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Meme kanseri, kadınlarda en yaygın görülen kanserlerden biridir ve dünyadaki en yüksek insidansa sahip kanser türüdür. Meme kanseri gelişiminde cinsiyet, yaş, östrojen düzeyi, aile öyküsü, gen mutasyon- ları ve sağlıksız yaşam tarzı gibi çok sayıda risk faktörü bulunmaktadır. Mevcut tedavi seçenekleri cerrahi, radyoterapi, hormonal tedaviler, kemoterapi ve hedefe yönelik tedavilerdir. Hedefe yönelik tedavilerin içinde immünoterapi son yıllarda oldukça yaygın bir tedavi stratejisi olarak karşımıza çıkmaktadır. Meme kanseri immün sistemden bağımsız bir kanser olduğu düşün- cesinin aksine, artık meme kanserinin immün temelli bir kanser türü olduğu bilinmektedir. Bu kapsamda diğer kanser türlerinde olduğu gibi, meme kanserinde de immünoterapinin hedeflediği moleküller- den programlanmış hücre ölümü-1 (PD-1) ve programlanmış hücre ölümü ligandı-1 (PD-L1) ile yapılan çok sayıda çalışma bulunmakta- dır. PD-1 ve PD-L1 hedefli tedaviler günümüzde meme kanseri tedavi- sinde uygulanmaktadır. Meme kanseri alt tipleri olarak ele alındığında; farklı alt tipler arasında heterojen bir dağılım olmakla birlikte tümör hücrelerinde artmış PD-L1 ekspresyonu gözlenmektedir. Ayrıca, PD- L1 ekspresyonu, genç yaş, ileri evre, tümör infiltre eden lenfositlerin (TIL’ler) varlığı ve agresif moleküler alt tipler ile pozitif korelasyon gös- termektedir. Şimdilik sadece üçlü negatif meme kanserinin (TNMK) tedavisinde yer alan immünoterapi, yapılacak daha fazla araştırma so- nucunda, diğer meme kanseri alt tiplerinde de kombinasyon ya da tek tedavi olarak yer alabilecektir. Meme kanseri tedavisinde, PD-1 ve PD-L1 düzenlemesinin ayrıntılı mekanizmasını anlamak; tedavilere direncin üstesinden gelinmesi ve daha iyi klinik sonuçlara ulaşılması açısından büyük önem taşımak- tadır. Bu derlemede meme kanserinde PD-1 ve PD-L1 hedefli tedavilerin incelenmesi hedeflenmiştir.

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Objectives The PI3K (Phosphatidylinositol 3-kinase) is the member of lipid kinase family that plays important roles in tumorigenesis, cancer development and cell proliferation. In our study, we aimed to investigate the relationships between breast cancer risk and prognosis with PIK3CA rs6443624 (C>A) intron region gene polymorphism and serum PI3K levels. Methods A total of 61-patients with breast cancer and 101 controls were included to the study. PIK3CA polymorphism was detected by Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) technique. Serum PI3K levels were measured by Enzyme-Linked Immuno Sorbent Assay (ELISA). Results PIK3CA (C>A) gene polymorphism genotype and allele distributions were no significant in cases and controls (p>0.05). The serum PI3K levels of breast cancer patients were found significantly higher than the control groups (p=0.033). There were not significant association between PIK3CA (C>A) gene polymorphism and clinic and prognostic parameters in our study group. We also evaluated serum PI3K levels in the term of tumor progression, but we did not observe any significant data. Conclusions We suggest that serum PI3K levels may play role in breast cancer risk and larger patient groups may have clinical value in assessment of the genetic risk and tumor progression of breast cancer.

Objective: Colorectal carcinoma (CRC) is the third most frequent cancer in the world and a heterogenious disease which aroze from one or a combination of different genetic mechanisms. The multiple drug resistance-1 (MDR1) gene which encodes P-glycoprotein (P-gp) plays a part in the bioavailability of drugs and cell toxicity. In the current study, we aimed to investigate the possible relation between the MDR1 gene C3435T polymorphism and CRC risk in the Turkish population. Material and Methods: Forty three patients (26 men, 17 women) with CRC and 48 healthy controls (34 men, 14 women) were included in the study. The MDR1 C3435T genotypes were determined by the Restriction Fragment Length Polymorphism (RFLP) method. Results: Statistical significance was obtained in terms of genotype distributions of MDR1 C3435T genotypes between study groups. The frequencies of MDR1 C3435T CC, TT and CT genotypes in the CRC patient group were found as 16.3%, 32.6% and 51.2%, respectively. The frequency of the homozygous TT genotype was found as 32.6% in CRC patients while it was identified as 14.6% in controls (p=0.04; OR=2.82, 95% CI: 1.01-7.87). When the patients were compared with the healthy population, TT genotype carriers of MDR1 C3435T polymorphism were found at 2.8-fold (p, Amaç: Bir veya çoklu genetik mekanizmaların kombinasyonuyla oluşan heterojen bir hastalık olan kolorektal kanser (KRK) dünyada en sık görülen üçüncü kanserdir. P-glikoproteini (P-gp) kodlayan çoklu ilaç direnci geni-1 (Multiple drug resistance-1 (MDR1)) ilaçların biyoyararlanımı ve hücre toksisitesinde rol oynar. Bu çalışmada, Türk popülasyonunda MDR1 geni C3435T polimorfizmi ve KRK riski arasındaki olası ilişkiyi araştırmayı amaçladık. Gereç ve Yöntemler: Çalışmamıza KRK hastası (26 erkek, 17 kadın) 43 kişi ve 48 sağlıklı kontrol (34 erkek, 14 kadın) dahil edilmiştir. MDR1 C3435T genotipleri Restriksiyon Fragman Uzunluk Polimorfizmi RFUP) yöntemiyle belirlenmiştir. Bulgular: MDR1 C3435T genotiplerinin dağılımı açısından çalışma grupları arasında istatistiksel anlamlılık elde edilmiştir. KRK hasta grubunda MDR1 C3435T CC, TT ve CT genotiplerinin sıklığı sırasıyla %16,3, %32,6 ve %51,2 olarak bulunmuştur. Homozigot TT genotipi frekansı KRK hastalarında %32,6 bulunurken kontrollerde %14,6 (p=0,04; OR=2,82, 95% CI: 1,01-7,87) olarak tespit edilmiştir. Hastalar ve sağlıklı kontroller karşılaştırıldığında MDR1 C3435T polimorfizmi TT genotipi taşıyıcıları KRK gelişimi için 2,8 kat (p

Objectives The accumulation of genetic damages in onset of cancer induce activation of protooncogenes or inactivation of tumor suppressor genes thus cause disruption of the balance between cell proliferation and programmed cell death. As a member of the apoptosis inhibitory protein family (IAP), survivin play important roles in carcinogenesis process. The evidence suggests that polymorphisms located in survivin promoter region may be important in determining genetic susceptibility of cancer. In this study, we aimed to examine a possible role of survivin −31 and −625 G/C gene polymorphisms in breast cancer. Methods A total of 160 breast cancer cases and 153 healthy controls were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methodology. Results Genotype and allele distributions and of −31 and −625 G/C polymorphisms were not significantly different between two groups. However, we observed the carriers of survivin −625 C/G polymorphism homozygous genotypes (GG/CC) were the significantly higher in patients with tumor necrosis (p=0.047). Conclusions Our results suggest that survivin −625 C/G polymorphism may be related with tumor prognosis, but we are opinion of that our result require to be validated in larger samples and further comprehensive research may explore the correlation.

© 2022 Informa UK Limited, trading as Taylor & Francis Group.Objective/Aim: Endometrisosis, one of the most common gynecological disease, is characterized by the presence of endometriotic tissue outside of uterine cavity. The development and the validation of a simple blood biomarker specific and sensitive for endometriosis may facilitate the rapid and the accurate diagnosis of the disease and thus early treatment. Cytokeratin expression changes during epithelial differentiation and this expression is important for the modulation and the control of cell cycle regulation, tumor cell motility and apoptosis. Cytokeratin 19 (CK-19) is expressed in most simple epithelial cells and their malignant counterparts. The aim of this study is to investigate serum CK-19 expression levels in patients with endometriosis and to determine the diagnostic role of CK-19 levels in differentiating various stage of endometriosis. Methods: Ctytokeratin-19 expression and level were studied in 70 endometriosis patients and 50 volunteers by ELISA and RT-PCR. ROC analysis was performed by comparing all stages with each other and with the control group. Results: The CK-19 levels were significantly higher in the endometriosis groups than that of the control group by ELISA and RT-PCR. A significant (p

Objectives Immunoregulatory GITR, OX40L and PD-1 molecules play an active role in the regulation of tumor microenvironment and have been shown in many cancer types. However, there are limited studies of these molecules in terms of gastric cancer. In our study, we aimed to determine the histopathological significance of sPD-1, sOX40L and sGITR levels in gastric cancer cases. Methods Serum samples were obtained from peripheral blood samples of 20 gastric cancer and 34 healthy controls and candidate biomarker levels were determined by ELISA. Results sGITR level was found to be 48.28 ± 2.66 pg/mL in the gastric cancers and 39.19 ± 2.01 pg/mL in the controls (p=0.014). sOX40L level was 6.13 ± 0.64 pg/mL in the patients and 8.68 ± 0.99 pg/mL in the control, and the sOX40L level was found to be 1.41 times higher in the control group compared to the patients (p=0.033). sGITR levels of signet-ring cell carcinoma were found to be higher than other adenocarcinomas (p=0.04). There was no difference between groups in sPD-1 (p=0.490). Conclusions We suggest that sGITR, sOX40L and molecules may play a role in tumor microenvironment regulation and histological type in gastric cancer.

Glioma is the most prevalent and lethal type of primary tumor of central nervous system. The regulatory role of calcitriol, the active form of vitamin D3, has been determined in various cellular processes including cell survival and apoptosis. To study the impact of AKT-pathway inhibition with or without calcitriol combination on glioma cell viability, the effects of AT7867 (AKT-pathway inhibitor) and calcitriol on cell viability and apoptosis were investigated in glioma C6 cell-line. Optimal doses of calcitriol and AT7867 were determined by MTT- and xCELLigence-assays. Both agents (alone/in combination) effectively suppressed the proliferation of C6 cells. While AT7867 inhibited glioma cell viability more effectively than calcitriol, this inhibitory action of AT7867 was not significantly increased by calcitriol combination. The expression levels of vitamin D receptor(VDR)-triggered molecules, AKT-pathway components and apoptosis factors were compared between calcitriol-, AT7867- and calcitriol + AT7867-treated and non-treated cells. CYP24A1 gene was upregulated and DBP, CYP1A1, CYP27B1, EGFRvIII, AKT-pathway (AKT1, MTOR, CREB, PTEN), apoptosis (BAD, CYC-C, CASP3, APAF-1, BCL2) and MMP3 genes were downregulated by calcitriol treatment.AT7867 treatment induced CYP27B1 upregulation, reduced VDR and AKT-pathway (PI3K, MTOR, CREB, PTEN) gene expression levels but showed a relatively less pronounced effect on apoptosis-related gene levels. The combination of calcitriol and AT7867 treatment generated an effect that was similar to that induced by calcitriol alone. Our results demonstrate that calcitriol and AT7867 have differing actions on AKT- and apoptotic-pathways of C6 glioma cell-line. Calcitriol has a lesser viability reducing impact than AT7867 putatively due to its apoptosis inhibiting action. Supplemental data for this article is available online at https://doi.org/10.1080/13102818.2021.1912641 .

Paraoxonase 1 (PON1) is a well recognised member of human endogeneous free radical scavenging systems and its polymorphism and enzyme activity are attributed to various different cancer formations. We aimed to study the Paraoxonase 1 (PON1) polymorphism and enzyme activity in colorectal cancer patients. Peripheral blood samples for DNA extraction were collected from 54 colorectal cancer patients and 85 healthy individuals. Polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) techniques were used for determination of the PON1192 polymorphism. The frequency of AA genotype was greater than BB and AB genotypes in all groups (n:65 with 46.8%; n:15 with 10.8% and n:59 with 42.4%, respectively). In both tumor groups, PON activities were significantly lower than the control group (p

Kan glukozunun yükselmesiyle karakterize olan diyabet, pankreastaki fonksiyon bozukluğu neticesinde oluşmaktadır ve bu durum insülin etkisine karşı dirence veya insülin üretiminin azalmasına neden olmaktadır. Diyabet, Tip-I ve Tip-II olmak üzere iki grupta incelenmektedir. Tip-I diyabet, pankreasın beta hücresinden salınan insülin hormonundaki yetersizlik neticesinde gelişim göstermektedir. Burada T-hücresi aracılığıyla gerçekleşen otoimmün yanıtın, pankreasın beta hücre fonksiyonunu etkilediği bilinmektedir. Tip-II diyabet sağlıksız beslenme, hareketsizlik, genetik-çevresel faktörlerden kaynaklı gelişim göstermektedir. Prevalansı yüksek Tip-II diyabette, insülin direnci oluşumu, beta hücre fonksiyonunda kayıp ile hiperglisemi gelişmektedir. Tümör nekroz faktör ilişkili apoptoz indükleyici ligand (TRAIL), tümör nekroz faktör (TNF)-süper ailesinin üyesi olup; Tip-II transmembran proteini olarak ifade edilmektedir. İmmün yanıt ve inflamasyonun düzenlenmesinde önemli fonksiyonlara sahiptir. Biyolojik etkilerini, hücre yüzeyindeki reseptörleri sayesinde gerçekleştirmektedir. TNF-alfa’nın senteziyle oluşan lenfosit infiltratları, Tip-I diyabete yol açmaktadır. TRAIL’in diyabet gelişimindeki rolüyle ilgili çalışmalar ilk olarak hayvan modellemeleriyle başlamıştır. TRAIL eksikliği olan hayvan çalışmalarında, otoimmün kaynaklı diyabetin ve pankreatik adacık inflamasyonunun arttığı kaydedilmiştir. Bu bulgular TRAIL’in diyabet patofizyolojisinde önemli bir rol oynadığını göstermektedir. Klinik veriler neticesinde TRAIL ekspresyonunun sağlıklı bireylerde yüksek olması obezite ve diyabette koruyucu bir rolü olduğunu düşündürmektedir. Bu derlemede, elde edilen bulgular temelinde TRAIL’in diyabetteki koruyucu rolünün incelenmesi hedeflenmiştir.

BACKGROUND Mesenchymal stem cells (MSCs) have gained remarkable attention because of their ability to dualistically regulate tumor growth. The main objective of this study was to evaluate the apoptotic effects of human bone marrow-derived (hBM) MSCs in combination with interferon gamma (IFN-γ) on MCF-7 breast cancer cells, and to determine the cytokines involved in the apoptotic process. MATERIALS AND METHODS hBM-MSCs were co-cultured with MCF-7 cells either directly and indirectly for 72 h in-vitro. Levels of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), apoptosis and cytokines were analyzed. RESULTS hBM-MSCs increased the apoptosis of MCF-7 cells partially through TRAIL in vitro. IFN-γ enhanced the apoptotic effect of hBM-MSCs (p

This study investigates whether the circulating miR-155, let-7c, miR-21, and PTEN levels to be used in the differential diagnosis of patients with idiopathic granulomatous mastitis (IGM) and breast cancer (BC). Forty-five patients with BC, 50 patients with IGM, and 48 healthy volunteers were included in the study. Serum miR-21 expression was significantly higher in BC (fold change = 2.42) and IGM group (fold change = 1.33) compared to control (p < .001). Serum miR-155 and let-7c expression levels were significantly lower in both groups compared to the control group (p < .001). miR-21 expression in BC was significantly higher than IGM (fold change = 1.976; p < .001). PTEN levels in BC were significantly higher than IGM (p < .001) and significantly lower than the control group (p < .001); the IGM group was significantly lower than the control group (p < .001). In addition to radiological data, serum miR-21 and PTEN levels may be noninvasive biomarkers that can help differentiate IGM from BC. The results of the study will lead to future studies in the differential diagnosis of IGM and BC.

Recent studies imply the effects of micronutrient intake on the development of several cancers including primary brain cancer (PBC). The biological effects of vitamin D, a member of the fat-soluble vitamin family acting as a steroid hormone, was carried out by binding its receptor (VDR) through vitamin D-binding-protein (VDBP). The present study aims to investigate the effects of vitamin D levels and VDR rs2228570, VDR rs731236, VDBP 7041 polymorphisms on PBC development. The study group consisted of 71 patients and 84 controls. Vitamin D levels were determined by high-pressure liquid chromatography where polymorphisms by polymerase-chain-reaction and restriction fragment length polymorphism methods. The distribution of VDR rs2228570 variants in PBC and its subgroups were determined as FF>Ff>ff; VDBP rs7041 variants were TG> GG>TT, however, VDR rs731236 variants were Tt>TT>tt in PBC and meningioma and TT>Tt>tt in glioma. Vitamin D levels were measured below normal levels in all patients and control groups, which shows the deficiency in Turkish society in line with the literature. Our results show that low serum vitamin D level may be an individual risk factor in the development of brain tumors, however, VDR rs2228570 and rs731236 and VDBP rs7041 polymorphisms have no effect on the risk of disease development., Son çalışmalar, mikrobesin alımının primer beyin kanseri (PBC) dahil olmak üzere çeşitli kanser türlerinin gelişimi üzerindeki etkilerine işaret etmektedir. Yağda çözünen vitaminler sınıfında yer alan ve steroid hormon olarak etki gösteren D vitamini biyolojik etkilerini reseptörü (VDR) ile vitamin D bağlayıcı protein (VDBP) aracılığıyla gerçeklestirmektedir. Çalışmamızda, D vitamini düzeyleri ile VDR rs2228570, VDR rs731236, VDBP 7041 polimorfizmlerinin PBC gelişimi üzerindeki etkilerinin araştırılması amaçlanmıştır. Çalışma grubu, beyin kanseri tanısı konmuş 71 hasta ile 84 sağlıklı bireyden oluşturulmuştur. D vitamini düzeyi, yüksek basınçlı sıvı kromatografisi yöntemiyle, VDR FokI (rs2228570), TaqI (rs731236) ve VDBP rs7041 polimorfizmleri polimeraz zincir reaksiyonu ve restriksiyon parça uzunluk polimorfizmi yöntemleriyle belirlenmiştir. Çalışmamızda VDR FokI gen varyantlarına ait dağılım primer beyin kanseri ve alt gruplarında FF>Ff>ff; VDBP rs7041 varyantları TG>GG>TT olarak, VDR TaqI varyantlarının ise primer beyin kanseri ve meningiomada Tt>TT>tt, gliomada TT>Tt>tt olduğu tespit edilmiştir. D Vitamini düzeyleri tüm hasta gruplarında ve kontrol grubunda normal düzeyinin altında ölçülmüş, bu durum Türk toplumundaki vitamin D düzeylerinin literatürle uyumlu bir şekilde düşük seviyede olduğunu göstermiştir. Çalışmamız sonuçları, beyin tümörleri gelişiminde düşük serum D vitamini seviyesinin bireysel bir risk faktörü olabileceğini, ancak VDR rs2228570 ile rs731236 ve VDBP rs7041 polimorfizmlerinin hastalık gelişim riskine etkisinin olmadığını göstermektedir.

Chronic hepatitis B virus (HBV) infection is a major cause of hepatocellular carcinoma (HCC). Circulating cell-free DNA (cfDNA) methylation of tumor suppressor genes are emerging potential biomarkers in HCC. We aimed to evaluate the cfDNA methylation status of RASSF1 and CDKN2AIP genes in patients with liver cirrhosis (LC) with or without HCC caused by HBV.A total of 47 patients with HBV cirrhosis were included in the study. Patients were divided into two groups: HCC and LC (HCC+LC, n=22) and HBV cirrhosis only (LC, n=25). cfDNA was isolated from the plasma samples of the patients. Methylation analysis was performed for RASSF1 and CDKN2AIP genes.Mean methylation percentage of CDKN2AIP gene was 0.001±0.004% in the HCC+LC group and 0.008±0.004 % in the LC only group. The mean methylation percentage of RASSF1 gene was 5.1±16.1% in the HCC+LC group and 9.7±25.9% in the LC only group. The methylation rate of CDKN2AIP was significantly lower in the HCC+LC group (p=0.027). A positive correlation was found with the absence of cfDNA methylation of CDKN2AIP gene in the presence of HCC (R=0.667, p=0.018).cfDNA methylation of CDKN2AIP and RASSF1 genes may provide important diagnostic information regarding the development of HCC in the setting of HBV cirrhosis.

Introduction: Although potential relationships with genetic variants of MLCK2, AMPD1 and COL5A1 have been detected in molecular studies evaluating sports performance from the genetic perspective, there are limited data in terms of muscle endurance and physical fitness. Materials and Methods: This study aimed to evaluate these variants in terms of lower limb muscle endurance and physical fitness in thirty-three soccer players. Genotypes were determined by High Resolution Melting (HRM) analysis in qPCR after genomic DNA was isolated from buccal swab samples from the participants. Measurements of lower limb muscle endurance, the dynamic leap and balance test (DLBT), and the standing broad jump test (SBJ) were taken for all the participants. Results: Greater height (p = 0.006), higher DLBT (p = 0.016) and SBJ (p = 0.033) scores, as well as greater left hip adduction (p

Objectives: Genetic variations of LGALS3 (Galectin-3) were found to be associated with treatment resistance, mortality, recurrence, high tumor volume and multiple tumor involvement in solid organ cancers. The modulators of extracellular matrix (ECM), which is a dynamic factor in the larynx tissue with high biomechanical and regenerating ability, can play an important role. We aimed to investigate the relationship between the genetic variants of LGALS3, one of these modulators, with Laryngeal Squamous Cell Carcinoma (LSCC). Methods: LGALS3 gene variations were genotyped by PCR-RFLP method using genomic DNA samples obtained from peripheral blood samples of 74 patients diagnosed with LSCC and 94 healthy controls. Results: The C allele carriage for the Rs4652 genetic variant was found to be higher (p=0.017) in patients with LSCC. Statistical relationships were found between homozygous genotypes of this variant (CC/AA) with advanced tumor stage (p=0.017) and presence of reflux (p=0.036). CC genotype for rs4644 was found to be higher in cases with positive family history (p=0.036). Conclusions: Our findings of LGALS3 gene variants, which are also found to be associated with other solid cancers, suggest that they may play a role in LSCC pathophysiology similarly., Amaç: LGALS3’ün (Galectin-3) genetik varyasyonlarının, solid organ kanserlerinde tedaviye direnç, ölüm oranı, nüks, yüksek tümör hacmi ve çoklu tümör tutulumu ile ilişkili olduğu bulunmuştur. Biyomekanik açıdan rejenerasyon kabiliyeti yüksek larinks dokusunda, dinamik bir faktör olarak ECM modülatörleri önemli rol oynayabilir. Bu modülatörlerden LGALS3’ün genetik varyantları ile LSCC (Laringeal Skuamöz Hücreli Karsinom) arasındaki ilişkiyi araştırmayı amaçladık. Gereç ve Yöntem: LSCC tanısı almış 74 hasta ve 94 sağlıklı kontrolün periferik kan örneklerinden elde edilen genomik DNA örnekleri kullanılarak LGALS3’ün genetik varyantları PCR-RFLP yöntemiyle genotiplendirildi. Bulgular: LSCC’li hastalarda Rs4652 genetik varyantı için C aleli taşıyıcılığının daha yüksek olduğu tespit edildi (p=0.017). Bu varyantın homozigot genotipleri (CC/AA) ile ileri tümör evresi (p=0.017) ve reflü varlığı (p=0.036) arasında istatistiksel ilişkiler bulundu. Aile öyküsü pozitif olan olgularda ise rs4644 genetik varyantı için CC genotipinin diğer genotiplere göre daha yüksek olduğu tespit edildi (p=0,036). Sonuç: Diğer solid kanserler tipleriyle de ilişkisi tespit edilen LGALS3 gen varyantlarına ait bulgularımız benzer şekilde LSCC patofizyolojisinde rol oynayabileceğini göstermektedir.

Inula viscosa is a type of Asteraceae family, which widely used for medicinal plant to treatment of different diseases. Inula viscosa contains many biological compounds, such as monoterpenes, sesquiterpenes, diterpenes, flavonoids. Our study aimed to investigate the cytotoxic effects of Inula viscosa extract on MCF-7 (breast carcinoma), C6 (glioblostoma cancer), MG63 (bone osteosarcoma), cancer cells and L929 (mouse fibroblostama) cell lines. Cytotoxic effects of the Inula viscosa extracts were performed by XTT assay. In this study, Inula viscosa extracts showed selective cytotoxic effect on MC-7 compared than L929 cells. The Inula viscosa extracts appear to be a promising source of new anticancer agent. Further studies are needed to identify the cytotoxic activity mechanisms on these cancer cell lines. Inula viscosa farklı hastalıkların tedavisinde medikal amaçlı kullanılan Asteraceae ailesine ait bir türdür. Inula viscosa monoterpene, seskiterpen, diterpen ve flavonoid gibi pek çok biyolojik bileşen içerir. Çalışmamızda Inula viscosa ekstraktlarının MCF-7, C6, MG63 ve L929 hücre hatlarında sitotoksik etkisinin incelenmesini amaçladık.Inula viscosa ekstraklarının sitotoksik etkisi XTT analizi ile yapıldı.Bu çalışmada Inula viscosa ekstrakları MCF-7 hücre hatlarında L929’a göre seçici sitotoksik etki gösterdi. Inula viscosa ekstrakları, ümit verici bir yeni antikanser ajan kaynağı olarak görünmektedir. Bu kanser hücre hatları üzerindeki sitotoksik aktivite mekanizmalarını tanımlamak için daha ileri araştırmalara ihtiyaç vardır.

DOI: 10.26650/experimed.2019.19014Human monocytes/macrophages produceneopterin when stimulated by the cytokine interferon-γ. The concentration ofneopterin in body fluids such as serum, cerebrospinal fluid and urine can bemeasured and increased concentrations of neopterin provides information aboutinfections states. Nowadays, neopterin is as a marker in neurological andcardiovascular diseases during cellular immune activation.Cite this article as: Hepokur C, Mısır S,Hepokur Aİ, Yaylım İ. Association of Neopterin and Wound Healing Process.Experimed 2019; 9(2): 65-8., DOI: 10.26650/experimed.2019.19014İnsan monositleri/makrofajları, sitokininterferon-γ tarafından uyarıldığında neopterin üretir. Serum, beyin omuriliksıvısı ve idrar gibi vücut sıvılarında neopterinin konsantrasyonu ölçülebilirve artan neopterin konsantrasyonları enfeksiyon durumları hakkında bilgisağlar. Günümüzde neopterin, hücresel immün aktivasyonu sırasındaki nörolojikve kardiyovasküler hastalıklarda bir belirteç olarak kullanılır.Cite this article as: Hepokur C, Mısır S,Hepokur Aİ, Yaylım İ. Association of Neopterin and Wound Healing Process.Experimed 2019; 9(2): 65-8.

Objevtive: Acromegaly is a rare disease characterized by growth hormone hypersecretion generally arising from pituitary adenomas. Survivin, an apoptosis inhibitor protein, plays an important role in cell cycle regulation and possibly involves hypophysis gland proliferation mechanisms. However, the underlying causes of somatotroph adenomas with different behaviors and useful prognostic markers are still not fully understood. We investigated possible associations between survivin gene promoter -31 G\C genotypes and serum survivin level and clinical prognostic factors in acromegaly. Material and Methods: Sixty-eight acromegaly patients and 171 age-sex matched control subjects were enrolled in the study. Survivin -31 G\C polymorphism was performed by using a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Blood GH and IGF1 levels were assayed using a chemiluminescence immunometric assay. Serum survivin levels were determined by ELISA. Results: Acromegaly patients had significantly higher serum survivin levels than controls (p=0.001). We found no significant association between acromegaly patients and controls in terms of survivin gene promoter -31 G\C genotype distribution and allele frequencies. No correlation was found between disease characteristics and survivin gene polymorphisms. Conclusion: Our study suggests that serum survivin levels might be associated with acromegaly, but survivin -31 G\C polymorphisms do not modify individual susceptibility to acromegaly in the Turkish population.

Detection of the circulating tumour cells (CTC) in dogs with a mammary tumour is a useful tool to reveal the micrometastases long before metastases are recognised clinically. The aim of this study was to evaluate the association of the epidermal growth factor receptor (EGFR), claudin 7 (CLND7) and epithelial cell adhesion molecule (EPCAM) with the clinical indices and to reveal the diagnostic importance of these biomarkers in canine mammary tumours (CMTs). Peripheral blood (PB) samples were collected from 45 bitches (group MT) which had single mass with malignant epithelial tumours and 9 healthy bitches (group H). Real time PCR (rt-PCR) was performed to determine the expression levels of EGFR, CLDN7, and EPCAM. Mean values of EGFR and CLDN7 expressions were significantly higher in group MT compared to group H (P < 0.01 and P < 0.001, respectively). The expression level of CLDN7 was positively correlated with EGFR and EPCAM (P < 0.001 and P < 0.05, respectively). The EPCAM expression was associated with increased tumour size (P < 0.05) and EPCAM tended to decrease in the presence of skin ulceration on tumour (P = 0.05). Furthermore, expression levels of EGFR in intact dogs were significantly higher compared to spayed dogs in group MT (P < 0.01). The EGFR expression was significantly higher in the presence of metastases (P < 0.05). Also, increased EGFR was determined in grade 2 compared to grade 1 (P < 0.05). In conclusion, these results show that EGFR, CLDN7, EPCAM markers are measureable in PB and they may provide valuable information about the clinical pathophysiology of CMT.

Colon and gastric cancers are the widespread benign types of cancers which are synchronous and metachronous neoplasms. In terms of the progression and progress of the disease, metabolic processes and differentiation in protein structures have an important role in for treatment of the disease. In this study we proposed to investigate the metabolic process and the differentiation of protein secondary structure among colon and gastric cancer as well as healthy controls using biochemistry and Fourier Transform InfraRed spectroscopy (FTIR) methods. For this purpose, we measured blood serum of 133 patients, which were conducted upon oncology department (45 colon cancer, 45 gastric cancer and 43 control individuals). The obtained spectroscopic results and biochemical assays showed significant reduction in the amount of functional groups in cancer groups contrary with total protein measurements and structure of protein differences between colon and gastric cancers. Differentiations were visible in serum levels of CEA, CA-125, CA-15-3, CA-19-9 AFP (Alpha fetoprotein) of gastric and colon cancer patients as well as in amide III and secondly described amide I regions. Our findings suggest that amide I bonds in colon cancer cells can be helpful in diagnosis of colon cancer. Indeed, our results showed that metabolic processes were higher in gastric cancer group than in colon cancer. Hence, FTIR spectroscopy and curve-fitting analysis of amide I profile can be successfully applied as tools for identifying quantitative and qualitative changes of proteins in human cancerous blood serum. However, what is very important, in PCA analysis we see, that the scatter plot of PC1 (variability 80%) and PC2 (variability 15%) show that the data related to the control and two cancer groups are clustered together with different magnitudes and directions. WOS:000658306800013 33965021 Q1

Background: The aim of this study was to investigate the possible relationship between galectin-3 gene variants, serum level, gene expression level, and the risks and survivals of resectable non-small cell lung cancer patients. Methods: The rs4644 and rs4652 variants of galectin-3 were genotyped by TaqMan single nucleotide polymorphism assay using genomic deoxyribonucleic acid isolated from the peripheral blood of 65 (54 males, 11 females; mean age: 60.1±11.9 years; range, 34 to 83 years) with Stage IA-IIIA non-small cell lung cancer who underwent primary surgical treatment and 95 healthy individuals (48 males, 47 females; mean age: 53.9±13.5 years; range, 32 to 87 years) between March 2017 and September 2018. Circulating galectin-3 levels in serum samples of the patient and control groups were assessed by enzyme-linked immunosorbent assay. Messenger ribonucleic acid expression of galectin-3 in tumor and surrounding tissues of the patient group was examined by real-time quantitative polymerase chain reaction. Both predictive and prognostic significance of the results were analyzed. Results: The presence of angiolymphatic invasion was significant in the patients with rs4652 AA genotype (p=0.04). Serum galectin-3 levels were significantly higher in the patients than the controls (p, Amaç: Bu çalışmada galektin-3 gen varyantları, serum düzeyi, gen ekspresyon düzeyi ile rezektabl küçük hücreli dışı akciğer kanseri hastalarının riskleri ve sağkalımları arasındaki olası ilişki araştırıldı. Ça­lış­ma pla­nı: Mart 2017 - Eylül 2018 tarihleri arasında galektin-3'ün rs4644 ve rs4652 varyantları, primer cerrahi tedavi yapılan küçük hücreli dışı akciğer kanserli 65 hastanın (54 erkek, 11 kadın; ort. yaş: 60.1±11.9 yıl; dağılım, 34-83 yıl) ve 95 sağlıklı bireyin (48 erkek, 47 kadın; ort. yaş: 53.9±13.5 yıl; dağılım, 32-87 yıl) periferik kanından izole edilen genomik deoksiribonükleik asitler kullanılarak TaqMan tek nükleotid polimorfizm testi ile genotiplendi. Hasta ve kontrol gruplarının serum örneklerinde dolaşımdaki galektin-3 düzeyi, enzim bağlı immünosorbent testi ile değerlendirildi. Hasta grubunda tümör ve çevre dokulardaki galektin-3’ün haberci ribonükleik asit ekspresyonu, gerçek zamanlı kantitatif polimeraz zincir reaksiyonu ile incelendi. Bu sonuçların hem prediktif, hem de prognostik önemi analiz edildi. Bulgular: Rs4652 AA genotipi olan hastalarda anjiyolenfatik invazyon varlığı anlamlı idi (p=0.04). Kontrol grubuna kıyasla, hastalarda serum galektin-3 düzeyleri anlamlı düzeyde yüksekti (p

The purpose of this study was to investigate the phenolic composition and antioxidant activity of Thymbra sintenisii subsp. isaurica extract (TSIE) and, to evaluate, for the first time, anticancer effect on human MCF-7 (breast carcinoma) cells.The antioxidant capacity of TSIE was evaluated using 2,2-diphenyl-1-picrylhydrazyl (DPPH) and total polyphenol assays. The anticancer activities of TSIE were tested on MCF-7 (breast carcinoma) cells.Total polyphenol value of extracts TSIE was found as 73.02 mg gallic acid /g powder. DPPH result of IC50 value of TSIE was found to be 27.15 μg/mL. To examine anticancer effect of TSIE at different concentrations were given on MCF-7 cells. TSIE was observed to reduce the cell viability in a dose-dependent manner. This anticancer property of the TSIE provides a highlights the importance of plant research for drug design.In this study, anticancer effects and antioxidant level of endemic species, that is TSIE, are evaluated on MCF-7 cells. Thus, an effective therapeutic agent for cancer treatment is aimed to develop. Further studies are needed to better understand the molecular mechanisms underlying this effect of TSIE.

ULKUSEVEN, BAHRI/0000-0001-6342-1505; Ozdemir, Namik/0000-0003-3371-9874; Yaylim, Ilhan/0000-0003-2615-0202; SULEYMANOGLU, MEDIHA/0000-0002-1401-4863 WOS: 000527699700001 PubMed: 32314849 Iron(III) and nickel(II) complexes bearing a thiosemicarbazone framework were synthesized by a one-pot synthesis method. The structures were characterized by elemental analysis, IR, H-1 NMR, APCI Mass, conductivity, magnetic moment measurements. Molecular and crystal structures of the iron(III) complex were obtained from single-crystal X-ray diffraction. The findings showed that the metal atom adopts a slightly distorted square-pyramidal coordination, with the four donor atoms of the thiosemicarbazone ligand defining the basal plane and a chloride atom occupying the apical position. In the crystal lattice, the structure is stabilized by intermolecular O & x2500;H center dot center dot center dot O and C & x2500;H center dot center dot center dot O interactions. The cytotoxic activity was studied by MTT assay, the expression levels of cytochrome P450 (CYP) enzymes by Western blot, and the lipophilicity (LogP) by using the shake-flask method, another pharmacokinetic parameter. The findings showed that the IC50 values decreased with the decrease of the LogP values of the substances. Cytochrome P450 expression levels were found specific for each compound and each cell line. As a result, the pharmacokinetic properties of the newly synthesized thiosemicarbazone compounds are crucial for oral administration and provide us with clues for prospective in vivo studies. Scientific Research Projects Coordination Unit of Istanbul UniversityIstanbul University [49111]; Ondokuz Mays UniversityOndokuz Mayis University [PYO.FEN.1906.19.001, 109S188] This study was supported by the Scientific Research Projects Coordination Unit of Istanbul University (Project number: 49111); the Ondokuz Mays University (Project No: PYO.FEN.1906.19.001); and TuBTAK-SBAG (Project Number: 109S188).

Introduction: The data suggesting that metabolites and genes of homocysteine may play a role in the pathogenesis of colorectal cancer are available in the literature. Similarly, selenium (Se) levels and SELENBP1, a member of the selenoprotein family characterized by selenium, have been evaluated for the etiopathology of colorectal cancer (CRC). In this study, we aimed to determine the levels of homocysteine (Hcy), Se, and SELENBP1 gene expression in tumor tissue according to histopathological stages in patients with CRC. Materials and methods: Hcy levels were determined by ELISA, and Se levels were determined by atomic absorption from serum samples isolated from peripheral blood of 56 colorectal cancer cases and 87 healthy controls. The expression of SELENBP1 gene in tumor samples was determined by RT-PCR method. The histopathological evaluations of the patients were evaluated according to the AJCC-8th staging system. Results: Se levels were 67.56 +/- 3.11 ng/mL in colorectal cancer patients and 61.92 +/- 21.26 ng/mL in control group patients (p = 0.078). Serum Hcy levels were 11.34 +/- 1.75 ng/mL in the patient group and 20.87 +/- 4.38 in the control group (p = 0.340). The SELENBP1 fold change was found to be 3.78 +/- 1.95-fold higher in tumor tissues compared to internal control (p = 0.755). Se levels were found to be 1.23 times lower in patients with distant metastasis than in patients without distant metastasis (p = 0.029). Similarly, Hcy level was found to be 1.79 times lower in patients with metastasis than in non-metastatic patients (p = 0.035). Conclusion: Our data suggest that low Se and Hcy levels may play an important role in the histopathological aspects of metastatic ability and CRC. Istanbul University Scientific Research Project UnitIstanbul University [TYO-2019-33675] This study was supported by Istanbul University Scientific Research Project Unit (Project No: TYO-2019-33675). WOS:000539395900002

INTRODUCTION: In the pathogenesis of Graves' disease (GD), which is the most common cause of hyperthyroidism, cellular and humoral immune systems are thought to play a role together. TNF-alpha, fibronectin and galectin-3 known to play an active role in inflammatory processes. The aim of this study was to investigate the relationship between galectin-3, fibronectin and TNF-alpha molecules with hyperthyroidism and GD. METHODS: The study included 108 volunteers, 50 Graves, 19 non-Graves hyperthyroid patients and 39 healthy controls. Galectin-3, fibronectin and TNF-alpha levels measured by enzyme-linked immunosorbent assay (ELISA). In the Graves group (Group 1) 32 women, 18 men; in the non-Graves hyperthyroidism group (Group 2) 13 women, 6 men; and there were age- and sex-matched 26 females and 13 males in the control group (Group 3). RESULTS: TNF-alpha levels were 22.7 ± 1.97 pg / ml in Group 1, 19.8 ± 2.56 pg / ml in Group 2, and 16.6 ± 2.29 pg / ml in the control group. TNF-alpha levels were significantly higher in GD group compared to healthy controls (p

Background: The purpose of this study was to investigate the phenolic composition and antioxidant activity of Thymbra sintenisii subsp. isaurica extract (TSIE) and, to evaluate, for the first time, anticancer effect on human MCF-7 (breast carcinoma) cells. Materials and Methods: The antioxidant capacity of TSIE was evaluated using 2,2-diphenyl-1-picrylhydrazyl (DPPH) and total polyphenol assays. The anticancer activities of TSIE were tested on MCF-7 (breast carcinoma) cells. Results: Total polyphenol value of extracts TSIE was found as 73.02 mg gallic acid /g powder. DPPH result of IC50 value of TSIE was found to be 27.15 μg/mL. To examine anticancer effect of TSIE at different concentrations were given on MCF-7 cells. TSIE was observed to reduce the cell viability in a dose-dependent manner. This anticancer property of the TSIE provides a highlights the importance of plant research for drug design. Conclusion: In this study, anticancer effects and antioxidant level of endemic species, that is TSIE, are evaluated on MCF-7 cells. Thus, an effective therapeutic agent for cancer treatment is aimed to develop. Further studies are needed to better understand the molecular mechanisms underlying this effect of TSIE. © 2020 Wolters Kluwer Medknow Publications. All rights reserved.

Background/aim The single nucleotide polymorphism -31C/G identified in the survivin gene promoter seems to be associated with over-expression of survivin, an anti-apoptotic protein. In gliomas, increased survivin expression correlated with decreased survival. The aim of the study was to investigate whether survivin gene polymorphism associates with benign and malignant brain tumors and whether it affects survivin serum levels. Patients and methods Survivin polymorphism -31C>G was genotyped in 82 patients with brain tumors and 65 healthy controls by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and survivin levels were evaluated by enzyme-linked immuno sorbent assay (ELISA) in patients and controls. Results Serum survivin levels in patients with malignant tumors were higher than patients with benign tumors (p G did not differ between patients and controls. Conclusion Survivin promoter -31C>G gene polymorphism seems to be associated with serum survivin levels in brain tumors of different grades and histologies.

Immunomodulatory signals regulate the self-tolerance, activation, priming and survival processes of T cells. Programmed cell death protein 1 (PD1), Programmed death-ligand 1 (PD-L1) inhibitory signals and CD27, CD28 costimulators have been detected for many solid organ cancers in tumor-infiltrating T cells. It was aimed to investigate the immune cell-based regulatory genetic variants in laryngeal squamous cell carcinoma (LSCC) in terms of clinicopathological features. Genotyping was performed by PCR-RFLP method for PD-1 rs2227981, PD-L1 rs2890658, CD28 rs3116496, CD27 rs2267966 genetic variants from genomic DNAs extracted from peripheral blood samples in One Hundred Thirty-Six individuals (Sixty-one LSCC and seventy-five controls). Analysis of SNPs was carried out according to multiple inheritance models (co-dominant, dominant, recessive, over-dominant and log-additive). There was no difference between LSCC and control groups in genotype/allele distribution for PD-1 and PD-L1 (p > 0.05). In the PD-1 overdominant model, the CT genotype was found to be high (p = 0.036) in those without a family history. The frequency of C allele (AC+CC) in the PD-L1 dominant model was higher in alcohol users and those with reflux (p = 0.024; p = 0.001 respectively). In the Dominant model for PD-L1, the AA genotype was lower in moderately and well-differentiated tumors than in poorly differentiated tumors (p = 0.02). CD27 AT and CD28 CT genotypes were found to be higher in LSCC patients compared to the control group (p = 0.009; p = 0.01 respectively), while linkage disequilibrium (LD) was detected between CD27 and CD28 (p = 0.02). In the CD28 dominant model, C allele (CT+CC) carriage was found to be high in those with family history and in those without reflux and perineural invasion (p = 0.01; p = 0.01; p = 0.03 respectively). In LSCC, PD-L1 rather than PD-1 has a prognostic effect in terms of clinicopathology, and the LD and clinicopathological relationships detected between CD28 and CD27 genotypes suggest that the hereditary immune checkpoint-dependent T cell traffic may be pathophysiologically important.

Laryngeal squamous cell carcinoma (LSCC) is a genomically complex disease that is difficult to target, and efforts have been made to identify new treatment strategies and molecular markers that might stratify patients and individualize options for treatment. miR-373 has diametrically opposed roles in different stages and types of cancers. miR-373 has been suggested to quantitatively control E-cadherin and CD44 expression. We studied the expression of miR-373, E-cadherin and CD44 in laryngeal squamous cell carcinoma and evaluated the association between the disease and clinical characteristics of patients. Tumor tissues were collected from 24 laryngeal cancer patients. Adjacent normal tissue samples were also obtained as controls. After RNA isolation, we assessed the miR-373, E-cadherin and CD44 levels. As endogenous controls, we used the small RNA U6 and GAPDH TaqMan® to normalize the levels of expression of miR-373, E-cadherin and CD44. The fold change in the expression of the genes in larynx tumor and control tissues was calculated using the 2-ΔΔCT method. miR-373 was significantly upregulated in seventeen tumor samples compared to controls. However, the expression levels of both E-cadherin and CD44 mRNA were found to be significantly downregulated in tumor versus control regions (p=0.026 and p=0.005, respectively). We did not find any significant difference in the expression levels of miR-373, E-cadherin or CD44 and cancer risk factors. miR-373, E-cadherin and CD44 may be involved in the etiopathogenesis of laryngeal cancer. It can be suggested that E-cadherin and CD44 are functional targets of miR-373, but we need further studies to investigate this hypothesis.

Blueberries belong to the genus Vaccinium of the family Ericaceae. Rapidly accumulating experimentally verified data is uncovering the tremendous pharmacological properties of biologically active constituents of blueberries against different diseases. Our rapidly evolving knowledge about the multifaceted nature of cancer has opened new horizons to search for different strategies to target multiple effectors of oncogenic networks to effectively inhibit cancer onset and progression. Excitingly, whole blueberry powder and various bioactive constituents (pterostilbene, malvidin-3-galactoside) of blueberries have been shown to efficiently inhibit metastasis in animal models. These results are encouraging and future studies must focus on the identification of cell signaling pathways effectively modulated by blueberries in different cancers. It seems exciting to note that researchers are focusing on metastasis inhibitory effects of blueberry; however, to reap full benefits, it is necessary to take a step back and critically re-interpret the mechanisms used by active components of blueberry to inhibit or prevent metastasis. JAK/STAT, TGF/SMAD, Notch, SHH/GLI, and Wnt/ β-Catenin have been shown to be directly involved in the regulation of metastasis. However, because of limited studies, it is difficult to critically assess the true potential of blueberry. Loss of apoptosis, metastasis and deregulation of signaling pathways are branching trajectories of molecular oncology. Accordingly, we have to emphasize on these essential facets to realistically claim blueberry as "Superfood". Different clinical trials have been conducted to gather clinical evidence about the chemopreventive role of blueberry or its bioactive components in cancer patients. But it seems clear that because of the lack of sufficient proof-of-concept studies, we cannot extract significant information about the transition of blueberry into the next phases of clinical trials. Overview of the existing scientific evidence revealed visible knowledge gaps and a better understanding of the targets of blueberry will be helpful in efficient and meaningful translation of laboratory findings to clinically effective therapeutics.

Massively parallel sequencing, genomic and proteomic technologies have provided near complete resolution of signaling landscape of breast cancer (BCa). NEDD4 family of E3-ubiquitin ligases comprises a large family of proteins particularly, SMURFs (SMURF1, SMURF2), WWPs and NEDD4 which are ideal candidates for targeted therapy. However, it is becoming progressively more understandable that SMURFs and NEDD4 have "split-personalities". These molecules behave dualistically in breast cancer and future studies must converge on detailed identification of context specific role of these proteins in BCa. Finally, we provide scattered clues of regulation of SMURF2 by oncogenic miRNAs, specifically considering longstanding questions related to regulation of SMURF1 and WWPs by miRNAs in BCa. SMURFS, WWPs and NEDD4 are versatile regulators and represent a fast-growing field in cancer research and better understanding of the underlying mechanisms will be helpful in transition of our knowledge from a segmented view to a more conceptual continuum.

Due to many biological cell functions of vitamin D including regulation of cell survival, proliferation and differentiation, the metabolism of itself gains importance in the development of several types of cancer. This case–control study was designed to evaluate the risk of gastric cancer development in terms of VDR rs2228570 & rs731236, and VDBP rs7041 polymorphisms, and serum levels of vitamin D. The study consists of 77 gastric cancer patients and 84 healthy individuals. VDR and VDBP gene polymorphisms and vitamin D levels were determined by using PCR–RFLP and HPLC methods. The distribution of VDR or VDBP gene variants were not different in study groups. The serum level of 25-hydroxyvitamin D was significantly lower in gastric cancer patients versus controls (16 ± 6 → 11 ± 6 ng/ml) in which male patients have higher levels than females. Although the whole study population lacks normal levels of 25-hydroxyvitamin D, it was found that the risk of the development of gastric cancer was approximately fourfold higher in cases with severe vitamin D (

Large-scale sequencing methodologies have helped us identify numerous genomic alterations and we have started to scratch the surface of many new targets for treatment of cancer and the associated predictive biomarkers. TRAIL (TNF-related apoptosis-inducing ligand) is a highly appreciated anti-cancer molecule because of its ability to selectively target cancer cells. However, confluence of information suggests that cancer cells develop resistance against TRAIL-based therapeutics. It is being realized that overexpression of anti-apoptotic proteins and inactivation of pro-apoptotic proteins significantly impairs TRAIL triggered apoptosis, particularly in clinical settings. Re-balancing of pro-and anti-apoptotic proteins and upregulation of death receptors with functionally active extrinsic and intrinsic apoptotic pathways are necessary to sensitize cancer cells to TRAIL based therapeutics. microRNAs (miRNAs) are involved in regulation of myriad of molecular processes and characterized into oncogenic and tumor suppressor miRNAs. Accumulating data has identified miRNAs which positively or negatively regulate TRAIL mediated signaling in cancer cells, helping us understand different steps at which TRAIL-mediated apoptotic signaling can be targeted. Here, we assess the status of our understanding of the mechanisms related to miRNA regulation of TRAIL mediated signaling, as well as the existing gaps therein, and discuss the challenges and opportunities that will help us get closer to personalized medicine.