Cancer is considered as the main public health problem and the second leading cause of morbidity and mortality worldwide. Numerous environmental-lifestyle related risk factors account for around one-third of cancer deaths. Recently, the key role of lncRNAs has been widely investigated in a variety of disorders, including cancer. The lncRNA GHET1 has been considered as an essential oncogenic lncRNA in many types of human cancers. Clinical investigations indicated that expression of lncRNA GHET1 is correlated with clinicopathological characteristics in cancer. This metaanalysis investigated the correlation between the lncRNA GHET1 expression and clinicopathological features in different types of cancers.

Mutations in the genes BRCA1 and BRCA2 represent a significant risk factor for ovarian and breast cancer. With increasing number and success rates, fertility protection and treatment are gaining importance also for BRCA1/2 mutation carriers. However, the effect on primary cancer risk and risk for recurrence remains unclear. This review analyses the published data on fertility treatment and risk of ovarian and breast cancer in BRCA1/2 mutation carriers.

Development of human genetic and proteomic research has increased the interest in alternative head-and-neck cancer (HNC) detection methods. The aim of this article, the second of two-part series, was to review the scientific literature about novel HNC genetic and proteomic biomarkers. A comprehensive review of the current literature was conducted according to the Preferred Reporting Item for Systematic Review and Meta-analyses guidelines by accessing the NCBI PubMed database. Authors conducted the search of articles in English language published from 2004 to 2015. A total of 50 relevant studies were included in the review. Thirty of them concerned proteomic and twenty genetic alterations in HNC. The present systematic review discovered 242 genes and 44 proteins associated with HNC. Due to inconsistent and sparse results, novel biomarkers cannot be firmly established. Prognostic capacity of genetic markers was not evaluated. Proteins (14-3-3γ, extracellular matrix metalloproteinase inducer, and PA28γ) were described as most valuable for prognostic observation of HNC. A strict methodological protocol for molecular studies must be established.

Tumour budding (TB) is an adverse histological feature in many epithelial cancers. It is thought to represent epithelial-mesenchymal transition, a key step in the metastatic process. The significance of TB in breast carcinoma (BC) remains unclear. The aim of this study is to investigate the relationship between TB and other histological and molecular features of BC.

Accumulating evidence indicates that aberrant regulation of metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1), a long noncoding RNA (lncRNA), plays a vital role in tumorigenesis. However, its association with breast cancer has not been systematically evaluated. In the current study, a meta-analysis was conducted to clarify the association between MALAT-1 and the prognosis and clinicopathological features of breast cancer. Relevant literature published in several databases was searched. Hazard ratio (HR) and odds ratio (OR) with 95% confidence interval (CI) were calculated to evaluate the effect of MALAT-1 expression on the survival outcomes and clinicopathological features of breast cancer. A total of 12 studies involving 4106 patients were identified. Pooled HR demonstrated that elevated MALAT-1 expression significantly predicted unfavorable overall survival (HR = 2.06, 95% CI: 1.66-2.56, P<0.0001) in patients with breast cancer. Subgroup analysis stratified by cancer type, sample size, and method of variance analysis also showed statistically significant associations. Additionally, the HR of patients with up-regulated MALAT-1 expression concerning disease-free survival (DFS), recurrence-free survival (RFS), and disease-specific survival (DSS) was 1.91 (95% CI: 1.53-2.39, P<0.0001). Further, elevated MALAT-1 expression was positively correlated with the progesterone receptor (PR) status (OR = 1.47, 95% CI: 1.18-1.82). Thus, MALAT-1 is a promising biomarker for predicting survival outcomes in patients with breast cancer.

To compare the survival outcomes of first-line treatment regimens for advanced epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer (NSCLC) patients with stable brain metastases.

The gene expression for interleukin-2 receptor subunit alpha (CD25/IL2RA) is frequently altered in adults with acute myeloid leukemia (AML). Increasing evidence indicates that the elevated expression of CD25 may be correlated with poor survival for AML patients. Thus, we performed this meta-analysis to further evaluate the prognostic value of elevated CD25 in AML. Eligible studies were gathered by searching on PubMed, Web of Science, and Embase. Using the R language 3.6.0 software, Pooled hazard ratios (HRs) with their corresponding 95% confidence intervals (CIs) of overall survival (OS) and disease-free survival (DFS)/relapse-free survival (RFS)/event-free survival (EFS) for total and subgroup analyses were calculated to investigate the association of elevated CD25 and outcomes of AML patients. Ten studies with a total of 1640 participants were enrolled in this meta-analysis. Pooled HRs suggested that overexpression of CD25 predicted poor outcomes on both OS (HR = 2.27, 95%CI 1.95-2.64) and DFS/RFS/EFS (HR = 1.77, 95%CI 1.44-2.17) in overall population. Subgroup analyses stratified by ethnicity, AML subtype, cut-off value, statistical methodologies and detection method draw similar results. Our meta-analysis indicates that elevated CD25 expression is a poor prognostic factor for AML patients. Considering limited number of samples, further relevant studies are warranted.

Previous studies have evaluated associations of XPG rs17655G&gt;C and XPF rs1799801T&gt;C polymorphisms with a risk of cutaneous malignant melanoma (CMM). However, their results thus remained inconsistent or even contradictory. Thus, the aim of this meta-analysis was to evaluate association of XPG rs17655G&gt;C and XPF rs1799801T&gt;C polymorphism with a risk of CMM.

Several studies have implicated the PIK3/AKT pathway in the pathophysiology of cancer progression as its activation seems to be aberrant in several forms of cancer. The purpose of the present systematic review is to evaluate the impact of PIK3CA mutations on survival outcomes of patients with cervical cancer.

mtDNA is the closed circular, ds-DNA present in mitochondria of eukaryotic cells and are inherited maternally. Besides being the power house of the cell, mitochondria are also responsible for the regulation of redox homeostasis, signaling, metabolism, immunity, survival and apoptosis. Lack of a 'Systematic Review' on mtDNA variations and cancers encouraged us to perform the present study. Pubmed', 'Embase' and 'Cochrane Library' databases were searched using keywords 'Mitochondrial DNA' OR 'mtDNA' OR 'mDNA' AND 'polymorphism' AND 'cancer' AND 'risk' to retrieve literature. Polymorphisms occupy first rank among mtDNA variations followed by CNV, MSI, mutations and hold a great potential to emerge as key predictors for human cancers.

Translation of survival benefits observed in glioblastoma clinical trials to populations and to longer-term survival remains uncertain. We aimed to assess if ≥ 2-year survival has changed in relation to the trial of radiotherapy plus concomitant and adjuvant temozolomide published in 2005. We searched MEDLINE and Embase for population-based studies with ≥ 50 patients published after 2002 reporting survival at ≥ 2 years following glioblastoma diagnosis. Primary endpoints were survival at 2-, 3- and 5-years stratified by recruitment period. We meta-analysed survival estimates using a random effects model stratified according to whether recruitment ended before 2005 (earlier) or started during or after 2005 (later). PROSPERO registration number CRD42019130035. Twenty-three populations from 63 potentially eligible studies contributed to the meta-analyses. Pooled 2-year overall survival estimates for the earlier and later study periods were 9% (95% confidence interval [CI] 6-12%; n/N = 1,488/17,507) and 18% (95% CI 14-22%; n/N = 5,670/32,390), respectively. Similarly, pooled 3-year survival estimates increased from 4% (95% CI 2-6%; n/N = 325/10,556) to 11% (95% CI 9-14%; n/N = 1900/16,397). One study with a within-population comparison showed similar improvement in survival among the older population. Pooled 5-year survival estimates were 3% (95% CI 1-5%; n/N = 401/14,919) and 4% (95% CI 2-5%; n/N = 1,291/28,748) for the earlier and later periods, respectively. Meta-analyses of real-world data suggested a doubling of 2- and 3-year survival in glioblastoma patients since 2005. However, 5-year survival remains poor with no apparent improvement. Detailed clinically annotated population-based data and further molecular characterization of longer-term survivors may explain the unchanged survival beyond 5 years.

Genetic biomarkers are a promising and growing field in the management of bladder cancer in all stages. The aim of this paper is to understand the role of genetic urinary biomarkers in the follow up of patients with non muscle invasive bladder cancer where there is increasing evidence that they can play a role in avoiding invasive techniques.

Test on the KRAS somatic mutation status is necessary before cetuximab and panitumumab treatments are given to colorectal cancer patients. Metastatic colorectal cancer patients sometimes lack tumor tissue samples, and the testing of KRAS mutation in plasma samples requires highly sensitive methods.

Epidermal growth factor receptor (EGFR) mutations are the most common carcinogenic driver mutations in non-small-cell lung cancer (NSCLC) patients, while invasive tissue biopsy has certain inherent defects. PubMed, Ovid Medline, Embase, and the Cochrane Library were systematically searched on January 4, 2020, using the keywords "liquid biopsy," "EGFR," and "NSCLC." The pooled sensitivity and specificity of EGFR mutations in paired tissue and blood were calculated. The accuracy was assessed by receiver operating characteristic curve. The meta-regression of the subgroup was performed to analyze the heterogeneity. Hazard ratio (HR) and 95% confidence interval (CI) were combined for evaluating the impact of EGFR mutation in tissue and liquid blood biopsy. A total of 40 studies with 5,995 patients were involved in the study. The pooled sensitivity was 68% (95% CI = 60-75%), and the specificity was 98% (95% CI = 95-99%). The diagnostic odds ratio was 88 (95% CI = 40-195), and the area under the curve was 0.91 (95% CI = 0.88-0.93). In the meta-regression, the sensitivity and specificity remain lower in the Asian studies than non-Asian studies (sensitivity: 66% vs. 73%, P = 0.04; specificity: 96% vs. 97%, P = 0.03, respectively). The EGFR mutation was associated with a better progression-free survival than wild type in both tissue (HR = 0.54, 95% CI = 0.34-0.85, P = 0.007) and blood (HR = 0.81, 95% CI = 0.71-0.92, P = 0.001) detection. Peripheral blood liquid biopsy had a better specificity for detecting EGFR mutation in NSCLC patients, while tissue biopsy still needs to be undertaken for negative blood biopsy patients due to its lower sensitivity.

Up to 70% of patients with advanced ovarian cancer have a relapse after primary therapy. New agents and approaches are urgently needed to avoid or slow down this recurrence.

We sought to analyze the association between miR-146a rs2910164 G > C polymorphism and susceptibility to lung cancer using a meta-analysis of case-control studies.

The Wilms tumor-1 (WT1) protein is an important regulator of malignant hematopoiesis and has been implicated in the pathogenesis of acute myeloid leukemia (AML). Recently special attention has been paid to the relationship of the WT1 single nucleotide polymorphism (SNP) rs16754 with AML risk and outcome, but the conflicting results made it difficult to draw definitive conclusions. In the present study, we systematically reviewed the literature and performed a meta-analysis of existing evidence. We searched Embase, Pubmed, Web of Science, Medline, Cochrane Library, Wanfang, and China National Knowledge Infrastructure databases using predefined search methodology for relevant studies. We pooled odd ratio (OR) with 95% confidence intervals (95% CI) to evaluate the association between SNP rs16754 and AML risk. In addition, we analyzed hazard ratio (HR) with 95% CI for overall survive, relapse-free survival, and disease-free survival. Q-statistic was used to assess the homogeneity and Egger test was used to evaluate publication bias. Eleven studies met the inclusion criteria for analysis. The results of fixed-effect meta-analyses revealed no association between SNP rs16754 and AML risk (AA + GA vs GG: OR = 0.92, 95% CI: 0.71-1.19, P = .518; AA vs GA + GG: OR = 1.23, 95% CI: 0.86-1.76, P = .262; AA vs GG: OR = 1.05, 95% CI: 0.68-1.63, P = .820; AG vs AA: OR = 0.77, 95% CI: 0.53-1.13, P = .186; AG vs GG: OR = 0.89, 95% CI: 0.68-1.16, P = .376). In subgroup analysis by race, age, and disease type, we did not find any significant association. However, the presence of rs16754 GA/GG genotype was associated with improved overall survive (HR = 0.48, 95% CI: 0.26-0.91, P = .024) and relapse-free survival (HR = 0.82, 95% CI: 0.68-1.00, P = .048) compared with the rs16754 AA. In summary, the WT1 SNP rs16754 was not associated with AML risk, but it had a significant impact on clinical outcome in AML patients.

N-acetyltransferase 2 (NAT2) polymorphism could participate in the metabolism of carcinogens through regulating the activity of a series of critical enzymes. However, the effects of NAT2 polymorphism on bladder cancer (BCa) risk were still inconclusive. In order to illustrate whether NAT2 polymorphism may influence the susceptibility to BCa, we conducted this updated meta-analysis.

Dysbiosis has been identified in oral squamous cell carcinoma (OSCC). The aim of this study was to carry out a systematic review of an electronic research that was carried out on articles published between January 2008 and September 2018.

Cyclooxygenase-2 (COX-2) is known as an important enzyme in the inflammation process that has tumorigenesis function in various cancers through the induction of epithelial-to-mesenchymal transition (EMT), cell proliferation, migration, and invasion that lead to metastasis. Celecoxib is a nonsteroidal anti-inflammatory drug (NSAID) that can selectively target COX-2, suppress downstream pathways, and finally lead to anticancer potentiality. microRNAs (miRNAs), as a class of small noncoding RNAs, play pivotal roles in cancers through the tumor-suppressive or oncogenic effects, by post-transcriptional regulation of their target genes. In this regard, shreds of evidence have shown that, COX-2 reveals its action through miRNA regulation. So, in this systematic review, we aimed to highlight the tumorigenic role of COX-2 in cancer development and the therapeutic effects of celecoxib, as a selective COX-2 drug, through the regulation of miRNAs.