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Purpose: We aimed to study the role of anoikis-related genes (ARGs) in colorectal cancer (CRC) using bioinformatics. Methods: GSE39582 and GSE39084, which collectively contain 363 CRC samples, were downloaded from the NCBI Gene Expression Omnibus (GEO) database as a test set. TCGA-COADREAD, with 376 CRC samples, was downloaded from the UCSC database as a validation set. Univariate Cox regression analysis was used to screen for ARGs that were significantly associated with prognosis. The top 10 ARGs were used to classify the samples into different subtypes based on unsupervised cluster analysis. The immune environments of the different subtypes were analyzed. ARGs that were significantly associated with CRC prognosis were used to construct a risk model. Univariate and multivariate Cox regression analyses were used to screen independent prognostic factors and construct a nomogram. Results: Four anoikis-related subtypes (ARSs) with differential prognoses and immune microenvironments were identified. KRAS and epithelial–mesenchymal transition pathways were enriched in subtype B, which had the worst prognosis. Three ARGs (DLG1, AKT3, and LPAR1) were used to construct the risk model. Both the test and validation sets showed worse outcomes for patients in the high-risk group than those in the low-risk group. Risk score was found to be an independent prognostic factor for CRC. Moreover, there was a difference in drug sensitivity between the high- and low-risk groups. Conclusion: The identified ARGs and risk scores were associated with CRC prognosis and could predict the responses of patients with CRC to immunotherapy strategies. [ABSTRACT FROM AUTHOR]

Background: Nab-paclitaxel plus gemcitabine (AG) and modified FOLFIRINOX (FFX) are two systemic therapies that have been widely used as standard first-line chemotherapy regimens in metastatic pancreatic cancer. However, since there is no clinical trial to directly compare the efficacy and safety of the two regimens, it is not clear which regimen is more effective. In this study, we aim to examine and compare the efficacy and safety of AG and FFX as first-line chemotherapy regimens in Chinese patients with metastatic pancreatic cancer in a real-world setting. Methods: We retrospectively evaluated the outcomes of 44 patients who were diagnosed with metastatic pancreatic cancer and were treated with either AG (n = 24) or FFX (n = 20) as first-line chemotherapy between March 2017 and February 2022 at Zhongnan Hospital of Wuhan University. Prognostic nutrition index (PNI) was calculated based on the serum albumin level and peripheral lymphocyte count. According to the optimal cutoff value of PNI, patients were divided into low PNI group (PNI < 43.70) and high PNI group (PNI ≥ 43.70). Results: Of 44 patients in this study, 24 were treated with AG, and 20 were treated with FFX as first-line chemotherapy. No significant differences in baseline characteristics were found between the two groups. The objective response rate (ORR) was 16.7% in the AG group and 20.0% in the FFX group. The disease control rate (DCR) was 70.8% in the AG group and 60.0% in the FFX group. There was no significant difference in PFS or OS between the AG group and the FFX group. The median progression-free survival (PFS) was 4.67 months (95% confidence interval [CI], 2.91–6.42) in the AG group and 3.33 months (95% CI, 1.87–4.79, p = 0.106) in the FFX group. The median overall survival (OS) was 9.00 months (95% CI, 7.86–12.19) in the AG group and 10.00 months (95% CI, 7.70–12.27, p = 0.608) in the FFX group. The second-line treatment rate was 62.5% in the AG group and 55.0% in the FFX group. Immune checkpoint inhibitors (ICIs) based regimens are common second-line treatment options whether in AG or FFX group. Significantly more grade 3–4 peripheral neuropathy occurred in the AG than FFX groups (4 (20.8%) vs 0 (0.0%), p = 0.030*). The patients in the PNI (Prognostic nutrition index) ≥ 43.7 group had a significant longer median OS (PNI ≥ 43.7 vs PNI < 43.7: 10.33 vs 8.00 months, p = 0.019). Conclusion: AG and FFX showed comparable efficacy outcomes in patients with metastatic pancreatic cancer. Pancreatic cancer patients receiving first-line chemotherapy with good nutritional status are likely to have a better prognosis. [ABSTRACT FROM AUTHOR]

Aims: This study was conducted to establish the potential competing endogeneous RNA (ceRNA) network for predicting prognoses in kidney papillary renal cell carcinoma (KIRP) and explore novel therapeutic targets.Methods: The edgeR package in R was used to determine differentially expressed messenger RNAs (mRNAs), long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), based on data from The Cancer Gene Atlas Program (TCGA) and the Genotype Expression (GTEx) databases. Weighted gene co-expression network analysis (WGCNA) was performed to filter out the mRNAs or lncRNAs that were strongly related to KIRP. The miRNAs that possibly sponged by differentially expressed RNAs lncRNAs (DElncRNAs) were screened using miRcode. Starbase, miRDB, and TargetScan sets were utilized to predict target mRNAs to corresponding miRNAs. LASSO and multivariate Cox regression analyses were applied for the determination of potential prognostic significance. Finally, the lncRNA-miRNA-mRNA ceRNA network was constructed.Results: A total of 1739 DEmRNAs and 1599 DElncRNAs were identified in KIRP. WGCNA analysis suggested that DEmRNAs in the blue module and DElncRNAs in the turquoise module were closely correlated with KIRP. An 8-gene signature was constructed, which had prognostic significance and predictive value in KIRP. Of note, a lncRNA-miRNA-mRNA ceRNA network (including 18 lncRNAs, 5 miRNAs, and 7 mRNAs) was established.Conclusion: This investigation constructed a new lncRNA-miRNA-mRNA ceRNA network, and proposed some genes that may be novel targets, as well as a theoretical basis for the treatment of patients with KIRP. [ABSTRACT FROM AUTHOR]

Background: Hypoxia plays a crucial role in immunotherapy of hepatocellular carcinoma (HCC) by changing the tumor microenvironment. Until now the association between hypoxia genes and prognosis of HCC remains obscure. We attempt to construct a hypoxia model to predict the prognosis in HCC.Results: We screened out 3 hypoxia genes (ENO1, UGP2, TPI1) to make the model, which can predict prognosis in HCC. And this model emerges as an independent prognostic factor for HCC. A Nomogram was drawn to evaluate the overall survival in a more accurate way. Furthermore, immune infiltration state and immunosuppressive microenvironment of the tumor were detected in high-risk patients.Conclusion: We establish and validate a risk prognostic model developed by 3 hypoxia genes, which could effectively evaluate the prognosis of HCC patients. This prognostic model can be used as a guidance for hypoxia modification in HCC patients undergoing immunotherapy. [ABSTRACT FROM AUTHOR]

Temporal muscle thickness measured on 3D MRI has recently been linked to prognosis in glioblastoma patients and may serve as an independent prognostic indicator. This single-center study looked at temporal muscle thickness and prognosis in patients with primary glioblastoma. Overall survival was the major study outcome. For a retrospective analysis from 2010 to 2020, clinical data from 102 patients with glioblastoma at the Department of Oncology Radiotherapy of the First Affiliated Hospital of Dalian Medical University were gathered. Fifty-five cases from 2016 to 2020 contained glioblastoma molecular typing data, of which 45 were IDH wild-type glioblastomas and were analysed separately. TMT was measured on enhanced T1-weighted magnetic resonance images in patients with newly diagnosed glioblastoma.Overall patient survival (OS) was calculated by the Kaplan–Meier method and survival curves were plotted using the log-rank-sum test to determine differences between groups, and multifactorial analyses were performed using a Cox proportional-risk model.The median TMT for 102 patients was 6.775 mm (range: 4.95–10.45 mm). Patients were grouped according to median TMT, and the median overall survival (23.0 months) was significantly longer in the TMT > median group than in the TMT median group (P 0.001; Log-rank test). Analysing 45 patients with IDH wild type alone, the median overall survival (12 months) of patients in the TMT > median group was significantly longer than that of patients in the TMT ≤ median group (8 months) (P < 0.001; Log-rank test).TMT can serve as an independent prognostic factor for glioblastoma. [ABSTRACT FROM AUTHOR]

Objective: To analyze the efficacy of high-intensity focused ultrasound (HIFU) for adenomyosis and postoperative recurrence and its influencing factors. Methods: Clinical and follow-up data of 308 patients with adenomyosis who were treated with HIFU in Haifu Center, Affiliated Hospital of Chengdu University of Traditional Chinese Medicine from September 2017 to January 2022 were retrospectively analyzed. The recurrence of adenomyosis and the efficacy of HIFU at 6 months after surgery were followed up. To explore factors influencing postoperative prognosis and recurrence, the following variables were analyzed: patients' age, course of disease, gravidity and parity, size of the uterus, duration of HIFU, duration of irradiation, treatment intensity, dysmenorrhea score, time of follow-up, combined treatment of traditional Chinese medicine (TCM), western medicine adjuvant treatment, lesion location and type, and menorrhagia. Results: Among the 308 patients, 238 (77%) were followed up from 6 to 36 months, with an average follow-up time of 15.24 ± 9.97 months. The other 70 (23%) were lost to follow-up. At 6-month after surgery, efficacy rates of dysmenorrhea and menorrhagia management were 86.7% and 89.3%, respectively. Postoperative recurrence rates were 4.8% (1–12 months), 9.0% (12–24 months), and 17.0% (24–36 months) for dysmenorrhea; and 6.3% (1–12 months), 2.4% (12–24 months), and 12.2% (24–36 months) for menorrhagia. Multivariate logistic regression analyses showed that parity (P = 0.043, OR = 1.773, 95% CI 1.018–3.087), uterine size (P = 0.019, OR = 1.004, 95% CI 1.001–1.007), combined treatment of TCM (P = 0.047, OR = 1.846, 95% CI 1.008–3.381), diffuse lesion type (P = 0.013, OR = 0.464, 95% CI 0.254–0.848) and ablation rate (P = 0.015, OR = 0.481, 95%CI 0.267–0.868) were prognostic factors (P < 0.05). Age, course of disease, gravidity, duration of HIFU, duration of irradiation, treatment intensity, preoperative dysmenorrhea score, time of follow-up, western medicine adjuvant therapy, lesion location, and preoperative menstrual volume had no effect on prognosis (P > 0.05). Conclusion: HIFU can effectively relieve dysmenorrhea and reduce menstrual volume in patients with adenomyosis. Parity, uterine size, lesion type (diffuse), and ablation rate are risk factors for symptom recurrence after HIFU, while the combination of TCM therapy is a protective factor for relapse. We, therefore, recommend TCM in the adjuvant setting after HIFU according to patient condition. [ABSTRACT FROM AUTHOR]

Background: Brain metastases were rare in esophageal cancer patients. Using the Surveillance, Epidemiology, and End Results (SEER) database, the present study investigated the incidence, risk and prognostic factors of brain metastases in esophageal cancer patients.Methods: Retrieving esophageal cancer patients diagnosed between 2010 and 2018 from the SEER database, univariable and multivariable logistic and cox regression models were used to investigate the risk factors for brain metastases development and prognosis, respectively. The brain metastases predicting nomogram was constructed, evaluated and validated. The overall survival (OS) of patients with brain metastases was analyzed by Kaplan-Meier method.Results: A total of 34,107 eligible esophageal cancer patients were included and 618 of them were diagnosed with brain metastases (1.8%). The median survival of the brain metastatic esophageal cancer patients was 5 (95% CI: 5-7) months. The presence of bone metastases and lung metastases were the homogeneously associated factors for the development and prognosis of brain metastases in esophageal cancer patients. Patients younger than 65 years, American Indian/Alaska Native race (vs. White), overlapping lesion (vs. Upper third), esophageal adenocarcinoma histology subtype, higher N stage, and liver metastases were positively associated with brain metastases occurrence. The calibration curve, ROC curve, and C-index exhibited good performance of the nomogram for predicting brain metastases.Conclusions: Homogeneous and heterogeneous factors were found for the development and prognosis of brain metastases in esophageal cancer patients. The nomogram had good calibration and discrimination for predicting brain metastases. [ABSTRACT FROM AUTHOR]

Studies on the association of elevated B‐type natriuretic peptide (BNP)/N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP) level with adverse clinical outcomes have yielded conflicting results in patients with atrial fibrillation (AF). This meta‐analysis aimed to assess the prognostic value of BNP/NT‐proBNP level in AF patients. A comprehensive literature search was conducted using PubMed and Embase databases up to July 1, 2020. Studies investigating the association between BNP/NT‐proBNP level and adverse clinical outcomes in patients with AF were eligible. Outcome measures were all‐cause mortality, stroke/systemic embolism, major bleed, and major adverse cardiovascular events (MACEs). Ten studies recruiting 29 543 patients with AF were included. Elevated BNP/NT‐proBNP level was independently associated with higher risk of all‐cause mortality (risk ratios [RR] 1.92; 95% confidence intervals [CI] 1.50–2.45), stroke/systemic embolism (risk ratio [RR] 2.53; 95% CI 2.00–3.19), and MACEs (RR 2.17; 95% CI 1.89–2.49). However, the association between elevated BNP/NT‐proBNP level and major bleed was not statistically significant (RR 1.14; 95% CI 0.92–1.40). Elevated BNP/NT‐proBNP level is significantly associated with higher risk of all‐cause mortality, stroke/systemic embolism, and MACEs. Determination of BNP/NT‐proBNP level may play an important role in risk stratification of AF patients. [ABSTRACT FROM AUTHOR]

Objectives: Interferon-induced protein with tetratricopeptide repeats 1 (IFIT1) and interferon-induced transmembrane protein 3 (IFITM3) are commonly induced by type I interferon. The study aims to investigate the expression and clinical significance of IFIT1 and IFITM3 in head and neck squamous cell carcinoma (HNSCC).Methods: Immunohistochemistry was applied on tissue microarray to reveal IFIT1 and IFITM3 expression in 275 HNSCC, 69 dysplasia, and 42 normal mucosa samples. The clinicopathologic features associated with IFIT1 and IFITM3 expression in HNSCC patients were analyzed.Results: IFIT1 and IFITM3 were highly expressed in HNSCC tissues. High expression of IFIT1 and IFITM3 predicts a negative prognosis for patients (P < .01). IFIT1 and IFITM3 expression was associated with programmed cell death ligand 1, B7-H4, V-domain Ig suppressor of T-cell activation, indoleamine 2,3-dioxygenase, and macrophage marker immunoreactivity.Conclusions: IFIT1 and IFITM3 were overexpressed in HNSCC and indicated poor prognoses for patients with HNSCC. IFIT1 and IFITM3 expression was correlated with several immune checkpoint molecules and tumor-associated macrophage markers. [ABSTRACT FROM AUTHOR]

Background: The KIF5B-RET fusion gene is a novel oncogene that has been observed in a subset of lung cancers in recent years. However, the results of related epidemiological studies remain unclear. Thus, a meta-analysis was conducted to evaluate the correlation of KIF5B-RET expression based on RT-PCR detection with clinicopathological features and prognosis of lung cancer. Methods: The PubMed, Google Scholar, Wiley Online, SpringerLink and Chinese National Knowledge Infrastructure databases were searched to identify the eligible studies. The association of the occurrence of KIF5B-RET fusion gene in lung cancer with age, gender, smoking status, histology type, differentiation and TNM stage was analyzed. HR, overall survival (OS) and progression-free survival (PFS) were used to describe the prognosis of patients with lung cancer. The OR and 95% CI were calculated to assess the correlations. Random- and fixed-effects models were used to analyze the data. Results: A total of 13 studies, which included 8,859 lung cancer patients, were included in the study based on the inclusion criteria. A total of 121 patients with positive KIF5B-RET fusion gene status were detected, with a positive expression rate of 1.36%. KIF5B-RET fusion gene status was identified at significantly higher frequencies in female (OR=0.67, 95% CI=0.48–0.94) than male patients, and the same trend was found in young (<60 years) patients (OR=0.08, 95% CI=0.01–0.45) compared with old patients (≥60 years). No differences were found in the TNM stage, histology, differentiation and smoking. Based on the prognosis, no difference was found between the status of the positive and negative KIF5B-RET fusion genes in OS and PFS of patients. Conclusion: The KIF5B-RET fusion gene occurred predominantly in young female patients with lung cancer. However, the relationship between the expression of the fusion gene and the prognosis of lung patients remains unclear. [ABSTRACT FROM AUTHOR]

Background: Lung is the most common extrahepatic metastatic organ of liver cancer. Surgical resection is a common local treatment for pulmonary metastasis. But the long-term prognosis of pulmonary metastasectomy varies greatly due to the small sample size and different results of previous studies. Therefore, we conducted this meta-analysis to evaluate the combined 5-year overall survival (OS) rate and prognostic factors after pulmonary metastasectomy in liver cancer.Methods: Key words such as liver cancer pulmonary metastasis and metastasectomy were retrieved firstly in PubMed, Cochrane Library, Embase and Chinese Wanfang databases. Eligible studies were identified by manual searches. Each included study should report 5-year OS rate and/or prognostic factors of pulmonary metastasectomy. Newcastle-Ottawa Scale was used for quality assessment, and heterogeneity was estimated by I2. We calculated the combined 5-year survival rates and determined the prognostic factors for OS by the hazard ratios (HR) and number of events.Results: Seventeen cohort studies with a total of 513 patients were included in this meta-analysis. The combined 5-year survival rates after pulmonary metastasectomy were 33% [95% confidence interval (95% CI) 29-37%]. The poor prognostic factors were disease-free interval (DFI) < 12 months (HR = 2.421 95% CI 1.384 4.236) and existence of cirrhosis (HR = 1.936 95% CI 1.031 3.636).Conclusion: The 5-year OS rate of patients with pulmonary metastasectomy after resection of primary liver cancer is 33%. DFI < 12 months and existence of cirrhosis are probably poor prognostic factors. [ABSTRACT FROM AUTHOR]

Objectives: The aims of this study were to investigate the relationship between Golgi phosphoprotein 2 (GOLPH2) and oral squamous cell carcinoma (OSCC) and explore the clinical significance of GOLPH2 in OSCC.Methods: Tissue microarrays from human OSCC samples were stained for GOLPH2 expression and clinicopathologic features. Kaplan-Meier analysis was used to compare the survival of patients with high GOLPH2 expression and patients with low GOLPH2 expression.Results: We found GOLPH2 is highly expressed in OSCC tissue, and the GOLPH2 expression in metastatic lymph nodes is higher than in tumor tissue. Our data indicate that patients with higher GOLPH2 expression have poor overall survival compared with those with lower GOLPH2 expression. This study demonstrated that GOLPH2 was associated with CD44, SOX2, Slug, B7-H3, B7-H4, TIM3, and VISTA.Conclusions: These findings suggest GOLPH2 is a potential marker for estimating the patient's prognosis and may be a target for molecular-targeted therapy against OSCC. [ABSTRACT FROM AUTHOR]

Accumulated evidence indicates that rare variants exert a vital role on predisposition and progression of human diseases, which provides neoteric insights into disease etiology. In the current study, based on three independently retrospective studies of 5,016 lung cancer patients and 5,181 controls, we analyzed the associations between five rare polymorphisms (i.e., p.Glu116Lys, p.Asn118Ser, p.Arg138Cys, p.Ala195Thr and p.Leu259Phe) in MKK7 and lung cancer risk and prognosis. To decipher the precise mechanisms of MKK7 rare variants on lung cancer, a series of biological experiments was further performed. We found that the MKK7 p.Glu116Lys rare polymorphism was significantly associated with lung cancer risk, progression and prognosis. Compared with Glu/Glu common genotype, the 116Lys rare variants (Lys/Glu/+ Lys/Lys) presented an adverse effect on lung cancer susceptibility (odds ratio [OR] = 3.29, 95% confidence interval [CI] = 2.70–4.01). These rare variants strengthened patients’ clinical progression that patients with 116Lys variants had a significantly higher metastasis rate and advanced N, M stages at diagnosis. In addition, the patients with 116Lys variants also contributed to worse cancer prognosis than those carriers with Glu/Glu genotype (hazard ratio [HR] = 1.53, 95% CI = 1.32–1.78). Functional experiments further verified that the MKK7 p.116Lys variants altered the expression of several cancer-related genes and thus affected lung cancer cells proliferation, tumor growth and metastasis in vivo and in vitro. Taken together, our findings proposed that the MKK7 p.Glu116Lys rare polymorphism incurred a pernicious impact on lung cancer risk and prognosis through modulating expressions of a serial of cancer-related genes. [ABSTRACT FROM AUTHOR]

Recent genome-wide association studies implicated that the nicotinic acetylcholine receptors (nAChRs) are common susceptible genes of two contextual diseases: chronic obstructive pulmonary disease (COPD) and lung cancer. We aimed to test whether the copy number variations (CNVs) in nAChRs have hereditary contributions to development of the two diseases. In two, two-stage, case-control studies of southern and eastern Chinese, a common CNV-3956 that duplicates the cholinergic receptor, nicotinic, α7 (CHRNA7) gene was genotyped in a total of 7880 subjects and its biological phenotype was assessed. The ≥4-copy of CNV-3956 increased COPD risk (≥4-copy vs 2/3-copy: OR=1.44, 95% CI=1.23-1.68) and caused poor lung function, and it similarly augmented risk (OR=1.49, 95% CI=1.29-1.73) and worsened prognosis (hazard ratio (HR)=1.25, 95% CI=1.07-1.45) of lung cancer. The ≥4-copy was estimated to account for 1.56% of COPD heritability and 1.87% of lung cancer heritability, respectively. Phenotypic analysis further showed that the ≥4-copy of CNV-3956 improved CHRNA7 expression in vivo and increased the carriers' smoking amount. The CNV-3956 of CHRNA7 contributed to increased risks and poor prognoses of both COPD and lung cancer, and this may be a genetic biomarker of the two diseases. [ABSTRACT FROM AUTHOR]

Abstract: Cancer cells adapt to chronic stress in the tumor microenvironment by inducing the expression of glucose-regulated protein 78 (GRP78), a major endoplasmic reticulum chaperone with Ca2+-binding and antiapoptotic properties. The effect in and potential role of its expression in progression of and prognosis for gastric cancer (GC) are unclear. In the present study, we investigated the clinical value of GRP78 expression in judgment of the severity of and prognosis for GC in a retrospective cohort study of 160 patients who underwent D2 radical gastrectomy and adjuvant chemotherapy. GRP78 expression was detected using immunohistochemistry. The relationships of GRP78 expression with age, sex, differentiation, invasion depth, disease stage, lymph node metastasis, and time to recurrence (TTR) were analyzed. The GRP78 expression was higher in tumors from patients with deep tumor infiltration, with poor differentiation, at late disease stages, and with lymph node metastasis than that in tumors from patients without. Also, GRP78 positivity was associated with short TTR (hazard ratio [HR], 1.75; 95% confidence interval [CI], 1.07–4.85; P =0.041). Subgroup analysis revealed that the HR in the GRP78-high group increased significantly in patients who did not receive taxane-containing regimens (HR, 2.21; 95% CI, 1.23–7.36; P =0.038). In contrast, in the patients who received taxane-based chemotherapy, the association between GRP78 positivity and increased risk of recurrence was not statistically significant (HR, 1.16; 95% CI, 0.81–2.98; P =0.111). In the patients with GRP78 expression, those who underwent taxane-containing chemotherapy had longer median TTRs than did those who did not undergo this treatment (P =0.017). Downregulation of GRP78 expression markedly inhibited proliferation of the GC cells at the G1 phase, whereas GRP78 overexpression promoted cell-cycle progression. These findings suggest that GRP78 overexpression promotes GC cells proliferation and is an independent indicator of poor prognosis for GC. [Copyright &y& Elsevier]

Background: Cellular senescence frequently occurs during anti-cancer treatment, and persistent senescent tumor cells (STCs) unfavorably promote tumor progression through paracrine secretion of the senescence-associated secretory phenotype (SASP). Extracellular vesicles (EVs) have recently emerged as a novel component of the SASP and primarily mediate the tumor-promoting effect of the SASP. Of note, the potential effect of EVs released from STCs on tumor progression remains largely unknown. Methods: We collected tumor tissues from two cohorts of colorectal cancer (CRC) patients to examine the expression of p16, p21, and SERPINE1 before and after anti-cancer treatment. Cohort 1 included 22 patients with locally advanced rectal cancer (LARC) who received neoadjuvant therapy before surgical resection. Cohort 2 included 30 patients with metastatic CRC (mCRC) who received first-line irinotecan-contained treatment. CCK-8, transwell, wound-healing assay, and tumor xenograft experiments were carried out to determine the impacts of EVs released from STCs on CRC progression in vitro and in vivo. Quantitative proteomic analysis was applied to identify protein cargo inside EVs secreted from STCs. Immunoprecipitation and mass spectrometer identification were utilized to explore the binding partners of SERPINE1. The interaction of SERPINE1 with p65 was verified by co-immunoprecipitation, and their co-localization was confirmed by immunofluorescence. Results: Chemotherapeutic agents and irradiation could potently induce senescence in CRC cells in vitro and in human CRC tissues. The more significant elevation of p16 and p21 expression in patients after anti-cancer treatment displayed shorter disease-free survival (DFS) for LARC or progression-free survival (PFS) for mCRC. We observed that compared to non-STCs, STCs released an increased number of EVs enriched in SERPINE1, which further promoted the progression of recipient cancer cells. Targeting SERPINE1 with a specific inhibitor, tiplaxtinin, markedly attenuated the tumor-promoting effect of STCs-derived EVs. Additionally, the patients with greater increment of SERPINE1 expression after anti-cancer treatment had shorter DFS for LARC or PFS for mCRC. Mechanistically, SERPINE1 bound to p65, promoting its nuclear translocation and subsequently activating the NF-κB signaling pathway. Conclusions: We provide the in vivo evidence of the clinical prognostic implications of therapy-induced senescence. Our results revealed that STCs were responsible for CRC progression by producing large amounts of EVs enriched in SERPINE1. These findings further confirm the crucial role of therapy-induced senescence in tumor progression and offer a potential therapeutic strategy for CRC treatment. [ABSTRACT FROM AUTHOR]

• A OS-related signature with robust predictive performance was developed based on proteomic profile of SARC patients from TPCA database. • The signature was validated from transcriptomic dataset of SARC patients from TCGA, and could be independent prognostic predictor after adjusting for clinicopathological parameters. • The signature has predictive capacity for predicting progression free intervals and disease free intervals for SARC patients. • Tumor infiltrating lymphocytes and immune checkpoint molecules analysis revealed distinctly immune landscapes of high- and low-risk patients. Sarcoma (SARC) represents a group of highly histological and molecular heterogeneous rare malignant tumors with poor prognosis. There are few proposed classifiers for predicting patient's outcome. The Cancer Proteome Atlas (TPCA) and The Cancer Genome Atlas (TCGA) databases provide multi-omics datasets that enable a comprehensive investigation for this disease. The proteomic expression profile of SARC patients along with the clinical information was downloaded. 55 proteins were found to be associated with overall survival (OS) of patients using univariate Cox regression analysis. We developed a prognostic risk signature that comprises seven proteins (AMPKALPHA, CHK1, S6, ARID1A, RBM15, ACETYLATUBULINLYS40, and MSH6) with robust predictive performance using multivariate Cox stepwise regression analysis. Additionally, the signature could be an independent prognostic predictor after adjusting for clinicopathological parameters. Patients in high-risk group also have worse progression free intervals (PFI) than that of patients in low-risk group, but not for disease free intervals (DFI). The signature was validated using transcriptomic profile of SARC patients from TCGA. Potential mechanisms between high- and low-risk groups were identified using differentially expressed genes (DEGs) analysis. These DEGs were primarily enriched in RAS and MPAK signaling pathways. The signature protein molecules are candidate biomarkers for SARC, and the analysis of computational biology in tumor infiltrating lymphocytes and immune checkpoint molecules revealed distinctly immune landscapes of high- and low-risk patients. Together, we constructed a prognostic signature for predicting outcomes for SARC integrating proteomic and transcriptomic profiles, this might have value in guiding clinical practice. [ABSTRACT FROM AUTHOR]

Purpose: There is an aberrant expression of NBAT-1 in various human cancers, which was proven to limit the proliferation, invasion, and metastasis of tumour cells via multiple approaches. Most existing research focuses on sample size and discrete outcomes. Thus, a quantitative meta-analysis was performed to elucidate the prognostic value of lncRNA NBAT-1 expression in cancer patients. Materials and methods: Using Web of Science and PubMed, two researchers independently identified relevant studies to explore the association between the pathological features of human cancers and NBAT-1 expression levels. Then two scholars conducted literature screening according to exclusion criteria and admission criteria, and finally conducted statistical analysis through data extraction with StataSE 12.0. Results: A total of 12 eligible studies with 1600 patients were included in the meta-analysis eventually. It is indicated that the low expression level of lncRNA NBAT-1 was closely related to distant metastasis [RR = 0.50, 95% CI (0.33, 0.76), and P = 0.00], deep tumour invasion [RR = 0.62, 95% CI (0.49,0.80), and P = 0.00], poor histological grade [RR = 0.68, 95% CI (0.57, 0.81), and P = 0.00], advanced TNM stage [RR = 0.66, 95% CI (0.55, 0.79), and P = 0.00], large tumour volume[RR = 0.72, 95% CI (0.55, 0.93), and P = 0.01], and lymph node metastasis [RR = 0.62, 95% CI (0.46, 0.84), and P = 0.00], suggesting that it may serve as biomarkers for patients with poor prognosis. Conclusion: Reduced expression of NBAT-1 can predict poor prognosis in several cancers, as found in the meta-analysis, demonstrating that NBAT-1 can serve as a promising prognostic factor of human cancers. [ABSTRACT FROM AUTHOR]

• RNAscope in situ hybridization was used to determine FAM83H-AS1 expression. • FAM83H-AS1 was significantly higher in cancer tissues than in paired normal mucosa from colon cancer patients. • High levels of FAM83H-AS1 predicts a poor prognosis in the patients with colon cancer. • FAM83H-AS1 downregulation promoted SMAD1 expression. Long noncoding RNAs (LncRNAs) have been proven to participate in many principal pathways during colonic mucosa tumourigenesis. FAM83H-AS1 has been identified as one of the LncRNAs that is dysregulated in multi-type cancers. Here, our purpose was to determine the expression pattern and clinical significance of FAM83H-AS1 and further analyse its prognostic value in colon cancer. FAM83H-AS1 expression was examined in 90 patients with colon cancer by RNAscope in situ hybridization, and the expression levels were analysed with the overall survival (OS) rates for patients with colon cancer. TCGA datasets derived from colon cancer (COAD) were used to further validate the main findings. We demonstrated that the expression of FAM83H-AS1 was significantly higher in cancer tissues than in paired normal mucosa from colon cancer patients (P < 0.001). The prognostic analysis indicated that the OS rates for colon cancer patients with high levels of FAM83H-AS1 were significantly lower than those for patients with low levels of FAM83H-AS1 (P = 0.013). The higher levels of FAM83H-AS1 were found to be associated with a lower expression of SMAD1/5/9, which is involved in TGF-β signalling in colon cancer tissues (P = 0.0174). In HCT116 and SW480 cell lines, the down regulation of FAM83H-AS1 promoted the expression of SMAD1. Our investigations suggest that the upregulation of FAM83H-AS1 serves as a promising predictor and might be conducive for clinicians to estimate OS time. FAM83H-AS1 might serve as an inhibitor of TGF-β signalling. [ABSTRACT FROM AUTHOR]

There are many factors that affect the survival of patients with gastric cancer, such as TNM stage, the patient's nutritional status, inflammation, and so on. In this study, the prognostic significance of preoperative fibrinogen-to-albumin ratio (FAR) and postoperative TNM staging in patients with gastric cancer was retrospectively studied. A total of 265 patients (surgery dates from January 2007 to December 2013) were included in this retrospective study. All the patients were confirmed by pathology after operation. Categorical variables were compared using the χ2 test. Kaplan–Meier and log-rank tests were used for survival analysis. Cox proportional hazard models were used to assess prognostic factors. Nomogram was applied to predict the prognosis of overall survival (OS). The higher the FAR value, the more lymph node metastasis, the later the TNM stage, and the shorter the survival time. We established a new scoring system, the FAR-TNM score, which combined FAR and TNM stage. The FAR-TNM score was significantly related to tumor location, tumor size, Bormann types, differentiation, operative type, vascular invasion, nerve invasion, depth of invasion, lymphatic metastasis, and advanced TNM stage. Multivariate Cox regression analysis demonstrated that tumor location, TNM stage, adjuvant chemotherapy, and FAR-TNM score were independent prognostic elements for OS in patients with GC. The FAR-TNM score was a valuable independent prognostic indicator for GC patients after surgery, which can help clinicians to assist the treatment and long-term management of patients with gastric cancer. [ABSTRACT FROM AUTHOR]

We retrospectively analyzed the treatment outcomes of elderly patients (aged ≥ 60 years) with extranodal natural killer/T-cell lymphoma, nasal type (ENKTL) and investigated the prognostic factors. Fifty-two elderly patients received chemotherapy alone, radiotherapy alone, or chemotherapy followed by radiotherapy ± consolidation chemotherapy as induction therapy. Overall, 97.26% patients in stage I/II had overall response (OR) and 86.1% had complete response (CR), whereas 71.4% of patients in stage III/IV had OR and 35.7% had CR. The 3-year freedom from progression (FFP) rate and overall survival (OS) rate of patients with stage I/II were 78.2% and 85.0%, respectively, and those with stage III/IV were 23.3% and 33.3%. Following multivariate analysis of Cox regression, ECOG performance status scores of 3–4 and stage III/IV were independent prognostic factors for elderly ENKTL patients. Elderly patients with stage I/II or stage III/IV and good or poor performance status can benefit from the commonly used or personalized treatment. [ABSTRACT FROM AUTHOR]

Objective. To determine prognostic role of endothelial progenitor cells (EPCs) in intensive care patients with acute myocardial infarction (AMI). Materials and Methods. From December 2018 to July 2021, a total of 91 eligible patients with AMI were consecutively examined in a single intensive care unit (ICU) in China. Patients with a history of acute coronary artery disease were excluded from the study. Samples were collected within 24 hr of onset of symptoms. EPCs, defined as coexpression of CD34+/CD133+ cells or CD133+/CD34+/KDR+, were studied using flow cytometry and categorized by quartiles. Based on the 28-days mortality outcome, the patients were further divided into two groups: death and survival. The study incorporated various variables, including cardiovascular risk factors such as body mass index, hypertension, diabetes, hypercholesterolemia, atherosclerotic burden, and medication history, as well as clinical characteristics such as APACHEⅡscore, central venous-arterial carbon dioxide difference (GAP), homocysteine, creatinine, C-reactive protein, HbAlc, and cardiac index. Cox regression analysis was employed to conduct a multivariate analysis. Results. A total of 91 patients with AMI who were admitted to the ICU were deemed eligible for inclusion in the study. Among these patients, 23 (25.3%) died from various causes during the follow-up period. The counts of EPCs were found to be significantly higher in the survival group compared to the death group (P < 0.05). In the univariate analysis, it was observed that the 28-days mortality rate was associated with the several factors, including the APACHEⅡscore (P = 0.00), vasoactive inotropic score (P = 0.03), GAP (P = 0.00), HCY (P = 0.00), creatinine (P = 0.00), C-reactive protein (P = 0.00), HbAlc (P = 0.00), CI (P = 0.01), quartiles of CD34+/CD133+ cells (P = 0.00), and quartiles of CD34+/CD133+/KDR+ cells (P = 0.00). CD34+/CD133+/KDR+ cells retained statistical significance in Cox regression models even after controlling for clinical variables (HR: 6.258 × 10−10 and P = 0.001). Nevertheless, no significant correlation was observed between CD34+/CD133+ cells and all-cause mortality. Conclusions. The decreased EPCs levels, especially for CD34+/CD133+/KDR+ cells subsets, were an independent risk factor for 28-days mortality in AMI patients. [ABSTRACT FROM AUTHOR]

Background: The epithelial-mesenchymal transition (EMT) plays an indispensable role in the development and progression of Endometrial cancer (EC). Nevertheless, little evidence is reported to uncover the functionality and application of EMT-related molecules in the prognosis of EC. This study aims to develop novel molecular markers for prognosis prediction in patients with EC. Methods: RNA sequencing profiles of EC patients obtained from The Cancer Genome Atlas (TCGA) database were used to screen differential expression genes (DEGs) between tumors and normal tissues. The Cox regression model with the LASSO method was utilized to identify survival-related DEGs and to establish a prognostic signature whose performance was evaluated by Kaplan–Meier curve, receiver operating characteristic (ROC) and calibration curve. Eventually, functional enrichment analysis and cellular experiments were performed to reveal the roles of prognosis-related genes in EC progression. Results: A total of 540 EMT-related DEGs in EC were screened, and subsequently a four-gene risk signature comprising SIRT2, SIX1, CDKN2A and PGR was established to predict overall survival of EC. This risk signature could serve as a meaningfully independent indicator for EC prognosis via multivariate Cox regression (HR = 2.002, 95%CI = 1.433–2.798; P < 0.001). The nomogram integrating the risk signature and clinical characteristics exhibited robust validity and performance at predicting EC overall survival indicated by ROC and calibration curve. Functional enrichment analysis revealed that the EMT-related genes risk signature was associated with extracellular matrix organization, mesenchymal development and cellular component morphogenesis, suggesting its possible relevance to epithelial-mesenchymal transition and cancer progression. Functionally, we demonstrated that the silencing of SIX1, SIRT2 and CDKN2A expression could accelerate the migratory and invasive capacities of tumor cells, whereas the downregulation of PGR dramatically inhibited cancer cells migration and invasion. Conclusions: Altogether, a novel four-EMT-related genes signature was a potential biomarker for EC prognosis. These findings might help to ameliorate the individualized prognostication and therapeutic treatment of EC patients. [ABSTRACT FROM AUTHOR]

Background: The incidence of cervical neuroendocrine carcinoma (CNECC) during pregnancy is extremely rare. Insufficient awareness of gynecological tumor screening, as well as atypical and insidious initial clinical symptoms, may result in diagnostic delays and misdiagnosis. There is no standardized treatment for cervical cancer in pregnancy. Herein, we present a case of cervical neuroendocrine carcinoma diagnosed in the third trimester of pregnancy. Case presentation: A 26-year-old female at 30 1/7 weeks of gestation presented with lower back and sacroiliac joint pain, abdominal distension, and lower limb dyskinesia. A pelvic examination revealed a large fungating gray mass that encompassed the entire cervix, with cervical contact bleeding testing positive. Imaging studies showed a significant cervical mass, diffuse liver changes, and metastasis to multiple sites. Biopsy results revealed poorly differentiated cervical carcinoma exhibiting high-grade neuroendocrine features, consistent with a diagnosis of large cell neuroendocrine carcinoma. The patient was diagnosed with stage IVB CNECC with HPV18 (+), and due to the gestational age of the fetus and her deteriorating condition, she underwent cesarean section delivery after receiving fetal lung maturation therapy. Following surgery, eight cycles of neoadjuvant chemotherapy were applied. Unfortunately, she succumbed to multiple tumor metastases six months post-treatment. Despite this tragic outcome, the infant was discharged in a healthy condition. Conclusions: CNECC during pregnancy, particularly the large-cell type, is an ultra-rare condition with poor prognosis. This case highlights the importance of individualized treatment approach and the need for better screening, early detection, and treatment. Given the rarity of the disease, further research is warranted to determine the prognostic factors and develop effective treatment strategies for this ultra-rare and aggressive malignancy. [ABSTRACT FROM AUTHOR]

Background: We screened out several hypermethylated solute carrier (SLC) family genes in acute myeloid leukemia by reduced representation bisulfite sequencing. SLC22A3 encodes an organic cation transport protein, which is critical for drug transportation and cellular detoxification. SLC22A3 is significantly downregulated and associated with tumor progression and worse prognosis in a variety of solid tumors. However, there are no data available regarding the role of SLC22 in AML. This study aimed to explore the regulatory mechanism of DNA methylation on SLC22A3 expression, as well as its clinical significance in AML prognosis. Results: SLC22A3 was identified as the sole prognosis-associated gene among SLCs based on TCGA and Beat AML databases. Bone marrow mononuclear cells (BMMNCs) from AML, MDS patients, and healthy donors were enrolled in this study. SLC22A3 methylation was significantly increased in AML compared with controls and MDS patients; meanwhile, the expression level of SLC22A3 was decreased. SLC22A3 hypermethylation presented an obvious association with some specific clinical characteristics and affected the survival time of AML patients as an independent risk indicator. SLC22A3 expression changed regularly as the disease complete remissions and relapses. Demethylation drug 5-aza-2′-deoxycytidine (DAC) activated transcription and increased mRNA expression of SLC22A3 in leukemia cell lines and AML fresh BMMNCs. Knockdown of SLC22A3 in leukemia cells enhanced cell proliferation and suppressed cell apoptosis. Data from public programs were used for auxiliary screening of probable molecular mechanisms of SLC22A3 in the antileukemia effect. Conclusions: Our results showed that increased methylation and decreased expression of SLC22A3 may be indicators of poor prognosis in AML. Methylation-silenced SLC22A3 expression may have potential guiding significance on antileukemia effect of DAC. [ABSTRACT FROM AUTHOR]

Background: Small intestine adenocarcinoma (SIA) is a scant disease that has no adequate clinical trials, so its prognostic factors are still unclear, especially in elderly patients. In this article, we aimed to explore the clinicopathology presentation, treatments, outcomes, and predictors of small intestine adenocarcinoma patients aged 65 years or older. Methods: We retrieved clinicopathology data of small intestine adenocarcinoma patients diagnosed between 2004 and 2015 from the Surveillance Epidemiology and End Results (SEER) database. We clarified patients into two groups: the surgery and the non-surgery group and conducted propensity score matching (PSM) to compare survival outcoming. We identified the prognostic indicators for cancer-specific survival (CSS) and overall survival (OS) by the Cox proportional hazards model. Results: In total, 1018 eligible cases were enrolled, with a median survival of 16 months; the 3-year OS and CSS rates were 36% and 41.7%, and the 5-year OS and CSS rates were 26.5% and 33.3%. Multivariate analyses revealed that age, grade, tumor stage, surgery, and chemotherapy were independent prognostic factors for OS, while grade, tumor stage, surgery, radiation, and chemotherapy were independent factors for CSS. After PSM, only surgery and tumor stage (AJCC 6th) were independent prognostic factors for OS and CSS. Conclusion: Surgery could bring benefit to survival for elderly SIA patients, and the early stage of the disease was another significant prognostic factor. [ABSTRACT FROM AUTHOR]

Abnormal methylation of let-7a-3 has been found in various cancers and may consequently affect their survival. In this study, real-time quantitative methylation specific PCR (RQ-MSP) was used to determine the unmethylation level of let-7a-3 in 95 patients with myelodysplastic syndrome (MDS). The hypomethylation of let-7a-3 promoter was detected in 22 of 95 (23.2%) patients with MDS compared to 4.2% (1/24) of controls (p= 0.0419). Moreover, the frequency of let-7a-3 hypomethylation was higher in older patients (≥70 years) than in younger patients (<70 years). No significant difference was observed in distribution of WHO, IPSS, and cytogenetic classification. However, hypomethylated patients had significantly shorter overall survival than those without hypomethylation (p= 0.007). Moreover both Kaplan–Meier and Multivariate Cox analyses confirmed that let-7a-3 hypomethylation was an independent prognostic risk factor in cohorts of MDS patients with lower-risk disease. Our study suggested that let-7a-3 hypomethylation may predict poor outcome in MDS. [ABSTRACT FROM PUBLISHER]

• Significantly different prognoses were found between two ABCB1 groups in breast cancer patients. • The expression level of ABCB1 gene was significantly correlated with several immune-related features in breast cancer patients. • The ABCB1 can be used to predict the therapeutic effect of immunotherapy in breast cancer patients. ABCB1 is an important gene that closely related to analgesic tolerance to opioids, and plays an important role in their postoperative treatment. Recent studies have demonstrated that ABCB1 genotype is significantly associated with the chemico-resistance and chemical sensitivity in breast cancer patients. So, it is become very important to investigate the important role of ABCB1 for predicting drug response in breast cancer patients. In this study, by conducting the Cox proportional hazards regression analysis in breast cancer patients, significant differences were found in prognosis between the ABCB1 high- and low-expression subtypes. Meanwhile, by using immune infiltration profiles as well as transcriptomics datasets, the ABCB1 high subtype was found to be significantly enriched in many immune-related KEGG pathways and biological processes, and was characterized by the high infiltration levels of immune cell types. Furthermore, bioinformatics inference revealed that the ABCB1 subtypes were associated with the therapeutic effect of immunotherapy, which would be important for patient prognosis. In conclusion, these findings may provide useful help for recognizing the diversity between ABCB1 subtypes in tumor immune microenvironment, and may unravel prognosis outcomes and immunotherapy utility for ABCB1 in breast cancer. [ABSTRACT FROM AUTHOR]

Circular RNAs (circRNAs) represent a novel class of non-coding RNAs that play significant roles in tumorigenesis and tumor progression. High-throughput sequencing of gastric cancer (GC) tissues has identified circRNA BIRC6 (circBIRC6) as a potential circRNA derived from the BIRC6 gene, exhibiting significant upregulation in GC tissues. The expression of circBIRC6 is notably elevated in GC patients. Functionally, it acts as a molecular sponge for miR-488, consequently upregulating GRIN2D expression and promoting GC proliferation, migration, and invasion. Moreover, overexpression of circBIRC6 leads to increased GRIN2D expression, which in turn enhances caveolin-1 (CAV1) expression, resulting in autophagy deficiency due to miR-488 sequestration. This cascade of events significantly influences tumorigenesis in vivo. Our findings collectively illustrate that the CircBIRC6-miR-488-GRIN2D axis fosters CAV1 expression in GC cells, thereby reducing autophagy levels. Both circBIRC6 and GRIN2D emerge as potential targets for treatment and independent prognostic factors for GC patients. [Display omitted] [ABSTRACT FROM AUTHOR]

Background: Long noncoding RNAs (lncRNAs) are emerging as master regulators for gene expression and thus play a vital role in human tumorigenesis and progression. But the involvement of novel lncRNAs in non-small cell lung cancer (NSCLC) remains largely unelucidated. Methods: A total of 170 NSCLC and their adjacent non-tumor tissues were enrolled to detect the expression of Lnc-LSAMP-1 by RT-qPCR. The effects of Lnc-LSAMP-1 on cell proliferation, migration, invasion and drug-sensitivity were determined by in vitro and in vivo experiments. The proteins that interact with Lnc-LSAMP-1were confirmed by RNA pull-down assay. RNA-sequencing were used to identify the potential targets of Lnc-LSAMP-1 in NSCLC. Results: We found that Lnc-LSAMP-1 was significantly down-regulated in 170 cases of NSCLC tissues when compared to their adjacent non-cancerous tissues. Loss expression of Lnc-LSAMP-1 was notably correlated with unfavorable prognosis of NSCLC patients. The ectopic expression of Lnc-LSAMP-1 drastically inhibited lung cancer cell proliferation, viability, invasion and migration ability, arrested cell cycle and facilitated apoptosis. Chemotherapy sensitization experiments showed that over-expressed Lnc-LSAMP-1 enhanced the inhibition of cell proliferation induced by TKI. Mechanistically, Lnc-LSAMP-1-LSAMP formed a complex which could protect the degradation of LSAMP gene, and thus exerted crucial roles in NSCLC progression and TKI targeted treatment. Conclusions: Consequently, our findings highlight the function and prognostic value of Lnc-LSAMP-1 in NSCLC and provide potential novel therapeutic targets and prognostic biomarkers for patients with NSCLC. [ABSTRACT FROM AUTHOR]

Breast cancer is a kind of malignant tumor that occurs in breast tissue, which is the most common cancer in women. Cellular metabolism is a critical determinant of the viability and function of cancer cells in tumor microenvironment. In this study, based on the gene expression profile of metabolism-related genes, the prognostic value of 20 metabolic pathways in patients with breast cancer was identified. A universal risk stratification signature that relies on 20 metabolic pathways was established and validated in training cohort, two testing cohorts and The Cancer Genome Atlas pan cancer cohort. Then, the relationship between metabolic risk score subtype, prognosis, immune infiltration level, cancer genotypes and their impact on therapeutic benefit were characterized. Results demonstrated that the patients with the low metabolic risk score subtype displayed good prognosis, high level of immune infiltration and exhibited a favorable response to neoadjuvant chemotherapy and immunotherapy. Taken together, the work presented in this study may deepen the understanding of metabolic hallmarks of breast cancer, and may provide some valuable information for personalized therapies in patients with breast cancer. [ABSTRACT FROM AUTHOR]

Objective: Upper urinary tract urothelial carcinoma (UTUC) is a relatively uncommon disease with few reported molecular markers. This study evaluated Tim-3 and PD-1 expression in primary UTUC and its impact on patients' clinical outcomes.Methods: Tim-3 and PD-1 protein expression was detected by immunohistochemistry in paraffin-embedded sections from 101 UTUC patients. The H-score was correlated with clinicopathologic outcomes and the long-term recurrence and survival rates.Results: T cell immunoglobulin mucin-3 (Tim-3) protein was overexpressed in UTUC cells, especially tumour-infiltrating lymphocytes (TILs) and endothelial cells. We found that 95% (95/101) of UTUC tissues had dysregulated Tim-3 expression, of which 44% (44/101) showed high expression. High Tim-3 expression (H-score≥100) was significantly correlated with advanced pathological grade, advanced T stage and tumour recurrence (P=0.016, 0.001 and < 0.001, respectively) and with poor intravesical recurrence-free survival (IRFS) and overall survival (OS) (P< 0.001 and 0.003). Moreover, another immune checkpoint molecule, programmed death receptor-1 (PD-1), was also assessed in our study. Among patients in the low Tim-3 expression subgroup, those with high PD-1 expression experienced intravesical recurrence (IVR) more often than those with low PD-1 expression (P< 0.001). However, the PD-1 expression level had no effect on prognosis in the high Tim-3 expression subgroup.Conclusion: We confirmed that high Tim-3 protein expression can be used as an indicator of earlier IVR and shorter OS in patients with UTUC, while high expression of PD-1 is only related to earlier IVR. We showed that Tim-3 plays a more important role in tumour recurrence and progression than PD-1. Collectively, our findings support the use of Tim-3 and PD-1 as clinical prognostic factors indicating poor patient survival. Tim-3, alone or in combination with PD-1, could become a target for future UTUC therapies, but further prospective studies are needed. [ABSTRACT FROM AUTHOR]

Background. In recent years, the incidence of colorectal cancer (CRC) has continued to increase. Although the overall prognosis of CRC has improved with the continuous improvement of the level of treatment, the prognosis of metastatic colorectal cancer (mCRC) is still poor. The purpose of our study is to explore the prognostic value of platelet to lymphocyte ratio (PLR) in mCRC. Methods. The PubMed, Web of Science, and Embase (via OVID) were systematically searched to obtain all relevant research. We used hazard ratio (HR) with 95% confidence interval (CI) to assess the associations of PLR and overall survival (OS) and progression free survival (PFS). Results. A total of twelve studies containing 1452 patients were included in this meta-analysis. Pooled analysis showed that high levels of PLR were associated with poor OS (HR: 1.72, 95% CI: 1.27–2.33, and P < 0.01) and PFS (HR: 1.64, 95% CI: 1.16–2.31, and P = 0.033). Conclusion. Our analysis suggested that high levels of PLR pretreatment may be an effective predictive biomarker for the prognosis of mCRC patients. [ABSTRACT FROM AUTHOR]

Background: Colorectal cancer is one of the most common malignancy in the world. It has been reported that cancer stem cells (CSCs) serve as the primary drivers of tumorigenesis and tumor progression. There is an urgent need to explore novel molecules that regulate CSCs or their signatures. Increasing evidence has shown that miRNAs are involved in tumorigenesis and progression. Here, we aim to explore the regulatory effect and mechanism of miR-3065-3p on the stemness of colorectal cancer.Methods: The expression of miR-3065-3p in colorectal cancer and the association of miR-3065-3p expression with prognosis of patients with colorectal cancer were analyzed using TCGA dataset or clinical cases. Gain or loss of function in different models, including colorectal cancer cell lines and orthotopic xenograft or liver metastatic mouse model, were used to investigate the effects of miR-3065-3p on colorectal cancer stemness and metastasis in vitro and in vivo. Cancer stemness was analyzed by detecting the ability of migration and invasion, NANOG, OCT4, and SOX2 expression, ALDH activity and sphere formation. In addition, the interaction of miR-3065-3p and cytokine receptor-like factor 1 (CRLF1) was analyzed theoretically and identified by the luciferase reporter assay. Moreover, the correlation between CRLF1 expression and miR-3065-3p was analyzed in colorectal cancer tissues. Finally, the effect of CRLF1 on the stemness and metastasis of colorectal cancer in vitro and in vivo was assessed.Results: In this report, we found that miR-3065-3p was overexpressed in colorectal cancer and that its high expression was associated with poor prognosis of patients with colorectal cancer. miR-3065-3p promotes the stemness and metastasis of colorectal cancer. Furthermore, CRLF1 was the downstream target of miR-3065-3p and inhibited the stemness of colorectal cancer. In addition, CRLF1 expression was negatively correlated with miR-3065-3p in colorectal cancer tissues. And, CRLF1 mediated the effects of miR-3065-3p on promoting stemness of colorectal cancer cells.Conclusion: Our data suggest that miR-3065-3p promoted the stemness and metastasis of colorectal cancer by targeting CRLF1. miR-3065-3p might serve as a promising prognostic marker as well as a therapeutic target for colorectal cancer. [ABSTRACT FROM AUTHOR]

Breast cancer is one of the most common types of cancers and the leading cause of death from malignancy among women worldwide. Tumor-infiltrating lymphocytes are a source of important prognostic biomarkers for breast cancer patients. In this study, based on the tumor-infiltrating lymphocytes in the tumor immune microenvironment, a risk score prognostic model was developed in the training cohort for risk stratification and prognosis prediction in breast cancer patients. The prognostic value of this risk score prognostic model was also verified in the two testing cohorts and the TCGA pan cancer cohort. Nomograms were also established in the training and testing cohorts to validate the clinical use of this model. Relationships between the risk score, intrinsic molecular subtypes, immune checkpoints, tumor-infiltrating immune cell abundances and the response to chemotherapy and immunotherapy were also evaluated. Based on these results, we can conclude that this risk score model could serve as a robust prognostic biomarker, provide therapeutic benefits for the development of novel chemotherapy and immunotherapy, and may be helpful for clinical decision making in breast cancer patients. [ABSTRACT FROM AUTHOR]

A non-invasive method to distinguish potential lung cancer patients would improve lung cancer prevention. We employed the RNA-sequencing analysis to profile serum exosomal long non-coding RNAs (lncRNAs) from non-small cell lung cancer (NSCLC) patients and pneumonia controls, and then determined the diagnostic and prognostic value of a promising lncRNA in four datasets. We identified 90 dysregulated lncRNAs for NSCLC and found the most significant lncRNA was a novel isoform of linc01125. Serum exosomal linc01125 could distinguish NSCLC cases from disease-free and tuberculosis controls, with the area under the curve values as 0.662 [95% confidence interval (CI) = 0.614–0.711] and 0.624 (95% CI = 0.522–0.725), respectively. High expression of exosomal linc01125 was also correlated with an unfavorable overall survival of NSCLC (hazard ratio = 1.48, 95% CI = 1.05–2.08). Clinic treatment decreased serum exosomal linc01125 in NSCLC patients (P = 0.036). Linc01125 functions to inhibit cancer growth and metastasis via acting as a competing endogenous RNA to up-regulate tumor necrosis factor alpha-induced protein 3 (TNFAIP3) expression by sponging miR-19b-3p. Notably, the oncogenic transformation of 16HBE led to decreased linc01125 in cells but increased linc01125 in cell-derived exosomes. The expression of linc01125 in total exosomes was highly correlated with that in tumor-associated exosomes in serum. Moreover, lung cancer cells were capable of releasing linc01125 into exosomes in vitro and in vivo. Our analyses suggest serum exosomal linc01125 as a promising biomarker for non-invasively diagnosing NSCLC and predicting the prognosis of NSCLC. [ABSTRACT FROM AUTHOR]

Breast cancer is one of the most human malignant diseases and the leading cause of cancer-related death in the world. However, the prognostic and therapeutic benefits of breast cancer patients cannot be predicted accurately by the current stratifying system. In this study, an immune-related prognostic score was established in 22 breast cancer cohorts with a total of 6415 samples. An extensive immunogenomic analysis was conducted to explore the relationships between immune score, prognostic significance, infiltrating immune cells, cancer genotypes and potential immune escape mechanisms. Our analysis revealed that this immune score was a promising biomarker for estimating overall survival in breast cancer. This immune score was associated with important immunophenotypic factors, such as immune escape and mutation load. Further analysis revealed that patients with high immune scores exhibited therapeutic benefits from chemotherapy and immunotherapy. Based on these results, we can conclude that this immune score may be a useful tool for overall survival prediction and treatment guidance for patients with breast cancer. [ABSTRACT FROM AUTHOR]

Background: Inflammation and nutrition are important causes contributing to the progression and poor survival of gastric cancer (GC). The objective of this study is to investigate the prognostic significance of the preoperative fibrinogen-to-pre-albumin ratio (FPR) and the prognostic nutritional index (PNI) in GC patients who have undergone gastrectomy. Methods: A total of 274 patients with resected pathological GC from January 2007 to December 2013 were enrolled in this retrospective study. Survival analysis was performed using Kaplan–Meier and log rank tests. Univariate and multivariate analyses were established to identify independent prognostic factors of 5-year survival. A predictive nomogram was used to predict prognosis of overall survival (OS), and its accuracy was determined by Harrell's concordance index (C index). Results: A high preoperative FPR-PNI score was significantly correlated with age, bigger tumor size, more lymphatic metastases and advanced TNM stage. Univariate analysis revealed that the GC patients with high FPR, low PNI and high FPR-PNI scores had shorter survival time. Multivariate analysis showed that FPR-PNI was an independent prognostic factor for OS in GC patients, especially in elderly patients. In the sub-analysis by age, the FPR-PNI score could significantly increase the accuracy of prognosis compared with the FPR and PNI alone in elderly GC patients. Conclusion: The preoperative FPR-PNI score is an effective independent prognostic index for GC patients after surgery, especially in elderly patients. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to explore the potential role and regulatory mechanism of microRNA (miR)-222-3p in oral squamous cell carcinoma (OSCC).Methods: The expression level and prognostic significance of miR-222-3p was detected in OSCC tissues. CCK-8, transwell, and flow cytometry assays were used to explore the effect of miR-222-3p on cell proliferation, migration, invasion, and apoptosis. The influence of miR-222-3p on cyclin-dependent kinase inhibitor 1B (CDKN1B) expression was evaluated by luciferase assays, real-time polymerase chain reaction, and Western blot.Results: We found that miR-222-3p was overexpressed in OSCC tissues, comparing with normal tissues. Kaplan-Meier curves showed that OSCC patients with high expression of miR-222-3p (P = .003) showed worse overall survival than those patients with low expression of miR-222-3p. Multivariate analysis showed that miR-222-3p (P = .037) expression was an independent prognostic factor of OSCC patients. miR-222-3p promoted cell proliferation, migration and invasion and induced the apoptosis of SCC-15 and Tca-83 cells. Furthermore, luciferase reporter assays indicated that CDKN1B is targeted by miR-222-3p in OSCC cells. Overexpression of CDKN1B inhibited OSCC cell proliferation, migration, and invasion and promoted cell apoptosis rate.Conclusions: miR-222-3p affects OSCC cell proliferation, migration, invasion, and apoptosis through targeting CDKN1B, and may be a potential prognostic biomarker for OSCC patients. [ABSTRACT FROM AUTHOR]

We retrospectively evaluated the long-term outcomes of patients receiving an EPOCHL (EPOCH + L-asparaginase) regimen as first-line chemotherapy for newly diagnosed extranodal natural killer/T cell lymphoma, nasal type (ENKTL). Ninety-six patients received 2–8 cycles of EPOCHL. After 2–4 cycles, 55.2% patients had complete response (CR) and 39.6% had partial response (PR). 42.7% patients developed progressive or relapsed disease. The 5-year progression-free survival (PFS) rates were 56.1% overall, 59.8% for stage I/II, and 34.9% for stage III/IV disease, and corresponding 5-year overall survival (OS) rates were 58.7, 65.3, and 39.8%, respectively. OS differed significantly between patients with stage I/II and those with stage III/IV disease (p = 0.018). Patients who achieved CR had better 3-year OS of 92.9%. Advanced stage disease was a poor prognostic factor for OS. All major adverse events associated with the EPOCHL regimen were reversible, and this first-line chemotherapy was safe and effective for patients with ENKTL. [ABSTRACT FROM AUTHOR]

Abstract PDH E1 component subunit alpha (PDHA1) has been reported to be biologically significant in several human tumors. The aim of this study was to investigate the expression of PDHA1 in gastric cancer (GC) and its relationship with clinicopathological characteristics and prognosis. Oncomine analysis of neoplastic vs. normal tissue showed that the mRNA levels of PDHA1 were significantly underexpressed in different types of GC across three analyses. Underexpression of PDHA1 was found in intestinal-type GC (P = 0.009), diffuse-type GC (P = 0.036), and mixed-type GC (P = 0.025). Immunohistochemical staining of the 174 GC tissue microarray showed that PDHA1 staining is much stronger in normal mucosa than in GC samples (P = 0.040). Furthermore, PDHA1 expression levels were found to be significantly lower in 69.05% (87/126) of poorly differentiated GCs as compared to the well or moderately differentiated ones (P = 0.037). Intriguingly, PDHA1 expression was significantly correlated with depth of invasion (P < 0.001), lymph node metastasis (P < 0.001), TNM stage (P < 0.001), and nerve invasion (P = 0.006). However, it was not correlated with gender, age, Lauren classification, and lymphovascular invasion (P > 0.05 for all). Kaplan-Meier analysis revealed that low tumor expression of PDHA1 was significantly correlated with a poorer overall survival in patients with GC (5-year overall survival rates for patients with low vs high PDHA1 expression = 49.8% vs 72.7%, hazard ratio of death from GC = 2.594, 95% CI = 1.527 to 4.408, P < 0.001). Multivariate analysis showed that PDHA1 (P = 0.025) was an independent predictor of overall survival. These findings are of potential clinical utility and merit further validation. [ABSTRACT FROM AUTHOR]

The chromosomal locations of lncRNAs (long non-coding RNAs, lncRNAs) infer their biological functions in cancer. Lnc-RAB1A-2, a Ras-related protein Rab-1A (RAB1A) upstream lncRNA, was chosen for assessment of its impact on lung cancer prognosis in a case-based analysis and investigation of its biological function though a series of functional assays. Lnc-RAB1A-2 was significantly upregulated in 276 lung cancer tissues compared with corresponding non-tumor tissues, and its expression level was significantly correlated with clinical stage and metastasis status in lung cancer patients. Patients with high expression levels of this lncRNA had a shorter median survival time (16.0 months vs. 23.0 months, P = 0.011 in southern samples; 8.0 months vs. 19.0 months, P = 0.020 in eastern samples; 13.0 months vs. 19.0 months, P = 0.002 in merged samples) and a higher risk of death than those with lower levels (HR = 1.52; 95% CI = 1.01-2.26, in merged samples). Additionally, overexpression of lnc-RAB1A-2 significantly promoted lung cancer cell proliferation in vitro and in vivo. Further analyses using digital gene expression tag profiling revealed that lnc-RAB1A-2 could affect the expression of fibroblast growth factor 1 (FGF1), a gene involved in the PI3K/AKT/mTOR pathway that is largely activated by RAB1A. FGF1 was confirmed to be a down-stream gene of lnc-RAB1A-2. Collectively, our study demonstrated that lnc-RAB1A-2 is associated with poor lung cancer prognosis by promoting lung cancer development. [ABSTRACT FROM AUTHOR]

TET2 (Ten‐Eleven Translocation 2) gene is a member of TET family that can modify DNA through catalyzing the conversion of 5‐methylcytosine (5‐mC) into 5‐hydroxymethylcytosine (5‐hmC). Although TET2 mutation has been disclosed in a variety of hematopoietic malignancies, the prognostic implication of TET2 expression in acute myeloid leukemia (AML) remains largely elusive. In this study, real‐time quantitative PCR was carried out to detect the level of TET2 transcript in 134 de novo AML patients and 35 healthy donors. TET2 mRNA level was significantly down‐regulated in AML patients compared with controls (p = 0.010). Among the French–American–British (FAB) subtypes, the incidence of TET2 under‐expression in M0/M1 subtypes was significantly higher than in the other subtypes M2/M3/M4/M5/M6 (p = 0.017), and also markedly higher than in the other granulocyte subtypes M2/M3 (p = 0.005). TET2 low‐expressed patients showed a significantly higher frequency of NPM1 mutations than TET2 high‐expressed patients. Although there was no significant difference in complete remission rate between two groups (low and high TET2 expression), patients with low TET2 expression had markedly shorter overall survival (OS) in both non‐M3 and cytogenetically normal AML (CN‐AML) (p = 0.016 and 0.044, respectively). Furthermore, multivariate analysis confirmed the prognostic value of TET2 expression on OS among CN‐AML patients (p = 0.049). Importantly, TET2 expression in complete remission (CR) time was significantly higher than newly diagnosis time (p = 0.001), and was returned to lower level when in relapse time (p < 0.001). These findings indicated that down‐regulation of TET2 expression was a common event and acted as a prognostic and predictive biomarker in CN‐AML patients. [ABSTRACT FROM AUTHOR]

Gastric cancer is one of the most common types of malignancy worldwide. However, the molecular mechanisms of cancer development remain unclear. Src-associated in mitosis of 68 kDa (Sam68) is involved in cell proliferation, transformation, tumorigenesis and metastasis in several types of cancer. The present study aimed to assess the expression and function of Sam68 in human gastric cancer. Western blot analysis and immunohistochemistry indicated that Sam68 expression was increased in tumor samples and the levels were associated with the grade of malignancy. High Sam68 expression was associated with the poor prognosis of patients with gastric cancer. In vitro, following knockdown of Sam68 by transfection of gastric cancer cells with small interfering RNA, the cell viability, cell cycle progress, migration and invasion were decreased. The results of the present study revealed that Sam68 may be a novel prognostic factor for, and is associated with cell growth, migration and invasion in, gastric cancer. [ABSTRACT FROM AUTHOR]

Background: Whether there are differences in pathogenesis among different types and subtypes of cerebral watershed infarction (WSI) is controversial since they have been combined into a single group in most previous studies.Methods: We prospectively identified 340 supratentorial WSI patients at Beijing Chao-Yang Hospital, Capital Medical University, China and classified them based on diffusion-weighted imaging(DWI) templates. Baseline characteristics, clinical courses and neuroradiological features were compared among patients with different types and subtypes of WSI.Results: We identified 92 patients with cortical watershed infarction (CWI), 112 with internal watershed infarction (IWI) and 136 with mixed-type infarction. Compared with CWI patients, more IWI patients had critical stenosis of internal carotid artery (ICA) (P < 0.001). For the CWI group, patients with anterior watershed infarction (AWI) were more prone to critical ICA stenosis than those with posterior watershed infarction (PWI) (P = 0.011). For the IWI group, critical ICA stenosis was more prevalent in patients with partial IWI (P-IWI) than in those with confluent IWI (C-IWI) (P = 0.026). IWI patients were more frequently found to have clinical deterioration during the first 7 days of hospitalization and a poor prognosis at the 90th day than in CWI patients (P = 0.003 and P = 0.014, respectively).Conclusions: IWI, especially the P-IWI subtype, is associated with hemodynamic impairment (HDI), whereas CWI has a weaker correlation with ICA steno-occlusion. Furthermore, IWI patients are more prone to poor prognosis. [ABSTRACT FROM AUTHOR]

Alterations in protein glycosylation affect tumor progression and immune responses in the tumor microenvironment. Keratinocyte-associated protein 2 (KRTCAP2) encodes the corresponding proteins involved in N-glycosylation. The clinical predictive significance and immune role of KRTCAP2 in hepatocellular carcinoma (HCC) largely remain elusive. Combining bioinformatics tools and multiplex immunohistochemistry analysis, we evaluated the KRTCAP2 expression in the HCC tumor microenvironment. The results showed that KRTCAP2 mRNA and protein expression were markedly increased in HCC tissues. Furthermore, high KRTCAP2 expression was an independent predictive factor of unfavorable prognosis in HCC. Moreover, high KRTCAP2 protein expression was associated with a lower proportion of CD8+ T cells and CD68+ macrophages in the stroma region. There was also a lower proportion of CD8+ T cells in the tumor region with high KRTCAP2 protein expression. Specifically, KRTCAP2 expression showed an inverse relationship with programmed cell death ligand-1 in HCC. Analysis of immunophenoscore showed that the low KRTCAP2 expression group had a stronger ability to predict response to immune checkpoint inhibitors. In conclusion, KRTCAP2 had a significant prognostic value for HCC and was correlated with the immune microenvironment. Our findings suggest that KRTCAP2 is a prognostic marker for HCC patients with potential clinical implications for predicting immunotherapeutic responsiveness. [Display omitted] • KRTCAP2 mRNA and protein expression were obviously increased in HCC tissues. • High KRTCAP2 expression was associated with poor prognosis in HCC. • CD8+ T cells were frequently found in both the tumor and stroma regions in KRTCAP2 low-expression group. • KRTCAP2 protein expression has an inverse relationship with PD-L1 in HCC. [ABSTRACT FROM AUTHOR]

Background: Mild encephalitis/encephalopathy with reversible splenial lesion (MERS) is a rare clinico-radiological entity characterized by the magnetic resonance imaging (MRI) finding of a reversible lesion in the corpus callosum, sometimes involved the symmetrical white matters. Many cases of child-onset MERS with various causes have been reported. However, adult-onset MERS is relatively rare. The clinical characteristics and pathophysiologiccal mechanisms of adult-onset MERS are not well understood. We reviewed the literature on adult-onset MERS in order to describe the characteristics of MERS in adults and to provide experiences for clinician.Methods: We reported a case of adult-onset MERS with acute urinary retension and performed literature search from PubMed and web of science databases to identify other adult-onset MERS reports from Januarary 2004 to March 2016. Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guideline was followed on selection process. And then we summarized the clinico-radiological features of adult-onset MERS.Results: Twenty-nine adult-onset MERS cases were reviewed from available literature including the case we have. 86.2% of the cases (25/29) were reported in Asia, especially in Japan. Ages varied between 18 and 59 years old with a 12:17 female-to-male ratio. The major cause was infection by virus or bacteria. Fever and headache were the most common clinical manifestation, and acute urinary retention was observed in 6 patients. All patients recovered completely within a month.Conclusion: Adult-onset MERS is an entity with a broad clinico-radiological spectrum because of the various diseases and conditions. There are similar characteristics between MERS in adults and children, also some differences. [ABSTRACT FROM AUTHOR]

Epigenetic inactivation of GPX3 has been identified in various cancers including leukemia. Moreover, aberrant DNA methylation was also found as a dominant mechanism of disease progression in myelodysplastic syndrome ( MDS). This study intended to explore GPX3 promoter methylation and its clinical relevance in 110 patients with MDS. GPX3 methylation was examined by real-time quantitative methylation-specific PCR ( RQ- MSP) and bisulfite sequencing PCR ( BSP). GPX3 methylation was identified in 15% (17/110) MDS patients, and significantly higher than controls, and lower than acute myeloid leukemia ( AML) patients ( P = 0.024 and 0.041). GPX3 methylated patients had older age and higher frequency of DNMT3A mutation ( P = 0.015 and 0.066). Cases with GPX3 methylation showed significantly shorter overall survival ( OS) time than those with GPX3 unmethylation analyzed with Kaplan-Meier analysis ( P = 0.012). Moreover, Cox regression analysis revealed that GPX3 methylation might act as an independent prognostic indicator in MDS ( HR = 1.847, P = 0.072). GPX3 methylation density was significantly increased during the progression from MDS to secondary acute myeloid leukemia ( sAML) in three follow-up paired patients. Our study concludes that GPX3 methylation in bone marrow is associated with adverse prognosis and leukemia transformation in MDS. [ABSTRACT FROM AUTHOR]

CDK7 has been known as a component of CDK activating kinase (CAK) complex, the complex was composed of CDK7, Cyclin H and RING finger protein Mat1 that contribute to cell cycle progression by phosphorylating other CDKs. In addition, the complex is also an essential component of general transcription factor TFIIH which controls transcription via activating RNA polymerase II by serines 5 and 7 phosphorylation of the carboxyl-terminal domain (CTD) of its largest subunit. However, the role of CDK7 in the pathogenesis of gastric cancer has not been identified. Our study showed that CDK7 was significantly upregulated and positively correlated with tumor grade, infiltration depth, lymph node, Ki-67, and predicted poor prognosis in 173 gastric cancer specimens by immunohistochemistrical analyses. Furthermore, in vitro results indicated that CDK7 promoted proliferation of gastric cancer cells by CCK8, clone formation analyses and flow cytometric analyses, while CDK7 knockdown led to decreased cell proliferation. Our study will provide a theoretical basis for the study of CDK7 in gastric cancer. [ABSTRACT FROM AUTHOR]

To investigateDLX4isoforms expression and their clinical significance in acute myeloid leukemia (AML).DLX4 transcript variant 1(BP1) expression was significantly up-regulated in AML patients compared with normal controls. However,DLX4 transcript variant 2(DLX7) was significantly down-regulated in AML patients. Both in the overall AML and the non-M3 AML cohorts, those patients with highBP1expression (BP1high) showed significantly lower rates of complete remission than those with lowBP1expression (BP1low).BP1highcases had significantly shorter overall survival thanBP1lowcases in the overall AML cohort, non-M3 AML, and cytogenetically normal AML (CN-AML). Multivariate analysis confirmed the independent prognostic value ofBP1expression among both the overall AML cohort and non-M3 AML as well as CN-AML patients. However, we did not observe the impact ofDLX7expression on prognosis in AML patients. Our study reveals thatBP1overexpression serves as an independent risk factor inde novoAML patients. [ABSTRACT FROM AUTHOR]