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1.
Eur Rev Med Pharmacol Sci ; 26(4): 1328-1340, 2022 Feb.
Article in English | MEDLINE | ID: mdl-35253189

ABSTRACT

OBJECTIVE: In this study, we aimed to evaluate the effect of tumor size and tumor sidedness on prognosis in patients with stage 2 colon cancer. PATIENTS AND METHODS: Data of 501 patients diagnosed with stage 2 colon cancer were evaluated retrospectively. It was evaluated whether the patients' age, gender, tumor differentiation, tumor node metastasis (TNM) stage, overall survival rate, and disease-free survival rate had any correlation with horizontal tumor diameter and tumor sidedness. In the ROC analysis performed to determine the cut-off value for the tumor diameter, which we think will predict survival, no significant results were obtained with maximum sensitivity and specificity. Therefore, the median value of the tumor diameter, which is 5 cm, was accepted as the cut-off value.  Kaplan-Meier method and Cox regression analysis were used for survival analysis and determination of prognostic factors. RESULTS: When the patients were evaluated in terms of tumor localization, 189 (37.7%) patients had right colon tumors and 312 (62.3%) patients had left colon tumors. There was no statistically significant difference in terms of disease-free survival and overall survival according to tumor localization. When the patients were analyzed by dividing them into two groups according to the horizontal tumor size (<5 cm and ≥5 cm), no statistically significant difference was found between the groups in terms of disease-free survival (DFS) and overall survival (OS) p=0.085, p=0.699, respectively. CONCLUSIONS: Our results suggest that the management of patients with stage 2 colon cancer requires a better understanding of tumor biology rather than features such as tumor size and localization.


Subject(s)
Colonic Neoplasms , Colonic Neoplasms/diagnosis , Colonic Neoplasms/pathology , Humans , Neoplasm Staging , Prognosis , Retrospective Studies , Survival Analysis
2.
J BUON ; 18(3): 619-22, 2013.
Article in English | MEDLINE | ID: mdl-24065473

ABSTRACT

PURPOSE: Hormone receptor (HR) status is a prognostic factor in women with breast cancer and differs among different ethnic groups. HR status among Turkish, Kurdish and Arabic women with breast cancer living in Turkey is unknown and in this study we investigated the relationship between HR and HER2 status and race. METHODS: FA total of 648 women with breast cancer (Turkish 438, Kurdish 174, Arabic 35 and Armenian 1) living in southeastern Turkey and referred to the Department of Radiation Oncology between July 2006-July 2012 were included in the study. Patients were categorized into 4 groups according to their HR status. Estrogen receptor (ER) and progesterone receptor (PR) positive (ER+/PR+), ER positive and PR negative (ER+/PR-), ER negative and PR positive (ER-/PR+) and ER and PR negative (ER-/PR-). Human epidermal growth factor receptor 2 (HER2) status was recorded immunohistochemically (IHC) as negative (0 and 1+), and positive (3+). Statistical analysis included ER, PR, HER2, triple subtypes (combination of ER, PR and HER2), and race. RESULTS: The median age at diagnosis was 48 years (range 20-83). ER+, PR+ and HER2+ patients were 453 (70%), 470 (72.6%) and 206 (32.1%), respectively. ER+/PR+ rates among Turkish and Arabic patients were similar, but were higher than Kurdish patients (p<0.002). Triple-negative (ER-/PR-/HER2-) rates among Kurdish and Arabic patients were similar, but were higher than Turkish patients (p=0.04). CONCLUSION: Turkish, Kurdish and Arabic women with breast cancer in southeastern Turkey differed by HR status. Compared to Turkish and Arabic patients, Kurdish patients had more unfavorable prognostic factors.


Subject(s)
Biomarkers, Tumor/metabolism , Breast Neoplasms/ethnology , Racial Groups/statistics & numerical data , Receptor, ErbB-2/metabolism , Receptors, Estrogen/metabolism , Receptors, Progesterone/metabolism , Adult , Aged , Aged, 80 and over , Arabia , Armenia , Breast Neoplasms/metabolism , Breast Neoplasms/pathology , Carcinoma, Ductal, Breast/ethnology , Carcinoma, Ductal, Breast/metabolism , Carcinoma, Ductal, Breast/pathology , Carcinoma, Lobular/ethnology , Carcinoma, Lobular/metabolism , Carcinoma, Lobular/pathology , Female , Follow-Up Studies , Humans , Immunoenzyme Techniques , Middle Aged , Neoplasm Grading , Neoplasm Staging , Prognosis , Survival Rate , Turkey , Young Adult
3.
Oncogene ; 32(47): 5409-20, 2013 Nov 21.
Article in English | MEDLINE | ID: mdl-23524585

ABSTRACT

Glioblastoma multiforme (GBM) is an aggressive brain malignancy characterized by high heterogeneity and invasiveness. It is increasingly accepted that the refractory feature of GBM to current therapies stems from the existence of few tumorigenic cells that sustain tumor growth and spreading, the so-called glioma-initiating cells (GICs). Previous studies showed that cytokines of the bone morphogenetic protein (BMP) family induce differentiation of the GICs, and thus act as tumor suppressors. Molecular pathways that explain this behavior of BMP cytokines remain largely elusive. Here, we show that BMP signaling induces Smad-dependent expression of the transcriptional regulator Snail in a rapid and sustained manner. Consistent with its already established promigratory function in other cell types, we report that Snail silencing decreases GBM cell migration. Consequently, overexpression of Snail increases GBM invasiveness in a mouse xenograft model. Surprisingly, we found that Snail depletes the GBM capacity to form gliomaspheres in vitro and to grow tumors in vivo, both of which are important features shared by GICs. Thus Snail, acting downstream of BMP signaling, dissociates the invasive capacity of GBM cells from their tumorigenic potential.


Subject(s)
Brain Neoplasms/pathology , Glioblastoma/pathology , Transcription Factors/metabolism , Animals , Bone Morphogenetic Proteins/metabolism , Brain Neoplasms/genetics , Brain Neoplasms/metabolism , Cell Differentiation/genetics , Cell Line, Tumor , Cell Movement/genetics , Cell Proliferation , Gene Expression Regulation, Neoplastic , Glioblastoma/genetics , Glioblastoma/metabolism , Humans , Mice , Neoplastic Stem Cells/metabolism , RNA Interference , RNA, Small Interfering , Signal Transduction/genetics , Smad1 Protein/genetics , Smad2 Protein/genetics , Smad3 Protein/genetics , Smad4 Protein/genetics , Smad5 Protein/genetics , Snail Family Transcription Factors , Transcription Factors/genetics
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