Objective: Lung cancer is characterized by uncontrolled proliferation, loss of apoptosis, angiogenesis, and metastatic potential. Caffeic acid phenethyl ester (CAPE), the major bioactive molecule of propolis, and epigallocatechin gallate (EGCG), a essential polyphenol of green tea, have documented antioxidant, anti-proliferative, and antiangiogenic effects. This study aimed to investigate the effects of EGCG and CAPE on VEGF and the PI3K/Akt/mTOR signaling pathway, key regulators of lung cancer progression, using in silico and in vitro models. Methods: This study Lung cancer cells (DSMZ/ACC-234) was conducted to demonstrate the inhibition of cell proliferation by the MTT method, molecular binding via autodock vina and protein expression by immunohistochemistry analysis, targeting the VEGF and PI3K/Akt/mTOR pathways with CAPE and EGCG treatment. Results: EGCG and CAPE treatments significantly reduced cell proliferation in lung cancer cells. Untreated cells exhibited strong to very strong immunoreactivity for VEGF and PI3K/Akt/mTOR pathway markers, whereas EGCG reduced these signals to mild- moderate levels and to CAPE moderate-strong levels. Since both treatments resulted in a statistically significant increase in mTORC1 immunoreactivity, molecular docking targeting was performed via it. Conclusion: EGCG and CAPE exhibit significant anti-proliferative and anti-angiogenic effects by adjusting the VEGF and PI3K/Akt/mTOR signaling pathways in lung cancer cells. mTORC1 activation molecular binding affinity is higher in the CAPE-treated group compared to the EGCG group. These findings highlight the therapeutic importance of targeting these pathways in developing novel treatment strategies for lung cancer.

Background/aim: Radiotherapy (RT) is a widely used treatment for non-small cell lung cancer (NSCLC), one of the most prevalent cancers globally. However, radioresistance (RR) remains a significant challenge, often leading to RT failure. The primary driver of RR is the enhanced DNA repair capability of tumor cells. Understanding the mechanisms underlying RR in NSCLC is essential for developing more effective therapeutic strategies. The ataxia-telangiectasia mutated (ATM) protein kinase is pivotal in responding to DNA double-strand breaks caused by RT. Additionally, cyclin-dependent kinase 1 (CDK1) and Ras-related nuclear protein (RAN) are crucial regulators of mitotic entry, G2 arrest, DNA repair, and cell cycle progression. Although these proteins are present in both cytosolic and mitochondrial forms, their specific roles in radiation response and RR remain poorly understood. Materials and methods: In this study, A549 cells were exposed to a single 5 Gy dose of ionizing radiation (IR) and analyzed at baseline and on days 1, 3, and 5 post-IR. The expression levels of ATM, CDK1, and RAN in cytosolic and mitochondrial fractions were assessed using immunohistochemical and Western blot analyses. Results: In immunohistochemical evaluations, ATM, CDK1, and RAN immunoreactivities A549 cancer cells were found to increase markedly on the 1st day, decreased on the 3rd day, and approached control group on the 5th day. Mitochondrial expressions of all three proteins increased significantly on day 1 but declined markedly by day 5. Conversely, altered cytosolic expressions returned to baseline levels by day 5. Conclusion: These results suggest that the early upregulation of mitochondrial ATM, CDK1, and RAN contributes to adaptive RR in A549 cancer cells, offering potential targets for overcoming RT resistance.

Anti-Mullerian hormone (AMH) has been implicated in the pathogenesis of preeclampsia. The present study was primarily designed to determine the placental tissue AMH, Anti-Mullerian hormone Receptor II (AMHRII), vascular endothelial growth factor (VEGF) and microRNA (miRNA) 26a/126/155/210 expressions and serum miRNA 26a/126/155/210 levels in patients with preeclampsia to examine their potential role in the pathogenesis of preeclampsia. Placental tissue samples from patients with preeclampsia (n = 20) and control subjects (n = 20) were examined by immunohistochemical staining and quantitative polymerase chain reaction (qPCR) for AMH, AMHRII, VEGF mRNA expression levels and miRNA 26a/126/155/210 expressions. Serum levels of miRNA 26a/126/155/210 were measured by qPCR. Patients with preeclampsia had lower AMH/AMHRII immunostaining, particularly in syncytiotrophoblastic cells compared to control subjects (p < 0.05). The relative mRNA expressions of AMH/AMHRII were increased (1.535 ± 0.121 and 1.155 ± 0.049 fold, p < 0.0002 and p < 0.033, respectively) and the relative mRNA expression of VEGF was decreased (4.878 ± 0.331 fold, p < 0.0002) in patients with preeclampsia compared to control subjects. The miR-26a expression was increased and miR-126 expression was decreased in serum samples of patients with preeclampsia compared to control subjects (p < 0.0002). miR-155 and miR-210 expressions were increased in serum and placental tissue samples of patients with preeclampsia compared to control subjects (p < 0.0002). In conclusion, reduced placental tissue immunostaining of AMH/AMHRII along with increased AMH/AMHRII mRNA expressions may indicate posttranscriptional dysregulation. Robust increase in expressions of hypoxia/inflammation-related miRNAs particularly miR-155 and miR-210 might have a role in this mechanistic pathway. Increased serum levels of miR 26a, 155 and 210 are potential early diagnostic markers for preeclampsia.

Objectives: The aim of this study is to investigate the immunomodulatory effects of MDA-MB-231 cells or MDA-MB231-derived exosome-mimetic nanovesicles (NVs) on CD4+ Jurkat cells. Methods: NVs were produced by the breakdown of MDA-MB-231 cells and the characterization of generated NVs were performed by using direct-ELISA and Flow cytometry methods. We co -cultured CD4+ Jurkat cells with MDA-MB-231 cells or MDA-MB-231-derived NVs for 48 h. Subsequently, expressions of pro -inflammatory and anti-inflammatory cytokines, and related transcription factors of CD4+ Jurkat cells were evaluated by qPCR method. Results: Clustering, which is the indicator of activation, was not seen in the CD4+ Jurkat cells co -cultured with MDAMB-231 cells. However, CD4+ Jurkat cell clusters were observed in the co -culture experiments with all NV concentrations. In addition, it was determined that the expressions of pro -inflammatory cytokines significantly increased while the expressions of anti-inflammatory cytokines was dramatically decreased in the NV -treated groups. On the contrary, opposite results were obtained in CD4+ Jurkat cells co -cultured with MDA-MB-231 cells. Moreover, TNF-alpha and Gata3 expressions were decreased in all groups. Conclusion: These preliminary findings from in -vitro experiments suggested that NVs could be a potential tool in cancer immunotherapy, but our data need to be supported by more comprehensive studies.

Objective:The implantation period of gestation is a complex process in which numerous molecular pathways play a role.The Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway is one of the evolutionarily conserved cascades used to transduce a multitude signals for several biological events such as implantation and uterine receptivity.Previous studies have indicated that the implantation process is disrupted by the lack of proteins involved in this pathway.However, our literature knowledge showed that there is no study evaluated the expression of JAK/STAT signaling pathwayassociated proteins during the implantation period.This study investigated the expression patterns of JAK/STAT signaling pathway-associated proteins in rats by immunohistochemical (IHC) staining according to gestational days. Methods:In this study, thirty Wistar Albino rats weighing 250-300 g, without any problems in their menstrual cycles, were used.The pregnant animals were sacrificed on the 4 th , 5 th , and 6 th days and histochemical and IHC analysis were performed on the uterine tissues taken from these animals.Results: In this study, protein expression of JAK1, JAK2, JAK3, STAT2, STAT3, STAT4, STAT5, and STAT6 belonging to the JAK/STAT pathway was evaluated in the uterine surface epithelium, gland structures, antimesometrial region, cells of the immune system, myometrium, mesometrial region and decidual cells, which are associated with the implantation process.The result of this evaluation reveals that the expression levels of these proteins in the JAK/STAT pathway vary in different days of the implantation period in implantation-related structures. Conclusion:This study indicates that JAK/STAT signaling pathway-associated proteins can function actively in the regulation of the immunological response of the uterus and embryo-uterus interaction during the implantation period in rats.However, the findings obtained from advanced research on JAK/STAT pathway can be used for treating recurrent pregnancy failures and in enhancing assisted reproductive technology.

The aim of this study was to evaluate testicular perfusion and vascularization with intraoperative ICG/NIR imaging in a testicular ischemia–reperfusion model and to investigate the effects of ICG on testicular tissue. 24 male rats were divided into four groups. In the ICG group, only ICG was given and images of the testicles were recorded with NIR camera. In the torsion group, the testicles were left in torsion for 4 h. ICG/NIR images were obtained after torsion and detorsion. In the reperfusion group, ICG/NIR images of the testicles were obtained at the 4th hour of reperfusion. After the procedures, testicles were collected and evaluated with histological, immunohistochemical examination and qRT-PCR. There was no histologically negative effect of ICG on testicular tissue. There was no testicular perfusion in the torsion group, but perfusion started after detorsion. At the 4th hour of reperfusion, testicular perfusion continued. TNF-a, IL-6, MCP-1 and caspase-3 immunoreactivity were found to be at low levels in the control and ICG groups, while high in the torsion and reperfusion groups (p < 0.05). In qRT-PCR, TNF-a, IL-6, MCP-1 and caspase-3 expressions were lower in the control and ICG groups, but higher in the torsion and reperfusion groups. There was no histologically negative effect of ICG on testicles. The ICG/NIR imaging technique seems to be a feasible method in testicular torsion and may contribute to the surgeon in the intraoperative management of testicular torsion. In testicles that started to be perfused after detorsion, perfusion still continued at the 4th hour of reperfusion. Our next goal is to test whether testicles showing ICG fluorescence in during reperfusion maintain their viability for long term.

Background : Non-small cell lung cancer (NSCLC) is the most commonly diagnosed cancer, and radiotherapy (RT) is used for the cancer therapy. RT affects DNA and causes DNA double-strand breaks which are repaired by DNA repair protein ataxia telangiectasia mutated (ATM). RT also affects the mitochondria which is a key player in mediating the radiation response in tumors and removing damaged mitochondria through mitophagy. During mitophagy, PARKIN accumulates on defective mitochondria to mediate the clearance of damaged mitochondria. This study examines the effect of radiation on mitophagy using PARKIN and ATM antibodies on the human NSCLC A549 line. Materials and Methods : A549 cells were treated with 2, 4, 6 and 8 Gy of radiation were analyzed on days 1 and 3 after a single dose of radiotherapy. PARKIN and ATM expressions of A549 cells were examined by using immunohistochemical technique. Results : In the control groups, weak immunoreactivity of ATM and PARKIN was observed on both days 1 and 3. The most intense ATM expression was seen in the 6 and 8 Gy groups after day 1. The most intense PARKIN expression was seen after the days 1 and 3 in the 2 Gy groups. PARKIN immunoreactivity decreased due to increasing radiation dose. Conclusion : It must be considered that mitophagy mechanisms are activated in RT applications. It must be considered that the activation of mitophagy mechanisms in RT and A549 lung cancer cell lines may provide hemostasis in cancer cells. Molecules targeting mitophagy must be developed for use with radiotherapy.

Автофагія — це катаболічний механізм, що направляє пошкоджені органели та непотрібні довгоживучі білки або токсичні молекули до лізосом для споживання, деградації, переробки, регулювання гомеостазу, контролю якості, клітинної адаптації, а також викликає апоптоз. Після радіаційного ураження активація мутантного при атаксії-телеангіектазії білка є найважливішою сигнальною реакцією ядра. Модифікації автофагії можуть впливати на покращення радіочутливості або ефективності променевої терапії за допомогою кількох способів активації автофагії. У тваринній моделі (миші) антитіла до GRP78, CHOP, MAP LC3β і LAMP1 аналізували, використовуючи імуногістохімічний метод, для дослідження стресу ендоплазматичного ретикулуму в легеневій тканині після променевої терапії 5 Гр. Низькі рівні антиапоптотичного фактора GRP78 і підвищені рівні апоптотичного білка CHOP вказували на ураження, викликане променевою терапією. Підвищена імунореактивність MAP LC3β, LAMP1 вказує на ретикулофагію та апоптоз. Клітинні лінії раку легенів A549, що опромінювали в дозі 2, 4, 6 і 8Гр, потім аналізували за допомогою імуногістохімічного методу на наявність експресії мутантного при атаксії-телеангіектазії білка та PARKIN. Найбільш інтенсивна експресія мутантного при атаксії-телеангіектазії білка спостерігається в групах 6 і 8 Гр. Імунореактивність PARKIN зменшувалася зі збільшенням дози опромінення, і вважається, що механізми мітофагії активуються під час променевої терапії. Слід враховувати, що механізми автофагії можуть бути активовані при застосуванні променевої терапії. Ракові клітини можуть бути знищені шляхом запуску апоптозу з посиленням стимуляції автофагії, але це може призвести до збільшення побічних ефектів променевої терапії. Розуміння автофагії та розробка цільових молекул за допомогою досліджень приведе до успіхів у радіотерапії раку.

Cyclophosphamide (CP) is commonly used as an anticancer agent but has been associated with high toxicity in several organs, including the testes. In this study, we aimed to evaluate the effects of CP-induced testicular toxicity, using glial cell line-derived neurotrophic factor (GDNF), occludin and transforming growth factor beta 3 (TGF-β3) primary antibodies, and miR-34b and miR-34c expressions. Eighteen young Balb/c male mice were divided into three groups. The control group received no treatment. The mice of CP group were injected 100 mg kg-1  day-1 CP for 5 days, and the same amount of saline was injected in the sham group. The animals were sacrificed 24 hr after the last injection. Immunohistochemical analysis of testicular tissues showed a decrease in both spermatogenic germ cell count and also GDNF, occludin expressions, but an increase in TGF-β3 expression in the CP group compared to the others group. The expressions of miR-34b and miR-34c were examined by qPCR technique, a significant decrease was observed in tissue samples in the CP-treated group. The expression of GDNF, occludin and TGF-β3 plays an important role in testicular injury caused by CP, and the decrease in the expression of miR-34b/c in tissue samples may be an important marker for the detection of testicular damage.

Background: Adrenomedullin (AM) and its receptor, receptor activity-modifying protein (RAMP) 2 have pleiotropic regulatory functions in normal tissue and cancer tissue. AM is produced and secreted both numerous stromal cells and tumor cells. This study aims to investigate a possible role of AM and RAMP2 in the radiation exposure in the normal lung tissue. Materials and Methods: Four groups with 6 male adult Swiss Albino mice per group were investigated. The mice were subjected to a 500 cGy single-dose radiation exposure in the total body radiation device and lung tissues were collected. 1, 2, and 7 days after radiation exposure, with 1 reference group which was not exposed to radiation. Results: The general histology and the immunohistochemistry of the tissue samples prepared with anti-AM, anti-RAMP2, and monoclonal antibodies were investigated, yielding a statistically significant increase for AM on day 3 and for RAMP2 on day 1 after radiation exposure. Conclusion: The observed increase of AM and RAMP2 concentrations in the normal tissue matrix after radiation exposure may play a role in the side effects of radiotherapy.

Background: Pentraxins (PTX) play key roles in innate immunity and inflammatory responses. An increase in PTX3 levels may be a marker of early radiation injury in the lung. Thus, we aimed to determine the effect of radiation on PTX3 expression in a lung injury mouse model. Materials and Methods: Twenty-four 6–8-week-old mice were divided into 4 groups, one control (group 1) and three experimental groups (groups 2–4) irradiated with 6 MV photons and 5 Gy in a single fraction. Groups 2, 3, and 4 were sedated and euthanized 24, 72, and 168 h after radiation, respectively. The right lung middle lobe was then removed for histochemical examination and immunostaining for PTX3 expression, which was evaluated semiquantitatively using H-SCORE analysis. Kolmogorov-Smirnov and Kruskal Wallis one-way analysis of variance were used for statistical analysis. Results: Immunohistochemistry of lung tissue samples showed different PTX3 expression levels across the four groups. Group 1 showed weak staining (232.50 ± 9.501), while group 2 (301.50 ± 7.472) and group 3 (283.50 ± 7.090) showed strong immunoreactivity. Group 4 showed moderate PTX3 immunoreactivity (271.50 ± 10.013). Moreover, H-score values between control and early radiation groups were statistically significant (group 1 vs. group 2, p < 0.001; group 1 vs. group 3, p = 0.002). Conclusion: PTX3 levels may be an early marker for long-term radiation effects. Our study provides insights into the pathological processes of pulmonary inflammation and acute radiation injury, and may provide novel therapeutic strategies for controlling pulmonary inflammation without eliciting radiation injury.

mTOR is a member of the PI3K/Akt/mTOR signaling pathway that participates in cell growth, proliferation, protein synthesis, transcription, angiogenesis, apoptosis and autophagy. mTOR and MAPK pahways are two important key signal pathways which are related to each other. We investigated the role of mTOR and other signaling molecules in rat ovaries and uteruses in stages of the estrous cycle. Young adult female rats were divided into four groups as proestrous, estrous, metestrous and diestrous according to vaginal smears. Immunohistochemical staining of mTORC1, IGF1, PI3K, pAKT1/2/3, ERK1 and pERK1/2 was performed and pAKT1/2/3 and ERK1 were also analyzed using western blotting on ovarian and uterine tissue samples. According to our results, PI3K/Akt/mTOR and ERK/pERK showed an increase in the rat ovulation period. When all the groups were evaluated the immunoreactivities for all of the antibodies were detected in the oocytes, granulosa and theca cells, corpus luteum and stroma of ovary and lamina propria, surface and glandular epithelium of uterus with the strongest observed with anti-ERK1 antibody and then with a decreasing trend with anti-mTORC1, anti-pAkt1/2/3, anti-IGF1, anti-PI3K and anti-pERK1/2 antibodies in the proestrus and estrus stages. Differently from other parts of the ovary, highest antibody expression in the corpus luteum was observed in the metestrous stage. Moreover, the existence of pAKT1/2/3 and ERK1 proteins was confirmed with the Western blotting technique. We suggest that mTOR and mTOR-related ERK signaling molecules may participate in the rat ovulation process.

The transmembrane protein zonula occludens of rectal tissue has function to prevents the spread of bacterial toxins into the intestinal mucosa and to systemic circulation. But radiotherapy causes ablation of crypt cell proliferation, mitotic catastrophe, and apoptosis leading to gastrointestinal mucositis. We investigated the acute radiation effect on gastrointestinal mucosa of rectum tissue thickness with immunohistochemistry method for zonula occludens-1 (ZO-1) protein in animal model. A total of 24 healthy Swiss Albino mice were divided into 4 groups, and except control group the groups of 1–3 was exposed to 500 cGy total body irradiation. All rectum tissue samples were taken from the groups of control, 24 h, 72 h, and 168 h after irradiation and stained with hematoxylin and eosin for histochemical examination, and for immunohistochemical staining with anti ZO-1 polyclonal antibody. We observed edema especially in the groups 2 and 3 but not in group 1. Immunohistochemical examination of staining of rectum tissue samples for ZO-1 showed poor staining for control group (1.48 ± 0.06) and group 1 (1.38 ± 0.09) and group 2 (1.50 ± 0.01) but the group 3 (2.12 ± 0.04) samples showed moderate ZO-1 immunostaining. It was found that the amount and thickness of ZO-1 expression increased in the late period for more than 24 hours. The comparison of the values of ZO-1 between the group 3 which is the group in the late period after radiation exposure and control group or group 1 or group 2, showed statistically significant differences (p <0.001). It was concluded that ZO-1 protein may have a role in the side effects of radiation injury, and the understanding of cellular and molecular activity will help us to develop pharmacological modulators to mitigate or treat the injury.

Photodynamic therapy works with a photosensitizer that is stimulated when exposed to a light source of a specific wavelength and produces a form of oxygen that can be used in cancer treatments. In this study, we investigated the effect of laser on apoptosis on breast cancer cell lines (MDA-MB-231) treated with verteporfin in cell culture media. Verteporfin added MDA-MB-231 cells were incubated without light for 24 hours after applying laser light at a wavelength of 695 nm at an intensity of 50 J/cm2 at various times. Anti-proliferative effects were evaluated by immunoreactivity of anti-Bcl-2 and anti-Bax antibodies by immunocytochemical staining. When anti-Bax/Anti-Bcl-2 ratio are compared, the ratio of 1.5 in the control group cells decreases in short-term laser applications, while it approaches normal values in the 7th min after longterm laser application and reaches a very high value in the 9th min. Therefore, our results suggest that verteporfin-mediated PDT may be a potential combined therapy strategy against breast carcinoma by increasing apoptosis.

Aim: In this research, we aimed to investigate the effects extremely low frequency electromagnetic fields (ELF-EMF) on proliferation and apoptosis during treatment of primary and metastatic colon cancer cell lines. Material and Methods: Colon cell lines; COLO-320, COLO-741 and as control mouse fibroblast (STO) cells were cultured in 24 wells of tissue culture plate. Both COLO-320 and COLO-741 cells were treated with α-lactalbumin, sulindac and α-lactalbumin + sulindac. The cells from all groups were exposed to 60 Hz ELF-EMF for 48 hours. For cytotoxicity analyses, the cells were collected and analyzed with ELISA. The cells were fixed in 4% paraformaldehyde for 30 minutes. Cell proliferation was analyzed by evaluating of anti-Ki-67 distribution using indirect immunohistochemistry, cell death were evaluated using TUNEL assay. Results: After TUNEL assay, the TUNEL positive cells were detected in all treated and control groups. However, the number of apoptotic cells was increased after treatment with α-lactalbumin and EMF exposure on COLO-320 cells. The apoptotic cells were less in STO cells. The distribution of Ki-67 was also detected in all groups, but, there were more Ki-67 immunoreactivity in COLO-741 cells than other groups. The cell cytotoxicity was also increased after EMF exposure in all groups. Discussion: Our results suggested that the EMF exposure may increase the effects of α-lactalbumin on primary colon cancer cell lines. However, the proliferation of both cancer and control cells were not affected. The EMF exposure may trigger apoptotic pathway in primary colon cancer cell lines.

Background: HAMLET (human alpha-lactalbumin made lethal to tumor cells) and sulindac are active ingredients which are used in the treatment of cancers. Under both in vivo and in vitro conditions, HAMLET binds to the surface of tumor cells and enters the cells. Sulindac is one of nonsteroidal anti-inflammatory drugs. It inhibits the growth of tumor cells by inducing the apoptosis. In our study, we aimed to investigate effects of alpha-lactalbumin and sulindac on COLO-320 primary and COLO-741 metastatic human colon carcinoma cell lines via mitochondrial apoptotic pathway by indirect immunocytochemistry and TUNEL assays. Materials and methods: The effects of alpha-lactalbumin and sulindac were assessed by using MTT assay at 24, 48 and 72 h and apoptosis markers caspase-3, caspase-9 and cytochrome-c were detected using immunocytochemistry and TUNEL methods. Results: It was appeared that alpha-lactalbumin and sulindac may triggger mechanisms of apoptosis in both primary and metastatic colon carcinoma cell lines and the primary colon carcinoma cell line was affected more than the metastatic cells. Conclusion: It is proposed that alpha-lactalbumin and sulindac can be used in cancer treatments and future in vivo experiments.

Amac:  Calismamizda, infantil hemanjiyom vakalarinda kullanilan propranolol (PR) ile antikemoterapotik bir ajan olarak yaygin kullanilan Paklitakselin (PX) kanser hucreleri uzerine etkisini incelemeyi amacladik. Gerec ve Yontem:  Tripan mavisi ile hucre sayimi yapilarak hucrelerin ikilenme zamanlari belirlendi. MTT testi ile de ilaclarin sitotoksik etkisi ve IC50 degerleri analiz edildi. Inva zyon yonunden farkli iki meme kanseri hucre hattinda (MDA-MB-231 ve MCF-7) anti-VEGF, anti-eNOS, anti-iNOS ve anti-ERK1/2 primer antikorlari indirek immunohistokimyasal yontemle incelendi. Immunoreaktivitenin degerlendirilmesi icin H skorlama sistemi kullanildi. Bulgular:  MTT testi ile hucrelere uygulanacak ilac dozlarinin IC 50 degerleri MDA icin; PX: 5 nmol, PR: 50 µm ve MCF- 7 icin; PX: 3,7 nmol, PR: 50 µm olarak bulundu. Immunohistokimyasal uygulamada kanser hucrelerinde kontrol gruplarinin immunoreaktivitesi siddetli ve/veya cok siddetli artmis iken PX, PR ve kombine uygulanan ilac gruplarinda boyanma siddeti anlamli veya cok anlamli olarak azaldi.  Sonuc:  Bu calisma ile kemoterapotik olarak uygulanan paklitaksele ek olarak anti anjiyogenik ilac uygulamalarinin damarlarda vazodilatasyon, hucre cogalmasi, gocu ve yasam suresini etkilemesi sonucunda anjiyogenezi azaltmasi veya onlemesi acisindan meme kanserinin tedavisinde onemli oldugu dusunulmustur.

Amaç: Bu çalışmanın amacı infantil hemanjiyom vakalarında kullanılan propranolol (PR) ile kemoterapötik bir ajan olarak yaygın kullanılan Paklitakselin (PX) kanser hücreleri üzerine etkisini incelenmesidir.Gereç ve Yöntem: Tripan mavisi ile hücre sayımı yapılarak hücrelerin ikilenme zamanları belirlendi. MTT testi ile de ilaçların sitotoksik etkisi ve IC50 değerleri analiz edildi. İnvazyon yönünden farklı iki meme kanseri hücre hattında (MDA-MB-231 ve MCF-7) anti-VEGF, anti-eNOS, anti-iNOS ve anti-ERK1/2 primer antikorları indirek immunohistokimyasal yöntemle incelendi. İmmunoreaktivitenin değerlendirilmesi için H skorlama sistemi kullanıldı.Bulgular: MTT testi ile hücrelere uygulanacak ilaç dozlarının IC50 değerleri MDA için; PX: 5 nmol, PR: 50 µm ve MCF- 7 için; PX: 3,7 nmol, PR: 50 µm olarak bulundu. İmmunohistokimyasal uygulamada kanser hücrelerinde kontrol gruplarının immunoreaktivitesi şiddetli ve/veya çok şiddetli artmış iken PX, PR ve kombine uygulanan ilaç gruplarında boyanma şiddeti anlamlı veya çok anlamlı olarak azaldı. Sonuç: Bu çalışma ile kemoterapötik olarak uygulanan paklitaksele ek olarak anti anjiyogenik ilaç uygulamalarının damarlarda vazodilatasyon, hücre çoğalması, göçü ve yaşam süresini etkilemesi sonucunda anjiyogenezi azaltması veya önlemesi açısından meme kanserinin tedavisinde önemli olduğu düşünülmüştür.