The emergence of antibody-drug conjugates (ADC) has ushered in a new era of precision therapy in lung cancer treatment. By conjugating highly selective monoclonal antibodies with highly potent cytotoxic payloads, ADC achieve precise targeting and killing of tumor cells while reducing systemic toxicity, facilitated by the bystander effect and other mechanisms. This article systematically reviews the latest advances in ADC for both non-small cell lung cancer and small cell lung cancer, and summarizes the latest data from key clinical trials,including the DESTINY-Lung series, TROPION-Lung series, and IDeate-Lung01, with a focus on the clinical efficacy of ADC targeting different key targets. Furthermore, this review analyzes the potential mechanisms of resistance to ADC and treatment-related adverse events, and summarizes the corresponding management strategies, providing a reference for the clinical application of ADC in lung cancer therapy.

BACKGROUND:Benign prostatic hyperplasia (BPH) is prevalent among aging men. Whether exposure to internet-derived health information is associated with disease awareness and symptom burden at initial diagnosis remains unclear. METHODS:We conducted a cross-sectional study of 400 newly diagnosed BPH outpatients. Participants were classified by prior exposure to internet-derived BPH content. BPH awareness and International Prostate Symptom Scores (IPSS) were compared using the Mann-Whitney U test and multivariate linear regression adjusted for age, education, and disposable income. Stratified analyses were performed according to educational attainment, disposable income, and content format. RESULTS:Exposure to internet-derived BPH content was independently associated with higher awareness and lower IPSS. Compared with unexposed participants, exposed participants had higher awareness (median 1.5 vs. 0) and lower IPSS (median 7.0 vs. 10.5) (both p < 0.001). In multivariable models, being unexposed was associated with a 1.39-point lower awareness score and a 2.20-point higher IPSS (both p < 0.001). In stratified analyses, the associations remained significant across education and income strata. Among exposed participants, those accessing text-based or mixed-format content had higher awareness and lower IPSS than those exposed to videos only (both p < 0.001). CONCLUSIONS:This study shows that exposure to internet-derived health content is significantly associated with higher BPH awareness and a lower symptom burden at initial presentation. Text-based or mixed-format content may be more effective than video-only formats.

Purpose: Posttraumatic growth (PTG) has been recognized as beneficial for the emotional well-being of cancer patients. However, the longitudinal relationship between PTG and emotional distress remains unclear and has rarely been investigated among patients undergoing neoadjuvant therapy. We investigated the linear and quadratic longitudinal associations between distress (depression, anxiety, and negative affect) and PTG in lung cancer patients undergoing neoadjuvant immunotherapy. We also tested individual variations in the longitudinal associations. Methods: Data were pooled from three clinical trials (n = 231) evaluating the efficacy of neoadjuvant immunotherapy in lung cancer patients. At the beginning of each treatment cycle, patients completed questionnaires assessing PTG and distress. Cross-lagged panel analysis was used to evaluate longitudinal associations, and multigroup structural equation modeling was conducted to examine individual variations in these relationships. Results: A unidirectional linear relationship was observed, with lower levels of distress predicting greater PTG over time. The impact of anxiety on PTG was more pronounced in patients with higher education or lower financial burdens, while the effect of negative affect was more salient in older patients. No significant quadratic effects of distress on PTG were observed. Conclusions: Lower emotional distress may facilitate the development of PTG over time. The longitudinal effect of distress on PTG varied on age, education, and financial burdens. Implications: Psychosocial interventions to promote PTG may be more effective by incorporating stress management and emotion regulation strategies, and need to be tailored to patients' socioeconomic characteristics.

This study aimed to evaluate the efficacy and safety of camrelizumab, an anti-PD-1 antibody, combined with either chemotherapy or apatinib, a VEGFR-2 inhibitor, as neoadjuvant treatment for stage IIA–IIIA NSCLC. This prospective, multicenter, dual-arm, non-randomized phase II trial enrolled participants from four hospitals in China between September 2020 and March 2022. Patients received 2–4 cycles of neoadjuvant treatment followed by surgery. Arm-AR (n = 28) included patients treated with camrelizumab (200 mg every 3 weeks) plus platinum-based chemotherapy, regardless of PD-L1 status. Arm-BR (n = 10) included PD-L1-positive patients treated with camrelizumab (200 mg every 3 weeks) plus apatinib (250 mg daily). The primary endpoint was the major pathological response (MPR) rate. Secondary endpoints included pathological complete response (pCR) rate, objective response rate (ORR), disease control rate (DCR), event-free survival (EFS), overall survival (OS), and safety profiles. In the ITT population, MPR rates were 25.0

Thymosin β10 (TMSB10) has emerged as a key player in the progression of prostate cancer, significantly influencing the tumor immune microenvironment. Pan-cancer analysis from The Cancer Genome Atlas (TCGA) revealed that TMSB10 is upregulated across multiple cancer types, particularly in prostate cancer, where high TMSB10 expression correlates with poorer patient outcomes. Functional assays using prostate cancer cell lines LNCaP and DU145 showed that TMSB10 silencing suppresses cell proliferation, migration, and invasion, while overexpression enhances these oncogenic processes. Furthermore, co-culture experiments demonstrated that TMSB10 overexpression skews macrophage polarization, decreasing the population of M1-type macrophages while increasing M2-type macrophages. This shift reduces immune cell cytotoxicity and alters cytokine secretion, highlighting TMSB10’s role in immune evasion. These findings establish TMSB10 as a pivotal factor in prostate cancer biology, promoting tumor aggressiveness and modulating the immune response within the tumor microenvironment. TMSB10 presents a promising therapeutic target for prostate cancer, offering new avenues for treatments aimed at altering the tumor immune landscape. This research also provides a foundation for further exploration of TMSB10’s role in other cancers.

This multicentre, two-arm, phase 2 study aimed to explore the efficacy and safety of neoadjuvant camrelizumab plus chemotherapy or apatinib in patients with initially unresectable stage II-III non-small-cell lung cancer (NSCLC). Eligible patients regardless of PD-L1 expression received neoadjuvant camrelizumab 200 mg and platinum-doublet chemotherapy every 3 weeks (arm A) or those with PD-L1-positive tumors received neoadjuvant camrelizumab and apatinib 250 mg once daily (arm B), for 2-4 cycles, followed by surgery. The primary endpoint was major pathological response (MPR) rate. Thirty patients in arm A and 21 in arm B were enrolled. Surgery rates were 50.0% (15/30) in arm A and 42.9% (9/21) in arm B, with all patients achieving R0 resections. Of these patients, the MPR and pathological complete response rates were both 20.0% (95% CI 4.3-48.1) in arm A and were 55.6% (95% CI 21.2-86.3) and 11.1% (95% CI 0.3-48.2) in arm B, respectively. The corresponding objective response rates were 33.3% (95% CI 11.8-61.6) and 55.6% (95% CI 21.2-86.3). With a median follow-up of 22.4 months (95% CI 19.0-26.0), the median event-free survival was not reached (NR; 95% CI 13.6-NR) in arm A and 16.8 months (95% CI 8.6-NR) in arm B. Grade 3 or above treatment-related adverse events occurred in eight (26.7%) patients in arm A and three (14.3%) in arm B. Biomarker analysis showed baseline TYROBP expression was predictive of treatment response in arm B. Neoadjuvant camrelizumab plus chemotherapy or apatinib exhibits preliminary efficacy and manageable toxicity in patients with initially unresectable stage II-III NSCLC.

Although immune checkpoint blockade (ICB) therapies have shifted the treatment paradigm for non-small-cell lung cancer (NSCLC), many patients remain resistant. Here we characterize the tumor cell states and spatial cellular compositions of the NSCLC tumor microenvironment (TME) by analyzing single-cell transcriptomes of 232,080 cells and spatially resolved transcriptomes of tumors from 19 patients before and after ICB–chemotherapy. We find that tumor cells and secreted phosphoprotein 1-positive macrophages interact with collagen type XI alpha 1 chain-positive cancer-associated fibroblasts to stimulate the deposition and entanglement of collagen fibers at tumor boundaries, obstructing T cell infiltration and leading to poor prognosis. We also reveal distinct states of tertiary lymphoid structures (TLSs) in the TME. Activated TLSs are associated with improved prognosis, whereas a hypoxic microenvironment appears to suppress TLS development and is associated with poor prognosis. Our study provides novel insights into different cellular and molecular components corresponding to NSCLC ICB–chemotherapeutic responsiveness, which will benefit future individualized immuno-chemotherapy. Samples from 19 patients with non-small-cell lung cancer treated with a combination of chemotherapy and immune checkpoint blockade are profiled with single-cell RNA sequencing and spatial transcriptomics to identify factors associated with treatment resistance.

Immunotherapy has revolutionized cancer treatment, but most patients are refractory to immunotherapy or acquire resistance, with the underlying mechanisms remaining to be explored. We characterized the transcriptomes of 92,000 single cells from 3 pre-treatment and 12 post-treatment patients with non-small cell lung cancer (NSCLC) who received neoadjuvant PD-1 blockade combined with chemotherapy. The 12 post-treatment samples were categorized into two groups based on pathologic response: major pathologic response (MPR; n = 4) and non-MPR (NMPR; n = 8). Distinct therapy-induced cancer cell transcriptomes were associated with clinical response. Cancer cells from MPR patients exhibited a signature of activated antigen presentation via major histocompatibility complex class II (MHC-II). Further, the transcriptional signatures of FCRL4+FCRL5+ memory B cells and CD16+CX3CR1+ monocytes were enriched in MPR patients and are predictors of immunotherapy response. Cancer cells from NMPR patients exhibited overexpression of estrogen metabolism enzymes and elevated serum estradiol. In all patients, therapy promoted expansion and activation of cytotoxic T cells and CD16+ NK cells, reduction of immunosuppressive Tregs, and activation of memory CD8+T cells into an effector phenotype. Tissue-resident macrophages were expanded after therapy, and tumor-associated macrophages (TAMs) were remodeled into a neutral instead of an anti-tumor phenotype. We revealed the heterogeneity of neutrophils during immunotherapy and identified an aged CCL3+ neutrophil subset was decreased in MPR patients. The aged CCL3+ neutrophils were predicted to interact with SPP1+ TAMs through a positive feedback loop to contribute to a poor therapy response. Neoadjuvant PD-1 blockade combined with chemotherapy led to distinct NSCLC tumor microenvironment transcriptomes that correlated with therapy response. Although limited by a small patient sample size subjected to combination therapy, this study provides novel biomarkers to predict therapy response and suggests potential strategies to overcome immunotherapy resistance.

BACKGROUND:The impact of evolving treatment strategies for metastatic prostate cancer (mPCa) on real-world survival is not well understood. We analyzed changes in mPCa survival over the past decade and discussed the potential driving factors behind these changes. METHODS:Our study involved 43,228 mPCa patients (2004-2020) from the SEER database, divided into 4 diagnostic periods. We used a multivariate Cox proportional hazards model to evaluate diagnostic periods' influence on overall mortality (OM) and prostate cancer-specific mortality (PSM), and calculated relative median survival improvements between adjacent periods. Subgroup analyses based on age and distant metastasis sites were conducted. RESULTS:Patients diagnosed in 2016 to 2020 experienced significantly reduced mortality risk compared to those in 2004 to 2007 (HR 0.64 for OM, HR 0.62 for CSM, both P < 0.001). The study period witnessed an absolute improvement in median overall survival (OS) and prostate cancer-specific survival (PCSS), 17 months (54.8%) and 25 months (67.6%) respectively. The most rapid relative survival improvement occurred post-2016, with a 29.7% increase in median OS and a 37.8% increase in PCSS compared to 2012 to 2015. There was a significant reduction in mortality risk throughout the study period in both age groups (age <75 and ≥75), but absolute survival gains were smaller in the older group (24 months [68.6%] vs. 8 months [32%] for OS, 36 months [90.0%] vs. 11 months [33.3%] for PCSS), with lower relative survival improvements after 2016 (37.2% vs. 17.9% for OS, 49% vs. 22.2% for PCSS). All metastasis site subgroups (except M1a) exhibited a significant reduction in mortality risk (all P < 0.001). Absolute survival improvements were 58 months (134.9%) for M1a, 16 months (50.0%) for M1b, and 17 months (54.8%) for M1c. CONCLUSION:The survival of mPCa have significantly improved over the past decade, although the progress is slower in elderly patients. Investigating the underlying reasons for survival differences among various patient profiles can further refine mPCa treatment strategies.

Background Prostate cancer (PCa) is a unique cancer from a metabolic perspective. Androgen receptor assumes a vital part in normal and malignant prostate cells regarding almost all aspects of cell metabolism, such as glucose, fat, amino acids, nucleotides, and so on. Methods We used The Cancer Genome Atlas database as training set, Memorial Sloan-Kettering Cancer Center cohort as validation set, and Gene Expression Omnibus database (GSE70769) as test set to identify the optimal prognostic signature. We evaluated the signature in terms of biochemical progression-free survival (bPFS), ROC curve, clinicopathological features, independent prognostic indicators, tumor microenvironment, and infiltrating immune cells. Nomogram was built dependent on the results of cox regression analyses. GSEA algorithm was used to evaluate differences in metabolism. The signature's prediction of androgen deprivation therapy (ADT) response was validated based on two groups of basic cytological experiments treat with ADT (GSE143408 and GSE120343) and the transcriptional information of pre-ADT/post-ADT of six local PCa patients. Results We finally input four screened genes into the stepwise regression model to construct metabolism-related signature. The signature shows good prediction performance in training set, verification set, and test set. A nomogram based on the PSA, Gleason score, T staging, and the signature risk score could predict 1-, 3-, and 5-year bPFS with the high area under curve values. Based on gene-set enrichment analysis, the characteristics of four genes signature could influence some important metabolic biological processes of PCa and were serendipitously found to be significantly related to androgen response. Subsequently, two cytological experimental data sets and our local patient sequencing data set verified that the signature may be helpful to evaluate the therapeutic response of PCa to ADT. Conclusions Our systematic study definite a metabolism-related gene signature to foresee prognosis of PCa patients which might add to individual prevention and treatment.

Abstract Bladder cancer (BLCA) is the common malignant urinary carcinoma and do not have uniformly poor prognosis. Hence, we focused on the function and prognostic value of fatty acid metabolism-related genes in bladder cancer patients. After obtained the fatty acid metabolism-related genes (FRGs), gene expression and corresponding clinical data were acquired from TCGA and GEO databases. Cox regression analysis and least absolute shrinkage and selection operator (LASSO) regression analysis were employed to establish the risk model to estimate the overall survival of BCLA patients. An eight-gene fatty acid metabolism-related risk signature was constructed to predict the overall survival (OS) of BLCA patients. Kaplan-Meier curves, tumor mutation burden, scatter diagram, ROC curves, nomogram were used to assess prognosis. The immunological features were estimated between different groups. IL6 and COL1A1 were considered to have important role in subgroups. Higher expression of IL6 and COL1A1 are positive correlation with higher grade, higher risk and poor prognosis. In conclusion, this risk model based on 8-FLGs is reliable to predict the prognosis and response to immunotherapy in BLCA patients. IL6 and COL1A1 are closely associated with higher risk score and poorer outcomes. This can provide a novel inspective in BLCA treatment.

In patients with castration-resistant prostate cancer (CRPC), clinical resistances such as androgen receptor (AR) mutation, AR overexpression, and AR splice variants (ARVs) limit the effectiveness of second-generation antiandrogens (SGAs). Several strategies have been implemented to develop novel antiandrogens to circumvent the occurring resistance. Here, we found and identified a bifunctional small molecule Z15, which is both an effective AR antagonist and a selective AR degrader. Z15 could directly interact with the ligand-binding domain (LBD) and activation function-1 region of AR, and promote AR degradation through the proteasome pathway. In vitro and in vivo studies showed that Z15 efficiently suppressed AR, AR mutants and ARVs transcription activity, downregulated mRNA and protein levels of AR downstream target genes, thereby overcoming AR LBD mutations, AR amplification, and ARVs-induced SGAs resistance in CRPC. In conclusion, our data illustrate the synergistic importance of AR antagonism and degradation in advanced prostate cancer treatment.

目的 比较一次性电子输尿管软镜与可重复使用电子输尿管软镜在治疗老年患者上尿路结石方面的安全性和有效性.方法 回顾性分析2020年3月至2022年11月北京医院因单侧上尿路结石行输尿管软镜碎石术的老年患者的临床资料,按照所使用软镜类别将符合入组条件的患者分为一次性软镜组和可重复使用软镜组,对两组患者结石完全清除率、手术时间、术后住院天数和术后全身炎症反应综合征(SIRS)发生率进行比较.结果 共纳入患者225例,其中一次性软镜组107例、可重复使用软镜组118例.一次性软镜组的手术时间短于可重复使用软镜组[60(40,97)min与75(60,110)min,Z=-2.947、P=0.003],一次性软镜组的术后住院时长短于可重复使用软镜组[1(1,2)d比1(1,2)d,Z=-2.554、P=0.011];两组患者在结石完全清除率[89/107(83.2％)与92/118(78.0％),x2=0.969、P=0.325]与术后 SIRS 发生率[8/107(7.5％)与 14/118(11.9％),x2=1.225、P=0.268]方面的差异均无统计学意义.结论 采用一次性电子输尿管软镜治疗老年患者上尿路结石的结石完全清除率、术后SIRS发生率与采用可重复使用电子输尿管软镜无明显差异,且手术时间和术后住院时长更短,一次性电子输尿管软镜用于治疗老年患者上尿路结石具有良好的安全性和有效性.

Afatinib, an irreversible ErbB-family blocker, could improve the survival of advanced epidermal growth factor receptor ( EGFR )-mutant non-small cell lung cancer patients (NSCLCm+). This phase II trial (NCT04201756) aimed to assess the feasibility of neoadjuvant Afatinib treatment for stage III NSCLCm+. Forty-seven patients received neoadjuvant Afatinib treatment (40 mg daily). The primary endpoint was objective response rate (ORR). Secondary endpoints included pathological complete response (pCR) rate, pathological downstaging rate, margin-free resection (R0) rate, event-free survival, disease-free survival, progression-free survival, overall survival, treatment-related adverse events (TRAEs). The ORR was 70.2% (95% CI: 56.5% to 84.0%), meeting the pre-specified endpoint. The major pathological response (MPR), pCR, pathological downstaging, and R0 rates were 9.1%, 3.0%, 57.6%, and 87.9%, respectively. The median survivals were not reached. The most common TRAEs were diarrhea (78.7%) and rash (78.7%). Only three patients experienced grade 3/4 TRAEs. Biomarker analysis and tumor microenvironment dynamics by bulk RNA sequencing were included as predefined exploratory endpoints. CISH expression was a promising marker for Afatinib response (AUC = 0.918). In responders, compared to baseline samples, increasing T-cell- and B-cell-related features were observed in post-treatment tumor and lymph-node samples, respectively. Neoadjuvant Afatinib is feasible for stage III NSCLC+ patients and leads to dynamic changes in the tumor microenvironment.

Background: Recently, a newly programmed cell death has been discovered, namely cuproptosis. It is considered a novel copper-dependent cell death model. Long non-coding RNA (lncRNA) influence the prognosis of bladder cancer. In this study, we established a scoring system based on 7 cuproptosis-related lncRNA to predict the prognosis and immune landscape of bladder cancer (BCa). Method: Gene expression and clinical data of 431 tissues were downloaded from The Cancer Genome Atlas (TCGA), including 19 normal samples and 419 cancer samples. All samples were randomly categorized into train and test cohorts. Cuproptosis-related lncRNA were distinguished. Then we conduct univariate COX and multivariate COX regression, paralleled with LASSO regression to cultivate a cuproptosis-related lncRNA risk model. Kaplan-Meier curves, scatter diagram, C-index, ROC curves, nomogram, PCA analysis and univariate and multivariate Cox regression were used to test the accuracy of risk model and to predict patient survival. Additional, gene mutation status between high- and low-risk groups was calculated.GO and KEGG were used to access the DEGs (different expression genes)-related pathway.The ssGSEA and ESTIMATE algorithms were used to assess the immune function in different tumor samples. Besides, patient's response to immunotherapy and drug susceptibility were also been estimated. Results: 7 cuproptosis-related lncRNA (LINC01184, LINC00513, LINC02443, SMARCA5-AS1, BDNF-AS, SOD2-OT1, HYI-AS1) were selected to construct the risk model in the train cohort. This model can well predict the overall survival (OS) in test group and entire cohort with different stage. Despite no significant different is observed in gene mutation between high- and low-risk group, different immune infiltration, different survival and sensitivity to drugs are discovered. Conclusion: We established a novel cuproptosis-related lncRNA risk model which can predict the outcome and immunotherapy response with satisfactory predictive effects. This risk model can provide a new insight into prognostic evaluation and may have potential to guide comprehensive treatment in bladder cancer.

Background: The effect of the adenoviral early region 2 binding factors (E2Fs) target pathway on prostate cancer is not clear. It is necessary to establish an E2F target-related gene signature to predict prognosis and facilitate clinical decision-making. Methods: An E2F target-related gene signature was established by univariate and LASSO Cox regression analyses, and its predictive ability was verified in multiple cohorts. Moreover, the enrichment pathway, immune microenvironment, and drug sensitivity of the activated E2F target pathway were also explored. Results: The E2F target-related gene signature consisted of MXD3, PLK1, EPHA10, and KIF4A. The patients with high-risk scores showed poor prognosis, therapeutic resistance, and immunosuppression, along with abnormal growth characteristics of cells. Tinib drugs showed high sensitivity to the expression of MXD3 and EPHA10 genes. Conclusion: Our research established an E2F target-related signature for predicting the prognosis of prostate cancer. This study provides insights into formulating individualized detection and treatment as well as provides a theoretical basis for future research.

Prostate cancer is one of the most common malignant tumors in men. Pyroptosis is related to tumor immune infiltration and tumor microenvironment (TME) and has been confirmed to be related to the progression of a variety of tumors. However, the relationship between prostate cancer and pyroptosis, as well as TME and tumor immune infiltration, has not been discussed yet. We obtained and combined the RNA-seq data of prostate cancer from TCGA and GEO databases, analyzed the differential expression of pyroptosis-related genes (PRGs), and divided them into two groups according to the PRG expression level. The relationship between pyroptosis subtypes and the TME of prostate cancer was further verified, and the differential expression genes (DEGs) in the two subtypes were identified. The relationship between the DEGs and clinicopathology was explored and KEGG and GO enrichment analysis was conducted; it was found that most DEGs were enriched in immune-related pathways. Then, we randomly divided datasets into training and testing sets, performed the LASSO and multicox progression analysis, selected eight genes as prognostic signatures and used the eight genes, calculated the risk score, and then separated the entire cohort into high- and low-risk groups. The prognosis between two groups and the 1-, 3-, and 5-year ROC curves of biochemical relapse (BCR) were verified in training, testing, and the entire cohort, respectively. The TME, CSC index, mutation, and drug susceptibility were also discussed.

BACKGROUND:Evidence of neoadjuvant chemoimmunotherapy for locally advanced non-small cell lung cancer remains investigational and requires prospective validation. This phase II trial (https://www.chictr.org.cn/historyversionpub.aspx?regno=ChiCTR1900023758) aimed to investigate the safety and effectiveness of neoadjuvant PD-1 inhibitor sintilimab in addition to chemotherapy in the management of resectable stage IIIA non-small cell lung cancer. METHODS:Eligible patients received two to four 21-day cycles of neoadjuvant therapy: sintilimab (200 mg) and carboplatin (area under the curve 5) on day 1, gemcitabine (1000 mg/m2) on day 1 and day 8 for squamous cell carcinoma, or pemetrexed (500 mg/m2) on day 1 for adenocarcinoma and non-small cell lung cancer not otherwise specified. The primary endpoints were adverse events and major pathological response. The secondary endpoint was disease-free survival at 1 year. RESULTS:Fifty patients were enrolled, and 23 (46%) achieved partial response after neoadjuvant chemoimmunotherapy. Four (8%) patients experienced grade 3 to 5 adverse events. Thirty patients received surgery, none of whom experienced treatment-related surgery delays, and 13 (43.3%) of 30 patients achieved major pathological response (viable tumor ≤10%). With a median follow-up of 13.6 months, 85.3% of patients were disease-free at 1 year (N = 50). CONCLUSIONS:Neoadjuvant sintilimab with platinum-containing dual-agent chemotherapy was feasible and safe for patients with resectable stage IIIA non-small cell lung cancer.

Purpose Early biochemical recurrence (eBCR) indicated a high risk for potential recurrence and metastasis in prostate cancer. The N6-methyladenosine (m6A) methylation modification played an important role in prostate cancer progression. This study aimed to develop a m6A lncRNA signature to accurately predict eBCR in prostate cancer. Methods Pearson correlation analysis was first conducted to explore m6A lncRNAs and univariate Cox regression analysis was further performed to identify m6A lncRNAs of prognostic roles for predicting eBCR in prostate cancer. The m6A lncRNA signature was constructed by least absolute shrinkage and selection operator analysis (LASSO) in training cohort and further validated in test cohort. Furthermore, half maximal inhibitory concentration (IC50) values were utilized to explore potential effective drugs for high-risk group in this study. Results Five hundred and thirty-eighth m6A lncRNAs were searched out through Pearson correlation analysis and 25 out of 538 m6A lncRNAs were identified to pose prediction roles for eBCR in prostate cancers. An m6A lncRNA signature including 5 lncRNAs was successfully built in training cohort. The high-risk group derived from m6A lncRNA signature could efficiently predict eBCR occurrence in both training (p < 0.001) and test cohort (p = 0.002). ROC analysis also confirmed that lncRNA signature in this study posed more accurate prediction roles for eBCR occurrence when compared with PSA, TNM stages and Gleason scores. Drug sensitivity analysis further discovered that various drugs could be potentially utilized to treat high-risk samples in this study. Conclusions The m6A lncRNA signature in this study could be utilized to efficiently predict eBCR occurrence, various clinical characteristic and immune microenvironment for prostate cancer.

Acute myeloid leukemia (AML) is a malignant hematological malignancy with a poor prognosis. Risk stratification of patients with AML is mainly based on the characteristics of cytogenetics and molecular genetics; however, patients with favorable genetics may have a poor prognosis. Here, we focused on the activity changes of immunologic and hallmark gene sets in the AML population. Based on the enrichment score of gene sets by gene set variation analysis (GSVA), we identified three AML subtypes by the nonnegative matrix factorization (NMF) algorithm in the TCGA cohort. AML patients in subgroup 1 had worse overall survival (OS) than subgroups 2 and 3 (P<0.001). The median overall survival (mOS) of subgroups 1–3 was 0.4, 2.2, and 1.7 years, respectively. Clinical characteristics, including age and FAB classification, were significantly different among each subgroup. Using the least absolute shrinkage and selection operator (LASSO) regression method, we discovered three prognostic gene sets and established the final prognostic model based on them. Patients in the high-risk group had significantly shorter OS than those in the low-risk group in the TCGA cohort (P<0.001) with mOS of 2.2 and 0.7 years in the low- and high-risk groups, respectively. The results were further validated in the GSE146173 and GSE12417 cohorts. We further identified the key genes of prognostic gene sets using a protein-protein interaction network. In conclusion, the study established and validated a novel prognostic model for risk stratification in AML, which provides a new perspective for accurate prognosis assessment.