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Leukotriene D4 (LTD4) is an inflammatory mediator synthesized in the arachidonic acid pathway and has been reported to induce cell proliferation and survival in cancer. LTD4 is synthesized from LTC4 by the enzyme gamma-glutamyltransferase (GGT). Here, we examined serum LTD4 levels and the relationship of LTD4 with GGT in patients with breast cancer. For that purpose, serum samples were taken from 43 patients diagnosed with breast cancer and 8 healthy controls. The patients were divided into five subgroups, as Luminal A, Luminal B, Luminal B-HER2(+), HER2(+) and triple negative. LTD4 levels were measured by ELISA method. Mean levels of LTD4 in the patients were significantly higher than in healthy controls [3,43 (2,21) ng/mL vs 1,47 (0,46) ng/mL; p < 0.05]. According to the molecular subtypes, serum LTD4 levels were found to be significantly higher in the Luminal A, Luminal B and Triple (-) subgroups than in the controls (p

One of the most important problems encountered in patients with triple-negative breast cancer (BC) treatment is the inadequate response of tumor tissueto treatment. The high expression of the Tip60, which is involved in the repair of DNA double-strand breaks, will increase the repair of DNA damage to becreated in tumor cells, especially during the radiotherapy treatment process, thus reducing the treatment response and having a negative effect. In thisstudy, the Tip60 gene was silenced using siRNA in MCF-7 and MDA-MB-231 cell lines, and their response to radiotherapy was monitored. To determinewhether gene silencing was successful or not, Tip60 mRNA and protein expression values were measured. Cytotoxicity and DNA damage in UV-treated cellswere analyzed by MTT and COMET methods, respectively. According to the results of the study, more DNA damage was observed in the MCF-7 in whichthe Tip60 gene was silenced and UV-treated compared to the non-Tip60 gene-silenced and UV-treated cells. On the other hand, more DNA damage wasobserved in the MDA-MB-321 in which the Tip60 gene was non-silenced and applied UV, compared to the cells in which the Tip60 gene was silenced.However, excessive DNA damage was already observed in the untreated MDA-MB-231. According to the results, silencing of the TiP60 gene in the MCF-7may be beneficial in reducing resistance to radiotherapy, but no effect is expected in the MDA-MB-231. This can be explained by the fact that they areheterogeneous tumors. These data could use for future treatment development studies., One of the most important problems encountered in patients with triple-negative breast cancer (BC) treatment is the inadequate response of tumor tissue to treatment. The high expression of the Tip60, which is involved in the repair of DNA double-strand breaks, will increase the repair of DNA damage to be created in tumor cells, especially during the radiotherapy treatment process, thus reducing the treatment response and having a negative effect. In this study, the Tip60 gene was silenced using siRNA in MCF-7 and MDA-MB-231 cell lines, and their response to radiotherapy was monitored. To determine whether gene silencing was successful or not, Tip60 mRNA and protein expression values were measured. Cytotoxicity and DNA damage in UV-treated cells were analyzed by MTT and COMET methods, respectively. According to the results of the study, more DNA damage was observed in the MCF-7 in which the Tip60 gene was silenced and UV-treated compared to the non-Tip60 gene-silenced and UV-treated cells. On the other hand, more DNA damage was observed in the MDA-MB-321 in which the Tip60 gene was non-silenced and applied UV, compared to the cells in which the Tip60 gene was silenced. However, excessive DNA damage was already observed in the untreated MDA-MB-231. According to the results, silencing of the TiP60 gene in the MCF-7 may be beneficial in reducing resistance to radiotherapy, but no effect is expected in the MDA-MB-231. This can be explained by the fact that they are heterogeneous tumors. These data could use for future treatment development studies.

Gama-glutamiltransferaz (GGT) düzeylerinde yükselme olan bireylerde meme kanseri riskinde artış olduğu bildirilmiştir. Genom araştırmaları, GGT1'in yanı sıra, insan genomunun ek ilgili genler veya diziler içerdiğini göstermiştir. Amino asit dizileri açısından, GGT1'e önemli benzerlik gösteren genler (GGT5 ve GGT7) tanımlanmıştır. Bu çalışmanın amacı, meme kanserinin moleküler alt tiplerinde GGT5 ve GGT7 gen ekspresyonlarını değerlendirmektir. Bu amaçla, meme kanseri tanısı konmuş 58 hastadan meme dokusu örnekleri alındı. Bu hastalar, östrojen reseptörü (ER), progesteron reseptörü (PR), İnsan epidermal büyüme faktör reseptör 2 (HER2) ve Ki67 antijeni moleküler belirteçleri kullanılarak; Luminal A, Luminal B, HER2(+), Luminal B-HER2(+) ve triple negatif olmak üzere beş alt gruba ayrıldı. Kontrol dokusu olarak, meme küçültme ameliyatı için kliniğe başvuran 8 sağlıklı kişiden alınmış meme dokuları da çalışmaya dahil edildi. Meme kanseri hastalarının ve sağlıklı kontrollerin normal ve tümörlü doku örneklerinde GGT5 ve GGT7 mRNA ekspresyonları qRT-PCR yöntemi ile incelenmiştir. Ayrıca, serum örneklerinde GGT aktivitesi ve glutatyon (GSH) düzeyleri sırasıyla spektrofotometrik ve ELISA yöntemleriyle ölçülmüştür. Tümör dokularının tamamında GGT5 ve GGT7'nin mRNA ekspresyonlarının aynı hastaların sağlıklı meme dokularındaki ekspresyondan fazla olduğu belirlendi (sırasıyla p

Aims: To investigate the changes in mRNA expression levels of telomerase-related significant proteins in several types of cancer. Methods: Human telomerase reverse transcriptase, pontin, reptin and dyskerin expressions were measured in normal and tumour tissues obtained from 26 patients with colorectal, breast and gastric cancers, using the realtime reverse transcriptase-polymerase chain reaction method. Results: For all patients, no significant difference was found in mRNA expressions of human telomerase reverse transcriptase and dyskerin (p>0.05), although their levels in tumour tissues were found to be higher than in normal tissues. However, pontin and reptin mRNA expressions were significantly higher in tumour tissues than in normal tissues (p

Oxidative stress is one of the pathophysiological pathways suggested for the development of cardiovascular diseases in obstructive sleep apnea. The recurrent nocturnal episodes of hypoxia/reoxygenation observed in patients with obstructive sleep apnea (OSA) appear to be partly responsible for the increased oxidative stress. We investigated the relationship between lipid peroxidation and DNA damage in OSA patients with or without metabolic syndrome (MetS). 117 patients that had recently diagnosed OSA with or without MetS, and 25 control subjects were studied. Plasma malondialdehyde (MDA) levels in fasting blood samples were measured by a high-performance liquid chromatography method and urine 8-hydroxydeoxyguanosine (8-OHdG) was accessed by a competitive ELISA kit method. The levels of MDA and 8-OHdG were significantly higher in total apnea patients than in the controls (P < 0.0001 and P < 0.005, respectively). Apnea patients with metabolic syndrome had slightly higher MDA and lower 8-OHdG levels than those in the patients without metabolic syndrome. The values of 8-OHdG was correlated with T%SaO2 < 90, T%SaO2 < %85, mean SaO2 (%), and the lowest SaO2 (%) (R = 0.511, P = 0.000, R = 0.420, P = 0.001, R = -0.448, P = 0.000, and R = -0.437, P = 0.001, respectively) in the severe apnea patients. Significant increases in the levels of MDA and 8-OHdG support the studies suggesting possible involvement of oxidative stress in OSA. According to the state of the MetS, there is no significant difference in the levels of oxidative stress markers in OSA patients with or without MetS. High correlations between 8-OHdG and oxygen saturation levels in severe apnea group indicate the role of hypoxia/reoxygenation in DNA damage.