Treatment and surveillance for non-muscle-invasive bladder cancer: a clinical practice guideline (2021 edition).

Non-muscle invasive bladder cancer (NMIBC) is a major type of bladder cancer with a high incidence worldwide, resulting in a great disease burden. Treatment and surveillance are the most important part of NIMBC management. In 2018, we issued "Treatment and surveillance for non-muscle-invasive bladder cancer in China: an evidence-based clinical practice guideline". Since then, various studies on the treatment and surveillance of NMIBC have been published. There is a need to incorporate these materials and also to take into account the relatively limited medical resources in primary medical institutions in China. Developing a version of guideline which takes these two issues into account to promote the management of NMIBC is therefore indicated. We formed a working group of clinical experts and methodologists. Through questionnaire investigation of clinicians including primary medical institutions, 24 clinically concerned issues, involving transurethral resection of bladder tumor (TURBT), intravesical chemotherapy and intravesical immunotherapy of NMIBC, and follow-up and surveillance of the NMIBC patients, were determined for this guideline. Researches and recommendations on the management of NMIBC in databases, guideline development professional societies and monographs were referred to, and the European Association of Urology was used to assess the certainty of generated recommendations. Finally, we issued 29 statements, among which 22 were strong recommendations, and 7 were weak recommendations. These recommendations cover the topics of TURBT, postoperative chemotherapy after TURBT, Bacillus Calmette-Guérin (BCG) immunotherapy after TURBT, combination treatment of BCG and chemotherapy after TURBT, treatment of carcinoma in situ, radical cystectomy, treatment of NMIBC recurrence, and follow-up and surveillance. We hope these recommendations can help promote the treatment and surveillance of NMIBC in China, especially for the primary medical institutions.

[Corrigendum] 5­bromo-3-(3-hydroxyprop-1-ynyl)-2H-pyran-2­one induces apoptosis in T24 human bladder cancer cells through mitochondria-dependent signaling pathways.

Following the publication of this article, an interested reader drew to our attention that Fig. 1, which described the effects of 5-bromo-3-(3-hydroxyprop-1-ynyl)-2H-pyran-2-one (BHP) on T24 bladder carcinoma cell morphology and viability, contained a pair of panels showing identical data. After having re-examined our original data, we realize that the control data (showing 0 µM BHP) were inadvertently also included in Fig. 1 for the panel that was intended to show the effect of adding 10 µM BHP to the cells. A corrected version of Fig. 1, featuring the correct data for the addition of 10 µM BHP to the cells, is shown here. The error did not affect the conclusions reported in this study. We sincerely apologize for this mistake, and thank the reader of our article who drew this matter to our attention. Furthermore, we regret any inconvenience this mistake has caused. [the original article was published in the Molecular Medicine Reports 15: 153-159, 2016; DOI: 10.3892/mmr.2016.5991].

5­bromo­3­(3­hydroxyprop­1­ynyl)­2H­pyran­2­one induces apoptosis in T24 human bladder cancer cells through mitochondria-dependent signaling pathways.

The present study was performed to investigate the effect of 5-bromo-3-(3-hydroxyprop-1-ynyl)-2H-pyran-2-one (BHP) on the induction of apoptosis and cell cycle arrest in T24 human bladder carcinoma cells. An MTT assay was used to investigate the inhibition of cell proliferation. Flow cytometry was used to observe alterations in the cell cycle, generation of reactive oxygen species (ROS), alterations in mitochondrial membrane potential (MMP) and induction of apoptosis in the T24 cells following BHP treatment. Western blot analysis was performed for the determination of expression levels of apoptotic proteins, and 4,6­diamidino­2­phenylindole dihydrochloride staining was used to observe apoptosis and DNA damage. The results demonstrated that treatment of the bladder cancer cells with BHP enhanced the activation of caspases and increased the production of ROS. It also caused damage to DNA, reduced MMP, and increased the secretion of endonuclease G and apoptosis­inducing factor from the mitochondria. The expression levels of cyclin E and cell division cycle 25C were reduced, whereas the expression levels of p21 and phosphorylated p53 were increased in the BHP­treated cells. In addition, treatment with BHP caused cell cycle arrest at the G0/G1 phase, increased the expression levels of B cell lymphoma­2 (Bcl­2)­associated X protein and poly(ADP­ribose) polymerase, decreased the expression of Bcl­2 and ultimately induced apoptosis of the T24 cells. Thus, BHP inhibited the proliferation of bladder cancer cells by inducing cell apoptosis through the mitochondrial pathway.