Amac: Anjiyogenez, endotelyal hücreler, malign durumlardaki tümör hücrelerinin yanı sıra kemik iliği kaynaklı hücreler ve stromal hücreleri içeren tumor mikrocevresindeki hucreleri kapsayan çok faktörlü ve çok hücreli bir kompleks (pato-)fizyolojik olaydır. Bu olayin ana faktoru, vasküler endotelyal büyüme faktörüdür (VEGFA). Son yillarda tümör hücrelerinde potansiyel damarlanma sinyalini bloke etmek icin VEGFA reseptorune karsi bevacizumab (anti-VEGF) ajani kullanilmaktadir ve akciğer kanseri (NSCLC), kolorektal kanser, meme kanseri ve renal hücreli karsinomada in vitro deneylerle farkli etkinlikleri belirlenmistir. Bu calismadaki temel hedef, Bevacizumab uygulanmis akciger kanser hucrelerinde damarlanma etkinligi ve mekanizmasinin normal hucrelerle karsilastirilarak belirlenmesidir.  Gerec ve yontemler: Ana uyarici VEGF ve anjiyogenez blokajini saglayan Bevacizumab uygulamalari ile hucre fonksiyonlari incelendi. Normal epithelial HUVEC hatti ile akciger kanser A549 hucre hatti kullanildi ve ATCC protokolune gore kulture edildi. Farkli dozlarda ajanlar uygulandiktan sonra, hucre canliligi, Sytox cogalma indeksi ve anjiyogenezden sorumlu basamak Notch etkinligi arastirildi. Bulgular: VEGF ile muamele edilen hucrelerde 24 saat inkubasyon ile hucre canliliginda belirgin artis saptandi. Iki hucre hattinda canlilik duzeyleri karsilastirildiginda VEGF etkisinin anlamli derecede farkli oldugu goruldu. Bevacizumab uygulamasinda ise, A549 hucrelerinin cogalma indeksi anlamli derece azaldi ve Notch mekanizmasi ile iliskili ADAM10 protein duzeyinin, HUVEC hucresine gore anlamli artis gosterdigi tespit edildi. Sonuc: Elde edilen bulgulara gore anjiyogenez molekuler mekanizmasinin aciklanmasi adina daha detayli calismalara ihtiyac oldugu gorulmektedir. Geleneksel kanser tedavi yontemleri yani sira etkisi bilinen antianjiyogenik ajanlarla kombine tedavilerin arttirilmasi basari sansini arttiracaktir

Objective: Angiogenesis is physiological event which involve endothelial cells and in malignant conditions involve bone-marrow derived cells, stromal cells related to tumor microenvironment is a multifactorial event. The main factor in this event is vascular endothelial growth factor (VEGFA). In recent years, bevacizumab (anti-VEGF) agent has been used against VEGFA receptor to block potential vascular signal in tumor cells and different activities were determined by in vitro experiments in lung cancer (NSCLC), colorectal cancer, breast cancer and renal cell carcinoma. The main objective of this study was to determine the vascularity and mechanism of vascular cancer in Bevacizumab-treated lung cancer cells compared to normal cells. Material-method: Study of cell functions with main stimulant VEGF and Bevacizumab applications which provide angiogenesis blockade. Normal epithelial HUVEC line and lung cancer A549 cell line were used and cultured according to ATCC protocol. After application of different doses of agents, cell viability, Sytox proliferation index and Notch pathway activity responsible for angiogenesis were investigated. Results: Cells treated with VEGF showed a significant increase in cell viability with incubation for 24 hours. VEGF effect was significantly different in two cell lines compared to viability. In the application of Bevacizumab, the proliferation index of A549 cells decreased significantly and the ADAM10 protein level associated with the Notch mechanism was found to increase significantly compared to HUVEC cell. Conclusion: According to the findings, it is seen that it needs more detailed studies to explain the molecular mechanism of angiogenesis. In addition to conventional cancer treatment methods, enhancing combined therapies with known antiangiogenic agents will increase the chances of success.