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The Association of cagA, vacA, babA2, babB and oipA of Helicobacter pylori with Risk of Gastric Carcinoma Development
Zainab H. Alsaadi, Nada Kadlim Hindi, Ali H. Al Marzoqi, Mojtaba Memariani, Maryam Kohansal , Abdolmajid Ghasemian,
Volume 12, Issue 4 (11-2022)
Abstract
Background & Objective: Helicobacter pylori (H. pylori), carried by more than half of the world population, is a major cause of chronic duodenal and gastric ulcers, gastritis and carcinoma. Colonization and toxin production include major virulence traits of H. pylori. The aim of this study was to assess the existence of H. pylori and virulence factors among patients with risk of gastrointestinal carcinoma (GC) in an Iraqi population.
Materials & Methods: During May 2016- October 2020 in Babylon, Iraq, a total of 500 biopsy samples were obtained from gastric tissue of patients with GC, gastritis, duodenitis, duodenal ulcer and gastric ulcer and cultured onto the Brucella agar. H. pylori isolates were identified using conventional biochemical and molecular tests. Molecular identification was conducted by amplification of glmM gene using the polymerase chain reaction (PCR) technique. The adhesin (babA2, babB and oipA) and toxin (cagA and vacA) genes were also amplified using PCR technique.
Results: Among 500 biopsy samples, 269 (110 from males and 159 from female patients) H. pylori isolates were identified. The age range of patients was 14-69 years (mean age=47.34±7.23). The babA2 and babB genes were detected in 59.47% and 59.10% of isolates, respectively. Notably, babA2 was observed in 89% of GC and 64% of DN strains being significantly more associated with GC and DN (<0.0001 and 0.028, respectively). Furthermore, babB-positive strains were significantly (0.042) more associated with PG. The rate of cagA and vacA was 44.60% and 48.32%, respectively. The cagA was detected in 64.73% of GC, and 100% of PG and DN strains with a significant association. We detected the oipA in 58.36% of strains which was significantly associated with GC (74%, P=0.0001), PG (88%, p<0.0001) and DN (84%, p<0.0001) as compared to oipA-negative strains.
Conclusion: The existence of H. pylori babA2, cagA and oipA virulence genes was associated with GC, DN and PG. As these genes play a crucial role in the development of gastric carcinoma, accurate control measure toward hindering the colonization of pathogenic strains is essential.

The Role of TP53 and Associated Pathways in Pancreatic Ductal Adenocarcinoma Progression
Mahdi Mokhtari Tabar, Mohammad Ghorbani, Abdolmajid Ghasemian,
Volume 15, Issue 1 (1-2025)
Abstract
The pancreas is an organ that conducts exocrine and endocrine activities in the body and plays an important role in digestive system and blood glucose regulation. Pancreatic cancer, particularly pancreatic ductal adenocarcinoma, is one of the most serious illnesses of this organ, killing many individuals each year due to the absence of an early detection method, making this cancer the third leading cause of death among malignancies. In up to 90% of cases, genetic abnormalities such as KRAS mutations and mutations in tumor suppressors such as CDKN2A, TP53, and SMAD4 can be detected, indicating the significance of additional studies in genetic diagnosis and therapy for this cancer. In this review, in addition to discovering information about the pancreas and its role in the body, an attempt has been made to determine the genetic origin of this malignancy. In addition, special consideration has been given to current therapeutic approaches and gene therapy-based therapies.
 

Cigarette Smoke-Induced Transcriptomic Alterations and Angiogenesis in Non-Small Cell Lung Cancer: An Integrative Analysis
Kianoush Mohammadi, Reza Safaralizadeh,
Volume 15, Issue 3 (6-2025)
Abstract

Background & Objectives: Cigarette smoke is a major risk factor for non-small cell lung cancer (NSCLC) and plays a pivotal role in tumor initiation and angiogenesis. This study aimed to elucidate the molecular mechanisms through which cigarette smoke influences angiogenesis in NSCLC by integrating transcriptomic data, with a particular emphasis on the regulatory role of microRNA-1 (miR-1) and its downstream targets.
Materials & Methods: We analyzed the Gene Expression Omnibus (GEO) dataset GSE290190, comprising gene expression profiles from 18 samples with different smoking statuses (9 normal and 9 tumor tissues). Differential expression analysis, Gene Set Enrichment Analysis (GSEA), Gene Ontology (GO) enrichment, and Protein–Protein Interaction (PPI) network analysis were conducted to identify critical genes and signaling pathways. Statistical analyses were employed to determine differentially expressed genes (DEGs) and to assess their biological relevance.
Results: Differential expression analysis identified 2,449 DEGs between normal and tumor tissues, with significant enrichment in angiogenesis, cell cycle regulation, and DNA repair pathways. Key angiogenesis-related genes—VEGFC, FGF2, and ANGPT1—were recognized as direct targets of miR-1. GSEA and GO analyses revealed marked alterations in biological processes such as chromosome segregation, mitotic nuclear division, and extracellular matrix organization. PPI network analysis identified E2F7, PLK1, and TOP2A as hub genes, suggesting their potential roles as key regulators in cell cycle progression and tumorigenesis.
Conclusion: This study highlights the transcriptomic heterogeneity of NSCLC and proposes miR-1 and its downstream targets—VEGFC, FGF2, and ANGPT1—as promising biomarkers and therapeutic targets. However, further validation using larger datasets and functional assays is essential to confirm these findings and facilitate their clinical translation.

 


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