The true rate of gastric cancer (GC) in juvenile polyposis syndrome (JPS) is unknown because of its rarity and ascertainment bias in published literature. To better assess this, we conducted a systematic review and meta-analysis.

The XRCC3 p.Thr241Met (rs861539) polymorphism has been extensively studied for its association with glioma risk, but results remain conflicting. Therefore, we performed a systematic review and meta-analysis to resolve this inconsistency.

Although neoadjuvant immunotherapy is being widely studied, there is no consensus on its efficacy in microsatellite-stable (MSS) or mismatch repair proficient (pMMR) colorectal cancer (CRC). This meta-analysis aimed to evaluate studies on neoadjuvant immunotherapy for advanced CRC to assess its efficacy and provide new clinical guidelines.

The aim is to evaluate the association of CDH1 methylation with esophageal cancer (EC) risk.

Objectives: The TNFAIP8 gene family and TNFAIP2 gene are inextricably linked to an elevated risk of cancer development. This systemic review and meta-analysis seeks to establish the relationship between TNFAIP8 (rs11064, rs1045241, rs1045242, and rs3813308), TNFAIP8L1 (rs1060555), and TNFAIP2 (rs710100 and rs8126) polymorphisms with the risk of cancer. Methods and Materials: A systematic search of multiple databases from January 2022 to April 2022 was used to identify relevant studies. Odds ratios (ORs) with corresponding 95% CI and p-value were calculated to assess the association. Bonferroni correction was performed to correct p-values. Trial sequential analysis (TSA) and in-silico messenger RNA expression were also performed. Review Manager 5.4 software was used for performing this meta-analysis. Results: This study comprised 6909 cancer patients and 7087 healthy participants from 14 studies. Four genetic models of rs11064 (codominant 2 [COD2]: OR = 2.30, p = 7.83 × 10-5; codominant 3 [COD3]: OR = 2.10, p = .0006; recessive model [RM]: OR = 2.24, p = .0001; AC: OR = 1.47, p = .037), two genetic models of rs1045241 (codominant 1 [COD1]: OR = 1.27, p = .009; overdominant model [ODM]: OR = 1.24, p = .018), four genetic models of rs1045242 (COD1: OR = 1.52, p = .005; dominant model (DM): OR = 1.56, p = .002; OD: OR = 1.48, p = .008; AC: OR = 1.48, p = .002), and three genetic models of rs8126 (COD2: OR = 1.41, p = .0005; COD3: OR = 1.44, p = .0002; RM: OR = 1.43, p = .0001) were statistically linked to cancer risk. Only one genetic model of rs1060555 polymorphism showed a significant protective association with cancer (COD2: OR = 0.80, p = .048). The outcomes of TSA also validated the findings of the meta-analysis. Conclusion: This study summarizes that rs11064, rs1045241, and rs1045242 polymorphisms of TNFAIP8 gene and rs8126 polymorphism of TNFAIP2 gene are significantly linked with the risk of cancer development. This meta-analysis was registered at INPLASY (registration number: INPLASY202270073).

Genome-wide association studies have revealed over 200 genetic susceptibility loci for prostate cancer (PCa). By combining them, polygenic risk scores (PRS) can be generated to predict risk of PCa. We summarize the published evidence and conduct meta-analyses of PRS as a predictor of PCa risk in Caucasian men.

Triple-negative breast cancer (TNBC), the subtype of breast cancer with the highest mortality rate, shows clinical characteristics of high heterogeneity, aggressiveness, easy recurrence, and poor prognosis, which is due to lack of expression of estrogen, progesterone receptor and human epidermal growth factor receptor 2. Currently, neoadjuvant chemotherapy (NAT) is still the major clinical treatment for triple-negative breast cancer. Chemotherapy drugs can be divided into platinum and non-platinum according to the presence of metal platinum ions in the structure. However, which kind is more suitable for treating TNBC remains to be determined.

Osimertinib is a recently approved third-generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) that selectively inhibits both EGFR-TKI-sensitizing and EGFR-T790M resistance mutations. The aim of the present meta-analysis was to investigate the efficacy and safety of osimertinib for patients with EGFR-mutated non-small-cell lung cancer (NSCLC).

Head and neck cancer (HNC) is an ascending and agressive disease. The search for new molecular markers is emerging to solve difficulties in diagnosis, risk management, prognosis and effectiveness of treatments. Proteins related to apoptotic machinery have been identified as potential biomarkers. Caspase 3 is the main effector caspase and has a key role in apoptosis. The objective of this systematic review and meta-analysis is to review studies that analyze changes in Caspase 3 and Cleaved Caspase 3 expression both in oral premalignant disorders (OPMD) as well as in head and neck cancer (HNC). This study also proposes to review the prognostic values associated with HNC according to the expression of Caspase 3. Medline (via PubMed), EMBASE, Scopus, Cochrane, Web of Science and Grey Literature Database were screened from inception to june of 2022 and 18 studies were selected and 8 were included in the prognostic meta-analysis. Results related to the comparison of Caspase 3 expression demonstrated similar expression of Caspase 3 in HNC, with an average of 51.9% (9.5-98.1) showing high/moderate expression compared to 45.7% (14.6-84.7) in OPMD. Of interest, Cleaved Caspase 3 resulted incresed in HNC when compared with OPMD, being 73.3% (38.6-88.3) versus 22.9% (7.1-38.7). Pooled Fixed effect of HR values (95% CI) for OS related to Caspase 3 IHC expression in HNC patients was 1.48 (95% CI 0.95-2.28); also, the rate of heterogeneity was low, as revealed by I2 = 31%. For DFS was 1.07 (95% CI 0.79-1.45) with I2 = 0% and DSS showed a HR of 0.88 (95% CI 0.69-1.12) with I2 = 37%. Caspase 3 and Cleaved Caspase 3 expression could be linked with malignancy progression, but the expression of Caspase 3 did not influence the prognosis of patients with HNC.

The biogenetic law (recapitulation law) states that ontogenesis recapitulates phylogenesis. However, this law can be distorted by the modification of development. We showed the recapitulation of phylogenesis during the differentiation of various cell types, using a meta-analysis of human single-cell transcriptomes, with the control for cell cycle activity and the improved phylostratigraphy (gene dating). The multipotent progenitors, differentiated from pluripotent embryonic stem cells (ESC), showed the downregulation of unicellular (UC) genes and the upregulation of multicellular (MC) genes, but only in the case of those originating up to the Euteleostomi (bony vertebrates). This picture strikingly resembles the evolutionary profile of regulatory gene expansion due to gene duplication in the human genome. The recapitulation of phylogenesis in the induced pluripotent stem cells (iPSC) during their differentiation resembles the ESC pattern. The unipotent erythroblasts differentiating into erythrocytes showed the downregulation of UC genes and the upregulation of MC genes originating after the Euteleostomi. The MC interactome neighborhood of a protein encoded by a UC gene reverses the gene expression pattern. The functional analysis showed that the evolved environment of the UC proteins is typical for protein modifiers and signaling-related proteins. Besides a fundamental aspect, this approach can provide a unified framework for cancer biology and regenerative/rejuvenation medicine because oncogenesis can be defined as an atavistic reversal to a UC state, while regeneration and rejuvenation require an ontogenetic reversal.

With the recent guideline change for individuals at average risk for colorectal cancer (CRC) to initiate colonoscopy at the age of 45 years, there is a need to provide an updated counseling framework for individuals with variants in moderate-penetrance CRC susceptibility genes.

Immune checkpoint inhibitors have shown promise in microsatellite instability-high/mismatch repair deficient (MSI-H/dMMR) advanced colorectal cancer (CRC) immunotherapy, and many clinical trials have been conducted.

T-cell immunoreceptor with Ig and ITIM domains (TIGIT) participates in tumor immune escape by delivering inhibitory signals to T cells. The purpose of this article was to assess the prognostic value of TIGIT and its immunological function in solid cancers.

Actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) is associated with prognosis in many cancers. The aim of this study was to systematically evaluate the potential correlation between AFAP1-AS1 and the prognosis of digestive system cancers (DSC).

Genetic variations like single nucleotide polymorphisms (SNPs) are associated with cervical carcinogenesis. In this study, SNPs have been identified that contribute toward changes in the function and stability of the proteins and show association with cervical cancer. Initially, literature mining identified 114 protein-coding polymorphisms with population-based evidence in cervical cancer. Subsequently, the functional assessment was performed using sequence-dependent tools, and thereafter, protein stability was analyzed using sequence and structural data. Twenty-three non-synonymous SNPs (nsSNPs) found to be damaging and destabilizing were then analyzed to check their risk association at the population level. The meta-analysis indicated that polymorphisms in DNA damage repair genes XRCC1 (rs25487 and rs1799782), ERCC5 (rs17655), and oxidative stress-related gene NQO1 (rs1800566) are significantly associated with increased cervical cancer risk. The XRCC1 rs25487 and rs1799782 polymorphisms showed the highest risk of cervical cancer in the homozygous model having odds ratio (OR) = 1.85, 95% confidence interval (CI) = 1.17-2.92, p = 0.01, and recessive model with OR = 1.81, 95% CI = 1.01-3.24, and p = 0.04 respectively. Similarly, rs17655 polymorphism of ERCC5 and rs1800566 polymorphism of NQO1 showed the highest pooled OR in the homozygous (OR = 1.70, 95% CI = 1.32-2.19, p = 0.00004) and heterozygous model (OR = 1.3, 95% CI = 1.06-1.58, p = 0.01) respectively. Thus, in this study, a comprehensive collection of nsSNPs was collated and assessed, leading to the identification of polymorphisms in DNA damage repair and oxidative stress-related genes, that destabilize the protein and shows increased risk associated with cervical cancer.

CRISPR is a customized genome-editing tool that snips DNA in a simpler, cheaper and more precise way than any other gene editing tool. In recent years CRISPR/Cas has completely transformed an existing discipline of genetic engineering. This 'review' focuses on the generations and modifications in CAR-T as an advanced cancer therapeutic tool and CAR-T-approved products. It also highlights three path-breaking successful autologous and allogenic ex vivo CAR-T clinical trials in treating cancer using CRISPR/Cas9 which reported successful results despite the controversies regarding the safety of this technique. Outcomes from the first successful clinical trial showed the beneficial long-term effect on genetically modified T-cells in targeting cancer cells which opens the door for CRISPR to be the most preferred technique to help treat cancer and other diseases in the future. We searched the MEDLINE, EMBASE and PUBMED databases for original studies and meta-analysis on the use of CRISPR/Cas9 to edit T-cells until 2021. We finally selected 15 pre-clinical and 26 clinical studies for the review.

Previous studies have shown that diffuse large B-cell lymphoma (DLBCL) subtype with both B-cell antigen receptor complex-associated protein beta chain (CD79B) and myeloid differentiation primary response 88 mutations (MYD88) had inferior outcome under standard immunochemotherapy. However, the prognostic significance of CD79B alone in DLBCL has not been fully elucidated. We conducted a meta-analysis to investigate the role of CD79B mutation on overall survival (OS) in patients with DLBCL.

colorectal cancer (CRC) is the most common carcinoma worldwide, but a lack of effective prognostic markers limits clinical diagnosis and treatment. Yes-associated protein 1 (YAP1) is an effector of the HIPPO-pathway, which plays a critical role in cancer development and prognosis, including CRC. However, previous reports have suggested that it plays a dual role in CRC.

Women with hereditary breast cancer factors are more likely to be infertile and tend to receive fertility treatments. The safety of fertility treatments that contain hormone-related medications for ovarian stimulation has gained wide attention; however, evidence of the safety of fertility treatments is limited. This study aims to assess the association between fertility treatments and the incidence rate of breast cancer in women with a family history of breast cancer or BRCA mutations. A literature search was conducted in PubMed, Cochrane Library, and Embase. Studies concerning the effect of fertility treatments on breast cancer risk in genetically susceptible women were included. The fixed and random effects models were used to estimate the summary effects. Risk Of Bias In Non-randomized Studies - of Interventions instrument was used to assess the risk of bias in the included studies. A total of 5,282 studies were screened. Five cohort studies and three case-control studies were included. Breast cancer risk was not significantly increased by fertility treatments in general genetically susceptible women [pooled odds ratio (OR) 1.18, 95% confidence interval (CI) 0.96-1.45], women with a family history of breast cancer (pooled OR 1.35, 95% CI 0.97-1.89), or women with BRCA mutations (pooled OR 1.02, 95% CI 0.74-1.4). In subgroup analyses, there was no significant increase in breast cancer risk whether in BRCA1 mutation carriers (pooled OR 1.18, 95% CI 0.81-1.72), BRCA2 mutation carriers (pooled OR 0.54, 95% CI 0.09-3.34), or in the women treated with in vitro fertilization (pooled OR 0.75, 95% CI 0.51-1.1), clomiphene citrate (pooled OR 1.07, 95% CI 0.78-1.45) or gonadotropins (pooled OR 1.32, 95% CI 0.8-2.18). This is the first meta-analysis concerning the impact of fertility treatments on breast cancer risk in genetically susceptible women. Despite the finding that fertility treatment did not significantly increase breast cancer risk in genetically susceptible women, large prospective cohorts with more detailed information are required. Further investigations are needed to explore subtypes of breast cancer, genetic background of hormone-related breast cancer, and the association between BRCA mutations and the incidence of hormone receptor-positive breast cancer.