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n-based neoadjuvant anti-HER2 therapy may be applied as an optimal treatment duration for screening high-risk HER2-positive breast cancer patients for escalation treatment. Further prospective study is warranted.

Four cycles of taxane/carboplatin-based neoadjuvant anti-HER2 therapy may be applied as an optimal treatment duration for screening high-risk HER2-positive breast cancer patients for escalation treatment. Further prospective study is warranted.The use of established drugs in new therapeutic applications has great potential for the treatment of cancers. Nanomedicine has the advantages of efficient cellular uptake and specific cell targeting. In this study, we investigate using lentinan-functionalized selenium nanoparticles (LET-SeNPs) for the treatment of prostate cancer (PCa). We used assays to demonstrate that a combination of LET-SeNPs and zoledronic acid (ZOL) can reduce PCa cell viability in vitro. Stability and hemocompatibility assays were used to determine the safety of the combination of LET-SeNPs and ZOL. The localization of LET-SeNPs was confirmed using fluorescence microscopy. JC-1 was used to measure the mitochondrial membrane potential, while the cellular uptake, cell cycle and apoptosis were evaluated by flow cytometry. Finally, cell migration and invasion assays were used to evaluate the effects of the combination treatment on cell migration and invasion. Under optimized conditions, we found that LET-SeNPs has good stability. The combination of LET-SeNPs and ZOL can effectively inhibit metastatic PCa cells in a concentration-dependent manner, as evidenced by cytotoxicity testing, flow cytometric analysis, and mitochondria functional test. The enhanced anti-cancer effect of LET-SeNPs and ZOL may be related to the regulation of BCL2 family proteins that could result in the release of cytochrome C from the inner membranes of mitochondria into the cytosol, accompanied by induction of cell cycle arrest at the S phase, leading to irreversible DNA damage and killing of PCa cells. Collectively, the results of this study suggest that the combination of SeNPs and ZOL can successfully inhibit the growth of PCa cells.

Immune-Oncology (IO) improves Overall Survival (OS) in metastatic Renal Cell Carcinoma (mRCC). The prognostic impact of previous Cytoreductive Nephrectomy (CN) and radical nephrectomy (RN), with curative intent, in patients treated with IO is not well defined. The aim of our paper is to evaluate the impact of previous nephrectomy on outcome of mRCC patients treated with IO.

287 eligible patients were retrospectively collected from 16 Italian referral centers adhering to the MeetUro association. buy Veliparib Patients treated with IO as second and third line were included, whereas patients treated with IO as first line were excluded. Kaplan-Meier method and log-rank test were performed to compare Progression Free Survival (PFS) and OS between groups. In our analysis, both CN and RN were included. The association between nephrectomy and other variables was analyzed in univariate and multivariate setting using the Cox proportional hazard model.

246/287 (85.7%) patients had nephrectomy before IO treatment. Median PFS in e in terms of OS. Further prospective trials would assess this issue in order to guide clinicians in real word practice.Diffuse large B-cell lymphoma (DLBCL) is the most frequent and commonly diagnosed subtype of NHL, which is characterized by high heterogeneity and malignancy, and most DLBCL patients are at advanced stages. The serine/threonine kinase NEK2 (NIMA-related kinase 2), a member of NIMA-related kinase (NEK) family that regulates cell cycle, is upregulated in a variety of malignancies, including diffuse large B-cell lymphoma. However, the role and underlying mechanisms of NEK2 in DLBCL have seldom been discussed. In this study, we identified that NEK2 is upregulated in DLBCL compared to normal lymphoid tissues, and overexpression of NEK2 predicted a worse prognosis of DLBCL patients. Gene set enrichment analysis indicates that NEK2 might participate in regulating glycolysis. Knockdown of NEK2 inhibited growth and glycolysis of DLBCL cells. The interaction between NEK2 and PKM2 was discovered by tandem affinity purification and then was confirmed by immunofluorescence staining, coimmunoprecipitation, and immunoprecipitation. NEK2 bounds to PKM2 and regulates PKM2 abundance via phosphorylation, which increases PKM2 stability. The xenograft tumor model checks the influence of NEK2 on tumor growth in vivo. Thus, NEK2 could be the novel biomarker and target of DLBCL, which remarkably ameliorates the diagnosis and treatment of DLBCL.

Tobacco smoking is a carcinogen for many cancers including bladder cancer. The microbiota is involved in the occurrence, development, and treatment of tumors. We explored the composition of male urinary microbiome and the correlation between tobacco smoking and microbiome in this study.

Alpha diversity, principal component analysis (PCA) and Adonis analysis, linear discriminant analysis (LDA) coupled with effect size measurement, and PICRUSt function predictive analysis were used to compare different microbiome between smokers and non-smokers in men.

There were 26 qualified samples included in the study. Eleven of them are healthy controls, and the others are from men with bladder cancer. Simpson index and the result of PCA analysis between smokers and non-smokers were not different (P > 0.05) in healthy men. However, the abundance of Bacteroidaceae, Erysipelotrichales, Lachnospiraceae, Bacteroides, and so on in the urinary tract of smokers is much higher than that of non-smokers. Compared to non-smokers, the alpha diversity in smokers was elevated in patients with bladder cancer (P < 0.05). PCA analysis showed a significant difference between smokers and non-smokers (P < 0.001), indicating that tobacco smoking plays a vital role in urinary tract microbial composition.

The composition of microbiome in the urinary tract is closely related to tobacco smoking. This phenomenon is more significant in patients with bladder cancer. This indicates tobacco smoking may promote the occurrence and development of bladder cancer by changing urinary tract microbiome.

The composition of microbiome in the urinary tract is closely related to tobacco smoking. This phenomenon is more significant in patients with bladder cancer. This indicates tobacco smoking may promote the occurrence and development of bladder cancer by changing urinary tract microbiome.