Therapeutic combinations of exosomes alongside cancer stem cells (CSCs) and of CSC-derived exosomes (CSCEXs) in cancer therapy.

Exosomes which are membrane vesicles released by cells have gained significant interest in the field of cancer therapy as a novel means of intercellular communication. Their role in immune activation and their pathophysiological functions in cancer therapy have been recognized. Exosomes carry diverse bioactive components including proteins, mRNA, microRNAs, and bioactive lipids. These molecules have therapeutic potential in promoting tissue regeneration, supporting stem cell activity, preventing cell death, modulating immune responses, and promoting the growth of new blood vessels. However, the precise roles of exosomes derived from mesenchymal stem cells (MSCs) in the treatment of various cancers are still not fully understood. Consequently, cancer stem cells (CSCs) can self-renew and differentiate into various cell types. Understanding the mechanisms that sustain their persistence is crucial for developing effective therapies. Exosomes have recently gained interest as vehicles for intercellular communication between CSCs and non-CSCs, influencing cancer progression and the microenvironment. Research is ongoing on the utilization of exosomes derived from cancer stem cells (CSC-Exosome) for cancer treatment. The composition of extracellular vesicles is influenced by the specific type and condition of the cells from which they are secreted. Circulating exosomes contain stable RNA molecules such as mRNAs, microRNAs, and long non-coding RNAs (lncRNAs). In this review, we will explore the significance of exosomes and their diverse cellular combinations in the context of cancer therapy.

Practical immunomodulatory landscape of glioblastoma multiforme (GBM) therapy.

Glioblastoma multiforme (GBM) is the most common harmful high-grade brain tumor with high mortality and low survival rate. Importantly, besides routine diagnostic and therapeutic methods, modern and useful practical techniques are urgently needed for this serious malignancy. Correspondingly, the translational medicine focusing on genetic and epigenetic profiles of glioblastoma, as well as the immune framework and brain microenvironment, based on these challenging findings, indicates that key clinical interventions include immunotherapy, such as immunoassay, oncolytic viral therapy, and chimeric antigen receptor T (CAR T) cell therapy, which are of great importance in both diagnosis and therapy. Relatively, vaccine therapy reflects the untapped confidence to enhance GBM outcomes. Ongoing advances in immunotherapy, which utilizes different methods to regenerate or modify the resistant body for cancer therapy, have revealed serious results with many different problems and difficulties for patients. Safe checkpoint inhibitors, adoptive cellular treatment, cellular and peptide antibodies, and other innovations give researchers an endless cluster of instruments to plan profoundly in personalized medicine and the potential for combination techniques. In this way, antibodies that block immune checkpoints, particularly those that target the program death 1 (PD-1)/PD-1 (PD-L1) ligand pathway, have improved prognosis in a wide range of diseases. However, its use in combination with chemotherapy, radiation therapy, or monotherapy is ineffective in treating GBM. The purpose of this review is to provide an up-to-date overview of the translational elements concentrating on the immunotherapeutic field of GBM alongside describing the molecular mechanism involved in GBM and related signaling pathways, presenting both historical perspectives and future directions underlying basic and clinical practice.

A critical review of the recent concept of regulatory performance of DNA Methylations, and DNA methyltransferase enzymes alongside the induction of immune microenvironment elements in recurrent pregnancy loss.

Recurrent pregnancy Loss (RPL)is a frequent and upsetting condition. Besides the prevalent cause of RPL including chromosomal defects in the embryo,the effect of translational elements like alterations of epigenetics are of great importance. The emergence of epigenetics has offered a fresh outlook on the causes and treatment of RPL by focusing on the examination of DNA methylation. RPL may arise as a result of aberrant DNA methylation of imprinted genes, placenta-specific genes, immune-related genes, and sperm DNA, which may have a direct or indirect impact on embryo implantation, growth, and development. Moreover, the distinct immunological tolerogenic milieu established at the interface between the mother and fetus plays a crucial role in sustaining pregnancy. Given this, there has been a great deal of interest in the regulation of DNA methylation and alterations in the cellular components of the maternal-fetal immunological milieu. The research on DNA methylation's role in RPL incidence and the control of the mother-fetal immunological milieu is summed up in this review.

The effects of the combination therapy of chemotherapy drugs on the fluctuations of genes involved in the TLR signaling pathway in glioblastoma multiforme therapy.

One of the most lethal and aggressive types of malignancies with a high mortality rate and poor response to treatment is glioblastoma multiforme (GBM). This means that modernizing the medications used in chemotherapy, in addition to medicines licensed for use in other illnesses and chosen using a rationale process, can be beneficial in treating this illness. Meaningly, drug combination therapy with chemical or herbal originations or implanting a drug wafer in tumors to control angiogenesis is of great importance. Importantly, the primary therapeutic hurdles in GBM are the development of angiogenesis and the blood-brain barrier (BBB), which keeps medications from getting to the tumor. This malignancy can be controlled if the drug's passage through the BBB and the VEGF (vascular endothelial growth factor), which promotes angiogenesis, are inhibited. In this way, the effect of combination therapy on the genes of different main signaling pathways like TLRs may be indicated as an impressive therapeutic strategy for treating GBM. This article aims to discuss the effects of chemotherapeutic drugs on the expression of various genes and associated translational factors involved in the TLR signaling pathway.

microRNAs, oxidative stress, and genotoxicity as the main inducers in the pathobiology of cancer development.

Cancer is one of the most serious leading causes of death in the world. Many eclectic factors are involved in cancer progression including genetic and epigenetic alongside environmental ones. In this account, the performance and fluctuations of microRNAs are significant in cancer diagnosis and treatment, particularly as diagnostic biomarkers in oncology. So, microRNAs manage and control the gene expression after transcription by mRNA degradation, or also they can inhibit their translation. Conspicuously, these molecular structures take part in controlling the cellular, physiological and pathological functions, which many of them can accomplish as tumor inhibitors or oncogenes. Relatively, Oxidative stress is defined as the inequality between the creation of reactive oxygen species (ROS) and the body's ability to detoxify the reactive mediators or repair the resulting injury. ROS and microRNAs have been recognized as main cancer promoters and possible treatment targets. Importantly, genotoxicity has been established as the primary reason for many diseases as well as several malignancies. The procedures have no obvious link with mutagenicity and influence the organization, accuracy of the information, or fragmentation of DNA. Conclusively, mutations in these patterns can lead to carcinogenesis. In this review article, we report the impressive and practical roles of microRNAs, oxidative stress, and genotoxicity in the pathobiology of cancer development in conjunction with their importance as reliable cancer biomarkers and their association with circulating miRNA, exosomes and exosomal miRNAs, RNA remodeling, DNA methylation, and other molecular elements in oncology.

Evaluation of Fluctuations of BRAF Gene Expression and its Polymorphism at rs1267623 in Colorectal Cancer.

BACKGROUND: Molecular markers in Colorectal Cancer (CRC) are needed for more ac-curate classification and personalized treatment. In this way, we investigated the effects of the BRAF gene on clinical outcomes of its expression fluctuations and its polymorphism at rs1267623 in CRC. METHODS: In this study, 36.36 percent of patients with CRC were women, and 63.63 percent were men. After the pathology department confirmed the tumor of the samples, the stage and grade of the tumor were determined according to the TNM system. Real-time PCR was used to check the expression of the BRAF gene in tumor and non-tumor tissues, and its polymorphism in rs1267623 was also checked using the Tetra-ARMs PCR technique. RESULTS: The expression of BRAF in tumor tissues was significantly higher than in non-tumoral tissues (P = 0.001), indicating an upregulation of BRAF gene expression in tumoral tissues. The user's text is empty. Furthermore, there was a significant correlation between BRAF expression and tumor stage (P = 0.001), as well as tumor grade (P = 0.003). However, no significant link was found between lymph node metastasis and distant metastasis of BRAF gene expression (P = 0.3). Additionally, no mutation was detected in the investigation of rs1267623 polymorphism. CONCLUSION: The BRAF gene was upregulated in tumoral tissues. Remarkably, no mutation was found in the rs1267623 polymorphism. As a result, this gene can be used as a biomarker in the diagnosis and treatment of CRC.

Bioinformatic-based Study to Investigate the Structure and Function of Pro-inflammatory Cytokines TNFα and IL-6 Involved in the Pathogenesis of COVID-19.

Background & Objective: Besides the clinical and laboratory research on the COVID-19 virus, the bioinformatics study in the field of genetics of immunity to COVID-19 is of particular importance. In this account, studies show that in patients with COVID-19, the level of tumor necrosis alpha (TNFα) and interleukin-6 (IL-6) is high and in severe cases of COVID-19, the production of IL-6, TNF-α, and other cytokines increases profoundly. On the other hand, investigating the molecular structure and receptors of IL-6 and TNFα and the structural analysis of the receptor proteins may potentially help to develop new therapeutic plans for COVID-19 infection. Methods: To identify genes with significant and different expressions in patients with COVID-19 in a microarray data set containing transcriptional profiles from GEO as a functional genomic database the GEO query package version 2.64.2 in a programming language R version 4.2.1 was downloaded. In this way, functional enrichment analysis for DEGs, WikiPathways, REGO, gene ontology, and STRING database was also investigated and employed. Results: The structure and function of pro-inflammatory cytokines TNFα and IL-6 involved in the pathogenesis of COVID-19 were investigated, and in general, after performing various analyses in this study and extracting A series of genes with different expressions from the KEGG database, the final 5 DEGs include CXCL14, CXCL6, CCL8, CXCR1, TNFRSF10, and the relationship and expression effects of them were observed in different pathways. Conclusion: IL-6 and TNFα were involved in immunological processes that had a direct and indirect relationship with the activation of cytokines, including IL6 and TNF-a, and cytokine storm, and this indicates their role in the formation of problems and complications, including ARDS, in COVID-19 patients. Of course, determining the effectiveness of each of these genes requires more specialized and clinical studies.

TLR signaling pathway and the effects of main immune cells and epigenetics factors on the diagnosis and treatment of infertility and sterility.

Recurrent pregnancy loss (RPL), often known as spontaneous miscarriages occurring two or more times in a row, is a reproductive disease that affects certain couples. The cause of RPL is unknown in many cases, leading to difficulties in therapy and increased psychological suffering in couples. Toll-like receptors (TLR) have been identified as crucial regulators of inflammation in various human tissues. The occurrence of inflammation during parturition indicates that Toll-like receptor activity in tissues related to pregnancy may play a crucial role in the onset and continuation of normal function, as well as in various pregnancy complications like infection-related preterm. TLRs or their signaling molecules may serve as effective therapeutic targets for inhibiting premature activity. At the maternal-fetal interface, TLRs are found in both immune and non-immune cells, such as trophoblasts and decidual cells. TLR expression patterns are influenced by the phases of pregnancy. In this way, translational combinations like epigenetics, have indicated their impact on the TLRs.Importantly, abnormal DNA methylation patterns and histone alterations have an impressive performance in decreasing fertility by influencing gene expression and required molecular and cellular activities which are vital for a normal pregnancy and embryonic process. TLRs, play a central duty in the innate immune system and can regulate epigenetic elements by many different signaling pathways. The potential roles of TLRs in cells, epigenetics factors their ability to identify and react to infections, and their place in the innate immune system will all be covered in this narrative review essay.

Analytical and therapeutic profiles of DNA methylation alterations in cancer; an overview of changes in chromatin arrangement and alterations in histone surfaces.

DNA methylation is the most important epigenetic element that activates the inhibition of gene transcription and is included in the pathogenesis of all types of malignancies. Remarkably, the effectors of DNA methylation are DNMTs (DNA methyltransferases) that catalyze de novo or keep methylation of hemimethylated DNA after the DNA replication process. DNA methylation structures in cancer are altered, with three procedures by which DNA methylation helps cancer development which are including direct mutagenesis, hypomethylation of the cancer genome, and also focal hypermethylation of the promoters of TSGs (tumor suppressor genes). Conspicuously, DNA methylation, nucleosome remodeling, RNA-mediated targeting, and histone modification balance modulate many biological activities that are essential and indispensable to the genesis of cancer and also can impact many epigenetic changes including DNA methylation and histone modifications as well as adjusting of non-coding miRNAs expression in prevention and treatment of many cancers. Epigenetics points to heritable modifications in gene expression that do not comprise alterations in the DNA sequence. The nucleosome is the basic unit of chromatin, consisting of 147 base pairs (bp) of DNA bound around a histone octamer comprised of one H3/H4 tetramer and two H2A/H2B dimers. DNA methylation is preferentially distributed over nucleosome regions and is less increased over flanking nucleosome-depleted DNA, implying a connection between nucleosome positioning and DNA methylation. In carcinogenesis, aberrations in the epigenome may also include in the progression of drug resistance. In this report, we report the rudimentary notes behind these epigenetic signaling pathways and emphasize the proofs recommending that their misregulation can conclude in cancer. These findings in conjunction with the promising preclinical and clinical consequences observed with epigenetic drugs against chromatin regulators, confirm the important role of epigenetics in cancer therapy.

Novel Biomarkers of microRNAs in Gastric Cancer: An Overview from Diagnosis to Treatment.

Gastric cancer (GC) is the fourth most frequent disease in the world and the second cause of cancer-related death. In this way, over 80% of diagnoses are made in the middle to advanced degrees of the disease, underscoring the requirement for innovative biomarkers that can be identified quickly. Meaningly, biomarkers that can complement endoscopic diagnosis and be used to detect patients with a high risk of GC are desperately needed. These biomarkers will allow for the accurate prediction of therapy response and prognosis in GC patients, as well as the development of an optimal treatment strategy for each individual. Conspicuously, microRNAs (miRNAs) and small noncoding RNA regulate the expression of target mRNA, thereby modifying critical biological mechanisms. According to the data, abnormally miRNAs expression in GC is linked to tumor growth, carcinogenesis, aggression, and distant metastasis. Importantly, miRNA expression patterns and nextgeneration sequencing (NGS) can also be applied to analyze different kinds of tissues and cancers. Given the high death rates and poor prognosis of GC, and the absence of a clinical diagnostic factor that is adequately sensitive to GC, research on novel sensitive and specific markers for GC diagnosis is critical. In this review, we examine the latest research findings that suggest the feasibility and clinical utility of miRNAs in GC.

MUTYH and KLF6 gene expression fluctuations in tumor tissue and tumor margins tissues of colorectal cancer.

BACKGROUND: Colorectal cancer (CRC) is one of the most important cancers in the world, and its prevalence varies depending on the geographical area. Genetically, tumor regeneration in CRC as a multi-step process involves activating mutations in protocogenes and losing the function of tumor suppressor genes as well as DNA repair and recovery genes. Occur in this way, our goal was to investigate the expression of KLF6 genes as a tumor suppressor and MUTYH involved in the DNA repair process in colorectal cancer. METHODS: This research was conducted during the years 2019-2018 in Razi Hospital, Rasht. The subjects included 30 tumoral and 30 non-tumoral tissues of colorectal cancer and 20 healthy controls. The real-time PCR method was used to investigate the gene expression. For data analysis by SPSS, parametric statistical tests ANOVA and T test and regression analysis were used and p value values less than 0.05 were considered significant. RESULTS: The expression of KLF6 gene in tumoral tissues showed a significant decrease compared to non-tumoral tissues (P = 0.04). Also, the expression of MUTYH gene in tumor tissue showed a significant decrease compared to non-tumoral (P = 0.02) and this decrease in MUTYH gene expression had a significant relationship with increasing tumor stage (P = 0.01). CONCLUSION: These findings suggest that decreased expression of KLF6 and MUTYH genes in the study population has a significant relationship with colorectal cancer and can be considered as tumor marker in diagnostic purpose.

Cell therapy for the treatment of reproductive diseases and infertility: an overview from the mechanism to the clinic alongside diagnostic methods.

Infertility is experienced by 8%-12% of adults in their reproductive period globally and has become a prevalent concern. Besides routine therapeutic methods, stem cells are rapidly being examined as viable alternative therapies in regenerative medicine and translational investigation. Remarkable progress has been made in understanding the biology and purpose of stem cells. The affected pluripotent stem cells (iPSCs) and mesenchymal stem cells (MSCs) are further studied for their possible use in reproductive medicine, particularly for infertility induced by premature ovarian insufficiency and azoospermia. Accordingly, this study discusses current developments in the use of some kinds of MSCs such as adipose-derived stem cells, bone marrow stromal cells, umbilical cord MSCs, and menstrual blood MSCs. These methods have been used to manage ovarian and uterine disorders, and each technique presents a novel method for the therapy of infertility.

Performance of DNA Methylation on the Molecular Pathogenesis of Helicobacter pylori in Gastric Cancer; targeted therapy approach.

Gastric cancer (GC) is a significant cause of cancer mortality which has led to focused exploration of the pathology of GC. The advent of genome-wide analysis methods has made it possible to uncover genetic and epigenetic fluctuation such as abnormal DNA methylation in gene promoter regions that is expected to play a key role in GC. The study of gastric malignancies requires an etiological perspective, and Helicobacter pylori (H. pylori) was identified to play a role in GC. H. pylori infection causes chronic inflammation of the gastric epithelium causing abnormal polyclonal methylation, which might raise the risk of GC. In the last two decades, various pathogenic factors by which H. pylori infection causes GC have been discovered. Abnormal DNA methylation is triggered in several genes, rendering them inactive. In GC, methylation patterns are linked to certain subtypes including microsatellite instability. Multiple cancer-related processes are more usually changed by abnormal DNA methylation than through mutations, according to current general and combined investigations. Furthermore, the amount of acquired abnormal DNA methylation is heavily linked to the chances of developing GC. Therefore, we investigated abnormal DNA methylation in GC and the link between methylation and H. pylori infection.

DNA Methylation Profiling of MYC, SMAD2/3 and DNMT3A in Colorectal Cancer.

Epigenetic modifications, particularly DNA methylation, is commonplace and a remarkable factor in carcinogenesis transformation. Conspicuously, previous findings have presented a cluster of irregular promoter methylation alterations related with silencing of tumor suppressor genes, little is accepted regarding their sequential DNA methylation (hypo and hyper) modifications during the cancer progression. In this way, fluctuations of DNA methylation of many genes, especially MYC, SMAD2/3, and DNMT3A, have an impressive central key role in many different cancers, including colorectal cancer (CRC). CRC is distinguished by DNA methylation, which is related to tumorigenesis and also genomic instability. Importantly, molecular heterogeneity between multiple adenomas in different patients with CRC may show diverse developmental phenotypes for these kinds of tumors. Conclusively, studying factors that are involved in CRC carcinogenesis, especially the alterations in epigenetic elements, such as DNA methylation besides RNA remodeling, and histone modification, acetylation and phosphorylation, can be influential to find new therapeutic and diagnostic biomarkers in this type of malignancy. In this account, we discuss and address the potential significant methylated modifications of these genes and their importance during the development of CRC carcinogenesis.

CAR T-cells profiling in carcinogenesis and tumorigenesis: An overview of CAR T-cells cancer therapy.

Immunotherapy of cancer by chimeric antigen receptors (CAR) modified T-cell has a remarkable clinical potential for malignancies. Meaningly, it is a suitable cancer therapy to treat different solid tumors. CAR is a special recombinant protein combination with an antibody targeting structure alongside with signaling domain capacity on order to activate T cells. It is confirmed that the CAR-modified T cells have this ability to terminate and remove B cell malignancies. So, methodologies for investigations the pro risks and also strategies for neutralizing possible off-tumor consequences of are great importance successful protocols and strategies of CAR T-cell therapy can improve the efficacy and safety of this type of cancers. In this review article, we try to classify and illustrate main optimized plans in cancer CAR T-cell therapy.

DNA Methylation Profiling of hTERT Gene Alongside with the Telomere Performance in Gastric Adenocarcinoma.

PURPOSE: Epigenetic modification including of DNA methylation, histone acetylation, histone methylation, histon phosphorylation and non-coding RNA can impress the gene expression and genomic stability and cause different types of malignancies and also main human disorder. Conspicuously, the epigenetic alteration special DNA methylation controls telomere length, telomerase activity and also function of different genes particularly hTERT expression. Telomeres are important in increasing the lifespan, health, aging, and the development and progression of some diseases like cancer. METHODS: This review provides an assessment of the epigenetic alterations of telomeres, telomerase and repression of its catalytic subunit, hTERT and function of long non-coding RNAs such as telomeric-repeat containing RNA (TERRA) in carcinogenesis and tumorgenesis of gastric cancer. RESULTS: hTERT expression is essential and indispensable in telomerase activation through immortality and malignancies and also plays an important role in maintaining telomere length. Telomeres and telomerase have been implicated in regulating epigenetic factors influencing certain gene expression. Correspondingly, these changes in the sub telomere and telomere regions are affected by the shortening of telomere length and increased telomerase activity and hTERT gene expression have been observed in many cancers, remarkably in gastric cancer. CONCLUSION: Epigenetic alteration and regulation of hTERT gene expression are critical in controlling telomerase activity and its expression. Graphical Abstract.

An insight of microRNAs performance in carcinogenesis and tumorigenesis; an overview of cancer therapy.

Importance of dysregulation and expression of microRNAs (miRNAs) has been confiemed in many disorders comprising cancer. In this way, different approaches to induce reprogramming from one cell type to another in oerder to control the cell normal mechanisem, comprising microRNAs, combinatorial small molecules, exosome-mediated reprogramming, embryonic microenvironment and also lineage-specific transcription agents, are involved in cell situation. Meaningly, besides the above factors, microRNAs are so special and have an impressive role in cell reprogramming. One of the main applications of cancer cell reprogramming is it's ability in therapeutic approach. Many insights in reprogramming mechanism have been recommended, and determining improvment has been aknolwged to develop reprogramming efficiency and possibility, permiting it to appear as practical therapy against all cancers. Conspiciously, the recent studies on the fluctuations and performance of microRNAs,small endogenous non-coding RNAs, as notable factors in carcinogenesis and tumorigenesis, therapy resistance and metastasis and as new non-invasive cancer biomarkers has a remarkable attention. This is due to their unique dysregulated signatures throughout tumor progression. Recognising miRNAs signatures capable of anticipating therapy response and metastatic onset in cancers might enhance diagnosis and therapy. According to the growing reports on miRNAs as novel non-invasive biomarkers in various cancers as a main regulators of cancers drug resistance or metastasis, the quest on whether some miRNAs have the ability to regulate both simultaneously is inevitable, yet understudied. The combination of genetic diagnosis using next generation sequencing and targeted therapy may contribute to the effective precision medicine for cancer therapy. Here, we want to review the practical application of microRNAs performance in carcinogenesis and tumorigenesis in cancer therapy.

Regulatory Fluctuation of WNT16 Gene Expression Is Associated with Human Gastric Adenocarcinoma.

INTRODUCTION: Gastric cancer is one of the most serious and lethal kinds of cancer in the world. It is a multi-step, multi-factor, and elaborated process that is associated to gene abnormal expression. This study intended to investigate the WNT16 gene's expression in human gastric tumor and the margin tissues of the stomach (normal tissues). METHODS: Correspondingly, 40 samples (20 tumoral tissues and 20 non tumoral or margins tissues) were investigated in Imam Khomeini Hospital in Sari City, Mazandaran Province, Iran. In this way, real-time PCR, Taqman assay was employed to evaluate the upregulation and downregulation of this gene in both tissues in triplicate form. The GAPDH gene was selected as housekeeping gene. RESULTS: Conspicuously, the results have shown a remarkable modification in tumoral tissues, and the gene expression increased significantly in tumoral tissue. CONCLUSIONS: Conclusively, the upregulation of WNTt16 gene expression in tumoral tissues was impressive and the P value was 0.005 and the SE range was 0.064-142.154.

Epigenetic profiling of MUTYH, KLF6, WNT1 and KLF4 genes in carcinogenesis and tumorigenesis of colorectal cancer.

Colorectal cancer (CRC) is distinguished by epigenetic elements like DNA methylation, histone modification, histone acetylation and RNA remodeling which is related with genomic instability and tumor initiation. Correspondingly, as a main epigenetic regulation, DNA methylation has an impressive ability in order to be used in CRC targeted therapy. Meaningly, DNA methylation is identified as one of most important epigenetic regulators in gene expression and is considered as a notable potential driver in tumorigenesis and carcinogenesis through gene-silencing of tumor suppressors genes. Abnormal methylation situation, even in the level of promoter regions, does not essentially change the gene expression levels, particularly if the gene was become silenced, leaving the mechanisms of methylation without any response. According to the methylation situation which has a strong eagerness to be highly altered on CpG islands in carcinogenesis and tumorigenesis, considering its epigenetic fluctuations in finding new biomarkers is of great importance. Modifications in DNA methylation pattern and also enrichment of methylated histone signs in the promoter regions of some certain genes like MUTYH, KLF4/6 and WNT1 in different signaling pathways could be a notable key contributors to the upregulation of tumor initiation in CRC. These epigenetic alterations could be employed as a practical diagnostic biomarkers for colorectal cancer. In this review, we will be discuss these fluctuations of MUTYH, KLF4/6 and WNT1 genes in CRC.

The fluctuation of APC gene in WNT signaling with adenine deletion of adenomatous polyposis coli, is associated in colorectal cancer / A flutuação do gene da APC na via de sinalização WNT com deleção de adenina na polipose adenomatosa do cólon está associada ao câncer colorretal

ABSTRACT Colorectal cancer is one of the most important malignancies in the classification of gastrointestinal cancers. One of the predisposing factors at molecular level for this cancer is via WNT signaling which is associated with the vast numbers of different genes. Thus, in this study, we aimed to investigate whether Adenomatous Polyposis Coli gene (APC) mutation of rs41115in two locations such as 132.002 and 131.989 acts as a trigger or cause of colorectal cancer. Relatively, 30 blood samples of colorectal cancer patients and 30 normal blood samples as control group after colonoscopy and also confirmation of pathology report at Rohani Hospital in Babol (Iran) were investigated. The primers were designed in order to be included the rs41115 to identify the particular polymorphisms of gene. The polymerase chain reaction (PCR direct sequencing method) was used. Conclusively, deletion of adenine in two specific locations such as 131.989 and 132.002 has been identified, but there was no relationship between rs41115 polymorphisms located in adenomatous polyposis coli gene and colorectal cancer.

RESUMO O câncer colorretal é uma das neoplasias malignas mais importantes na classificação dos cânceres gastrointestinais. Um dos fatores predisponentes no âmbito molecular para esse câncer é através da via de sinalização WNT, que está associada a um grande número de genes diferentes. Portanto, neste estudo, objetivamos investigar se a mutação rs41115 do gene da polipose adenomatosa do cólon (Adenomatous Polyposis Coli - APC) em dois locais como 132.002 e 131.989 atua como gatilho ou como causa do câncer colorretal. Relativamente, 30 amostras de sangue de pacientes com câncer colorretal e 30 amostras de sangue normal (grupo controle) foram analisadas após a colonoscopia, bem como a confirmação do laudo da patologia no Rohani Hospital em Babol (Irã). Os primers foram projetados de modo a incluir o rs41115 para identificar os polimorfismos particulares do gene. A reação em cadeia da polimerase (método de sequenciamento direto por PCR) foi utilizada. Conclusivamente, a deleção de adenina em dois locais específicos, como 131.989 e 132.002, foi identificada, mas não houve relação entre o polimorfismo rs41115 localizado no gene da polipose adenomatosa do cólon e o câncer colorretal.