Volume 16, Issue 3 (September 2024 2024)                   Iranian Journal of Blood and Cancer 2024, 16(3): 32-39 | Back to browse issues page

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Moonesi M, Mehdizade H, Zakakhosravi S, Molaei Ramshe S, Allahbakhshian M, Solali S et al . IGF Gene Family Expression: A Comparative Study in Acute Myeloid Leukemia (AML) and Healthy Bone Marrow. Iranian Journal of Blood and Cancer 2024; 16 (3) :32-39
URL: http://ijbc.ir/article-1-1619-en.html
1- Tabriz University of Medical Sciences, Tabriz, Iran.
2- Shahid Beheshti University of Medical Sciences, Tehran, Iran.
3- Tabriz University of Medical Sciences, Tabriz, Iran. , mfarshdoustihagh@gmail.com
Abstract:   (55 Views)
Background:  One of the most common types of leukemia is acute myeloid leukemia (AML). Intrinsic and extrinsic factors may lead to AML. Insulin-like growth factor (IGF) is a mitogenic intermediate from the liver that regulates growth and proliferation in response to GH. In this study, we examined the expression of IGF family genes in bone marrow of AML patients (M3 and Non-M3) and compared them with normal samples.
Methods: Forty bone marrow samples from recently diagnosed AML patients along with 15 samples from subjects without hematological malignancies were collected. For molecular tests, RNA extraction and cDNA synthesis were performed. Finally, IGF1, IGF2, IGFBP3, IGF1R, and IGF2R gene expression were examined by Real-Time PCR.
Results: IGF1, IGF1R, and IGFBP3 gene expression were significantly increased in patients with AML. In contrast, IGF2 and IGF2R genes did not show significant expression changes between the two groups.
Conclusion: The expression in this gene family soared in AML patients' bone marrow, compared to normal subjects. This can be caused by malignant cells in the bone marrow. These malignant cells express proteins that increase the number of malignant cells. Moreover, they can be considered as diagnostic biomarkers or therapeutic targets with further research.
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: Original Article | Subject: Adults Hematology & Oncology
Received: 2024/07/1 | Accepted: 2024/08/29 | Published: 2024/09/30

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