Occurrence Of Malignant Tumors Research Articles

Idiopathic inflammatory myopathies : An interdisciplinary challenge

Idiopathic inflammatory myopathies (IIM) are rare diseases (incidence 1:100,000) with awide range of clinical symptoms and manifestations. Typical indicators of IIM are proximally emphasized muscle weakness and myalgias, which are usually accompanied by elevated creatine kinase levels and muscle atrophy. The autoantibody diagnostics separate IIM into different entities, which are each associated with atypical risk of organ manifestations and the occurrence of tumors. The IIM represents an interdisciplinary challenge and the diagnostics and treatment require the involvement of several disciplines including rheumatology, neurology, neuropathology, dermatology and pneumology. An accurate diagnosis and careful tumor screening are essential because of the association between certain subgroups of IIM and the occurrence of malignant tumors.

High-grade sinonasal adenocarcinoma as an unusual presentation: A case report

The occurrence of malignant tumors, such as adenocarcinoma, is commonplace in the nasal region, characterized by a notably low incidence. This rarity often contributes to delayed diagnosis, rendering the condition challenging to manage. Here, we present the case of a 70-year-old man who presented with chronic left nasal obstruction, accompanied by headaches and recurrent epistaxis. The diagnostic investigation revealed an extensive and aggressive nasal adenocarcinoma, necessitating a hemi-maxillectomy for tumor excision. Subsequent reconstruction of the ipsilateral cheek was accomplished using a pectoralis major flap. Despite the initial intervention, the patient experienced a recurrence 1 year later. In sinonasal adenocarcinoma, nasal obstruction stands out as the predominant symptom, complemented by potential manifestations of swelling and facial deformation. The inherently aggressive nature of this tumor underscores the imperative for early diagnosis and meticulous management to achieve optimal therapeutic outcomes. The comprehensive approach involving surgical intervention and reconstruction reflects the complexity in treating advanced nasal adenocarcinomas.

The relationship between metabolite mediated immune regulatory imbalance and the occurrence of malignant tumors of bone and articular cartilage: a Mendelian randomization study.

This study aims to assess the causal relationship between immune cell characteristics and malignant tumors of bone and articular cartilage, focusing on the mediating role of metabolites. Using Mendelian randomization, we evaluated these relationships based on genetic variations to identify potential biomarkers and therapeutic targets. A two-sample Mendelian randomization analysis was conducted using GWAS data for immune cell features and 1,400 metabolites to investigate direct and mediating effects. Effective instrumental variables (IVs) were selected, and statistical analyses-including inverse variance weighting (IVW), weighted median, and mode-based methods-were performed using R software. This approach enabled the assessment of direct causal relationships as well as the potential mediating role of metabolites in the association between immune cell features and malignancies. Significant causal relationships were identified between 26 immune phenotypes and the risk of malignant tumors of bone and articular cartilage. Notably, the HLA DR+ NK cell phenotype SSC-A showed a positive correlation with the risk of these malignancies. Further analysis revealed causal relationships with 67 metabolites, 38 of which were positively correlated and 29 negatively correlated. Mediation analysis highlighted the role of immune surveillance and metabolic dysregulation in tumor development, as evidenced by the association between the immune phenotype SSC-A on HLA DR+ NK cells and the metabolite 5-hydroxyhexanoate. The findings suggest significant causal relationships between immune phenotypes and malignant tumors of bone and articular cartilage, with metabolites potentially mediating these relationships. These insights lay the groundwork for further research and could contribute to the development of new biomarkers and treatment strategies.

Relationship between sex differences in drinking, smoking, and exercising and the incidence of malignancies and medical procedures: a cross-sectional study of 21,916 participants in China.

Objectives: The unresolved issue of the relationship between sex differences in tea, coffee, and beverage consumption and malignancy risk prompted our study in 2022. Methods: Logistic proportional hazards models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) in our investigation of the associations between cancer risk and tea, coffee, and beverage consumption. Results: Our findings revealed that frequent consumption of white tea significantly reduced the occurrence of malignant tumours, but this effect was detected only in the fully adjusted model for males (OR: 0.736, 95% CI: 0.095-5.704). The amount of sugar added to coffee was associated with an increased risk of malignancy in a dose-dependent manner (P for trend = 0.001), with significance observed for both men (P for trend = 0.049) and women (P for trend = 0.005) in the final model. Notably, individuals who consumed more than 2100 ml of sugary beverages daily had a statistically significant reduction in malignancy risk (OR: 0.219, 95% CI: 0.052-0.917). Interestingly, the intake of sugary beverages had a protective effect on cancer incidence, with a significant effect on males (P for trend = 0.031) but not females (P for trend = 0.096) in the final model. Conclusions: Our study highlights the substantial impact of regular white tea consumption on reducing the risk of malignant tumours in males. This study first reported that the potential protective effect of consuming sugary beverages is predominantly observed in males, and a correlation between the amount of sugar added to coffee and a heightened risk of malignancy.

Non B Cell-Derived Immunoglobulin, A Brighter Horizon for the Future.

The canonical theory of immunology stating that "Immunoglobulin (Ig) is produced by B lymphocytes and exerts antibody activity" has been established since the 1970s. However, the discovery of nonB cell-derived Igs (nonB-Igs), which can exert multiple biological activities in addition to their antibody activities, necessitates a reevaluation of the classic concept of Ig. This has been documented with a number of characteristics related to their structure, modification, genetic regulation as well as the functions associated with clinical conditions, particularly multiple cancers. The discovery of nonB-Ig provides us with a new perspective to better understand not only basic immunology, but also various Ig-related clinical manifestations including autoimmune diseases, chronic inflammation, and anaphylaxis. Notably, nonB-Ig can directly promote the occurrence of malignant tumours.

Malignant Neoplasms Arising in the Cardiac Pacemaker Cavity: A Systematic Review.

Cancer is the abnormal proliferation of physiologically inadequate cells. Studies have identified the cardiac pacemaker pocket as a site of rare neoplasms. To evaluate the clinical outcomes, treatment, prognosis, and individualized management of tumors originating in the cardiac pacemaker pocket, a systematic review was conducted using case reports and case series available in the PubMed/Medline, Science Direct, Cochrane Central, LILACS, and Scientific Electronic Library Online (Scielo) databases. Pacemaker pocket tumors affected patients with a mean age of 72.9 years, with a higher incidence in males (76.9%, n = 10). The average time for neoplasm development was 4.4 years (54.07 months). The most prevalent model was Medtronic (38.4%, n = 5), with titanium (83.3%) being the most common metal composition. Chemotherapy was the most performed procedure among patients (38.4%), followed by radiation therapy (38.4%) and surgical tumor resection (30.7%). Six analyzed cases (46.1%) resulted in death, and four patients (30.7%) achieved a cure. Patients with pacemakers should be routinely evaluated for the occurrence of malignant tumors at the site of device implantation.

Previous, simultaneous, or subsequent occurrence of malignant tumours in patients with primary hyperparathyroidism: a closer look at the single-tertiary-centre cases.

Our aims were to explore the relationship between primary hyperparathyroidism (pHPT) and malignant tumour development, to determine the frequency and the time of occurrence of malignant tumours in patients with pHPT, and to evaluate the characteristics of pHPT in these patients. This retrospective cohort study included consecutive individuals who were diagnosed with pHPT aged 18 years or older in a university hospital during a 7-year period. A total of 198 patients with pHPT were reviewed retrospectively. Demographic, clinical, biochemical, radiologic findings, and histopathological diagnosis were collected from the electronic medical records of the hospital system. The mean age of the study population was 58 ± 13 years and was predominantly female (female/male: 162/36). There were 42 (21.2%) patients with malignant tumours. Five (12%) out of 42 patients had metachronous double malignancies. The most common 2 concurrent malignancies were breast (36.1%) and thyroid (17.0%). Sixty-eight per cent of the malignant tumours occurred before the diagnosis of pHPT. A higher percentage (87.5%) of simultaneous tumours was seen in the thyroid gland. No statistically significant differences were observed between patients with and without malignant tumours in terms of demographic, clinical, biochemical, radiological, and histopathological features. The median follow-up duration was 24 months after parathyroid surgery. The results of this study revealed that pHPT was associated with various tumour types. The frequency of malignant tumours was 21.2%. Breast and thyroid cancers were the most common 2 cancers coexisting with pHPT. A large percentage of malignant tumours occurred before the diagnosis of pHPT. A higher percentage of simultaneous tumours was seen in the thyroid gland. pHPT patients with and without malignant tumours seemed to have similar characteristics.

Construction of a prognostic model based on genes associated with mitochondrial energy metabolic pathway in colon adenocarcinoma and its clinical significance.

Mitochondria are the main sites of oxidative metabolism and energy release of sugars, fats and amino acids in the body. According to studies, malignant tumor occurrence and development have been linked to abnormal mitochondrial energy metabolism (MEM). However, the feasible role of abnormal MEM in colon adenocarcinoma (COAD) is poorly understood. In this work, we obtained COAD patient data from The Cancer Genome Atlas (TCGA) as the training set, and GSE103479 from Gene Expression Omnibus (GEO) as the validation set. Combined with the mitochondrial energy metabolic pathway (MEMP)-related genes in Kyoto Encyclopedia of Genes and Genomes (KEGG) database, a risk prognostic model was constructed by utilizing Cox regression analysis to identify 6 feature genes (CYP4A11, PGM2, PKLR, PPARGC1A, CPT2 and ACAT2) that were significantly associated with MEMP in COAD. By stratifying the samples based on riskscore, two distinct groups, namely the high- and low-risk groups, were identified. The model demonstrated accurate assessment of the prognosis risk in COAD patients and exhibited independent prognostic capability, as evidenced by the survival curve and receiver operating characteristic (ROC) curve analysis. A nomogram was plotted based on clinical information and riskscore. We proved it could predict the survival time of COAD patients effectively combined with the calibration curve of risk prediction. Subsequently, based on the immune evaluation and mutation frequency analysis performed on COAD patients, patients in high-risk group had observably higher immune scores, immune activity and PDCD1 expression level than low-risk group. In general, the prognostic model developed using MEMP-related genes served as a valuable biomarker for forecasting the prognosis of COAD patients, which offered a reference for the prognosis evaluation and clinical cure of COAD patients.

Integrative Identification by Hi-C Revealed Distinct Advanced Structural Variations in Lung Adenocarcinoma Tissue.

Advanced three-dimensional structure variations of chromatin in large genome fragments, such as conversion of A/B compartment, topologically associated domains (TADs) and chromatin loops are related closely to occurrence of malignant tumors. However, the structural characteristics of lung cancer still remain uncovered. In this study, we used high-throughput chromosome (Hi-C) conformation capture technology to detect the advanced structural variations in chromatin of two non-smoking lung adenocarcinoma (LUAD) tumor and paired normal tissues. The results indicate that significant chromatin variations are detected in tumor tissues compared with normal tissues. At compartment scale, the main conversion type of compartment is A → B in tumor tissues, which are concentrated mainly on chromosome 3 (Chr3) (33.6%). A total of 216 tumor-specific TADs are identified in tumor tissues, which are distributed mainly in Chr1 (19), Chr2 (15) and Chr3 (17). Forty-one distinct enhancer-promoter loops are observed in tumor tissue, which are associated closely to tumor-related pathways including mitogen-activated protein kinase (MAPK), Phosphatidylinositol-3-kinase-Protein kinase B (PI3K-AKT), Ras, Wnt and Ras1. The most important observation in this study is that we identify five important genes (SYT16, NCEH1, NXPE3, MB21D2, and DZIP1L), which are detected in both A → B compartment, TADs and chromatin loops in tumor samples, and four of these genes (NCEH1, NXPE3, MB21D2, and DZIP1L) locate on q arm of Chr3. Further gene expression and invasion experiment analysis show that NCEH1, MB21D2 and SYT16 are involved in the tumor development. Thus, we provide a comprehensive overview ofadvanced structures in LUAD for the first time and provide a basis for further research on the genetic variation of this tumor.

Identification of potentially high drug-like VEGFR2/c-Met dual-target type II kinase inhibitors with symmetric skeletons based on structural screening

Vascular endothelial growth factor receptor 2 (VEGFR2) and c-Mesenchymal epithelial transition factor (c-Met) are tyrosine kinase receptors associated with the occurrence of malignant tumors. Studies have shown that inhibition of VEGFR2 promotes a feedback increase in c-Met, a mechanism linked to the emergence of resistance to VEGFR2 inhibitors. Therefore, treatment targeting both VEGFR2 and c-Met will have better application prospects. In this study, hierarchical virtual screening was performed on ZINC15, Molport and Mcule-ULTIMATE databases to identify potential VEGFR2/c-Met dual inhibitors. Firstly, the best pharmacophore model for each target was used to cross-screen the three databases, and the compounds that could match the two pharmacophore models were then retained based on the Fit Value of the respective crystal ligands. Compounds ZINC, MOL, and MLB named after their database sources were retained by binding pattern analysis and docking assessment. ADMET predictions indicated that ZINC had significantly higher oral bioavailability compared to the approved drug cabozantinib. This is likely due to ZINC's unique symmetrical backbone with less structure complexity, which may reduce the occurrence of adverse effects. Molecular dynamics simulations and binding free energy analysis showed that all three hit compounds were able to stably bind at the active site, but only ZINC could form high occupancy of hydrogen bonds with both VEGFR2 and c-Met, and also only ZINC had a higher binding free energy than crystal ligands, suggesting that ZINC was the most likely potential VEGFR2/c-Met dual-target inhibitor. This finding provides a promising starting point for the development of VEGFR2/c-Met dual-target inhibitors. Communicated by Ramaswamy H. Sarma

Хондробластна остеосаркома проксимального відділу лівої великогомілкової кістки на тлі муковісцидоз-асоційованого цукрового діабету. Клінічний випадок

Cystic fibrosis related diabetes (CFRD) is a rare pathology that combines genetically determined systemicity with damage to the exocrine glands, which leads to early manifestations of the disease, a clear exacerbation and chronicity of the process, with possible complications in bone remodeling with the occurrence of malignant tumors. Purpose - to acquaint practitioners with the peculiarities of manifestations, diagnosis and course of chondroblastic osteosarcoma in a child with CFRD. Features of the clinical course and differential diagnosis are described and given osteosarcoma of the proximal part of the left tibia against the background of CFRD in a child. The main diagnostic value of history, clinical picture, laboratory, instrumental, immunohistochemical and microscopic research methods was highlighted, in particular, a biopsy of this tumor. Microscopic examination of tissue biopsy revealed alternating areas of atypical cartilaginous tissue corresponding to the structure of chondrosarcoma 1-2 cm, solid proliferates of atypical fibroblast-like cells and areas of atypical and fibroblastic tissue containing elements of atypical osteogenesis. Periosteally - randomly oriented bone fragments at the place of the cortical plate, as well as impressions of the lower metaphysis of the thigh and the upper metaphysis of the tibia, near the knee joint. The immunohistochemical examination showed a clear differential diagnosis of the existing CD99-positive tumor cells (DAKO, clone 12E7). Some cells were positive for SATB2 (Cell Marque, clone EP281); tumor cells were negative for S-100 - SOX-10. The histological picture and immunophenotype of the tumor cells correspond to chondroblastic osteosarcoma. Osteosarcoma with genetic, metabolic and aplastic features developing in the setting of a comorbid background significantly complicates diagnosis and requires certain changes in the treatment tactics of CFRD (correction of prophylactic and basic therapy, metabolic and toxic disorders, including those caused by chemotherapy). The research was carried out in accordance with the principles of the Helsinki Declaration. The informed consent of the patient was obtained for conducting the studies. No conflict of interests was declared by the authors.

MiR-338-3p acts as a tumor suppressor in lung squamous cell carcinoma by targeting FGFR2/FRS2

BackgroundLung cancer refers to the occurrence of malignant tumors in the lung, and squamous cell carcinoma is one of the most common pathological types of non-small cell lung cancer. Studies have shown that microRNAs (miRNAs) play an important role in the occurrence, development, early diagnosis, and treatment of lung cancer. This study aimed to explore the role and possible mechanism of MicroRNA-338-3p (miR-338-3p) in lung squamous cell carcinoma (LUSC). MethodIn this study, we compared 238 LUSC patients with relatively high miR-338-3p expression levels with 238 miR-338-3p expression levels in The Cancer Genome Atlas (TCGA)-LUSC dataset using first-line gene set enrichment analysis (GSEA). Second, the mRNA expression of miR-338-3p, FGFR2, and fibroblast growth factor receptor substrate 2 (FRS2) in 30 lung cancers and adjacent lung tissues was detected using quantitative real-time polymerase chain reaction (qRT-PCR). Finally, in vitro experiments were conducted, whereby the expression levels of miR-338-3p in lung cancer cells (H1703, SKMES1, H2170, H520) and normal lung epithelial cells (16HBE) were detected using qRT-PCR. miR-338-3p was overexpressed in lung cancer cells (H1703), and the cell proliferation (cell counting kit-8 [CCK8] assay), colony formation, cell apoptosis, cell cycle (BD-FACSVerse assay, Becton Dickinson, Bedford, MA, USA), cell invasion, and migration (Transwell assay, Thermo Fischer Corporation, Waltham, MA, USA) were detected. ResultsWe found that the expression of miR-338-3p was significantly reduced in LUSC tissues (p ​< ​0.001) and cancer cell lines (P < 0.01), and miR-338-3p was significantly negatively correlated with the expression of FGFR2 (P < 0.001) and FRS2 (P < 0.01). Furthermore, overexpression of miR-338-3p inhibited proliferation (P < 0.001), migration, and invasion (P < 0.001) of LUSC cell lines and increased apoptosis in the G1 phase (P < 0.001) and cell cycle arrest (P < 0.05). ConclusionsOur study demonstrates that miR-338-3p inhibits tumor cell proliferation and migration by targeting FGFR2 and FRS2 in LUSC. We believe that miR-338-3p may be a promising target for the treatment of LUSC.

Comprehensive analyses reveal the role of histone deacetylase genes in prognosis and immune response in low-grade glioma.

Many studies have shown that Histone deacetylases (HDAC) is involved in the occurrence of malignant tumors and regulates the occurrence, proliferation, invasion, and migration of malignant tumors through a variety of signaling pathways. In the present, we explored the role of Histone deacetylases genes in prognosis and immune response in low-grade glioma. Using consensus clustering, we built the new molecular clusters. Using HDAC genes, we constructed and validated the prognostic model in two independent cohort datasets. Patients were divided into high-risk and low-risk groups. Then, we explored the molecular characteristics, clinical characteristics, tumor microenvironment and immune infiltration levels of two clusters and risk groups. Receiver operating characteristic analyses were built for model assessment. We finally detected the expression levels of signature genes between tumor and normal tissues. Low-grade can be separated into two molecular clusters using 11 HDACs genes. Two clusters had different clinical characteristics and prognosis. Nex, we constructed a prognosis model using six HDAC genes (HDAC1, HDAC4, HDAC5, HDAC7, HDAC9, and HDAC10), which was also validated in an independent cohort dataset. Furthermore, multivariate cox regression indicated that the calculated risk score was independently associated with prognosis in low-grade glioma, and risk score can predict the five-year survival probability of low-grade glioma well. High-risk patients can be attributed to multiple complex function and molecular signaling pathways, and the genes alterations of high- and low-risk patients were significantly different. We also found that different survival outcomes of high- and low- risk patients could be involved in the differences of immune filtration level and tumor microenvironment. Subsequently, using signature genes, we identified several small molecular compounds that could be useful for low-grade glioma patients' treatment. Finally, we detected the expression levels of signature genes in tumor tissues. our study uncovers the biology function role of HDAC genes in low-grade glioma. We identified new molecular subtypes and established a prognostic model based on six HDAC genes, which was well applied in two independent cohort data. The regulation of HDAC genes in low-grade glioma involved in multiple molecular function and signaling pathways and immune infiltration levels. Further experiments in vivo and vitro were required to confirm the present findings.

Characterization of glucose metabolism in breast cancer to guide clinical therapy

BackgroundBreast cancer (BRCA) ranks as a leading cause of cancer death in women worldwide. Glucose metabolism is a noticeable characteristic of the occurrence of malignant tumors. In this study, we aimed to construct a novel glycometabolism-related gene (GRG) signature to predict overall survival (OS), immune infiltration and therapeutic response in BRCA patients.Materials and methodsThe mRNA sequencing and corresponding clinical data of BRCA patients were obtained from public cohorts. Lasso regression was applied to establish a GRG signature. The immune infiltration was evaluated with the ESTIMATE and CIBERSORT algorithms. The drug sensitivity was estimated using the value of IC50, and further forecasted the therapeutic response of each patient. The candidate target was selected in Cytoscape. A nomogram was constructed via the R package of “rms”.ResultsWe constructed a six-GRG signature based on CACNA1H, CHPF, IRS2, NT5E, SDC1 and ATP6AP1, and the high-risk patients were correlated with poorer OS (P = 2.515 × 10−7). M2 macrophage infiltration was considerably superior in high-risk patients, and CD8+ T cell infiltration was significantly higher in low-risk patients. Additionally, the high-risk group was more sensitive to Lapatinib. Fortunately, SDC1 was recognized as candidate target and patients had a better OS in the low-SDC1 group. A nomogram integrating the GRG signature was developed, and calibration curves were consistent between the actual and predicted OS.ConclusionsWe identified a novel GRG signature complementing the present understanding of the targeted therapy and immune biomarker in breast cancer. The GRGs may provide fresh insights for individualized management of BRCA patients.

Regulation of SUMOylation Targets Associated With Wnt/β-Catenin Pathway

Wnt/β-catenin signaling is a delicate and complex signal transduction pathway mediated by multiple signaling molecules, which plays a significant role in regulating human physiology and pathology. Abnormally activated Wnt/β-catenin signaling pathway plays a crucial role in promoting malignant tumor occurrence, development, recurrence, and metastasis, particularly in cancer stem cells. Studies have shown that the Wnt/β-catenin signaling pathway controls cell fate and function through the transcriptional and post-translational regulation of omics networks. Therefore, precise regulation of Wnt/β-catenin signaling as a cancer-targeting strategy may contribute to the treatment of some malignancies. SUMOylation is a post-translational modification of proteins that has been found to play a major role in the Wnt/β-catenin signaling pathway. Here, we review the complex regulation of Wnt/β-catenin signaling by SUMOylation and discuss the potential targets of SUMOylation therapy.

Cryotherapy as a method of treating diseases of the pancreas

The problem of treating diseases of the pancreas remains highly relevant. Despite the large arsenal of methods of surgical treatment of this pathology, even the introduction of endoscopic, minimally invasive and organpreserving technologies does not allow us to speak unambiguously about solving the problem. The high incidence of acute and chronic forms of pancreatitis, the frequent occurrence of malignant neoplasms of the pancreas, in which it is not possible to carry out radical operations, determined the need for the use of cryosurgical technologies both for open interventions on the pancreas and for laparoscopic operations. In an experiment on animals, the effectiveness of the use of ultra-low temperatures in the pathology of the pancreas was proved. The developed methods of cryotherapy began to be used in the clinic not only as independent surgical interventions, but also in combined operations with good immediate and long-term results.

Retrospective analysis of 9 cases of appendiceal mucocele in 3,071 cases of appendicitis

Appendiceal mucocele is a rare disease. Due to the lack of specific clinical symptoms, and the high misdiagnosis rate before operation, in the present study, the clinical data were assessed to determine a potential basis for the diagnosis and treatment of appendiceal mucocele. The clinical data of 3,071 patients with appendicitis admitted between January 2014 and July 2021, including 9 patients with appendiceal mucoceles were retrospectively analyzed. The data were retrieved from the hospital records and included the patients' age, sex, leukocyte counts (measured in the peripheral venous blood sample), the surgical methods, the pathological results and the postoperative follow-up information. Among the 3,071 patients with appendicitis, 9 cases were appendiceal mucocele. These 9 were treated by laparoscopic surgery in 6 cases (2 laparoscopic appendectomy, 2 laparoscopic partial cecectomy plus appendectomy, and 2 laparoscopic right hemicolectomy) and laparotomy in 3 cases (partial cecectomy plus appendectomy). Pathological examination was performed on the surgically resected specimens of all patients. The results showed that 7 cases were appendiceal mucoceles, and 2 cases were low-grade appendiceal mucoceles. During the follow-up after surgery, one patient with exploratory laparotomy plus partial cecectomy and appendectomy was pathologically diagnosed with low-grade appendiceal myxoma. The patient developed peritoneal implants appeared 2 years later, and the remaining patients are still alive, without any postoperative complications or obvious signs of recurrence. Appendiceal mucocele is a disease that usually causes clinical manifestations of acute appendicitis. Ultrasound and CT scans can be used for preoperative diagnosis. The surgical treatment options for mucoceles are open or laparoscopic appendectomy, cecectomy, and right hemicolectomy. Although the incidence of appendiceal mucocele is low, special attention should be paid to surgery due to its predisposition to peritoneal implantation and metastasis. Laparoscopic appendectomy with partial cecectomy is not a difficult procedure and is not likely to cause abdominal implantation metastasis, thus it should be the preferred surgical method. When conditions permit, intraoperative rapid cryotherapy can quickly identify the occurrence of malignant tumors.

Promoter methylation-regulated miR-148a-3p inhibits lung adenocarcinoma (LUAD) progression by targeting MAP3K9.

Lung adenocarcinoma (LUAD) characterized by high metastasis and mortality is the leading subtype of non-small cell lung cancer. Evidence shows that some microRNAs (miRNAs) may act as oncogenes or tumor suppressor genes, leading to malignant tumor occurrence and progression. To better understand the molecular mechanism associated with miRNA methylation in LUAD progression and clinical outcomes, we investigated the correlation between miR-148a-3p methylation and the clinical features of LUAD. In the LUAD cell lines and tumor tissues from patients, miR-148a-3p was found to be significantly downregulated, while the methylation of miR-148a-3p promoter was notably increased. Importantly, miR-148a-3p hypermethylation was closely associated with lymph node metastasis. We demonstrated that mitogen-activated protein (MAP) kinase kinase kinase 9 (MAP3K9) was the target of miR-148a-3p and that MAP3K9 levels were significantly increased in both LUAD cell lines and clinical tumor tissues. In A549 and NCI-H1299 cells, overexpression of miR-148a-3p or silencing MAP3K9 significantly inhibited cell growth, migration, invasion and cytoskeleton reorganization accompanied by suppressing the epithelial-mesenchymal transition. In a nude mouse xenograft assay we found that tumor growth was effectively inhibited by miR-148a-3p overexpression. Taken together, the promoter methylation-associated decrease in miR-148a-3p could lead to lung cancer metastasis by targeting MAP3K9. This study suggests that miR-148a-3p and MAP3K9 may act as novel therapeutic targets for the treatment of LUAD and have potential clinical applications.

Гигиеническая оценка канцерогенного риска здоровью населения, ассоциированного с загрязнением депонирующих сред тяжелыми металлами

In nature there are depositing media which are relatively stable macrosystems. Their contamination that occurs due to long-term exposure to contaminants influences population health and this is especially vital for urbanized territories with large city-forming enterprises. Our research goal was to perform hygienic assessment of carcinogenic risks for population health under exposure to heavy metals contained in depositing media. We analyzed long-term data on contents of heavy metals in such accumulating media as soils and foods collected in 2005–2018. The data were taken from the reports on social and hygienic monitoring and statistical reports provided by the Orenburg Regional Office of the Federal State Statistics Service. Carcinogenic risks were assessed in accordance with the Guide R 2.1.10.1920-04. We used data provided by the territorial section of the National Cancer Registry to analyze prevalence of oncologic diseases of the digestive organs. We performed correlation analysis to examine correlations between the analyzed factors. The total carcinogenic risk under multi-route introduction of heavy metals from such depositing media as soils and foods has turned out to be unacceptable and amounts to 1.5E-04. The total population carcinogenic risk caused by exposure to heavy metals can reach 85 additional cases of malignant neoplasms over an averaged exposure period which is equal to 70 years. Heavy metals were detected in soils, nickel, cadmium, and chromium VI included, that produced statistically authentic effects on occurrence of malignant neoplasms in the digestive organs. We established an authentic correlation between developing malignant neoplasms in the digestive organs and concentrations of arsenic in foods. We didn’t detect any heavy metals with carcinogenic properties in such accumulating media as soils and foods in concentrations deviating from hygienic standards. But still, it doesn’t mean there is no negative influence on population health, notably long-term effects and developing malignant neoplasms.

Hygienic assessment of carcinogenic health risks associated with contamination of depositing media with heavy metals

In nature there are depositing media which are relatively stable macrosystems. Their contamination that occurs due to long-term exposure to contaminants influences population health and this is especially vital for urbanized territories with large city-forming enterprises. Our research goal was to perform hygienic assessment of carcinogenic risks for population health under exposure to heavy metals contained in depositing media. We analyzed long-term data on contents of heavy metals in such accumulating media as soils and foods collected in 2005–2018. The data were taken from the reports on social and hygienic monitoring and statistical reports provided by the Orenburg Regional Office of the Federal State Statistics Service. Carcinogenic risks were assessed in accordance with the Guide R 2.1.10.1920-04. We used data provided by the territorial section of the National Cancer Registry to analyze prevalence of oncologic diseases of the digestive organs. We performed correlation analysis to examine correlations between the analyzed factors. The total carcinogenic risk under multi-route introduction of heavy metals from such depositing media as soils and foods has turned out to be unacceptable and amounts to 1.5E-04. The total population carcinogenic risk caused by exposure to heavy metals can reach 85 additional cases of malignant neoplasms over an averaged exposure period which is equal to 70 years. Heavy metals were detected in soils, nickel, cadmium, and chromium VI included, that produced statistically authentic effects on occurrence of malignant neoplasms in the digestive organs. We established an authentic correlation between developing malignant neoplasms in the digestive organs and concentrations of arsenic in foods. We didn’t detect any heavy metals with carcinogenic properties in such accumulating media as soils and foods in concentrations deviating from hygienic standards. But still, it doesn’t mean there is no negative influence on population health, notably long-term effects and developing malignant neoplasms.