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Peer-reviewedCC BY-NC 4.0Asian Pacific Journal of Cancer Prevention : APJCP

Gene Expression Alterations of TIMP3, ELASTIN, K-RAS, and BRAF in Colorectal Cancer Patients with H. pylori Infection

  • Ayat Majeed Zeadan1,2
  • Tarek A.A. Mousaa1
  • Ahmed Rushdi Abdullah2
  1. 1Botany and Microbiology Department, Faculty of science, Cairo University, Egypt.
  2. 2Microbiology Department, Collage of Medicine, Al-Iraqia University, Iraq.
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Abstract

Objective:: Colorectal cancer (CRC) is the third most common malignancy and the second leading cause of cancer-related mortality worldwide, with over 1.9 million new cases and 0.9 million deaths reported in 2020. The role of Helicobacter pylori infection in CRC pathogenesis remains a significant area of research. This study aimed to investigate the association between H. pylori infection, and genetic alterations in CRC patients.

Methods:: A total of 110 blood and tissue biopsy samples were collected from CRC patients at Ghazi AL-Hariri Specialized Surgery Hospital in Baghdad, Iraq, between November 2023 and August 2024. An additional 36 samples from non-cancer patients were used as controls. Enzyme-linked immunosorbent assay (ELISA) was employed to detect H. pylori-specific immunoglobulins (IgG). Gene expression analysis of ELASTIN, TIMP3, K-RAS, and BRAF was performed using RT-qPCR.

Results:: The study found that H. pylori infection was present in 79.5% of CRC patients, with significant IgG seropositivity (p < 0.05). Gene expression analysis revealed a significant downregulation of TIMP3 and alterations in ELASTIN, K-RAS, and BRAF (p < 0.01).

Conclusion:: In conclusion, chronic H. pylori infection may contribute to CRC pathogenesis through sustained inflammation and genetic dysregulation. The study highlights TIMP3 suppression as a potential factor in CRC progression, warranting further investigation into its clinical implications.

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Cite

BibTeXRIS
BibTeX
@article{zeadan2026gene,
  title = {{Gene Expression Alterations of TIMP3, ELASTIN, K-RAS, and BRAF in Colorectal Cancer Patients with H. pylori Infection}},
  author = {Ayat Majeed Zeadan and Tarek A.A. Mousaa and Ahmed Rushdi Abdullah},
  journal = {Asian Pacific Journal of Cancer Prevention : APJCP},
  year = {2026},
  month = jun,
  doi = {10.31557/apjcp.2026.27.6.2287},
  url = {https://doi.org/10.31557/apjcp.2026.27.6.2287},
  note = {CC BY-NC 4.0},
}
RIS
TY  - JOUR
TI  - Gene Expression Alterations of TIMP3, ELASTIN, K-RAS, and BRAF in Colorectal Cancer Patients with H. pylori Infection
AU  - Ayat Majeed Zeadan
AU  - Tarek A.A. Mousaa
AU  - Ahmed Rushdi Abdullah
PY  - 2026
DA  - 2026/06/22
JO  - Asian Pacific Journal of Cancer Prevention : APJCP
DO  - 10.31557/apjcp.2026.27.6.2287
UR  - https://doi.org/10.31557/apjcp.2026.27.6.2287
AB  - Objective:: Colorectal cancer (CRC) is the third most common malignancy and the second leading cause of cancer-related mortality worldwide, with over 1.9 million new cases and 0.9 million deaths reported in 2020. The role of Helicobacter pylori infection in CRC pathogenesis remains a significant area of research. This study aimed to investigate the association between H. pylori infection, and genetic alterations in CRC patients.  Methods:: A total of 110 blood and tissue biopsy samples were collected from CRC patients at Ghazi AL-Hariri Specialized Surgery Hospital in Baghdad, Iraq, between November 2023 and August 2024. An additional 36 samples from non-cancer patients were used as controls. Enzyme-linked immunosorbent assay (ELISA) was employed to detect H. pylori-specific immunoglobulins (IgG). Gene expression analysis of ELASTIN, TIMP3, K-RAS, and BRAF was performed using RT-qPCR.  Results:: The study found that H. pylori infection was present in 79.5% of CRC patients, with significant IgG seropositivity (p < 0.05). Gene expression analysis revealed a significant downregulation of TIMP3 and alterations in ELASTIN, K-RAS, and BRAF (p < 0.01).  Conclusion:: In conclusion, chronic H. pylori infection may contribute to CRC pathogenesis through sustained inflammation and genetic dysregulation. The study highlights TIMP3 suppression as a potential factor in CRC progression, warranting further investigation into its clinical implications.
SN  - 1513-7368
SN  - 2476-762X
ER  -