It has been reported that the encapsulated miRNAs from exosomes are potential biomarkers of tumors prognosis. Yet, the results are controversial, so it is obliged to do a meta-analysis to reach a definite conclusion.

Number of studies have been performed to evaluate the relationship between prostate stem cell antigen (PSCA) variation rs2294008 and bladder cancer risk, but the sample size was small and the results were conflicting. This meta-analysis was conducted to comprehensively evaluate the overall association.

Nuclear Yes-associated protein 1 (YAP1) has often been regarded as an adverse prognostic indicator in various tumors. Recent studies have associated YAP1 with unfavorable prognosis in nonsmall cell lung cancer (NSCLC). However, due to small sample sizes, the prognostic value of nuclear YAP1 in NSCLC patients is not well understood. In the present study, we evaluated the prognostic role of nuclear YAP1 in NSCLC patients via a systematic review and meta-analysis.

Objective: In this work, the relationship between octamer binding transcription factor 4 (OCT-4) expression and the clinicopathological features of cervical cancer (CC) is evaluated in detail.Methods: The library databases Pubmed, Embase, Cochrane library, Wan Fang and Chinese National Knowledge Infrastructure (CNKI) were searched for research related to these concepts published from the time the databases were established until May 2018. The obtained studies are screened, extracted, and evaluated according to the inclusion and exclusion criteria, and meta-analysis is carried out via RevMan 5.3.Results: Ten case-control studies, including 408 cases of CC, 164 cases of cervical intraepithelial neoplasia (CIN), and 148 cases of normal cervix, are included in the analysis. Results show that OCT-4 levels are statistically significantly different between the CC and normal cervical tissue groups (odds ratio (OR) = 15.59, 95% confidence interval (CI): 8.70, 27.94), the CC and CIN groups (OR = 5.64, 95% CI: 3.23, 9.86), the CIN and normal cervical tissues groups (OR = 7.13, 95% CI: 2.41, 21.05), and the CC well/moderately differentiated and poorly differentiated groups (OR = 0.44, 95% CI: 0.24, 0.81). OCT-4 is not statistically significantly different between CIN I + II and CIN III tissues (OR = 0.40, 95% CI: -0.02, 0.81), the CC lymphatic and non-lymphatic metastasis groups (OR = 1.93, 95% CI: 0.83, 4.47), the FIGO I and FIGO II groups (OR = 0.79, 95% CI: 0.29, 2.13), and the adenocarcinoma and squamous cell carcinoma groups (OR = 1.55, 95% CI: 0.70, 3.44).Conclusions: The available evidence suggests that OCT-4 expression is associated with CC malignancy and histological differentiation. This finding, however, is subject to quantitative studies and quality tests.

Mucinous differentiation occurs in 5-15 per cent of colorectal adenocarcinomas. This subtype of colorectal cancer responds poorly to chemoradiotherapy and has a worse prognosis. The genetic aetiology underpinning this cancer subtype lacks consensus. The aim of this study was to use meta-analytical techniques to clarify the molecular associations of mucinous colorectal cancer.

Human endogenous retroviruses (HERVs) are genetic elements in the human genome, which resulted from ancient retroviral germline infections. HERVs have strong transcriptional promoters and enhancers that affect a cell's transcriptome. They also encode proteins that can exert effects in human cells. This review examines how our increased understanding of HERVs have led to their potential use as biomarkers and immunologic targets.

The rise in cancer survival rates has raised concerns about the long-term adverse effects of cancer treatment, including neurocognitive impairment. Neurocognitive deficits such as attention and processing speed are frequently observed and can have a profound, lifelong impact in daily life of cancer patients. Interestingly, large interpatient variability exists in cognitive outcomes. Emerging evidence indicates that such differences may be related to genetic variation. The aim of our review was to systematically summarize the current literature on the modulatory effects of germline genetic polymorphisms on cancer treatment-induced cognitive changes and the potential age-dependent impact in cancer survivors. The PubMed/Medline database was screened using an extensive search string focusing on four components: "cancer", "cancer treatment", "neurocognitive outcome" and "germline genetic variation". Seventeen studies meeting predefined eligibility criteria were analyzed, including sixteen candidate gene studies and one genome-wide association study. 38 polymorphisms in 15 genes across proposed pathophysiological pathways, including (1) neural plasticity and repair, (2) neuroinflammation and defenses against oxidative stress, (3) neurotransmission, and (4) folate metabolism pathway, were reported to be significantly associated with treatment-related neurocognitive dysfunction or neuroimaging abnormalities. Still, some study results remained discordant, partly due to the methodological heterogeneity (i.e. in test assessments, age, cancer-type populations). Future large-scale, (epi-)genome studies integrating neurocognitive assessments and advanced neuroimaging techniques, are recommended in order to investigate neurotoxicity throughout the lifespan. Hence, adverse neurodevelopmental problems during childhood and neurodegenerative processes later in life could be minimized based on genetic risk classifications.

Prostate cancer (PCa) is a major health risk for older men worldwide. Existing systemic therapies mostly target androgen receptor (AR). Although treatments are initially effective, the disease always recurs. A potential mechanism for the treatment failure is that PCa contains, in addition to the AR-positive luminal type tumor cells, a small component of neuroendocrine (NE) cells. The function of NE cells in PCa remains poorly understood, and one important characteristic of these cells is their lack of expression of AR and resistance to hormonal therapy. In addition, many patients develop the more aggressive small-cell neuroendocrine carcinoma (SCNC) after hormonal therapy. Although this clinical phenomenon of disease transformation from adenocarcinoma to SCNC is well established, the cell of origin for SCNC remains unclear. Recently, loss of function of Rb and TP53 and amplification and overexpression of MYCN and Aurora A kinase have been identified as important biomarkers and potential disease drivers. In this article, we systematically review the histology of normal prostate and prostate cancer including the main histologic types: adenocarcinoma and SCNC. We also review the findings from many studies using cellular and animal models as well as human specimens that attempt to understand the molecular mechanisms of treatment failure, disease progression, and tumor transformation from adenocarcinoma to SCNC.

A first-line biologic treatment for metastatic colorectal cancer (mCRC) is still controversial. We, therefore, performed a meta-analysis to determine the efficacy of first-line cetuximab versus bevacizumab for RAS and BRAF wild-type mCRC.

Although the prognostic value of microRNA-122 (miR-122) for hepatocellular carcinoma (HCC) patients have been evaluated by numerous studies, the results of them were not completely consistent. The present study aims to comprehensively evaluate the predicting value of miR-122 on the prognosis of patients with HCC based on all eligible literatures.

The role of adjuvant tyrosine kinase inhibitors (TKIs) in non-small cell lung cancer (NSCLC) is not well defined. Recent randomized controlled trials showed a disease-free survival (DFS) benefit in patients harboring an epidermal growth factor receptor (EGFR) mutation. Yet, older trials on patients with any EGFR status did not demonstrate the same benefit. We aimed to assess the efficacy and safety of adjuvant TKIs in NSCLC patients. The electronic databases Medline (PubMed) and EMBASE were searched for relevant randomized controlled trials. Random effect models were used. The primary outcome was DFS measured as hazard ratio (HR). The secondary outcomes were overall survival (OS) measured as HR, 2-year DFS and toxicity expressed as risk ratio and odds ratio (OR), respectively. Subgroup analyses assessed DFS by trial design. Six trials incorporating 1860 patients were included. In patients harboring an EGFR mutation, adjuvant TKIs decreased the risk of disease recurrence by 48% (HR: 0.52, 95% confidence interval [CI]: 0.35-0.78), improved 2-year DFS (HR: 0.53, 95% CI: 0.43-0.66) but did not improve OS (HR: 0.64, 95% CI: 0.22-1.89). The risk of developing ≥grade 3 skin toxicity (OR: 6.07, 95% CI: 4.34-8.51) and diarrhea (OR: 4.05; 95% CI: 2.44-6.74) was increased. In subgroup analyses, the DFS benefit was more pronounced in trials using TKIs over chemotherapy compared with trials using TKIs postchemotherapy. In conclusion, adjuvant TKIs decrease the risk of recurrence in NSCLC patients harboring an EGFR mutation but do not improve OS. Longer follow-up is needed for a definitive assessment of OS and to define the role of adjuvant TKI for NSCLC in the clinical practice.

Several studies demonstrated that lncRNA differentiation antagonizing non-protein coding RNA (lncRNA DANCR) expression might have the potential capacity to predict the cancer prognosis; however, definite conclusion has not been obtained. The aim of this meta-analysis was to evaluate the prognostic value of lncRNA DANCR expression in cancers. PubMed, Web of Science, Scopus, and Embase were comprehensively searched for relevant studies. Studies meeting all inclusion standards were included into this meta-analysis. The analysis of overall survival (OS), disease-free survival (DFS), or clinicopathological features was conducted. Total 11 studies containing 1154 cancer patients were analyzed in this meta-analysis. The results showed, compared with low lncRNA DANCR expression, high lncRNA DANCR expression was significantly associated with shorter OS (hazard ratio [HR] = 1.85; 95% CI = 1.52-2.26; P<0.01) and DFS (HR = 1.82; 95% CI = 1.43-2.32; P<0.01) in cancers. Besides, high lncRNA DANCR expression predicted deeper tumor invasion (P<0.01), earlier lymph node metastasis (P<0.01), earlier distant metastasis (P<0.01), and more advanced clinical stage (P<0.01) compared with low lncRNA DANCR expression in cancer populations. High lncRNA DANCR expression was associated with worse prognosis compared with low lncRNA DANCR expression in cancers. LncRNA DANCR expression could serve as a prognostic factor of human cancers.

Long non-coding RNA (lncRNA) prostate cancer associated transcript 1 (PCAT-1) has been identified as a potential biomarker for the diagnosis and prognosis of various cancers. We performed this systematic review and meta-analysis to evaluate the role of dysregulation as well as the biological and clinical significance of lnc-PCAT-1 for predicting the malignancy status in several cancers. Two independent reviewers conducted an extensive search in electronic databases of Medline, Embase, Scopus, Web of Science and PubMed until the December of 2017. Five articles investigating the clinical significance of lncRNA PCAT-1, including 996 patients, were analyzed. Our results revealed that the increased PCAT-1 expression was related to overall survival (OS) (HR = 1.9, 95%CI: 1.13-3.18, P=0.015). Also, pooled results of the diagnostic data analysis demonstrated that PCAT-1 has a sensitivity of 0.59 and specificity of 0.66 for cancer diagnosis. Moreover, pooled area under curve was 0.62 (95% CI: 0.58–0.69). This meta-analysis revealed that lncRNA PCAT-1 could be served as a potential diagnostic and prognostic biomarker in various solid tumors.

Background: Women at high risk to develop ovarian cancer opt for risk-reducing salpingo-oophorectomy (RRSO) to reduce the risk by 80-96%. RRSO leads to a direct onset of menopause in premenopausal women. Hormone replacement therapy (HRT) can be used to mitigate menopausal symptoms after RRSO. However, it is unclear whether HRT in these women is safe in terms of breast cancer (BC) risk. Methods: We performed a literature search and investigated national guidelines on the use of HRT following RRSO in BRCA1 and BRCA2 mutation carriers. We analyzed differences and similarities between the guidelines and describe what these guidelines were based upon. Results: Seven articles regarding HRT following RRSO in BRCA1 and BRCA2 mutation carriers were identified. None of the included studies yielded any evidence that short-term use of HRT following RRSO increases the risk of developing BC or negates the protective effect of RRSO in BRCA1/2 mutation carriers without a personal history of BC. Eleven national guidelines were found and described. Conclusion: Short-term use of HRT after RRSO seems to be safe. The literature is more favorable toward estrogen alone. The ideal dosage and duration of use are unknown and remain to be investigated in future studies.

To estimate association between androgen receptor (AR) gene polymorphisms and testicular germ cell tumor (TGCT) susceptibility.

A prior meta-analysis found no association between BRCA1 mutation and prostate cancer (PCa). Subsequent BRCA2 mutation studies have shown an association with PCa risk and mortality. We conducted a meta-analysis of overall BRCA mutation carriers and in subgroups to (1) estimate PCa risk in BRCA mutation carriers, (2) evaluate the frequency of BRCA mutation carriers in patients with PCa, and (3) compare cancer-specific survival (CSS) and overall survival (OS) among BRCA mutation carriers and noncarriers.

To systematically assess the prevalence of BRCA1 and BRCA2 gene mutations in women with Hereditary Breast and/or Ovarian Cancer (HBOC) in Arab countries and to describe the variability in the BRCA gene mutations in different regions of the Arab world.

Circular RNAs (circRNAs) have spurred considerable interest in numerous tumors. We aimed to investigate the clinical, prognostic, and diagnostic roles of circRNAs in human lung cancer. We systematically searched PubMed, Web of Science, EMBASE, Scopus, CBM, and the Cochrane Library databases up to July 24, 2018. Eligible studies about the relationship between circRNAs expression and clinical, prognostic, and diagnostic outcomes in patients with lung cancer were in our study. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were to investigate clinical parameters, and hazard ratios (HRs) and 95% CIs to estimate overall survival (OS). A total of 23 relevant studies were eligible, with 15 on clinicopathological features, 14 on prognosis, and six on diagnosis. For clinical features, high expression of oncogenic circRNAs was remarkably related to poor clinical parameters. Whereas, the results of tumor-suppressor circRNAs were the complete opposite. For the prognostic roles, oncogenic circRNAs had an unfavorable impact on overall survival (OS: HR = 3.24, 95% Cl: 2.70-3.77), and elevated level of tumor-suppressor circRNAs was correlated with longer survival (OS: HR = 0.57, 95% Cl: 0.43-0.70). For the diagnostic values, the pooled result showed an area under the curve (AUC) of 0.86, with 77% sensitivity and 81% specificity in distinguishing patients with lung cancer from healthy ones. The above results suggested that circRNAs have the potential to be novel indicators for prognostic and diagnostic evaluation of patients with lung cancer.

Pheochromocytoma and paraganglioma (PPGL) can be divided into at least four molecular subgroups. Whether such categorizations are independent factors for prognosis or metastatic disease is unknown. We performed a systematic review and individual patient meta-analysis aiming to estimate if driver mutation status can predict metastatic disease and survival. Driver mutations were used to categorize patients according to three different molecular systems: two subgroups (SDHB mutated or wild type), three subgroups (pseudohypoxia, kinase signaling or Wnt/unknown) and four subgroups (tricarboxylic acid cycle, VHL/EPAS1, kinase signaling or Wnt/unknown). Twenty-one studies and 703 patients were analyzed. Multivariate models for association with metastasis showed correlation with SDHB mutation (OR 5.68 (95% CI 1.79-18.06)) as well as norepinephrine (OR 3.01 (95% CI 1.02-8.79)) and dopamine (OR 6.39 (95% CI 1.62-25.24)) but not to PPGL location. Other molecular systems were not associated with metastasis. In multivariate models for association with survival, age (HR 1.04 (95% CI 1.02-1.06)) and metastases (HR 6.13 (95% CI 2.86-13.13)) but neither paraganglioma nor SDHB mutation remained significant. Other molecular subgroups did not correlate with survival. We conclude that molecular categorization accordingly to SDHB provided independent information on the risk of metastasis. Driver mutations status did not correlate independently with survival. These data may ultimately be used to guide current and future risk stratification of PPGL.

Surveillance of Barrett's esophagus (BE) is a clinical challenge; metaplasia of the distal esophagus increases a patient's risk of esophageal adenocarcinoma (EAC) significantly but the actual percentage of patients who progress is low. The current screening recommendations require frequent endoscopy and biopsy, which has inherent risk, high cost, and operator variation. Identifying BE patients genetically who are at high risk of progressing could deemphasize the role of endoscopic screening and create an opportunity for early therapeutic intervention. Genetic alterations in germline DNA have been identified in other disease processes and allow for early intervention or surveillance well before disease develops. The genetic component of BE remains mostly unknown and only a few genome-wide association studies exist on this topic. This review summarizes the current literature available that examines genetic alterations in BE and EAC with a particular emphasis on clinical implications.