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Objective: Ankylosing spondylitis (AS) is a chronic inflammatory disorder. MicroRNAs (miRNAs) can function as either oncogenes or tumor suppressor genes. Altered miRNA expression has been implicated in the pathogenesis of several diseases. Therefore, we aimed to explore the effects of miR-196a2T/C (rs11614913) variant profile on susceptibility to AS in a Turkish population.Materials and Methods: Blood samples were collected from 78 AS patients and 79 healthy controls. miR-196a2T/C variant was genotyped by PCR-RFLP. Odds ratio (OR) with 95% confidence interval (95%CI) were calculated using the chi(2) test.Results: The frequency of T/C and T/T genotypes of the miR196a2T/C were higher in AS patients compared to healthy controls (p=0.034 and p=0.028, respectively). The subjects carrying the miR-196a2T/C variant T/T genotype showed a 2.542-fold increased AS risk than the control group. However, no difference was observed in the allele frequencies of miR-196a2T/C between AS patients and the controls. It was found that C/C genotype of miR-196a2T/C variant was more frequent in AS patients with enthesitis than AS patients without enthesitis (p=0.042).Conclusion: The miR-196a2T/C variant represents a genetic risk factor for increased susceptibility to AS and is associated with enthesitis in the Turkish population. Amaç: Ankilozan spondilit (AS) kronik, enflamatuar bir hastalıktır. MikroRNA’lar (miRNA’,lar) onkogen veya tümör baskılayıcıgenler olarak fonksiyon yapabilirler. Çeşitli hastalıkların patogenezinde miRNA ekspresyonu’nun değişmesi bulunmaktadır.Bu nedenle, Türk toplumunda AS yatkınlığında miR-196a2T/C(rs11614913) varyant profilinin etkilerini araştırmayı amaçladık.Gereç ve Yöntem: 78 AS hastası ve 79 kontrolden kan örnekleritoplandı. miR-196a2T/C varyantı PCR-RFLP ile genotiplendi. χ2testi kullanılarak %95 güven aralığı ile Odds oranı (OR) hesaplandı.Bulgular: miR-196a2T/C T/C ve T/T genotipleri AS hastalarında sağlıklı kontrollere kıyasla daha yüksekti (sırasıyla, p=0.034and p=0.028). miR-196a2T/C varyant T/T genotipini taşıyankişiler kontrol grubundan 2,542 kat artmış AS riski gösterdiler.Ancak, miR-196a2T/C allele frekansları açısından AS hastalarıve kontroller arasında fark saptanmadı. miR-196a2T/C varyant C/C genotipinin entezitli AS hastalarında entezit bulunmayan AS hastalarından daha çok olduğu bulundu (p=0.042).Sonuç: miR-196a2T/C varyantı Türk toplumunda AS ve hastalığın entezit ile ilişkisine yatkınlık sağlayan genetik risk faktörü rolü göstermektedir.

WOS: 000537954700007 OBJECTIVE Oral squamous cell carcinoma (OSCC) is the most frequently seen oral malignancy and accounts for up to 80-90% of all malignant neoplasms that occurin the oral cavity. The p53 tumor suppressor gene plays a crucial role in the regulation of the cell cycle. Mutations of the p53 gene havean important role in OSCC carcinogenesis. In this study, we aimed to evaluate the C-deletion mutation in exon 4 codon 63 of p53 gene in Turkish patients with OSCC. METHODS A total of 60 subjects were enrolled in this study, 30 patients with a pathologic diagnosis of OSCC and 30 cases of age and sex-matched healthy controls. Genotyping was performed for all individuals using polymerase chain reaction (PCR) analysis. RESULTS The findings showed that the distribution of p53 exon 4 codon 63 C-deletion was significantly different between patient group and control group (p=0.000). It was detected that all patients had C-deletion mutation in exon 4 codon 63 of p53. CONCLUSION Our results suggest that C-deletion in exon 4 codon 63 deletion of the p53 gene may play a role in the pathogenesis of human OSCC in a Turkish cohort. Ahi Evran University BAPAhi Evran University [SYO.A4.16.002] This study was supported by Ahi Evran University BAP (SYO.A4.16.002) program.

Objective: Glycogen storage disease type 5, also known as McArdle disease, is a hereditary disorder with progressive myopathy. It is characterized by onset of exercise intolerance with premature fatigue and painful muscle cramps in childhood or adolescence. Temporary myoglobinuria may occur after exercise due to rhabdomyolysis. Patients may have mild muscle weakness since childhood. Muscular atrophy with fatty replacement may develop in adult life. McArdle disease is a relatively benign disease and rarely severe myoglobinuria can cause acute renal failure as a complication of widespread rhabdomyolysis. This autosomal recessive disease is caused a homozygous mutation of the PYGM gene encoding muscle enzyme myophosphorylase C. Case: A 36-year-old woman admitted to the Physical Medicine and Rehabilitation polyclinic of Giresun University Hospital with a complaint of gradually increasing progressive weakness and tiredness since 13 years age. CK serum level has been found to in normal range; even after exercise. The findings demonstrated myogenic abnormalities on electromyography, multiple glycogen-containing vacuoles and undetectable muscle myophosphorylase activity on muscle biopsy. The genetic analysis revealed no pathogenic mutations in exon regions of PYGM gene. But in sequencing analysis, the rs71049658, insertion/ deletion variation in intron 17 was determined. Coenzyme Q10 (CoQ-10) 30mg/day, vitamin B6 250mg/day and L-carnitine 1gr/day treatment protocol has been applied and after two months the treatment, clinical improvement has been achieved. Conclusion: In this case report, an atypical McArdle case with a diagnostic challenge has been presented. We thought that this polymorphism in the myophosphorylase gene may lead to a severe mosaic alteration in mRNA splicing, including exon skipping, activation of cryptic splice-sites, and exon-intron reorganizations.

Objective: Ankylosing spondylitis (AS) is a chronic inflammatory disorder. Micro RNAs (miRNAs) can function as either oncogenes or tumor suppressor genes. Altered miRNA expression has been implicated in the pathogenesis of several diseases. Therefore, we aimed to explore the effects of miR-196a2T/C (rs11614913) variant profile on susceptibility to AS in a Turkish population. Materials and Methods: Blood samples were collected from 78 AS patients and 79 healthy controls. miR-196a2T/C variant was genotyped by PCR-RFLP. Odds ratio (OR) with 95% confidence interval (95%CI) were calculated using the χ2 test. Results: The frequency of T/C and T/T genotypes of the miR196a2T/C were higher in AS patients compared to healthy controls (p=0.034 and p=0.028, respectively). The subjects carrying the miR-196a2T/C variant T/T genotype showed a 2.542-fold increased AS risk than the control group. However, no difference was observed in the allele frequencies of miR-196a2T/C between AS patients and the controls. It was found that C/C genotype of miR-196a2T/C variant was more frequent in AS patients with enthesitis than AS patients without enthesitis (p=0.042). Conclusion: The miR-196a2T/C variant represents a genetic risk factor for increased susceptibility to AS and is associated with enthesitis in the Turkish population., Amaç: Ankilozan spondilit (AS) kronik, enflamatuar bir hastalıktır. MikroRNA’lar (miRNAlar) onkogen veya tümör baskılayıcı genler olarak fonksiyon yapabilirler. Çeşitli hastalıkların patogenezinde miRNA ekspresyonunun değişmesi bulunmaktadır. Bu nedenle, Türk toplumunda AS yatkınlığında miR-196a2T/C (rs11614913) varyant profilinin etkilerini araştırmayı amaçladık. Gereç ve Yöntem: 78 AS hastası ve 79 kontrolden kan örnekleri toplandı. miR-196a2T/C varyantı PCR-RFLP ile genotiplendi. χ2 testi kullanılarak %95 güven aralığı ile Odds oranı (OR) hesaplandı. Bulgular: miR-196a2T/C T/C ve T/T genotipleri AS hastalarında sağlıklı kontrollere kıyasla daha yüksekti (sırasıyla, p=0.034 and p=0.028). miR-196a2T/C varyant T/T genotipini taşıyan kişiler kontrol grubundan 2,542 kat artmış AS riski gösterdiler. Ancak, miR-196a2T/C allele frekansları açısından AS hastaları ve kontroller arasında fark saptanmadı. miR-196a2T/C varyant C/C genotipinin entezitli AS hastalarında entezit bulunmayan AS hastalarından daha çok olduğu bulundu (p=0.042). Sonuç: miR-196a2T/C varyantı Türk toplumunda AS ve hastalığın entezit ile ilişkisine yatkınlık sağlayan genetik risk faktörü rolü göstermektedir.

[Abstract Not Available] WOS:000505772700275

ViralApert's syndrome (AS) is a rare congenital disorder with autosomal dominantinheritance and is characterized by irregular craniosynostosis, syndactylia ofhands and feet, mid-face hypoplasia, hypertelorism and anomalies of centralnervous system, heart and kidneys. AS has been associated with mutations inFibroblast growth factor receptor 2 (FGFR2) located on chromosome 10q (10q26).Dental anomalies are common in AS. We report on a 6-year-old AS patient withcomplex dental anomalies. A 6 year-old female patient with AS was presented tothe dental clinic with complaints of teeth decay and embedded teeth. She haddysmorphic facial symptoms including mid-face hypoplasia, low-set ears,hypertelorism, prognathic mandible, steep wide forehead, down-slanting lateralcanthi and palpebral fissures. She had syndactyly of third and fourth digits ofboth hands. Arachnoidal cyst was diagnosed previously. She had intellectualdisability. Radiography showed that there were more than one embedded teeth.Upper first premolar and canine teeth were displaced. She had teeth agenesis ofthe maxillary lateral incisor. Her maxilla and mandible were narrow. Themaxillary dental arch was v-shaped. Orthodontic treatment was planned for thefuture because the patient was too young. The aim of the present report is toshow the dental manifestations in case with AS. The treatment and management ofAS require a multidisciplinary approach.

WOS: 000472755200014, …

WOS: 000411861000184 …

The journey of nucleic acid isolation and characterization has been a long one starting in the late 1800s. DNA isolation has led the way due to its stable chemical characteristic. Since its initial implementation the demand of molecular studies has evolved rapidly into studying a wide range of nucleic acids, including all types of RNAs, mitochondrial DNA, and nucleic acid materials of other organisms. The scientific advancements and the "omics" era certainly brought new challenges, forcing the technology to go into an enormous advancement in a relatively short period. In the early 1900s the range of methods, the material, and the field of applications were limited. During, nearly, the last three decades the procedures became automated, standardized, economic, user-friendly, nonhazardous, and less time-consuming. The manual organic or inorganic procedures had left their place to more robust and reliable solid-phase extraction techniques. There are a wide range of samples in which high-quality and high-yield nucleic acid isolation is carried out. These samples vary from whole blood to different types of tissues, hair, bones, saliva, urine, and many more. We are going to explore the principles of nucleic acid isolation, the basics of chemistry behind the scenery, manual and advanced techniques of isolation and quality check, and the means of good laboratory practice. © 2018 Elsevier Inc. All rights reserved.

research Sitokin gen varyantları/ekspresyonları ve non-sendromik mikrotia - Bir ilişki var mıdır?Amaç: Mikrotianın etyopatogenezinde birçok genetik ve çevreselfaktörler araştırılmasına rağmen hala belirsizlik vardır. Bu çalışmadabir Türk kohortunda pro- ve anti-enflamatuar sitokinlerin [interlökin(IL) 6, IL-10, tümör nekroz faktör alfa (TNF-?), transforme edici büyüme faktörü beta (TGF-?1), İnterferon gama (IFN-?)] varyant/ekspresyonu ve sendromik-olmayan mikrotiaya yatkınlık arasındaki ilişkiyi araştırdık.Yöntem:Çalışmaya akraba olmayan 19 mikrotiyalı olgu ve 40 sağlıklı gönüllü kontrol dahil edildi. Sitokin varyantları dizi spesifik primerpolimeraz zincir reaksiyonu (PCR-SSP) metodu kullanılarak analizedildi. Bulgular:IL-6 (-174) GC genotipi (yüksek ekspresyon) mikrotia vakalarında daha düşükken (p=0.003), IL-6 (-174) GG genotipi (yüksekekspresyon) mikrotia vakalarında kontrolden daha yüksek olarak bulundu (p=0.010). IL-6 (-174) için, GG genotipi taşıyan hastalar mikrotia için 5895 kat yüksek riske sahipti. IFN-? (+874) varyant AA genotip (düşük ekspresyon) mikrotia vakalarında düşüktü (p=0.009). IL6 (-174) C alleli hastalarda kontrollere göre düşükken, G alleli hastagrubunda kontrole göre daha yaygındı (p=0.003). IFN-? (+874) varyant A alleli hastalarda düşükken, T alleli hastalarda daha yaygındı(p=0.017). Sonuç:Burada mikrotia gelişimi için sitokin varyantlarının risk faktörü teşkil edeceğini ilk defa gösterdik. Sonuçlarımız IFN-? (+874) veIL-6 (-174) varyantlarının Türk toplumunda mikrotia gelişimi ile ilişkili olabileceğini öne sürmektedir. Objective:Although many genetic and environmental factors areinvestigated the etiopathogenesis of microtia, it still remains unclear.We investigated the relationship between the variants/expression ofpro- and anti-inflammatory cytokines [interleukin (IL) 6, IL-10,tumor necrosis factor-alpha (TNF-?), transforming growth factorbeta (TGF-?1), interferon gamma (IFN-?)] and susceptibility nonsyndromic microtia in a Turkish cohort. Methods:Nineteen unrelated cases with microtia and 40 healthycontrols were included in the present study. Cytokine variants weretested by polymerase chain reaction with sequence-specific primers(PCR-SSP) method. Results: It was found that IL-6 (-174) GG genotype (high expression) was higher in microtia cases than the controls (p=0.010) whileIL-6 (-174) GC (high expression) genotype was lower in patients(p=0.003). For IL-6 (-174), patients with GG genotype had a 5895fold increased risk for microtia. IFN-? (+874) variant AA genotype(low expression) was lower in microtia cases (p=0.009). IL-6 (-174) Gallele was more prevalent in patient group compared to controls whileC allele was lower in patients than controls (p=0.003). IFN-? (+874)variant T allele was more prevalent in cases while A allele was lowerin cases (p=0.017). Conclusion:We have demonstrated for the first time that thecytokine variants constitute risk factors for developing microtia. Ourstudy suggests that the IFN-? (+874) and IL-6 (-174) variants may beconsidered as a risk factor for microtia in a Turkish cohorts.

Amaç: Bu çalışmanın amacı, adenozin deaminaz (ADA) genindeki G22A polimorfizminin Türk popülasyonunda şizofreni ile ilişkisinin araştırılmasıdır. Yöntemler: Bu çalışmada biz 113 şizofreni tanısı almış hasta ve 121 sağlıklı kontrol bireylerini inceledik. ADA geni G22A polimorfizmi allel spesifik-polimeraz zincir reaksiyonu (AS-PCR) yöntemi kullanılarak belirlendi. Bulgular: ADA genindeki G22A polimorfizmi için GG, GA ve AA genotip sıklıkları sırası ile kontrol grubu için %79.3 (96/121), %20,3 (25/121), %0 (0) ve hasta grubu için %87,6 (99/113), %10,6 (12/113), %1,8 (2/113) olarak belirlendi. Genotip dağılım bakımından hasta ve kontrol grupları arasında anlamlı fark bulundu (p=0,017). Ayrıca GA genotipinin sıklığı hastalarda kontrole nazaran anlamlı düzeyde düşük bulundu (p=0,048, OR=0.46, 95%CI 0.22- 0.96). Fakat allel sıklıkları bakımından iki grup arasında anlamlı fark bulunamadı. Cinsiyet bakımından karşılaştırma yaptığımız zaman, erkek hastalarda GG genotipinin anlamlı düzeyde yüksek, GA genotipinin ise düşük olduğu gözlendi (sırası ile p=0,036 ve p=0,005). Kadın hastalarda herhangi bir anlamlı fark gözlenmedi. Sonuç: Bizim sonuçlar ADA genindeki G22A polimorfizminin Türk popülasyonunda şizofreni hastalığı ile ilişkili olabileceğini gösterdi. ADA genindeki GA genotipinin özellikle erkeklerde şizofreniye yatkınlığı düşürdüğü, buna karşın GG genotipinin yatkınlığı arttırdığı muhtemeldir. Farklı hasta ve etnik gruplar ile gelecekte yapılacak çalışmalar, elde ettiğimiz sonuçların kesinleşmesine yardımcı olur, Objective: The aim of this study was to investigate whether the G22A polymorphism of adenosine deami­nase (ADA) gene is associated with schizophrenia in Turkish population. Methods: In this study, we evaluated 113 patients with schizophrenia and 121 individuals without the disease. The ADA G22A polymorphism was examined using allele specific-polymerase chain reaction (PCR). Results: The ADA G22A genotype frequencies of GG, GA, and AA were 79.3% (96/121), 20.7% (25/121) and 0% (0) in the control group, while 87.6 % (99/113), 10.6% (12/113), 1.8% (2/113) in the patient group, respectively. There was a statistically significant difference in genotype distribution between patients and controls (p=0.017). Also the frequency of GA genotype was found significantly low­er in patients compared with healthy controls (OR = 0.46, 95% Cl 0.22-0.96, p =0.048). However, there was not any noticeable difference in allele distribution between the groups (p>0.05). In addition, the frequency of GG geno­type in the male patient group significantly higher, and GA genotype significantly lower compared to the male control group, were found (p=0.036, p=0.005, respectively). No association was found for the female group. Conclusion: Our results show that, the G22A polymor­phism of ADA gene may be associated with schizophrenia in Turkish population. The ADA GA genotype is likely to reduce, whereas GG genotype increased genetic sus­ceptibility to schizophrenia, especially in males. Further studies should be repeated with different study subjects and/or other ethnic subjects to generalize the conclusion of this study.

research Akciğer kanseri tüm dünyada kansere bağlı ölüm sebepleri içinde ilk sırada yer alır. Tedavi alanında tüm gelişmelere rağmen hala kötü prognoza sahiptir. Akciğer kanseri histolojik tipine göre küçük hücreli akciğer kanseri (KHAK) ve küçük hücreli dışı akciğer kanseri (KHDAK) olarak iki ana tipe ayrılır. KHDAK tüm vakaların yaklaşık %85'ni oluşturur. MET proto-onkogeni birçok hücresel olayda rol oynayan tirozin kinaz reseptörüdür ve KHDAK'inde overeksprese olur. Güncel KHDAK tedavisinde MET inhibitörleri kullanılmaktadır. KHDAK'de sık görülen epidermal büyüme faktör reseptör (EBFR) mutasyonlarına karşı kullanılan tirozin kinaz inhibitörleri (TKI) tedavisinin başlangıcından bir süre sonra direnç ortaya çıkmaktadır. Bunun oluşmasındaki faktörlerden biri MET amplifikasyonlarıdır. Bu derlemede MET geninin KHDAK'indeki rolü gözden geçirilecektir. Lung cancer is the most common cause of cancer mortality all over the world. Despite the fact that there has been a progress in lung cancer, it still has a poor prognosis. Lung cancer is classified into two major histological types; small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). NSCLC accounts for approximately 85% of all cases of lung cancer. MET proto-oncogene is a tyrosine kinase receptor that plays a role in various cellular events and it is overexpressed in NSCLC. MET kinase inhibitors are currently used in the treatment of NSCLC. The resistance emerges upon the initiation of the treatment with tyrosine kinase inhibitors (TKI) against EGFR mutations frequently seen in NSCLC. One of the reasons for this resistance is MET amplifications. In this review, the role of the MET gene in NSCLC will be evaluated.

Amaç: Bu çalışmanın amacı, adenozin deaminaz (ADA) genindeki G22A polimorfizminin Türk popülasyonunda şizofreni ile ilişkisinin araştırılmasıdır.Yöntemler: Bu çalışmada biz 113 şizofreni tanısı almış hasta ve 121 sağlıklı kontrol bireylerini inceledik. ADA geni G22A polimorfizmi allel spesifik-polimeraz zincir reaksiyonu (AS-PCR) yöntemi kullanılarak belirlendi.Bulgular: ADA genindeki G22A polimorfizmi için GG, GA ve AA genotip sıklıkları sırası ile kontrol grubu için %79.3 (96/121), %20,3 (25/121), %0 (0) ve hasta grubu için %87,6 (99/113), %10,6 (12/113), %1,8 (2/113) olarak belirlendi. Genotip dağılım bakımından hasta ve kontrol grupları arasında anlamlı fark bulundu (p=0,017). Ayrıca GA genotipinin sıklığı hastalarda kontrole nazaran anlamlı düzeyde düşük bulundu (p=0,048, OR=0.46, 95%CI 0.220.96). Fakat allel sıklıkları bakımından iki grup arasında anlamlı fark bulunamadı. Cinsiyet bakımından karşılaştırma yaptığımız zaman, erkek hastalarda GG genotipinin anlamlı düzeyde yüksek, GA genotipinin ise düşük olduğu gözlendi (sırası ile p=0,036 ve p=0,005). Kadın hastalarda herhangi bir anlamlı fark gözlenmedi.Sonuç: Bizim sonuçlar ADA genindeki G22A polimorfizminin Türk popülasyonunda şizofreni hastalığı ile ilişkili olabileceğini gösterdi. ADA genindeki GA genotipinin özellikle erkeklerde şizofreniye yatkınlığı düşürdüğü, buna karşın GG genotipinin yatkınlığı arttırdığı muhtemeldir. Farklı hasta ve etnik gruplar ile gelecekte yapılacak çalışmalar, elde ettiğimiz sonuçların kesinleşmesine yardımcı olur. Objective: The aim of this study was to investigate whether the G22A polymorphism of adenosine deaminase (ADA) gene is associated with schizophrenia in Turkish population.Methods: In this study, we evaluated 113 patients with schizophrenia and 121 individuals without the disease. The ADA G22A polymorphism was examined using allele specific-polymerase chain reaction (PCR).Results: The ADA G22A genotype frequencies of GG, GA, and AA were 79.3% (96/121), 20.7% (25/121) and 0% (0) in the control group, while 87.6 % (99/113), 10.6% (12/113), 1.8% (2/113) in the patient group, respectively. There was a statistically significant difference in genotype distribution between patients and controls (p=0.017). Also the frequency of GA genotype was found significantly lower in patients compared with healthy controls (OR = 0.46, 95% Cl 0.22-0.96, p =0.048). However, there was not any noticeable difference in allele distribution between the groups (p>0.05). In addition, the frequency of GG genotype in the male patient group significantly higher, and GA genotype significantly lower compared to the male control group, were found (p=0.036, p=0.005, respectively). No association was found for the female group.Conclusion: Our results show that, the G22A polymorphism of ADA gene may be associated with schizophrenia in Turkish population. The ADA GA genotype is likely to reduce, whereas GG genotype increased genetic susceptibility to schizophrenia, especially in males. Further studies should be repeated with different study subjects and/or other ethnic subjects to generalize the conclusion of this study.

Tedavi alanındaki tüm gelişmelere rağmen, akciğer kanseri halatüm dünyada kanserle ilişkili ölüm nedenlerinin başında gelmektedir.Etyolojisinde sigaranın yanı sıra çevresel, mesleksel ve genetikfaktörler rol oynamaktadır. Akciğer kanserleri genellikle kü-çük hücreli akciğer kanseri (KHAK) ve küçük hücreli dışı akciğerkanseri (KHDAK) olmak üzere iki ana histolojik tipe ayrılır. Tümakciğer kanserlerinin yaklaşık %85’ini oluşturan KHDAK’inde bir-çok gen anomalisi saptanır. Anaplastik lenfoma kinaz (ALK) geniinsülin reseptör tirozin kinaz süper ailesinin bir üyesidir. ALK geniakciğer kanseri, lenfoma gibi çeşitli malignitelerde füsyon proteinoluşumuna yol açan translokasyonlara dahil olur. Bu derlemedeKHDAK’inde görülen ALK yeniden düzenlenmelerine ait son literatürgözden geçirilecektir., Despite all improvements in treatment modalities, lung canceris the leading cause of death related to cancers worldwide.Environmental, occupational and genetic factors, as well as smokingplay role in the etiology. Lung cancers are generally dividedinto two main histologic categories: small cell lung cancer (SCLC)and non-small cell lung cancer (NSCLC). Several gene aberrationsare detected in NSCLC, which constitute approximately 85% ofall lung cancers. The Anaplastic lymphoma kinase (ALK) gene is amember of insulin receptor tyrosine kinase super family. ALK geneinvolves with translocation those results in formation of fusion proteinin various malignancies such as lung cancer and lymphoma. Inthis article, latest literature regarding re-arrangement of ALK seenin NSCLC will be reviewed.

Akciğer kanseri tüm dünyada en yaygın görülen kanser nedenli ölüm sebebidir. Etyolojide sigara en önemli risk faktörü olmasına karşın çevresel, genetik, mesleki faktörlerin de hastalığa katkıda bulunur. Tedavi alanında son yıllardaki tüm gelişmelere rağmen kötü prognoza sahiptir. Akciğer kanseri genellikle histolojik tipine göre küçük hücreli akciğer kanseri ve küçük hücreli olmayan akciğer kanseri olarak iki ana tipe ayrılır. Küçük hücreli olmayan akciğer kanseri tüm vakaların yaklaşık %85ni oluşturur. Küçük hücreli olmayan akciğer kanserinde en sık rastlanılan mutasyonlardan biri epidermal büyüme faktör reseptör mutasyonlarıdır. Bu mutasyonlar sigara içmeyenlerde, kadınlarda ve Asya ırkında daha fazladır ve bu mutasyona sahip tümörler tirozin kinaz inhibitörlerine daha iyi cevap verir. Bu derlemede epidermal büyüme faktörün küçük hücreli olmayan akciğer kanserindeki öngörüsel ve prognostik rolü değerlendirilecektir. Lung cancer is the most common reason of cancer mortality all over the world. Although smoking is the most important factor in lung cancer etiology, additionally, environmental, genetic and occupational factors also contribute to this disease. Despite the fact that there havebeen progress in lung cancer area in terms of treatments, it has still poor prognosis. Lung cancer is generally classifed into two major histological types; small cell lung cancer and non-small cell lung cancer. Non-small cell lung cancer (NSCLC) accounts for approximately 85% of all cases of lung cancer. Epithelial growth factor receptor mutations are among the most common mutations in NSCLC. These mutations are more prevalent in lung cancer patients who are non-smokers, female, and of Asian ethnicity and tumors which have these mutations response better to tyrosine kinase inhibitors in NSCLC. In this review, the prognostic and predictive role of EGFR will be evaluated in NSCLC.