Effect of Smoking on Outcomes of Urothelial Carcinoma: A Systematic Review of the Literature

Crivelli, Joseph J.; Xylinas, Évanguelos; Kluth, Luis A.; Rieken, Malte; Rink, Michael; Shariat, Shahrokh F.

doi:10.1016/j.eururo.2013.06.010

Cited by 167 publications

(106 citation statements)

References 46 publications

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“…Several recent retrospective studies reported that tumor progression and cancer-specific survival were significantly associated with the duration and intensity of cigarette smoking in patients with urothelial carcinoma (7,8,31). Rink and colleagues reported that cumulative smoking exposure based upon duration of smoking and quantity smoked was independently associated with worse prognosis in patients treated with radical cystectomy and that smoking cessation for more than 10 years mitigated the risk of tumor recurrence (32).…”

Section: Discussionmentioning

confidence: 99%

Nicotine Induces Tumor Growth and Chemoresistance through Activation of the PI3K/Akt/mTOR Pathway in Bladder Cancer

Yuge

Kikuchi

Yasumizu

et al. 2015

Molecular Cancer Therapeutics

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Continued smoking is highly associated with not only a higher incidence but also greater risk of tumor recurrence, progression, and acquired chemoresistance of urothelial carcinoma. We investigated whether nicotine affects urothelial carcinoma, and the detailed mechanism by which nicotine could induce tumor growth and any associated chemoresistance. Cell viability was evaluated in the human bladder cancer cell line T24 exposed to nicotine with or without cisplatin (CDDP) and NVP-BEZ235 as a PI3K/mTOR dual inhibitor by the WST-1 assay. Protein expression of the PI3K/Akt/mTOR pathway was investigated by Western blotting or immunohistochemical analysis. The influence of nicotine on tumor growth was also evaluated with or without CDDP and/or NVP-BEZ235 in a subcutaneous bladder tumor model. The result demonstrated that cell proliferation was increased in T24 cells after exposure to nicotine. Phospho-specific Akt (pAkt) and phospho-specific p70 S6 kinase (pS6) were significantly upregulated by nicotine exposure. Tumor growth in vivo was significantly induced by nicotine exposure in accordance with increased pS6 expression. Nicotine attenuated inhibition of T24 cell growth by CDDP and further upregulated pS6 expression in vitro and in vivo. NVP-BZE235 inhibited T24 cell proliferation and pAkt and pS6 expression induced after exposure to nicotine and/or CDDP. In conclusion, nicotine increases tumor growth and induces acquired chemoresistance through activation of the PI3K/Akt/mTOR pathway in bladder cancer.

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Section: Discussionmentioning

confidence: 99%

Nicotine Induces Tumor Growth and Chemoresistance through Activation of the PI3K/Akt/mTOR Pathway in Bladder Cancer

Yuge

Kikuchi

Yasumizu

et al. 2015

Molecular Cancer Therapeutics

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“…UC is associated with a number of risk factors, with tobacco smoking considered to be the most important (10,11). A previous study confirms that smoking exposure confers risk to the recurrence rate for smokers and non-smokers (12).…”

Section: Introductionmentioning

confidence: 92%

Prospective evaluation of fluorescence in situ hybridization for diagnosing urothelial carcinoma

Lin

Liu

et al. 2017

Oncology Letters

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Abstract. Urothelial carcinoma (UC) is the most common type of cancer of the bladder and upper urinary tract, and is characterized by a high risk of recurrence and progression. Urine fluorescence in situ hybridization (FISH) is a technique that detects genetic aberrations in exfoliated cells in the urine, with specific probes for chromosomes 3, 7 and 17 and the p16 gene. To evaluate the diagnostic value of FISH in UC, 119 patients from November 2010 to June 2012 with suspected UC were recruited into a prospective, cross-sectional study and were followed up for 12-30 months. These patients received voided urine cytology and FISH tests, and underwent cystoscopy and/or ureteroscopy as a reference standard. The final diagnoses confirmed 73 patients with UC, located in the bladder, upper urinary tracts or the two. The sensitivity of FISH for detecting UC was superior to cytology, irrespective of tumor grade and stage: Overall, 80.8 vs. 32.9% (P<0.001); low grade, 75.8 vs. 12.1% (P<0.001); high grade, 85 vs. 50% (P<0.005); non-muscle-invasive, 81.1 vs. 28.3% (P<0.001) and muscle-invasive, 80 vs. 45% (P<0.05), respectively. The specificities of the two tests were similar; overall, the specificity was 89.1% for cytology vs. 100% for FISH, and no significant difference was observed between the methods. Notably, FISH exhibited 100% sensitivity for cytologically non-diagnostic UC, but 33.3% specificity. In conclusion, FISH is a reliable and non-invasive diagnostic tool for bladder and upper urinary tract UC, particularly in patients with low-grade or early stage

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“…Several studies demonstrated that smoking intensity is a significant predictor for prognosis and survival in patients with UTUC (6,7). However, a recent review demonstrated that there is a lack of consensus regarding the association between smoking status and cancer outcome, including cancer recurrence, progression and survival, in UTUC patients following nephroureterectomy (9).…”

Section: Positive Expression Presence -------------------------------mentioning

confidence: 99%

“…The effect of smoking on the carcinogenesis, pathological characteristics and prognosis of UTUC has been reported and reviewed in earlier studies (5)(6)(7)(8)(9). Therefore, the main objective of this study was to elucidate the association between the smoking status of patients and the malignant aggressiveness of UTUC at the molecular level.…”

Section: Introductionmentioning

confidence: 97%

“…In addition to carcinogenesis, cigarette smoking plays an important role in cancer progression and the prognosis of patients with bladder cancer (2)(3)(4). Although a similar role for smoking has been reported in patients with upper tract (UT) UC, there are conflicting opinions regarding the pathological significance and prognostic role of smoking status in these patients (5)(6)(7)(8)(9). In addition, it was previously suggested that the changes in the malignant potential of UTUC induced by cigarette smoke were different from those in bladder cancer (4).…”

Section: Introductionmentioning

confidence: 99%

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Smoking-induced changes in cancer-related factors in patients with upper tract urothelial cancer

Miyata

Mitsunari

Asai

et al. 2014

Molecular and Clinical Oncology

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Abstract. Cigarette smoking is a major risk factor for urothelial cancer (UC) development. However, the associations between smoking and changes in the pathological characteristics and molecular expression of cancer-related molecules in upper tract (UT) UC have not been fully elucidated. We investigated the associations between smoking status and cancer-related factors, including cancer cell proliferation, apoptosis, angiogenesis, lymphangiogenesis and expression of vascular endothelial growth factor-A and -C, matrix metalloproteinase (MMP)-2 and -9, cyclooxygenase (COX)-2 and urokinase-type plasminogen activator, in patients with UTUC. A total of 134 patients who underwent nephroureterectomy were retrospectively investigated. Proliferation index (PI), microvessel density and lymphatic vessel density (LVD) were measured using anti-Ki-67, anti-CD105 and anti-D2-40 antibodies in formalin-fixed specimens. The apoptotic index was evaluated using the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling method. Other cancer-related molecules were investigated by immunohistochemistry in similar specimens. The patients were divided into three groups; non-smoker (n=54, 40.3%), former smoker (n=46, 34.3%) and current smoker (n=34, 25.4%). The PI and the apoptotic index were not found to be correlated with smoking status; however, the mean/standard deviation level of LVD in current smokers (40.9/12.9) was significantly higher (P= 0.034) compared to that in patients who had never smoked (34.4/10.6). In addition, smoking status was positively correlated with the presence of intratumoral lymphatic vessels (iLV) (P=0.010) and the expression of COX-2 and MMP-9 (P=0.032). The multivariate analysis demonstrated that current smoking was independently associated with all the abovementioned smoking-related factors. However, former smoking was correlated with LVD and the presence of iLV. In the survival analysis, LVD, the presence of iLV and the expression of COX-2 and MMP-9 were identified as predictive factors for metastasis following surgery. In conclusion, lymphangiogenesis and the expression levels of COX-2 and MMP-9 were found to be associated with the smoking status of UTUC patients. Our results may provide important insights into the pathological changes precipitated by smoking in these patients.

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Effect of Smoking on Outcomes of Urothelial Carcinoma: A Systematic Review of the Literature

Cited by 167 publications

References 46 publications

Nicotine Induces Tumor Growth and Chemoresistance through Activation of the PI3K/Akt/mTOR Pathway in Bladder Cancer

Nicotine Induces Tumor Growth and Chemoresistance through Activation of the PI3K/Akt/mTOR Pathway in Bladder Cancer

Prospective evaluation of fluorescence in situ hybridization for diagnosing urothelial carcinoma

Smoking-induced changes in cancer-related factors in patients with upper tract urothelial cancer

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