Mohammad Atefi
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Explore the profile of Mohammad Atefi including associated specialties, affiliations and a list of published articles.
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Articles
23
Citations
2686
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Recent Articles
1.
Movahedi M, Arianfar H, Atefi M, Tavakoli Golpaygani A, Gheisari F, Mahmoudi T
J Biomed Phys Eng
. 2024 Dec;
14(6):561-568.
PMID: 39726883
Background: Coronary heart disease the most prevalent form of cardiovascular disease, results from the blockage of blood flow through arteries. The Myocardial Perfusion Scan (MPS) is considered a non-invasive method...
2.
Movahedi M, Karimaghaei G, Noori A, Atefi M, Mahmoudi T, Gheisari F
Galen Med J
. 2023 Jan;
11:e2397.
PMID: 36698694
Despite the benefits of radioactive iodine (RAI) therapy as an adjunctive treatment for thyroid cancer, it can be associated with several side effects. The main purpose of this study was...
3.
Tsoi J, Robert L, Paraiso K, Galvan C, Sheu K, Lay J, et al.
Cancer Cell
. 2018 Apr;
33(5):890-904.e5.
PMID: 29657129
Malignant transformation can result in melanoma cells that resemble different stages of their embryonic development. Our gene expression analysis of human melanoma cell lines and patient tumors revealed that melanoma...
4.
Chung S, Wu Y, Okobi Q, Adekoya D, Atefi M, Clarke O, et al.
Mediators Inflamm
. 2017 Jul;
2017:5958429.
PMID: 28676732
There are increasing evidences of proinflammatory cytokine involvement in cancer development. Here, we found that two cytokines, IL-6 and TNF-, activated colorectal cancer cells to be more invasive and stem-like....
5.
Wu Y, Yu X, Yi X, Wu K, Dwabe S, Atefi M, et al.
Cancer Res
. 2017 Jan;
77(6):1383-1394.
PMID: 28115363
Obesity increases the risk of distant metastatic recurrence and reduces breast cancer survival. However, the mechanisms behind this pathology and identification of relevant therapeutic targets are poorly defined. Plasma free...
6.
Wu Y, Dong Y, Atefi M, Liu Y, Elshimali Y, Vadgama J
Mediators Inflamm
. 2017 Jan;
2016:6456018.
PMID: 28077918
Increasing body of evidence suggests that there exists a connection between diabetes and cancer. Nevertheless, to date, the potential reasons for this association are still poorly understood and currently there...
7.
Titz B, Lomova A, Le A, Hugo W, Kong X, Hoeve J, et al.
Cell Discov
. 2016 Sep;
2:16028.
PMID: 27648299
A prominent mechanism of acquired resistance to BRAF inhibitors in BRAF (V600) -mutant melanoma is associated with the upregulation of receptor tyrosine kinases. Evidences suggested that this resistance mechanism is...
8.
Escuin-Ordinas H, Li S, Xie M, Sun L, Hugo W, Huang R, et al.
Nat Commun
. 2016 Aug;
7:12348.
PMID: 27476449
BRAF inhibitors are highly effective therapies for the treatment of BRAF(V600)-mutated melanoma, with the main toxicity being a variety of hyperproliferative skin conditions due to paradoxical activation of the mitogen-activated...
9.
Atefi M, Titz B, Tsoi J, Avramis E, Le A, Ng C, et al.
Sci Rep
. 2016 Jun;
6:27454.
PMID: 27273450
Approximately 75% of melanomas have known driver oncogenic mutations in BRAF, NRAS, GNA11 or GNAQ, while the mutations providing constitutive oncogenic signaling in the remaining melanomas are not known. We...
10.
Atefi M, Titz B, Avramis E, Ng C, Wong D, Lassen A, et al.
Mol Cancer
. 2015 Feb;
14:27.
PMID: 25645078
Background: Approximately 20% of melanomas contain a mutation in NRAS. However no direct inhibitor of NRAS is available. One of the main signaling pathways downstream of NRAS is the MAPK...