Zeybek Kuyucu, Ayça

Profile URL
https://hdl.handle.net/11147/16219
Name Variants
Zeybek Kuyucu, Ayca
Kuyucu, Ayca Zeybek
Zeybek Kuyucu, A.
Zeybek Kuyucu, Ayça
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Email Address
Main Affiliation
03.01. Department of Bioengineering
Status
Former Staff
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ORCID ID
Scopus Author ID
57195971193
Turkish CoHE Profile ID
Google Scholar ID
Fs1R2O8AAAAJ
WoS Researcher ID

Sustainable Development Goals

NO POVERTY1
NO POVERTY
0
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ZERO HUNGER2
ZERO HUNGER
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GOOD HEALTH AND WELL-BEING3
GOOD HEALTH AND WELL-BEING
2
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QUALITY EDUCATION4
QUALITY EDUCATION
0
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GENDER EQUALITY5
GENDER EQUALITY
0
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CLEAN WATER AND SANITATION6
CLEAN WATER AND SANITATION
0
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AFFORDABLE AND CLEAN ENERGY7
AFFORDABLE AND CLEAN ENERGY
0
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DECENT WORK AND ECONOMIC GROWTH8
DECENT WORK AND ECONOMIC GROWTH
0
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INDUSTRY, INNOVATION AND INFRASTRUCTURE9
INDUSTRY, INNOVATION AND INFRASTRUCTURE
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REDUCED INEQUALITIES10
REDUCED INEQUALITIES
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SUSTAINABLE CITIES AND COMMUNITIES11
SUSTAINABLE CITIES AND COMMUNITIES
0
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RESPONSIBLE CONSUMPTION AND PRODUCTION12
RESPONSIBLE CONSUMPTION AND PRODUCTION
0
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CLIMATE ACTION13
CLIMATE ACTION
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LIFE BELOW WATER14
LIFE BELOW WATER
0
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LIFE ON LAND15
LIFE ON LAND
0
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PEACE, JUSTICE AND STRONG INSTITUTIONS16
PEACE, JUSTICE AND STRONG INSTITUTIONS
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PARTNERSHIPS FOR THE GOALS17
PARTNERSHIPS FOR THE GOALS
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Documents

3

Citations

16

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1

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Scholarly Output

3

Articles

1

Views / Downloads

2361/1184

Supervised MSc Theses

0

Supervised PhD Theses

1

WoS Citation Count

0

Scopus Citation Count

36

Patents

0

Projects

0

WoS Citations per Publication

0.00

Scopus Citations per Publication

12.00

Open Access Source

3

Supervised Theses

1

JournalCount
Journal of Hepatology1
Oncotarget1
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2017 - 20183

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Scholarly Output Search Results

Now showing 1 - 3 of 3
  • Doctoral Thesis
    Pre-Clinical Trial Treatment of Hepatocellular Carcinoma on Cirrhosis in a Rat Model
    (İzmir Institute of Technology, 2017) Zeybek Kuyucu, Ayça; Şanlı Mohamed, Gülşah
    Hepatocellular carcinoma (HCC) is the second most common cause of cancer related mortality worldwide. AKT pathway has been found activated in 50% of HCC cases, making it promising target. Therefore we assess efficacy of the allosteric AKT inhibitor or the combination of Sorafenib with AKT inhibitor compared to untreated control and to standard treatment, Sorafenib, in vitro and in vivo. AKT inhibitor blocked phosphorylation of AKT in vitro and strongly inhibited cell growth and migration with significantly higher potency than Sorafenib. Similarly, apoptotic cell was strongly increased by AKT inhibitor in vitro. To mimic human advanced HCC, we used diethylnitrosamine-induced cirrhotic rat model with fully developed HCC. MRI analyses showed that AKT inhibitor significantly reduced overall tumor size. Furthermore, number of tumors was decreased by AKT inhibitor, which was associated with increased apoptosis and decreased proliferation. Tumor contrast enhancement was significantly decreased in the AKT inhibitor group. Moreover, on tumor tissue sections, we observed a vascular normalization and a significant decrease in fibrosis in surrounding liver of animals treated with AKT inhibitor. Finally, pAKT/AKT levels in AKT inhibitor treated tumors were reduced, followed by down regulation of actors of AKT downstream signaling pathway: pmTOR, pPRAS40, pPLCγ1 and pS6K1. In conclusion, we demonstrated that AKT inhibitor blocks AKT phosphorylation in vitro and in vivo. In HCC-rat model, AKT inhibitor was well tolerated, showed anti-fibrotic effect and had stronger antitumor effect than Sorafenib. Our results confirm the importance of targeting AKT in HCC.
  • Conference Object
    Akt Inhibitor Arq 092 and Sorafenib Additively Inhibit Progression of Hepatocellular Carcinoma and Improve Immune System in Cirrhotic Rat Model
    (Elsevier, 2017) Jilkova, Z. M.; Zeybek Kuyucu, Ayça; Kurma, K.; Pour, S. T. A.; Roth, G. S.; Abbadessa, G.; Decaens, T.
    Background and Aims: Hepatocellular carcinoma (HCC) is often diagnosed at advanced stages with limited number of therapeutic options. Longer exposure to classical treatment of advanced HCC, sorafenib, often over-activates AKT pathway, leading to HCC resistance. Moreover, AKT pathway itself is activated in almost half of HCC cases. Therefore, we investigated the efficacy of combination of Sorafenib with allosteric Akt inhibitor ARQ 092 in a DEN-induced cirrhotic rat model with HCC.
  • Article
    Citation - Scopus: 36
    Combination of Akt Inhibitor Arq 092 and Sorafenib Potentiates Inhibition of Tumor Progression in Cirrhotic Rat Model of Hepatocellular Carcinoma
    (Impact Journals, 2018) Macek Jilkova, Zuzana; Zeybek Kuyucu, Ayça; Kurma, Keerthi; Tayébéh, Séyédéh; Pour, Ahmad; Roth, Gaël S.; Abbadessa, Giovanni; Yu, Yi; Schwartz, Brian; Sturm, Nathalie; Marche, Patrice N.; Hainaut, Pierre; Decaens, Thomas
    The prognosis of patients with advanced hepatocellular carcinoma (HCC) is very poor. The AKT pathway is activated in almost half of HCC cases and in addition, long term exposure to conventional drug treatment of HCC, sorafenib, often results in overactivation of AKT, leading to HCC resistance. Therefore, it is important to assess the safety and the efficacy of selective allosteric AKT inhibitor ARQ 092 (Miransertib) in combination with sorafenib. Here, we demonstrated in vitro that the combination of ARQ 092 with sorafenib synergistically suppressed proliferation, promoted apoptosis, and reduced migration. To test the effect of the combination in vivo, rats with diethylnitrosamine-induced cirrhosis and fully developed HCC were randomized and treated with vehicle, sorafenib, ARQ 092 or the combination of ARQ 092 with sorafenib; (n=7/group) for 6 weeks. Tumor progression, size of tumors and the mean tumor number were significantly reduced by the combination treatment compared to the control or single treatments. This effect was associated with a significant increase in apoptotic response and reduction in proliferation and angiogenesis. Sirius red staining showed a decrease in liver fibrosis. Moreover, treatments improved immune response in blood and in tumor microenvironment. Thus, the combination of ARQ 092 with sorafenib potentiates inhibition of tumor progression and gives the possibility of therapeutic improvement for patients with advanced HCC.