دکتر صادق ولیان بروجنی

استاد

گروه زیست‌شناسی سلولی مولکولی و میکروبیولوژی
دانشکده علوم و فناوری‌های زیستی

پست الکترونیکی

svallian@sci.ui.ac.ir

تلفن

03136245219

آدرس

دانشگاه اصفهان میدان آزادی اصفهان، ایران
کد پستی : 8174673441

2009

2025

فعالیت های پژوهشی بر اساس سال

معرفی کلی

درباره من

دکتر صادق ولیان بروجنی کارشناسی خود را در رشته ژنتیک از دانشگاه جندی شاپور اهواز (شهید چمران) و کارشناسی ارشد را در رشته بیوشیمی بالینی از دانشگاه علوم پزشکی اهواز دریافت نمودند. سپس تحصیلات خود را در سطح دکتری در دانشگاه لندن انگلستان دانشکده پزشکی و دندان پزشکی (کالج سلطنتی) در رشته پزشکی مولکولی به اتمام رساندند. سپس دوره فلوشیپ پسا دکتری خود را در دپارتمان پزشکی آزمایشگاهی مرکز سرطان شناسی ام دی اندرسن دانشگاه تگزاس امریکا گذراندند. نامبرده از سال 1379 در دانشگاه اصفهان به عنوان عضو هیات علمی مشغول به کار است. در سال 1390 به درجه استاد تمام نائل شده و هم اکنون در بخش ژنتیک گروه زیست شناسی سلولی مولکولی این دانشگاه مشغول به تدریس و پژوهش می باشند. محور تحقیقاتی نامبرده عبارت است از: مطالعه مولکولی و تشخیص بیماری های ژنتیک و سرطان بویژه الف) مطالعه و شناسایی مارکرهای مرتبط با مقاومت دارویی در سرطان های خون و پستان ب) جهش های مرتبط با بیماریهای ژنتیک در جمعیت ایران

علاقه مندی پژوهشی

محور تحقیقاتی دکتر ولیان عبارت است از: مطالعه مولکولی و تشخیص بیماری های ژنتیک و سرطان بویژه الف) مطالعه و شناسایی مارکرهای مرتبط با مقاومت دارویی در سرطان های خون و پستان ب) جهش های مرتبط با بیماریهای ژنتیک در جمعیت ایران

برونداد‌های پژوهشی

همه موارد

مقالات

1996

2026

مقالات لاتین

2026

Noncoding RNAs and DNA methylation as epigenetic modulators of breast cancer: mechanisms and clinical perspectives in the Iranian population, a systematic review

( Article . Gold • Green )

Mashayekh, Z., Fard, R.F., Vallian borujeni, S.

Publication Date: 2026

Bmc Cancer (14712407)26(1)

2025

Bi-Allelic Variants in MICU1 Cause Myopathy With Extrapyramidal Signs: Case Series, Phenotypic Spectrum, and Genotype–Phenotype Correlations From 61 Patients

( Article )

Beheshti, P., Akbarian, F., Esmaeilzadeh, E., Galehdari, H., Khorrami, M., Vallian borujeni, S., Abdi, A., Güngör, Ö., Tuncel, R., Aykut, A.

Publication Date: 2025

Clinical Genetics (00099163)

Dissecting lncRNA-mRNA regulatory network in type 2 diabetes as the risk factor of pancreatic cancer

( Article . Green • Gold )

Nilchi, A.N., Dehghanian, F., Vallian borujeni, S., Bahreini, A.

Publication Date: 2025

Scientific Reports (20452322)15(1)

Emerging evidence supports the role of type 2 diabetes (T2D) mellitus as a risk factor for cancer progression. In this study, we investigated and identified biomarkers related to diabetes and pancreatic ductal adenocarcinoma (PDAC) using systems biology to understand better the molecular landscape of PDAC and its connections with T2D. RNA-seq data related to blood samples of diabetes and pancreatic cancer were analyzed using bioinformatics tools in the Galaxy platform. After differential expression analysis using the DESeq2, the co-expression network associated with T2D and PDAC data was reconstructed using the WGCNA. Then, by visualizing the protein-protein interaction network in modules specifically related to T2D and PDAC, the key genes involved in these two diseases were identified, and their interaction network with long non-coding RNAs was reconstructed. Finally, the results of bioinformatics analysis were verified by qPCR in four groups, including T2D, PDAC, PDAC-T2D, and control groups. In this study, 1905 and 18,558 genes with significant differential expression were identified in the data of T2D and PDAC, respectively (|logFC| > 0.58, adj. p value < 0.05). The WGCNA showed 32 and 20 co-expression modules in diabetes and pancreatic cancer data, respectively. Among these, 303 genes were co-expressed, related to diabetes and pancreatic cancer. Based on the protein-protein interaction pattern, five hub genes were identified (using the CytoHubba Cytoscape plugin and the Maximal Clique Centrality (MCC) parameter). Finally, the co-expression network was reconstructed between these five genes and other lncRNAs. The qPCR showed that the expression of the CEBPZ gene was significantly increased in the blood samples of the diabetic (log2FC = 1.163, adj. p value = 0.0006), pancreatic cancer (log2FC = 3.22, adj. p value < 0.0001), and pancreatic cancer-diabetic (log2FC = 2.73, adj. p value < 0.0001) groups compared to the control group. For the first time, this study suggested that CEBPZ expression may serve as a diagnostic biomarker for assessing PDAC in individuals with T2D, given its differential expression in this specific cohort. © The Author(s) 2025.

Molecular signatures of breast cancer in the Iranian population: a review of cell growth and cell cycle regulators

( Article . Green • Gold )

Mashayekh, Z., Broojeni, J.V., Fard, R.F., Vallian borujeni, S.

Publication Date: 2025

Journal Of Cancer Research And Clinical Oncology (01715216)151(9)

Mutations in the Key Autophagy Tethering Factor EPG5 Link Neurodevelopmental and Neurodegenerative Disorders Including Early-Onset Parkinsonism

( Article . Green • Hybrid Gold )

Vallian borujeni, S., Vallian borujeni, S., Dafsari, H.S., Deneubourg, C., Singh, K., Maroofian, R., Suprenant, Z., Kho, A.L., Ingham, N.J., Steel, K.P., Sheshadri, P., Baur, F.

Publication Date: 2025

Annals of Neurology (0364-5134)98(5)pp. 932-950

Objective: Autophagy is a fundamental biological pathway with vital roles in intracellular homeostasis. During autophagy, defective cargoes including mitochondria are targeted to lysosomes for clearance and recycling. Recessive truncating variants in the autophagy gene EPG5 have been associated with Vici syndrome, a severe early-onset neurodevelopmental disorder with extensive multisystem involvement. Here, we aimed to delineate the extended, age-dependent EPG5-related disease spectrum. Methods: We investigated clinical, radiological, and molecular features from the largest cohort of EPG5-related patients identified to date, complemented by experimental investigation of cellular and animal models of EPG5 defects. Results: Through worldwide collaboration, we identified 211 patients, 97 of them previously unpublished, with recessive EPG5 variants. The phenotypic spectrum ranged from antenatally lethal presentations to milder isolated neurodevelopmental disorders. A novel Epg5 knock-in mouse model of a recurrent EPG5 missense variant featured motor impairments and defective autophagy in brain areas particularly relevant for the neurological disorders in milder presentations. Novel age-dependent neurodegenerative manifestations in our cohort included adolescent-onset parkinsonism and dystonia with cognitive decline, and myoclonus. Radiological features suggested an emerging continuum with brain iron accumulation disorders. Patient fibroblasts showed defects in PINK1-Parkin-dependent mitophagic clearance and α-synuclein overexpression, indicating a cellular basis for the observed neurodegenerative phenotypes. In Caenorhabditis elegans, EPG5 knockdown caused motor impairments, defective mitophagic clearance, and changes in mitochondrial respiration comparable to observations in C. elegans knockdown of parkinsonism-related genes. Interpretation: Our findings illustrate a lifetime neurological disease continuum associated with pathogenic EPG5 variants, linking neurodevelopmental and neurodegenerative disorders through the common denominator of defective autophagy. ANN NEUROL 2025;98:932–950. © 2025 The Author(s). Annals of Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.