The neoplastic changes in the urothelium Selleckchem EPZ015666 of bladder is a multistep phenomenon [2]. The exact genetic events leading to urothelial transformation involve the activation of oncogenes, inactivation or loss of tumor suppressor genes, and alterations in the apoptotic

gene products [3]. One of the conditions leads to bladder cancer in Africa, the Middle East, and Asia is schistosomiasis [4, 5]. S. haematobium is the most predominant species in the Middle East, Asia, and Africa and the most implicated in the schistosomal bladder tumors (SBT) in these regions [6, 7]. C-myc is implicated in bladder cancer, the genetic mechanism causing overexpression of the c-myc gene in bladder cancer is unknown. It could be related to hypomethylation [8] and its overexpression has been TGF-beta/Smad inhibitor shown to be associated with high-grade bladder cancer [9]. Another oncogene implicated in bladder cancer, namely epidermal growth factor receptor (EGFR). Overexpression of EGFR has been described in several solid tumors including bladder, breast, colorectal, prostate, and ovarian cancers [10]. And 70% of muscle-invasive bladder cancers express EGFR, which is associated with poor prognosis [11]. The majority of aggressive and invasive bladder carcinomas have alterations in the tumor suppressor genes products such as retinoblastoma (Rb) [12]. A study revealed that tumor

expression of Rb proteins in locally advanced bladder cancers was found abnormal [13]. Another tumor suppressor protein, p53, plays a vital role in the regulation of cell cycle. The defective p53 in human cancer leads to the loss of p53-dependent apoptosis, proliferative advantage, genomic instability and DNA repair and angiogenic control loss [14]. Mutations in the p53 gene result in the production of dysfunctional protein product with a prolonged half-life compared to the wild-type protein [14]. On the other hand, p16, which is a tumor suppressor protein,

was found almost abnormal in the advanced bladder cancers where it was severely lowered and impaired in function. [12]. Overexpression of bcl-2 has been reported in a wide variety of cancers including prostate, colorectal, lung, renal, bladder and leukemia [15]. Vildagliptin Several studies have provided conclusive evidence that elevations in bcl-2 expression cause resistance to chemotherapy and radiotherapy and increases the proliferation [16]. On the other hand, Ki 67 is used to evaluate the proliferative potential of any tumor as it is one of the important markers for cell proliferation [17]. There was no previous study explored the profiling of molecular markers in SBT and NSBT with respect to tumor suppressor proteins: p53, Rb, and p16, oncogenes: c-myc, and EGFR, an antiapoptotic protein: bcl-2, and a proliferative protein, ki-67 together in one study.