Bladder cancer is one of the most prevalent genitourinary cancers responsible for about 150,000 deaths per year worldwide. Currently, several treatments, such as endoscopic and open surgery, appended by local or systemic immunotherapy, chemotherapy, and radiotherapy are used to treat this malignancy. However, the differences in treatment outcome among patients suffering from bladder cancer are considered as one of the important challenges. In recent years, cancer stem cells, representing a population of undifferentiated cells with stem-cell like properties, have been eyed as a major culprit for the high recurrence rate in superficial papillary bladder cancer.Cancer stem cells have been reported to be resistant to conventional treatments, such as chemotherapy, radiation, and immunotherapy, which induce selective pressure on tumoral populations resulting in selection and growth of the resistant cells. Therefore, targeting the therapeutic aspects of cancer stem cells in bladder cancer may be promising.In this study, we briefly discuss the biology of bladder cancer and then address the possible relationship between molecular biology of bladder cancer and cancer stem cells. Subsequently, the mechanisms of resistance applied by cancer stem cells against the conventional therapeutic tools, especially chemotherapy, are discussed.Moreover, by emphasizing the biomarkers described for cancer stem cells in bladder cancer, we have provided, described, and proposed targets on cancer stem cells for therapeutic interventions and, finally, reviewed some immunotargeting strategies against bladder cancer stem cells.cancer stem cells, drug resistance, immunotherapy, transitional cell carcinoma, urinary bladder neoplasms a higher rate of recurrence was associated with variants in the aldehyde dehydrogenase (ALDH2) enzyme (Andrew et al., 2015). Also, CD44 polymorphisms may have a crucial role in the development of bladder cancer and may have a clinical significance as molecular prognostic markers. Indeed, current evidence indicates that

The presence of inflammatory cells and their products in the tumor microenvironment plays a crucial role in the pathogenesis of a tumor. Releasing the cytokines from a host in response to infection and inflammation can inhibit tumor growth and progression. However, tumor cells can also respond to the host cytokines with increasing the growth/invasion/metastasis. Bladder cancer (BC) is one of the most common cancers in the world. The microenvironment of a bladder tumor has been indicated to be rich in growth factors/inflammatory cytokines that can induce the tumor growth/progression and also suppress the immune system. On the contrary, modulate of the cancer progression has been shown following upregulation of the cytokines‐related pathways that suggested the cytokines as potential therapeutic targets. In this study, we provide a summary of cytokines that are involved in BC formation/regression with both inflammatory and anti‐inflammatory properties. A more accurate understanding of tumor microenvironment creates favorable conditions for cytokines targeting to treat BC.

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Background: Several studies have shown association of fatty acids with type 2 diabetes (T2D), as well as metformin effects on blood glucose concentrations through affecting lipid metabolism. Objectives: Since the exact therapeutic mechanism of metformin is not clear, in this study we investigated effects of different doses of metformin on serum fatty acids in rats with T2D. Materials and Methods: Twenty-five adult albino male Wistar rats were divided into the following groups: Healthy, untreated T2D, and T2D rats receiving metformin for 4 weeks with doses of 100, 150, and 200 mg/kg/d. Serum insulin and triglyceride (TG) were measured using commercial kits. Serum total lipids were extracted by the Bligh-Dyer method and then compositions of fatty acids were evaluated using gas chromatograph. Results: Monounsaturated fatty acid (MUFA) levels in T2D rats were lower than those in healthy rats (P < 0.05). We also observed that diabetic rats treated with 100 or 150 mg/kg/d of metformin had higher levels of arachidonic acid and polyunsaturated fatty acids (PUFA) in comparison with the healthy group (P < 0.05). Moreover, the T2D+Met (150 mg/kg) group showed increased levels of MUFA compared with the T2D group. Such a difference was seen in levels of arachidonic acid between the T2D+Met 100 mg/ kg group and untreated T2D group. In the group treated with high doses of metformin (200 mg/kg/d), levels of palmitic acid, palmitoleic acid, and saturated fatty acid (SFA) were higher and levels of oleic acid, linoleic acid, arachidonic acid, MUFA, PUFA, and also SFA/UFA ratio were lower compared with other metformin treated and untreated groups (P < .05). In untreated T2D group, there were positive correlations between glucose levels and linoleic acid and PUFA levels (r = 0.707, P = .049 and r = 0.726, P = .041 respectively). Arachidonic acid levels were positively correlated with glucose levels in T2D rats treated with 100 mg/kg/d of metformin (r = 0.969, P = .031). Conclusions: Our study showed that different doses of metformin could have different effects on serum levels of saturated and unsaturated fatty acids, as 200 mg/kg/d of metformin could increase and decrease saturated and unsaturated fatty acids respectively, while lower doses increased unsaturated fatty acids, particularly arachidonic acid.