Ibrahimpollock5104

To compare the efficacy and safety of hyperthermic intravesical chemotherapy (HIVEC) and intravesical chemotherapy (IVEC) in patients with intermediate and high risk nonmuscle-invasive bladder cancer (NMIBC) after transurethral resection.

We included 560 patients diagnosed with primary or recurrent NMIBC between April 2009 and December 2015 at 1 of 6 tertiary centers. We matched 364 intermediate or high risk cases and divided them into 2 groups the HIVEC+IVEC group [chemohyperthermia (CHT) composed of 3 consecutive sessions followed by intravesical instillation without hyperthermia] and the IVEC group (intravesical instillation without hyperthermia). The data were recorded in the database. The primary endpoint was 2-year recurrence-free survival (RFS) in all NMIBC patients (

= 364), whereas the secondary endpoints were the assessment of radical cystectomy (RC) and 5-year overall survival (OS).

There was a significant difference in the 2-year RFS between the two groups in all patients (

= 364; HIVEC+IVEC 82.42%

IVEC 74.18%,

= 0.038). Compared with the IVEC group, the HIVEC+IVEC group had a lower incidence of RC (

= 0.0274). However, the 5-year OS was the same between the 2 groups (

= 0.1434). Adverse events (AEs) occurred in 32.7% of all patients, but none of the events was serious (grades 3-4). No difference in the incidence or severity of AEs between each treatment modality was observed.

This retrospective study showed that HIVEC+IVEC had a higher 2-year RFS and a lower incidence of RC than IVEC therapy in intermediate and high risk NMIBC patients. Both treatments were well-tolerated in a similar manner.

This retrospective study showed that HIVEC+IVEC had a higher 2-year RFS and a lower incidence of RC than IVEC therapy in intermediate and high risk NMIBC patients. Both treatments were well-tolerated in a similar manner.

Patients with underlying diseases are more vulnerable to coronavirus disease 2019 (COVID-19). The purpose of this study was to investigate cancer incidence in patients with COVID-19 and to determine whether cancer was associated with mortality among patients with COVID-19.

Electronic searches of PubMed, Embase, Cochrane, Web of Science, and medRxiv were conducted to collect studies that provided data regarding the incidence and mortality of cancer patients with COVID-19. Meta-analyses were used to estimate pooled incidences, risk ratios (RRs), and 95% confidence intervals (CIs) using a random-effects model. Heterogeneity among studies was detected using



statistics.

A total of 19 retrospective studies involving 63,019 patients (2,682 patients with cancer) were included. Meta-analysis showed that the pooled incidence of cancer in COVID-19 patients was 6% (95% CI 3%-9%). The mortality rate of COVID-19 patients with cancer was higher than that of those without cancer [risk ratio (RR) 1.8, 95% CI 1.38-ion for their clinical management.

The systemic inflammation index and body mass index (BMI) are easily accessible markers that can predict mortality. However, the prognostic value of the combined use of these two markers remains unclear. The goal of this study was therefore to evaluate the association of these markers with outcomes based on a large cohort of patients with gastric cancer.

A total of 2,542 consecutive patients undergoing radical surgery for gastric or gastroesophageal junction adenocarcinoma between 2009 and 2014 were included. Systemic inflammation was quantified by the preoperative neutrophil-to-lymphocyte ratio (NLR). High systemic inflammation was defined as NLR ≥ 3, and underweight was defined as BMI < 18.5 kg/m

.

Among 2,542 patients, NLR ≥ 3 and underweight were common [627 (25%) and 349 (14%), respectively]. In the entire cohort, NLR ≥ 3 or underweight independently predicted overall survival (OS) [hazard ratio (HR) 1.236, 95% confidence interval (95% CI) 1.069-1.430; and HR 1.600, 95% CI 1.350-1.897, respectively] and recurrence-free survival (RFS) (HR 1.230, 95% CI 1.054-1.434; and HR 1.658, 95% CI 1.389-1.979, respectively). Patients with both NLR ≥ 3 and underweight (

neither) had much worse OS (HR 2.445, 95% CI 1.853-3.225) and RFS (HR 2.405, 95% CI 1.802-3.209). Furthermore, we observed similar results in subgroup analyses according to pathological stage, age, and postoperative chemotherapy.

Our results showed that preoperative elevated NLR and decreased BMI had a significant negative effect on survival. Underweight combined with severe inflammation could enhance prognostication. Taking active therapeutic measures to reduce inflammation and increase nutrition may help improve outcomes.

Our results showed that preoperative elevated NLR and decreased BMI had a significant negative effect on survival. Underweight combined with severe inflammation could enhance prognostication. Taking active therapeutic measures to reduce inflammation and increase nutrition may help improve outcomes.

O6methylguanine-DNA methyltransferase (

) promoter methylation is a biomarker widely used to predict the sensitivity of

-wildtype glioblastoma to temozolomide therapy. Given that the

status has critical effects on the survival and epigenetic features of glioblastoma, we aimed to assess the role of

promoter methylation in

-mutant glioblastoma.

This study included 187

-mutant glioblastomas and used 173

-wildtype glioblastomas for comparison. Kaplan-Meier curves and multivariate Cox regression were used to study the predictive effects.

Compared with

-wildtype glioblastomas,

-mutant glioblastomas showed significantly higher (

< 0.0001)

promoter methylation. We demonstrated that

promoter methylation status, as determined by a high cutoff value (≥30%) in pyrosequencing, could be used to significantly stratify the survival of 50

-mutant glioblastomas receiving temozolomide therapy (cohort A); this result was validated in another cohort of 25

-mutant glioblastomas (cohort B). The median progression-free survival and median overall survival in cohort A were 9.33 and 13.76 months for unmethylated cases, and 18.37 and 41.61 months for methylated cases, and in cohort B were 6.97 and 9.10 months for unmethylated cases, and 23.40 and 26.40 months for methylated cases. In addition, we confirmed that the

promoter methylation was significantly (

= 0.0001) correlated with longer OS in

-mutant patients with GBM, independently of age, gender distribution, tumor type (primary or recurrent/secondary), and the extent of resection.

promoter methylation has predictive value in

-mutant glioblastoma, but its cutoff value should be higher than that for

-wildtype glioblastoma.

MGMT promoter methylation has predictive value in IDH-mutant glioblastoma, but its cutoff value should be higher than that for IDH-wildtype glioblastoma.

Hepatocellular carcinoma (HCC) is a lethal global disease that requires an accurate diagnosis. We assessed the potential of 5 serum biomarkers (AFP, AFU, GGT-II, GPC3, and HGF) in the diagnosis of HCC.

In this retrospective study, we measured the serum levels of each biomarker using ELISAs in 921 participants, including 298 patients with HCC, 154 patients with chronic hepatitis (CH), 122 patients with liver cirrhosis (LC), and 347 healthy controls from 3 hospitals. Patients negative for hepatitis B surface antigen and hepatitis C antibody (called "NBNC-HCC") and patients positive for the above indices (called "HBV-HCC and HCV-HCC") were enrolled. The selected diagnostic model was constructed using a training cohort (

= 468), and a validation cohort (

= 453) was used to validate our results. Receiver operating characteristic analysis was used to evaluate the diagnostic accuracy.

The α-L-fucosidase (AFU)/α-fetoprotein (AFP) combination was best able to distinguish NBNC-HCC [area under the curve 0.986 (95% confidence interval 0.958-0.997), sensitivity 92.6%, specificity 98.9%] from healthy controls in the test cohort. For screening populations at risk of developing HCC (CH and LC), the AFP/AFU combination improved the diagnostic specificity for early-stage HCC [area under the curve 0.776 (0.712-0.831), sensitivity 52.5%, specificity 91.6% in the test group]. In all-stage HBV-HCC and HCV-HCC, AFU was also the best candidate biomarker combined with AFP [area under the curve 0.835 (0.784-0.877), sensitivity 69.1%, specificity 87.4% in the test group]. selleck products All results were verified in the validation group.

The AFP/AFU combination could be used to identify NBNC-HCC from healthy controls and hepatitis-related HCC from at-risk patients.

The AFP/AFU combination could be used to identify NBNC-HCC from healthy controls and hepatitis-related HCC from at-risk patients.

Anoctamin 7 (ANO7) is a calcium

-dependent chloride ion channel protein. Its expression is restricted to prostate epithelial cells. The exact function is unknown. This study aimed to analyze ANO7 expression and its clinical significance in prostate cancer (PCa).

ANO7 expression was assessed by immunohistochemistry in 17,747 clinical PCa specimens.

ANO7 was strongly expressed in normal prostate glandular cells but often less abundant in cancer cells. ANO7 staining was interpretable in 13,594 cancer tissues and considered strong in 34.4%, moderate in 48.7%, weak in 9.3%, and negative in 7.6%. Reduced staining was tightly linked to adverse tumor features [high classical and quantitative Gleason grade, lymph node metastasis, advanced tumor stage, high Ki67 labeling index, positive surgical margin, and early biochemical recurrence (

< 0.0001 each)]. The univariate Cox hazard ratio for prostate-specific antigen (PSA) recurrence after prostatectomy in patients with negative

strong ANO7 expression was ion in PCa.

Natural extracts, including nobiletin, have been reported to enhance the efficacy and sensitivity of chemotherapeutic drugs. However, whether and how nobiletin affects tumor growth and progression in renal cell carcinoma (RCC) are still unclear.

Cell proliferation, cell cycle and apoptosis analyses, colony-formation assays, immunoblotting analysis, and qRT-PCR analysis were performed to investigate how nobiletin affected RCC cell proliferation

. The nude mouse model was used to test the efficacy of nobiletin alone or in combination with palbociclib.

Nobiletin inhibited cell proliferation by inducing G1 cell cycle arrest and cell apoptosis in RCC cells. Mechanistically, nobiletin decreased SKP2 protein expression by reducing its transcriptional level. The downregulated SKP2 caused accumulation of its substrates, p27 and p21, which further inhibited the activity of the G1 phase-related protein, CDK2, leading to inhibition of cell proliferation and tumor formation. A higher SKP2 protein level indicated less sensitivity to the CDK4/6 inhibitor, palbociclib. A combination of nobiletin and palbociclib showed a synergistic tumor inhibition

and in an

model.

Nobiletin downregulated the SKP2-p21/p27-CDK2 axis to inhibit tumor progression and showed synergistic tumor inhibition effects with the CDK4/6 inhibitor, palbociclib, on RCC, which indicates a potential new therapeutic strategy.

Nobiletin downregulated the SKP2-p21/p27-CDK2 axis to inhibit tumor progression and showed synergistic tumor inhibition effects with the CDK4/6 inhibitor, palbociclib, on RCC, which indicates a potential new therapeutic strategy.