expression was not associated with pathological complete response.

Effects of enhancer of zeste homolog 2 and mucin 1 expressions on treatment response in breast cancer

SUMMARY OBJECTIVE: Breast cancer is the most common malignancy in women. In the treatment of these patients, pathological complete response is defined as the absence of invasive cancer in breast or lymph node tissue after the completion of neoadjuvant chemotherapy. In this study, we aimed to investigate the relationship of enhancer of zeste homolog 2 and mucin 1 expressions with pathological complete response in patients with breast cancer receiving neoadjuvant chemotherapy. METHODS: A total of 151 patients were included in the study. Enhancer of zeste homolog 2 and mucin 1 expressions were evaluated in the biopsy materials pre-neoadjuvant chemotherapy and post-neoadjuvant chemotherapy surgical material, and their relationship with pathological complete response was investigated. RESULTS: The pathological complete response rates were significantly higher among the hormone receptor-negative patients, those with a high Ki-67 score, and patients with HER2-positive. Higher pathological complete response rates were obtained from patients with enhancer of zeste homolog 2 expression positivity pre-neoadjuvant chemotherapy. In addition, after neoadjuvant chemotherapy, enhancer of zeste homolog 2 expression was found to be completely negative in materials with pathological complete response; that is, in breast tissues considered to be tumor-free. While there was no significant relationship between mucin 1 expression and pathological complete response pre-neoadjuvant chemotherapy, mucin 1 expression was determined to significantly differ between the tissues with and without pathological complete response among the surgical materials examined. CONCLUSION: In our study investigating the relationship between enhancer of zeste homolog 2 and mucin 1 expression and pathological complete response in patients who received neoadjuvant chemotherapy, we found that enhancer of zeste homolog 2 expression could be used as a predictive marker for pathological complete response. However, mucin 1 expression was not associated with pathological complete response.

Symptomatic bilateral choroid plexus xanthogranuloma in a pediatric patient.

INTRODUCTION: Central nervous system xanthogranulomas are uncommon clinical entities, and symptomatic bilateral choroid plexus xanthogranulomas are rare. CASE PRESENTATION: We present the case of a 15-year-old male patient with bilateral choroid plexus xanthogranulomas with symptoms of increased intracranial pressure. Gross total resection of the tumor in the left lateral ventricle was performed. The patient improved, and asymptomatic right-sided tumor was monitored at follow-up. CONCLUSION: The main treatment objective in these tumors is gross total resection. Asymptomatic tumors can be followed without intervention. However, surgery should be performed for symptomatic tumors that cause hydrocephalus or symptoms of increased intracranial pressure.

The effects of exercise on skeletal and heart muscle citrate synthase and carnitine palmitoyltransferase mRNA expressions in high-calorie fed rats.

In this study, the effect of high-calorie feeding and aerobic exercise on skeletal and cardiac muscle citrate synthase (CS), carnitine palmitoyltransferase-I (CPT-I), and -II (CPT-II) mRNA expressions were evaluated. Genetically non-obese rats were grouped as normal-high calorie and sedentary-exercising. Gastrocnemius-soleus and heart muscles' CS, CPT-I, and CPT-II expressions and skeletal muscles' histopathological characteristics were evaluated. High-fat diet had increased body weight by 10% and aerobic exercise did not make any difference. Skeletal muscle CS expression was increased significantly in normal-calorie exercising group. Exercise and high-fat diet did not change CPT-I and CPT-II expressions in both heart and skeletal muscle. Histopathological evaluations demonstrated increased cytoplasmic lipid droplets in high-calorie fed sedentary rats, and exercise had reduced lipid droplets in skeletal muscle. Also, both mitochondria and nuclei distribution were impaired in high-calorie groups. In conclusion, aerobic exercise without food restriction was not enough to make significant changes in fat transportation mechanism into skeletal and heart muscle.

Clinical Relevance and Immunohistochemical Patterns of Silent Pituitary Adenomas: 10 Years of Single-centre Experience.

BACKGROUND: Silent pituitary adenomas are clinically non-functional (i.e., without clinically evident pituitary hormone production). INTRODUCTION: The aim of this study was to investigate subjects with silent pituitary adenomas for possible variations in their clinical status. METHODS: A total of 102 patients who had undergone surgery for pituitary adenoma and had been diagnosed with silent pituitary adenoma was included in the study. The patients' preoperative and postoperative hormonal parameters and magnetic resonance imaging (MRI) features were collected, and pathological specimens were re-evaluated. RESULTS: Immunohistochemistry results of the 102 patients were as follows: hormone-negative adenomas (n=35) 35.5%; FSH+LH-positivity (n=32) 31.3%; ACTH-positivity (n=11) 10.7%; α-subunit- positivity (n= 9) 8.8%; prolactin-positivity (n=8) 7.8%; GH-positivity (n=6) 5.4%; and plurihormonal adenoma (n=1). The mean sizes of SGA, SGHA, and SCA were 28.0±12.7, 30.0±16.0, and 27.7±8.9mm (p>0.05), respectively. With the exception of silent gonadotroph adenomas (SGAs), female gender dominance was shown in patients with silent growth hormone adenoma (SGHA) and silent corticotroph adenoma (SCA). Although no clinical relevance was observed in relation to hormonal excess, preoperative GH (4.21±4.6, vs. 0.27±0.36 p=0.00) was slightly more elevated in SGHA than in GH-negative adenomas. Additionally, preoperative basal ACTH values (47.3±28.7 vs. 23.9±14.4, p=0.003) were also higher in SCA compared to the other types. Our findings revealed SCAs to be of more aggressive behaviour than SGHAs and SGAs due to invasiveness in radiological imaging, their elevated re-operation, and postoperative ACTH values. CONCLUSION: Silent pituitary adenomas represent a challenging diagnostic tumour group. Careful initial evaluation of patients with pituitary adenomas should consider any mild signs and symptoms of functionality, particularly in cases of GH- and ACTH-secreting adenomas.

Prognostic significance of EGFR, MUC1 and PD-L1 expressions in cases with triple negative breast cancer.

PURPOSE: Twenty percent of the breast cancers are triple negative (TNBC). Despite the impressive progression in the biology of this subgroup, data is limited as compared to hormone and/or HER2 positive cases. Thus, the aim of this study was to detect the expression levels and to identify the prognostic values of MUC1, EGFR and PD-L1 in TNBC. METHODS: MUC1, EGFR and PD-L1 expressions were detected by immunohistochemistry in 97 cases with TNBC. Associations between clinical and histopathological parameters with overall survival (OS) and progression-free survival (PFS) were analyzed using the Kaplan-Meier method and compared by the log-rank test. Prognostic effects were analyzed by Cox proportional hazard models. RESULTS: During a median follow-up of 93 months (0.6-168.7) the mean PFS was 110.1 and OS was 121.8 months. Tumor diameter (T), involved lymph node status (N) and TNM were found to be prognostic for PFS and OS. PD-L1 in microenvironment (PD-L1 ME) and EGFR expression were found to be associated with longer PFS and OS, but MUC1 and tumor PD-L1 (PD-L1 TM) expressions were not. All combined analyses showed that in the subgroups of MUC1, PD-L1 TM or ME positive, EGFR expression was correlated with longer PFS and OS than those who were not. Older age (≥70 years), T and N status and also EGFR expression were found to be independent prognostic factors for OS in Cox regression analysis. CONCLUSION: EGFR expression was found to be one of the most important prognostic factors in addition to T and N status in cases with TNBC.

Insights from genotype-phenotype correlations by novel SPEG mutations causing centronuclear myopathy.

Centronuclear myopathies (CNM) are a clinically and genetically heterogeneous group of congenital myopathies, defined histologically by increased number of fibres with centrally located nuclei, and type I fibre predominance in muscle biopsy. Myotubular myopathy, the X-linked form of CNM caused by mutations in the phosphoinositide phosphatase MTM1, is histologically characteristic since muscle fibres resemble myotubes. Here we present two unrelated patients with CNM and typical myotubular fibres in the muscle biopsy caused by mutations in striated muscle preferentially expressed protein kinase (SPEG). Next generation sequencing revealed novel biallelic homozygous mutations in SPEG in both cases. Patient 1 showed the c.1627_1628insA (p.Thr544Aspfs*48) mutation and patient 2 the c.9586C>T (p.Arg3196*) mutation. The clinical phenotype was distinctive in the two patients since patient 2 developed a dilated cardiomyopathy with milder myopathy features, while patient 1 showed only myopathic features without cardiac involvement. These findings expand the genotype-phenotype correlations after the initial report. Additionally, we describe whole body muscle MRI of patient 2 and we argue on the different SPEG isoforms in skeletal muscle and heart as the possible explanation leading to variable phenotypes of SPEG mutations.

Impacts of ß-estradiol on intestinal injury in newborn rats.

OBJECTIVE: Necrotizing enterocolitis has been investigated and debated extensively in recent years; however, there is still no effective treatment. The aim of this study was thus to examine the effects of ß-estradiol on intestinal injury in rats. METHODS: Twenty-four newborn female rat pups were divided into three groups. In group 1 (sham), hypoxia-re-oxygenation was not performed. In group 2 (saline), the rats were injected with saline after hypoxia-re-oxygenation, and the process was repeated for 5 d. In group 3 (ß-estradiol treatment), the rats were subjected to hypoxia-re-oxygenation and then given ß-estradiol intraperitoneally once a day for 5 d. After these procedures, the terminal ileum was removed for analysis. RESULTS: Statistically significant differences in histological grades were found between groups 1 and 2 (p = 0.000), groups 1 and 3 (p = 0.028), and groups 2 and 3 (p = 0.021). There were also differences in TNF-α and IL-6 levels between groups 2 and 3 (p = 0.000 and p = 0.038, respectively) and between groups 1 and 2 (p = 0.000 and p = 0.000); there was no difference between groups 1 and 3 (p = 0.574 and p = 0.195, respectively). Electron microscopy examination revealed a decrease in lipid droplets at the apical cytoplasm of the columnar cells in group 2; in group 3, the absorption of the lipids as lipid droplets was similar to that of group 1. CONCLUSION: In this study, ß-estradiol was found to decrease the intensity of intestinal injury significantly by inhibiting TNF-α and IL-6.

Intestinal ischemia-reperfusion induced diaphragm contractility dysfunction: Electrophysiological and ultrastructural study in a neonatal rat model.

AIM: To evaluate the remote effect of intestinal ischemia reperfusion (IR) injury mediated by tumor necrosis factor alpha (TNF-α) on diaphragm contractility functions and whether administration of NAC may counteract the possible detrimental effects in an experimental neonatal rat model. METHODS: 40 Wistar rat pups were randomized into four groups; ten animals in each. Intestinal ischemia was conducted by obstructing mesentery of intestines by a silk loop. In the control group; only laparotomy was performed. After 1h ischemia, reperfusion was conducted for 1h in 1h group, 24h for 24h group and 24h for 24h+NAC group but administration of NAC (150mg/kg/day) intraperitoneally twice a day was performed. Inflammatory response was evaluated by tissue TNF-α level and contractility functions by mechanic activity studies of the diaphragm. Electrophysiology of the diaphragm and the phrenic nerve was conducted to determine neuropathy or myopathy and transmission electron microscopy was performed to evaluate ultrastructural changes in the phrenic nerve. RESULTS: Diaphragm tissue TNF-α level significantly increased in 1h and 24h groups (P=0.004, P=0.0001; respectively). Diaphragm mechanic activation force and duration significantly decreased at 1h and 24h (P=0.004, P=0.02 and P=0.0001, P=0.0001; respectively). NAC administration significantly prevented decrease in the maximal contraction and the duration (P<0.001). Phrenic nerve compound action potential (CMAP) amplitude significantly decreased in 1h group (P<0.0001) and NAC administration significantly prevented this decrease when compared with 24h group (P<0.001). In diaphragmatic needle electromyography, the duration of motor unit potentials (MUP) was prolonged significantly when compared with control group. Contractility and electrophysiological studies were indicating primarily neuropathy in diaphragm dysfunction. Histopathology revealed axonal and myelin degeneration in the 1h and 24h group, but less injury in the NAC administered group. CONCLUSIONS: Intestinal IR induced elevation of TNF-α level in the diaphragm. Impairment in the diaphragm contractility and neuropathic changes in the phrenic nerve occurred even in the first hour of reperfusion. NAC administration prevented these detrimental effects.

Effects of intraperitoneally administered folic acid on the healing of repaired tibial nerves in rats.

BACKGROUND: Complete nerve regeneration and clinical healing remain a challenge despite considerable advances in the treatment of peripheral nerve injuries. To improve nerve regeneration, several experimental molecular procedures have been attempted. This study aimed to investigate the effects of folic acid on peripheral nerve healing after transection and end-to-end suture repair of the tibial nerve in rats. METHODS: In this study, 20 adult male Wistar Albino rats weighing 225 to 250 g were used. The right tibial nerves of 20 rats were explored, transected, and sutured using the end-to-end technique. The rats were randomly allocated to either the intraperitoneally administered folic acid group (test group) or the control group. Preoperative and 6-week postoperative neurophysiological studies were performed by the same researcher. Myelin-sheathed axons were counted. RESULTS: The results demonstrated that the folic acid-treated group exhibited improved electromyographic results compared with the control group. Histological evaluation revealed that the axons were well preserved and that the axon quantity and density were increased in the test group compared with the control group. Quantitative results also increased in the test group compared with the control group (p = 0.001). CONCLUSION: In this study, 6-week intraperitoneal administration of 80 µg/kg of folic acid significantly improved peripheral nerve healing. Histological analysis of the group that received folic acid revealed increased axon myelination with little granular tissue or fibrosis. We propose that folic acid supplementation may be an effective component of peripheral nerve injury treatment.

Giant axonal disease: Report of eight cases.

BACKGROUND: Giant axonal neuropathy (GAN) is an autosomal recessive inherited progressive motor and sensory neuropathy with typical onset in early childhood. The disease is caused by GAN gene mutations on chromosome 16q24.1. To determine clinical and genetic results in Turkish patients with GAN. METHODS: Eight children with GAN were retrospectively analyzed. Five (62.5%) were girls and 3 (37.5%) were boys with the mean age on admission 10.13±3.8 years (range: 5-15 years). RESULTS: Parental consanguinity was found in all the families. The patients had the classical clinical phenotype characterized by a severe axonal neuropathy with kinky hair. Two patients had contractures of extremities, and not walking. One patient was walking with aid. The other patients were walking without aid. Mutation analysis was performed in two patients and IVS9 (+1G>T) (homozygous) mutation was detected. CONCLUSION: The classical clinical findings allowed considering the GAN diagnosis, but, in atypical cases and milder phenotypes, the presence of giant axons in nerve biopsy was helpful to specify molecular analysis.

Well-differentiated papillary mesothelioma of the tunica vaginalis: a case study and review of the literature.

Well-differentiated papillary mesothelioma is an uncommon tumor of the testes that usually presents as a hydrocele. Here, we present the case of one patient who did not have a history of asbestos exposure. The tumor was localized in the tunica vaginalis and was composed of three pedunculated masses macroscopically. Microscopically, branching papillary structures with focal coagulative necrosis were present. In addition to immunohistochemistry, simian virus 40 DNA was also tested by polymerase chain reaction. This report presents one case of this rare entity, its clinical and macroscopic features, and follow-up results.

In situ hybridization analysis of invasive breast carcinomas with immunohistochemically negative Her-2 status (a national multicenter study).

OBJECTIVE: The aim of this study was to determine the rate of Her-2 gene amplification in breast cancer cases with a previous negative Her-2 result as determined by immunohistochemistry (score 0 or 1). MATERIAL AND METHOD: 552 cases of invasive breast carcinoma were assessed with the contribution of 9 centers. Previous immunohistochemistry score was either 0 or 1+ in all cases. These cases were re-tested by Her-2 silver in situ hybridization in the central laboratory. Her-2 gene amplification was defined as Her-2/CEP 17 ratio of more than 2.2. Cases with a ratio between 1.8 and 2.0 were defined as equivocal and cases with a ratio of less than 1.8 were defined as negative. RESULTS: Re-testing of the 552 cases with silver in situ hybridization showed a total of 22 cases with Her-2 gene amplification, of which 11 (3.2%) were found to be score 0, and 11 were found to be score 1+ (5.3%) by immunohistochemistry previously. Her-2 gene amplification rate of cases (score 0 and 1+) ranged from 0% to 10.48% among the centers. Polysomy was found in 28 (8.1%) of the score 0 cases and 25 (12.1%) among the score 1+ cases. Five (9.4%) of the cases with polysomy were found to be amplified, and 48 (90.6%) were not. CONCLUSION: The results of the study show that a group of cases (3.98%) with a potential to benefit from anti-Her-2 therapy may be missed with the immunohistochemical method. This indicates the importance of quality assurance, especially in central laboratories with many breast cancer cases in daily practice.

Effects of caffeine on neuronal apoptosis in neonatal hypoxic-ischemic brain injury.

OBJECTIVE: Hypoxia-ischemia (HI) in rat pups leads to strong activation of apoptosis, and apoptosis contributes significantly to cerebral damage in the perinatal period. Caffeine displays a broad array of actions on the brain. The aim of this study was to investigate the effects of caffeine on neuronal apoptosis in a hypoxic-ischemic neonatal model. METHODS: Twenty-four seven-day-old Wistar rat pups were subjected to right common carotid artery ligation and hypoxia for 2 h. Sham group (n = 8) had a median neck incision, but the rats were not subjected to ligation or hypoxia. The pups were treated with 20 mg/kg/day caffeine citrate (n = 8) or saline (n = 8) immediately before HI and at 0, 24, 48 and 72 h post-hypoxia. Neuronal apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) and caspase-3 in the hippocampus and parietal cortex of both hemispheres. RESULTS: The numbers of apoptotic cells in the hippocampus and parietal cortex were significantly higher in the saline group than they were in the sham group (p < 0.0001). The number of apoptotic cells in the hippocampus (p < 0.0001) and parietal cortex (p < 0.0001, TUNEL and p = 0.001, caspase-3) were higher in the caffeine-treated group than they were in the sham group, but the number of apoptotic cells decreased significantly in the caffeine-treated group compared with the saline group in the hippocampus (p < 0.0001, TUNEL and p = 0.001, caspase-3) and parietal cortex (p = 0.001, TUNEL and p = 0.002, caspase-3). CONCLUSIONS: We show that caffeine administration in hypoxic-ischemic brain injury reduces neuronal apoptosis in the developing brain. We suggest that caffeine may be effective in reducing brain injury.

The first report of cabergoline-induced immune hemolytic anemia in an adolescent with prolactinoma.

Prolactinomas are common pituitary tumors that can cause gonadal dysfunction and infertility related to hyperprolactinemia. Dopamine agonists are the first-line treatment in these patients. Cabergoline leads to significant reduction in serum prolactin levels and tumor size in patients with prolactinoma. Dopamine agonists have been associated with adverse effects such as nausea, vomiting and psychosis. We report here a case with cabergoline-induced immune hemolytic anemia. The patient had cabergoline treatment history for prolactinoma and presented with weakness, fatigue, nausea, and paleness. Laboratory findings revealed severe anemia-related immune hemolysis. There were no causes identified to explain hemolytic anemia except cabergoline. Therefore, cabergoline therapy was stopped and subsequently hemolytic anemia resolved and did not occur again. This is the first reported pediatric case with prolactinoma and cabergoline-induced hemolytic anemia. Clinicians should be watchful for this rare side effect induced by cabergoline.

Sweet syndrome in a patient with chronic lymphocytic leukemia/small lymphocytic lymphoma: curious lymphocyte/neutrophil fluctuations.

UNLABELLED: Sweet syndrome, also referred to as acute febrile neutrophilic dermatosis, is characterized by tender, red inflammatory nodules or papules that occur in association with infection, malignancy, connective tissue disease, or following exposure to certain drugs. Here, we present Sweet syndrome in a case with small lymphocytic lymphoma/chronic lymphocytic leukemia (SLL/CLL) which is a relatively rare co-occurrence. CONFLICT OF INTEREST: None declared.

The effect of levetiracetam on neuronal apoptosis in neonatal rat model of hypoxic ischemic brain injury.

BACKGROUND: Hypoxic-ischemic brain injury (HIBI) is a common cause of neonatal mortality and morbidity. The use of levetiracetam (LEV), as a potential neuroprotective in brain ischemia, receives an increasingly high attention, and it could have a crucial role in the regulation of epileptogenesis and neuroprotection. Potential effects of LEV on neuronal apoptosis in HIBI have not previously been reported in literature. OBJECTIVES: The aim of this study is to evaluate the possible effects of LEV on neuronal apoptosis in neonatal rat model of HIBI. METHODS: Seven-day-old Wistar rat pups were subjected to right common carotid artery ligation and hypoxia (92% nitrogen and 8% oxygen) for 2h. The pups were treated with LEV or saline after hypoxia. In sham group rats, neither ligation, nor hypoxia was performed. Neuronal apoptosis was evaluated by the terminal deoxynucleotidyl-transferase- mediated dUTP nick-end labeling (TUNEL) methods. RESULTS: The counts of apoptotic cells in both hippocampus and cerebral cortex were significantly higher in the saline treatment group than in the sham group. The counts of apoptotic cells in both hippocampus and cerebral cortex were similar to those in the sham group and in the LEV treatment group. The number of apoptotic cells decreased significantly in the LEV-treated group compared with the saline group. CONCLUSIONS: These results show that LEV administration after hypoxia reduces neuronal apoptosis. Thus, we propose that LEV, as an effective antiepileptic and antiapoptotic drug, may be a viable choice for the control of seizure activity in neonates with HIBI.

Impairment of peripheral nerve healing after nerve repair in rats chronically exposed to alcohol.

BACKGROUND AND AIMS: The aim of this study was to determine the effect of chronic alcoholism on the healing of repaired peripheral nerve and muscle. METHODS: Group 1 rats (n = 9) were fed with an alcohol-free modified liquid diet (MLD) throughout the experiment and received no nerve transection or repair. Group 2 rats (n = 9) were fed the same isocaloric MLD and underwent nerve transection and repair. Group 3 (n = 7) consisted of alcoholic rats without nerve transection and repair and Group 4 (n = 8) consisted of alcoholic rats with nerve transection and repair. To assess the effects of chronic alcoholism on nerve healing, surgical procedures were applied to rats in Groups 2 and 4. After 2 months, posterior tibial nerve and gastrocnemius muscle samples were taken for histological analysis. RESULTS: Group 2 rats displayed a group of atrophic fibers, whereas Group 3 rats showed myophagocytosis and endomysial mononuclear infiltration and type 2 fiber atrophy. Group 4 rats displayed a large section of atrophic fibres. Axonal loss, prominent regenerative clusters and endoneural fibrosis occurred in Group 2 rats. Axonal and myelin degeneration, myelin remnants and thinly myelinated axons were exhibited in Group 3 rats, whereas severe axonal loss, myelin degeneration, regenerative clusters and endoneural fibrosis were discovered in Group 4. There was a significant difference in the number of myelinated axons among the various groups of rats. CONCLUSIONS: Our findings show that chronic alcoholism has a negative influence on peripheral nerve regeneration associated with a significant decrease in axon number and increased axonal degeneration.

Antioxidant enzyme levels in cases with gastrointesinal cancer.

UNLABELLED: The aim is to evaluate the antioxidant enzyme levels in tumoral tissues and accompanying normal tissues in gastrointestinal cancer; and compare the colorectal cancer (CRC) with gastric cancer (GC). METHOD: Antioxidant enzymes including glutathione reductase (GR), glutathione peroxidase (GPX), superoxide dismutase (SOD), malondialdehyde (MDA) and glucose 6 phosphate dehyrogenase (G6PD) which are important for anti-oxidant functions were evaluated in fresh tumor tissues and adjacent normal tissues obtained from a total of 58 patients. RESULTS: All the enzyme levels were higher in tumoral tissues compared to normal tissue from non-cancerous disease. There was not a significant difference for enzyme levels between CRC and GC groups except GPx. GPx activity tended to be higher in cases without serosal involvement (SI), and this activity was higher in cases without lymph node (LN) involvement in normal tissue (p=0.012). MDA activity was higher in cases without serosal involvement compared to with SI groups in tumor tissue (p=0.050). G6PD activity in normal tissue was higher in cases with serosal involvement and LN involvement (p=0.064, 0.046, respectively). GR activity was higher in signet ring cell cancer (SRC) than adeno cancer. In GC, G6PD activity in tumor was tended to be higher in undifferentiated cancer (p=0.071). CONCLUSION: The antioxidant enzymes activities such as GPX, SOD, G6PD, MDA and GR were found to be related with malignant phenotype in gastrointestinal cancers. We need further studies to understand the biologic and clinical importance of these enzymes in GI cancers.