Saeid Ghavami

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Dr. Ghavami got his BSc. in Chemistry in 1989 (Shiraz University, Shiraz, Iran), MSc. and PhD (1995, 2004, TMU University, Tehran, Iran) in Clinical Biochemistry. His Postdoctoral training was focused on the application of apoptosis/autophagy/unfolded protein response (UPR) in regulation of cell fate. His research program is focused on regulation of cellular phenotype via targeting autophagy and UPR at the Department of Human Anatomy and Cell Science, University of Manitoba, He has been the recipient of a number of prestigious awards including CIHR/GSK/CLA postdoctoral award (No

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Soykan Arikan

Istanbul Education and Research Hospital

Behzad Narouie

Shahid Beheshti University of Medical Sciences

mohsen saravani

dr yousef Alalawi

majid mojarrad

Mashhad University of Medical Sciences, Mashhad. Iran.

Mirela Petrulea

Parham Jabbarzadeh Kaboli

UPM - Universiti Putra Malaysia

sara samadi

Mashhad University of Medical Sciences, Mashhad. Iran.

Tahereh Mazoochi

Amedeo Carraro

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02:58

Simvastatin Boosts Chemotherapy by cutting autophagic lifeline in Glioblastoma

Temozolomide (TMZ) is a chemotherapy agent used to treat Grade IV astrocytoma, also known as glio... more Temozolomide (TMZ) is a chemotherapy agent used to treat Grade IV astrocytoma, also known as glioblastoma (GBM). TMZ treatment causes DNA damage that results in tumor cell apoptosis and increases the survival rate of GBM patients. However, chemoresistance as a result of TMZ-induced autophagy significantly reduces this anticancer effects over time. Statins are competitive inhibitors of HMG-CoA reductase, the rate-limiting enzyme of the mevalonate (MEV) cascade. Statins are best known for their cholesterol (CH)-lowering effect. Long-term consumption of statins, prior to and in parallel with other cancer therapeutic approaches, has been reported to increase the survival rate of patients with various forms of cancers. In this study, we investigated the potentiation of TMZ-induced apoptosis by simvastatin (Simva) in human GBM cell lines and patient GBM cells, using cell monolayers and three-dimensional cell culture systems.

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Papers by Saeid Ghavami

Association between single nucleotide polymorphisms in the PI3K/AKT/mTOR pathway and bladder cancer risk in a sample of Iranian population

PubMed, 2018

In the past few years several investigations have focused on the role of PI3K/AKT/mTOR pathway an... more In the past few years several investigations have focused on the role of PI3K/AKT/mTOR pathway and its deregulations in different cancers. This study aimed to examine genetic polymorphisms of this pathway in bladder cancer (BC). In this case-control study, 235 patients with pathologically confirmed bladder cancer and 254 control subjects were examined. PIK3CA, AKT1 and mTOR variants were analyzed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The findings proposed that the PIK3CA rs6443624 SNP significantly decreased the risk of BC (OR=0.44, 95 % CI=0.30-0.65, p<0.0001 CA vs CC; OR=0.35, 95 % CI=0.16-0.78, p=0.0107, AA vs CC; OR=0.60, 95 % CI=0.46-0.79, p=0.0002, A vs T). The AKT1 rs2498801 variant is associated with a decreased risk of BC (OR=0.57, 95 % CI=0.39-0.82, p=0.003, AG vs AA; OR=0.74, 95 % CI=0.56-0.97, p=0.032, G vs A) while, AKT1 rs1130233 polymorphism considerably increased the risk of BC (OR=3.70, 95 % CI=2.52-5.43, p<0.0001, GA vs GG; OR=5.81, 95 % CI=1.53-21.97, p=0.010, AA vs GG; OR=2.71, 95 % CI=1.98-3.70, p<0.0001, A vs G). Additionally, mTOR rs2295080 variant notably increased the risk of BC (OR=2.25, 95 % CI=1.50-3.38, p<0.0001, GT vs GG; OR=4.75, 95 % CI=2.80-8.06, p<0.0001, TT vs GG; OR=3.10, 95 % CI=2.34-4.10, p<0.0001, T vs G). None of the other examined polymorphisms (AKT1 rs1130214, AKT1 rs3730358, mTOR rs1883965) revealed significant association with BC. In conclusion, our findings suggest that PIK3CA rs6443624, AKT1 rs2498801, AKT1 rs1130233, as well mTOR rs2295080 polymorphism may be related to bladder cancer development in a sample of Iranian population. Validation of our findings in larger sample sizes of different ethnicities would provide evidence on the role of variants of PI3K/AKT/mTOR pathway in developing BC.

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