br References br Behrouz Sharif S Hashemzadeh
2. Behrouz Sharif S, Hashemzadeh S, Mousavi Ardehaie R, et al. Detection of aberrant methylated SEPT9 and NTRK3 genes in sporadic colorectal cancer patients as a potential diagnostic biomarker. Oncol Lett. 2016;12:5335–5343.
3. Ushijima T. Detection and interpretation of altered methylation patterns in cancer cells. Nat Rev Cancer. 2005;5:223.
4. Mousavi Ardehaie R, Hashemzadeh S, Behrouz Sharif S, Ghojazadeh M, Teimoori-Toolabi L, Sakhinia E. Aberrant methylated EDNRB can act as a potential diagnostic biomarker in sporadic colorectal cancer while KISS1 is con-troversial. Bioengineered. 2017:1–10.
10. Chowdhury I, Tharakan B, Bhat GK. Current concepts in apoptosis: the physiological suicide program revisited. Cell Mol Biol Lett. 2006;11:506.
12. Gao J, Li N, Dong Y, et al. miR-34a-5p suppresses colorectal cancer metastasis and predicts recurrence in patients with stage II/III colorectal cancer. Oncogene. 2015;34:4142.
13. Fedorova M, Kudryavtseva A, Lakunina V, et al. Downregulation of OGDHL expression is associated with promoter hypermethylation in colorectal cancer. Mol Biol. 2015;49:608–617.
14. Ng EK, Leung CP, Shin VY, et al. Quantitative analysis and diagnostic significance of methylated SLC19A3 DNA in the plasma of breast and gastric cancer patients. PLoS One. 2011;6:e22233.
17. Bunik VI, Degtyarev D. Structure–function relationships in the 2-oxo Concanamycin A dehydrogenase family: substrate-specific
signatures and functional predictions for the 2-oxoglutarate dehydrogenase-like proteins. Proteins: Struct Funct Bioinf. 2008;71:874–890.
Please cite this article as: M. Khalaj-kondori, M. Hosseinnejad and A. Hosseinzadeh et al., Aberrant hypermethyla-tion of OGDHL gene promoter in sporadic colorectal cancer, Current Problems in Cancer, https://doi.org/10.1016/j. currproblcancer.2019.03.001 Advances in Biological Regulation 71 (2019) 172–182
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Advances in Biological Regulation
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Abilities of berberine and chemically modified berberines to inhibit
T proliferation of pancreatic cancer cells
Stephen L. Abramsa, Matilde Y. Follob,∗∗, Linda S. Steelmana, Kvin Lertpiriyapongc,d, Lucio Coccob, Stefano Rattib, Alberto M. Martellib, Saverio Candidoe, Massimo Librae, Ramiro M. Murataa,f, Pedro L. Rosaleng, Giuseppe Montaltoh,i, Melchiorre Cervelloi, Agnieszka Gizakj, Dariusz Rakusj, Weifeng Maok, Paolo Lombardil,
James A. McCubreya,∗ a Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC, 27858, USA
b Dipartimento di Scienze Biomediche e Neuromotorie, Università di Bologna, Bologna, Italy
c Department of Comparative Medicine, Brody School of Medicine at East Carolina University, USA
d Center of Comparative Medicine and Pathology, Memorial Sloan-Kettering Cancer Center, Weill Cornell Medicine and the protozoa Hospital for Special Surgery, New York City, NY, USA
e Department of Biomedical and Biotechnological Sciences – Oncological, Clinical and General Pathology Section, University of Catania, Catania, Italy
f Department of Foundational Sciences, School of Dental Medicine, East Carolina University, USA
g Department of Physiological Sciences, Piracicaba Dental School, State University of Campinas, Piracicaba, Brazil
h Biomedical Department of Internal Medicine and Specialties, University of Palermo, Palermo, Italy
i Consiglio Nazionale delle Ricerche, Istituto di Biomedicina e Immunologia Molecolare “Alberto Monroy”, Palermo, Italy
j Department of Molecular Physiology and Neurobiology, Wroclaw University, Wroclaw, Poland
k College of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning, China
l Naxospharma, Via Giuseppe di Vittorio 70, Novate Milanese, 20026, Italy