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Evaluation of Serum IL-7 as a Biomarker in Breast Cancer

Assiut University · 2025
ClinicalTrials.gov · Datasets · License: Public Domain · 2025
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breast-cancer
Breast cancer is one of the most commonly diagnosed cancers and leading cause of cancer-related mortality in women worldwide, posing a serious threat to their health (1). It is a heterogeneous disease, characterized by varying molecular subtypes such as hormone receptor-positive (HR+), human epidermal growth factor receptor 2 (HER2-positive), and triple-negative breast cancer (TNBC) (2). Breast cancer develops as a result of several internal and external factors (3-5). Poor lifestyle choices, environmental factors, and social-psychological factors are all linked to its occurrence. It has been demonstrated that 5% to 10% of breast cancers can be attributed to genetic mutations and family history, while 20% to 30% of breast cancers can be attributed to factors that may be modifiable (6). An early and accurate diagnosis is essential for effective treatment and improved patient survival. The human immune system plays a fundamental role in the defense against malignant diseases by recognizing and eliminating cancerous cells at the early stages of tumor development. Many research has been conducted on various cytokines to assess their role in the development of various tumors. IL-7 is an essential cytokine for the adaptive immune system, which is crucial for the development of B cells, the proliferation and survival of memory T cells and naive T cells, as well as the development of thymic T cells (7). IL-7 action is realized through two main signaling pathways: (Jak-Stat and PI3K-Akt) (8). Through these pathways, it has an impact on the development, survival, proliferation, differentiation and maturity of immune cells such as T-lymphocytes, B-lymphocytes, and natural killer cells (9). IL-7 has strong immunomodulatory act on tumor cells and exerts anti-tumor effects by enhancing tumor eradication or adoptive immunity (10). However, IL-7 may also facilitate tumor progression by activating the same downstream AKT pathways .
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