الفهرس 
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Abstract
Introduction:
Breast cancer (BC) is the most common malignancy among women worldwide and is one of the major contributors to the global death burden. Therefore, it is critical to discover prognostic factors as well as therapeutic target for breast cancer.There is increasing evidence suggests that the existence of a small population of specialized cancer cells that display stem-cell properties, commonly referred to as cancer stem cells (CSCs) or cancer initiating cells.
DCLK1 is a cancer stem cell marker over expressed in many cancers.Studies showed that DCLK1 expression is critical for cancer growth, epithelial to mesenchymal transition (EMT), metastasis, and cancer cell self-renewal.Epithelial to mesenchymal transition is the loss of epithelial differentiation and gain the mesenchymal phenotype.Epithelial-mesenchymal transition has been considered to be one of the critical steps involved in cancer metastasis.
Core elements of EMT include reduction of cell–cell adherence via the transcriptional repression of cadherins, and functional loss of E-Cadherin is a well-known hallmark of EMT. Expression of epithelial intermediate filaments is typically reduced and the equivalent mesenchymal filament protein vimentin increased.EMT can be triggered by a diverse set of stimuli that includes growth factor signaling. The most classical experimental model is the induction of EMT by transforming growth factor-beta (TGF-β) in epithelial cell culture. Recently, it has also been reported that TGF-β can induce the CSC phenotype and cause EMT in vitro.
Aim of the Work
The aim of the present study was to detect the level of DCLK1 in breast cancer and to study its role in tumorigensis of breast cancer through its possible association with clinicopathological features and other biochemical parameters (E-cadherin, vimentin and transforming growth factor-beta)as well as the relationship with breast cancer output.
Subjects and Methods:
100 female patientswere divided into two groups:
group I: Included 40 apparently normal healthy female volunteers clinically free from any diseases, and served as control group.
group II: Included 60 females of matched age, menstrual state and socisaconomic status as the previous group having breast carcinoma of clinical stage II- III.
Tumor tissue and adjacent normal breast tissue were collected from patients with breast cancer. A single venous blood sample (5ml) was collected concurrently from breast cancer patients (Before surgery) and from the control group. Tissue expression of Doublecortin-like kinase 1, E-cadherin and vimentin were evaluated in breast carcinoma tissue and adjacent normal breast tissue by real-time reverse transcription polymerase chain reaction (RT-PCR). Serum level of TGF-β was assayed by enzyme linked-immunossorbant assay.