ALDOA Expression in Bladder Urothelial Carcinoma

Overview

1. Study the immunohistochemical expression of ALDOA in bladder urothelial cancer. 2. Correlate between ALDOA expression in specimens and different cilnicopathological factors. 3. Correlate between ALDOA expression and urothelial cancer prognosis and survival.

Bladder cancer is the 7th most prevalent malignancy and the 13th cause of cancer related death worldwide1. In Egypt, it's the third most common tumor2. The most common histologic subtype of bladder cancer is urothelial carcinoma3. Bladder cancer is divided according to absence or presence of muscle invasion into non-muscle invasive bladder cancer and muscle invasive bladder cancer 3. Despite the advance in diagnosis and development of therapeutic options of urothelial cancer, the recurrence and progression rate remains high4. The conventional histopathological evaluation of urothelial cancer is vital for diagnosis and prediction of patient's prognosis. However, it doesn't fully reflect the biological behavior of the tumor or the clinical outcome of the patient5. Under hypoxic conditions, cancer cells produce ATP by glycolysis, which provide energy for tumor proliferation and dissemination6,7. Glycolytic enzymes are abnormally activated in cancer cells8,9. Thus, several studies have identified glycolytic enzymes or related metabolic pathways as potential drug targets. One of the typical glycolytic enzymes is Aldolase A (ALDOA) 6 which is the most abundant glycolytic enzyme detected in tumors10. Several studies have identified ALDOA as an oncogene in different types of malignancy 6,8,10-12. The oncogenic potential of ALDOA contributed to its ability to stimulate DNA synthesis and accelerate S phase in tumor cell cycle6-8. In addition, studies have shown that ALDOA promotes tumor cell invasion by negative regulation of E-cadherin and by activation of MAPK, AKT and EGFR signaling pathways7,11,13. Thus, increased expression of ALDOA in tumor predicts a bad prognosis and poor survival of patients13-15.

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Central Contacts