Development Of Malignant Tumors Research Articles

An intravenous anesthetic drug-propofol, influences the biological characteristics of malignant tumors and reshapes the tumor microenvironment: A narrative literature review.

Malignant tumors are the second leading cause of death worldwide. This is a public health concern that negatively impacts human health and poses a threat to the safety of life. Although there are several treatment approaches for malignant tumors, surgical resection remains the primary and direct treatment for malignant solid tumors. Anesthesia is an integral part of the operation process. Different anesthesia techniques and drugs have different effects on the operation and the postoperative prognosis. Propofol is an intravenous anesthetic that is commonly used in surgery. A substantial number of studies have shown that propofol participates in the pathophysiological process related to malignant tumors and affects the occurrence and development of malignant tumors, including anti-tumor effect, pro-tumor effect, and regulation of drug resistance. Propofol can also reshape the tumor microenvironment, including anti-angiogenesis, regulation of immunity, reduction of inflammation and remodeling of the extracellular matrix. Furthermore, most clinical studies have also indicated that propofol may contribute to a better postoperative outcome in some malignant tumor surgeries. Therefore, the author reviewed the chemical properties, pharmacokinetics, clinical application and limitations, mechanism of influencing the biological characteristics of malignant tumors and reshaping the tumor microenvironment, studies of propofol in animal tumor models and its relationship with postoperative prognosis of propofol in combination with the relevant literature in recent years, to lay a foundation for further study on the correlation between propofol and malignant tumor and provide theoretical guidance for the selection of anesthetics in malignant tumor surgery.

Circ_0007534 as new emerging target in cancer: Biological functions and molecular interactions.

Circular RNA (circRNAs), an important member of the non-coding RNA (ncRNA) family, are widely expressed in a variety of biological cells. Owing to their stable structures, sequence conservations, and cell- or tissue-specific expressions, these RNA have become a popular subject of scientific research. With the development of sequencing methods, it has been revealed that circRNAs exert their biological function by sponging microRNAs (miRNAs), regulating transcription, or binding to proteins. Humans have historically been significantly impacted by various types of cancer. Studies have shown that circRNAs are abnormally expressed in various cancers and are involved in the occurrence and development of malignant tumors, such as tumor cell proliferation, migration, and invasion. As one of its star molecules, circ_0007534 is upregulated in colorectal, cervical, and pancreatic cancers; is closely related to the occurrence, development, and prognosis of tumors; and is expected to become a novel tumor marker and therapeutic target. This article briefly reviews the expression and mechanism of circ_0007534 in malignant tumors based on the domestic and foreign literature.

Lentigo melanoma associated with Leser–Trélat syndrome

LeserTrlat syndrome is characterized by the sudden appearance of a large amount of elements of seborrheic keratosis. The syndrome is associated with the development of malignant tumors of internal organs. The reason for the development of the syndrome is probably the production of cytokines by cells of malignant tumors of internal organs (transforming growth factor alpha (TGF-), epidermal growth factor (EGF), etc.) endogenous mediators that affect the proliferation of keratinocytes and cause rapid growth of seborrheic keratosis. Currently, the question of the paraneoplastic nature of multiple seborrheic keratosis remains open. The article presents the observation of an 82-year-old patient with lentigo-melanoma, who developed multiple elements of seborrheic keratosis within a short time, discusses the question of how in this case it is possible to consider this as a paraneoplastic process. This case is interesting for the atypical clinical picture of seborrheic keratosis and the association with lentigo-melanoma.

Comprehensive analysis of the potential role and prognostic value of sine oculis homeobox homolog family in colorectal cancer.

Several genes, important for development, are reduced or silenced in adulthood, and their abnormal expression has been related to the occurrence and development of malignant tumors. Human sine oculis homeobox homolog (SIX) proteins belong to the homeobox family and play important roles in the development of different organs. Importantly, SIXs are predicted to have chromatin-binding and DNA-binding transcription factor activity with reported roles in cancers. However, a comprehensive analysis of SIXs in colorectal cancers (CRCs) has not been performed. To explore the expression pattern of six SIX proteins in CRCs and their relationship with the clinicopathological parameters of CRC patients as well as investigate the potential utilization of SIXs as novel prognostic indicators in CRCs. The expression level of SIXs in normal tissues of different organs and related cancerous tissues was analyzed in the Human Protein Atlas. Kaplan-Meier Plotter and GEPIA2 were used to analyze the prognostic values of SIXs. To analyze the potential signaling pathways with SIX family involvement, LinkedOmics was used to perform Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses of SIX4-related genes. Subsequently, immunohistochemical experiments were performed on CRC tissues and adjacent normal tissues, and we examined the SIX4 expression level in 87 pairs of patients with tissue microarray. The relationship between SIX4 and clinicopathological parameters in CRC patients was tested using the χ 2 test and Fisher's exact probability to verify the results of the database analysis. The RNA levels of SIX1-4 and SIX6 were relatively low in normal human tissues, while SIX5 was highly expressed at both the RNA and protein levels. However, the protein level of SIX4 was found to be elevated in various malignancies. In CRC tissues, SIX1, SIX2 and SIX4 were elevated in cancer tissues compared with adjacent normal tissue. Among all SIXs, a high level of SIX4 was found to be associated with poor overall and disease-free survival in patients with CRC. For different clinicopathological parameters, increased SIX4 expression was positively correlated with advanced CRC. The top 50 SIX4-related genes were involved with oxidative phosphorylation and the respiratory chain signaling pathways. The current results provided a comprehensive analysis of the expression and prognostic values of SIX family members in CRC. Among different SIXs, SIX4 plays an oncogenic role in CRC to promote the development of malignancy. In CRC, SIX4 mRNA and protein expression is higher than that in normal tissues and associated with shorter CRC patient survival, suggesting that SIX4 may be a potential therapeutic target for treatment of CRC patients.

HAPLN3 inhibits apoptosis and promotes EMT of clear cell renal cell carcinoma via ERK and Bcl-2 signal pathways.

Hyaluronan and proteoglycan link protein 3 (HAPLN3) is a member of the hyaluronan and proteoglycan link protein family expressed in the extracellular matrix closely associated with the development and occurrence of various malignant tumors; yet, its function in clear cell renal cell cancer (ccRCC) is still poorly understood. The following study investigated the progress and mechanism of HAPLN3 on ccRCC using bioinformatics analysis and in vitro experiments. In order to determine whether HAPLN3 is differentially expressed in ccRCC, we analyzed data from the Cancer Genome Atlas (TCGA) and GSE40435 and further validated them in the Human Protein Atlas (HPA) database. Simultaneously, the TCGA dataset was utilized to study the relationship between HAPLN3 expression and the progression of ccRCC and its prognostic value in ccRCC. Gene enrichment analysis (GSEA) was used to explore HAPLN3-related signaling pathways in ccRCC. The TIMER database investigates the link for both HAPLN3 and immune cell infiltration. Different ccRCC cell lines the role of HAPLN3 on cell biological behavior in vitro. HAPLN3 was increased in ccRCC, and its high expression was related to the patients' survival rates and clinical characteristics. GSEA showed that HAPLN3 is mainly enriched in proliferative and metastatic pathways. In addition, HAPLN3 was an independently associated significant predictor in patients with ccRCC. Functional experiments demonstrated that HAPLN3 could promote the proliferation, migration, and invasion of ccRCC cells through the ERK1/2 signaling pathway. To sum up, our data suggest that HAPLN3 may serve as a new prognostic biomarker and potential therapeutic target for ccRCC.

Four circadian rhythm-related genes predict incidence and prognosis in hepatocellular carcinoma.

Circadian dysregulation can be involved in the development of malignant tumors, though its relationship with the progression of hepatocellular carcinoma is not yet fully understood. We identified genes related to circadian rhythms from the Cancer Genome Atlas (TCGA), measured gene expression, and conducted genomic difference analysis to construct a circadian rhythm-related signature. The resulting prognosis model proved to be an effective biomarker, as demonstrated by Kaplan-Meier survival analysis for both the training (n = 370, P = 2.687e-10) and external validation cohorts (n = 230, P = 1.45e-02). Further, we found that patients considered 'high risk', with an associated poor prognosis, displayed elevated levels of immune checkpoint genes and immune filtration. We also conducted functional enrichment, which indicated that the risk model showed a significant positive correlation with certain malignant phenotypes, including G2M checkpoint, MYC targets, and the MTORC1 signaling pathway. In summary, we identified a novel circadian rhythm-related signature allowing assessment of prognosis for hepatocellular carcinoma patients, and further can be used to predict immune infiltration sensitivity.

Inhibition of Angiogenesis by MiR-524-5p through Suppression of AKT and ERK Activation by Targeting CXCR7 in Colon Cancer Cells.

Increasing evidence shows that alterations in microRNA (miRNA) expression are involved in the occurrence and development of various malignant tumors, including colon cancer. MiRNA-524-5p has been reported to have anticancer activity in colon cancer. This study explored the influence of the miRNA-524-5p/CXCR7 axis on angiogenesis using colon cancer cells and further studied the mechanisms involved. We found that changing the expression of miRNA-524-5p can affect colonic proliferation, migration, and angiogenesis. Furthermore, angiogenesis induced by miRNA-524-5p overexpression was reversed by overexpression of CXCR7 in HT-29 cells, while the opposite was observed in Caco-2 cells. Furthermore, miRNA-524-5p inhibited the activation of AKT and ERK signaling by targeting CXCR7. Overall, our results indicated that the miRNA-524-5p/CXCR7 axis regulated angiogenesis in colon cancer cells through the AKT and ERK pathways.

A comprehensive pan-cancer analysis of necroptosis molecules in four gynecologic cancers

BackgroundIn recent years, it has been proved that necroptosis plays an important role in the occurrence, development, invasion, metastasis and drug resistance of malignant tumors. Hence, further evaluation and targeting of necroptosis may be of clinical benefit for gynecologic cancers (GCs).MethodsTo compare consistency and difference, we explored the expression pattern and prognostic value of necroptosis-related genes (NRGs) in pan-GC analysis through Linear regression and Empirical Bayesian, Univariate Cox analysis, and public databases from TCGA and Genotype-Tissue Expression (GTEx), including CESC, OV, UCEC, and UCS. We explored the copy number variation (CNV), methylation level and enrichment pathways of NRGs in the four GCs. Based on LASSO Cox regression analysis or principal component analysis, we established the prognostic NRG-signature or necroptosis-score for the four GCs. In addition, we predicted and compared functional pathways, tumor mutational burden (TMB), somatic mutation features, immunity status, immunotherapy, chemotherapeutic drug sensitivity of the NRG-signature based on NRGs. We also examined the expression level of several NRGs in OV samples that we collected using Quantitative Real-time PCR.ResultsWe confirmed the presence of NRGs in expression, prognosis, CNV, and methylation for four GCs, thus comparing the consistency and difference among the four GCs. The prognosis and independent prognostic value of the risk signatures based on NRGs were determined. Through the results of subclass mapping, we found that GC patients with lower risk score may be more sensitive to PDL1 response and more sensitive to immune checkpoint blockade therapy. Drug susceptibility analysis showed that, 51, 45, 64, and 29 drugs with differences between risk groups were yielded in CESC, OV, UCEC, and UCS respectively. For OV, the expression differences of several NRGs in the tissues we collected were similar to that in TCGA.ConclusionOur comprehensive analysis of NRGs and NRG-signature demonstrated their similarity and difference, as well as their potential roles in prognosis and could guide therapeutic strategies, thus improving the outcome of GC patients.

TAM-targeted reeducation for enhanced cancer immunotherapy: Mechanism and recent progress.

Tumor-associated macrophage (TAM) as an important component of tumor microenvironment (TME) are closely related with the occurrence, development, and metastasis of malignant tumors. TAMs are generally identified as two distinct functional populations in TME, i.e., inflammatory/anti-tumorigenic (M1) and regenerative/pro-tumorigenic (M2) phenotype. Evidence suggests that occupation of the TME by M2-TAMs is closely related to the inactivation of anti-tumor immune cells such as T cells in TME. Recently, efforts have been made to reeducate TAMs from M2- to M1- phenotype to enhance cancer immunotherapy, and great progress has been made in realizing efficient modulation of TAMs using nanomedicines. To help readers better understand this emerging field, the potential TAM reeducation targets for potentiating cancer immunotherapy and the underlying mechanisms are summarized in this review. Moreover, the most recent advances in utilizing nanomedicine for the TAM immunomodulation for augmented cancer immunotherapy are introduced. Finally, we conclude with our perspectives on the future development in this field.

RNA m6A methylation regulators in endometrial cancer (Review).

As one of the three major malignant tumor types of the female reproductive system, endometrial cancer (EC) is the most prevalent gynecologic cancer in developed countries. In recent years, the incidence of EC has increased worldwide, threatening the health and well‑being of women. Recent research has indicated that the expression of multiple N6‑methyladenosine (m6A) regulators is up‑ or downregulated in EC and that abnormalities in m6A methylation and the expression of associated regulators are critical to the pathogenesis and progression of EC. m6A is the most abundant internal modification of mRNA. Several studies have demonstrated a close association between the development and progression of malignant tumors and the epigenetic phenomenon of m6A methylation. In the present study, the current status of research on m6A methylation in EC was reviewed. The mechanisms of methyltransferase, demethylase and m6A binding protein in regulating the development and progression of EC by modifying mRNA were introduced. The related research results will provide novel methods and approaches for the prevention and treatment of EC.

Role of Tumor Suppressor PTEN and Its Regulation in Malignant Transformation of Endometrium.

Tumor-suppressive effects of PTEN are well-known, but modern evidence suggest that they are not limited to its ability to inhibit pro-oncogenic PI3K/AKT signaling pathway. Features of PTEN structure facilitate its interaction with substrates of different nature and display its activity in various ways both in the cytoplasm and in cell nuclei, which makes it possible to take a broader look at its ability to suppress tumor growth. The possible mechanisms of the loss of PTEN effects are also diverse - PTEN can be regulated at many levels, leading to change in the protein activity or its amount in the cell, while their significance for the development of malignant tumors has yet to be studied. Here we summarize the current data on the PTEN structure, its functions and changes in its regulatory mechanisms during malignant transformation of the cells, focusing on one of the most sensitive to the loss of PTEN types of malignant tumors - endometrial cancer.

Hereditary ovarian cancer

Background. Hereditary genetic mutations are a significant risk factor for malignant transformation of cells and cancer development. Hereditary genetic mutations account for 15 to 25 % of all ovarian carcinomas. Purpose of the study: to summarize data on hereditary ovarian malignancies, namely: genetic defects, features of the clinical course, treatment options, and disease prevention. Material and methods. A systemic search was undertaken using PubMed, Medline, Cochrane Library databases for publications from 1999 to 2021. Results. The review describes the main genetic defects and hereditary cancer syndromes predisposing to the development of hereditary malignant ovarian tumors. The features of the clinical course and response to drug therapy have been presented. This article summarizes clinical guidelines of the professional communities (National Comprehensive Cancer Network (NCCN), American Society Of Clinical Oncology (ASCO), The U.S. Preventive Services Task Force, and European Society For Medical Oncology (ESMO). These guidelines contain early detection strategies and approaches to prevent the development of cancers in mutation carriers. Conclusion. Detection of hereditary cancer syndromes is important for patients and their families. Recognizing hereditary predisposition to cancer is important to allow timely surveillance and preventative interventions for both patients and family members.

High DAPK1 Expression Promotes Tumor Metastasis of Gastric Cancer.

Simple SummaryGastric cancer is a common upper gastrointestinal tumor. Death-associated protein kinase (DAPK1) was found to participate in the development of various malignant tumors. However, there are few reports on DAPK1 in gastric cancer. In this study, we found that the expression of DAPK1 was up-regulated in gastric cancer tissues. Survival analysis showed that low expression of DAPK1 was a favorable prognostic factor of overall survival and disease-free survival for gastric cancer patients. The functional experiments demonstrated that DAPK1 can promote the migration and invasion of gastric cancer cells. Meanwhile, a risk score module for four DAPK1-related genes was constructed and validated. In conclusion, these results indicated that DAPK1 can promote gastric cancer cell migration and invasion and established a signature of four DAPK1-related genes for gastric cancer that could independently predict the survival of gastric cancer patients.Gastric cancer (GC) is a common upper gastrointestinal tumor. Death-associated protein kinase (DAPK1) was found to participate in the development of various malignant tumors. However, there are few reports on DAPK1 in gastric cancer. In this study, the TCGA and GEO datasets were used to explore the expression and role of DAPK1 in gastric cancer. The functions of DAPK1 in gastric cancer were determined by proliferation, migration and invasion assays. In addition, genes co-expressed with DAPK1 in gastric cancer were estimated through the WGCNA and correlation analysis. A DAPK1-related gene prognostic model was constructed using the Cox regression and lasso analyses. The expression of DAPK1 was significantly up-regulated in gastric cancer tissues. Kaplan–Meier analysis showed that low expression of DAPK1 was a favorable prognostic factor of overall survival and disease-free survival for gastric cancer patients. Functional experiments demonstrated that DAPK1 can promote the migration and invasion of gastric cancer cells. WGCNA, correlation analysis, Cox regression, and lasso analyses were applied to construct the DAPK1-related prognostic model. The prognostic value of this prognostic model of DAPK1-related genes was further successfully validated in an independent database. Our results indicated that DAPK1 can promote gastric cancer cell migration and invasion and established four DAPK1-related signature genes for gastric cancer that could independently predict the survival of GC patients.

HOXD11 upregulates JAM-A and exerts oncogenic properties via NF-κB signaling pathway in esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma (ESCC) is a tumor with high incidence and poor prognosis in developing countries. Junctional adhesion molecule A (JAM-A, also known as F11R) affects numerous biological processes, which is a vital regulator of the development of malignant tumors. However, its exact role and underlying mechanism in ESCC remain obscure. Our present study demonstrated that JAM-A was upregulated in ESCC tissues and cell lines by RNA sequencing and immunohistochemistry (IHC). JAM-A knockdown significantly suppressed the proliferation of the ESCC cells, induced cell cycle arrest at the G1 and promoted apoptosis, and suppressed the ability of invasion and migration in vivo and in vitro. Mechanistically, JAM-A may activate the NF-κB signaling pathway to regulate malignant behavior of ESCC. Further research showed that Homeobox D11 (HOXD11) could directly regulate JAM-A transcription by binding to specific sequences of JAM-A promoter region, thereby activating NF-κB signaling pathway to regulate malignant behavior of ESCC. Functional experiments indicated that HOXD11 could exert an oncogenic role in ESCC. Collectively, our findings support the hypothesis that the HOXD11/JAM-A/NF-κB signal axis plays a role in regulating malignant behavior in ESCC patients, highlighting its potential therapeutic value for ESCC.

Imaging manifestations of von Hippel-Lindau disease: an illustrated guide focusing on abdominal manifestations.

Von Hippel-Lindau (VHL) disease is a monogenic autosomal dominant disorder with germline mutations of the VHL anti-oncogene on the short arm of chromosome 3 (3p25-26). It affects 1:36,000-50,000 individuals, with a penetrance greater than 90% at 65 years of age. Although of variable onset and presentation, with pleiotropism even among members of the same family who share a specific mutation, VHL disease usually manifests initially in young adults. It predisposes to the development of benign and malignant tumors of the central nervous system (CNS) and visceral organs. The clinical diagnosis of VHL disease can be made in the following circumstances: a) in patients with a family history of the disease and at least one of the tumors characteristic of it (e.g., retinal or CNS hemangioblastomas, clear cell renal cell carcinoma, pancreatic neuroendocrine tumors, and endolymphatic sac tumors); b) in patients with two or more CNS hemangioblastomas; c) or in patients with a retinal or CNS hemangioblastoma plus at least one visceral tumor characteristic of the disease, excluding renal and epididymal cysts. Imaging plays an important role in the diagnosis and follow-up of patients with VHL disease. This pictorial essay presents characteristic images of abdominal manifestations of VHL disease-related tumors that all radiologists should be aware of.

Research progress on microRNA-1258 in the development of human cancer.

microRNAs (miRNAs) are small endogenous RNAs composed of 20-22 nucleotides that do not encode proteins, which regulate the expression of downstream genes by targeting the 3’ untranslated region of mRNA. Plentiful research has demonstrated that miRNAs participate in the initiation and development of diverse diseases and malignant tumors. miR-1258 exerts great influence on tumors, including tumor growth, distant metastasis, migration, invasion, chemosensitivity, cell glycolysis, apoptosis, and stemness. Interestingly, miR-1258 is a miRNA with explicit functions and has been investigated to act as a tumor suppressor in studies on various types of tumors. With accumulating research on miR-1258, it has been found to be used as a biomarker in the early diagnosis and prognosis prediction of tumor patients. In this review, we outline the development of miR-1258 research, describe its regulatory network, and discuss its roles in cancer. Additionally, we generalize the potential clinical applications of miR-1258. This review offers emerging perspectives and orientations for further comprehending the function of miR-1258 as a diagnostic and prognostic biomarker and potent therapeutic target in cancer.

LEVELS OF CERTAIN HORMONES AND RECEPTORS IN TUMOR AND PERITUMORAL AREA IN BALB/C NUDE FEMALE MICE WITH MULTIPLE PRIMARY MALIGNANT PROCESS DEVELOPING ON THE BACKGROUND OF PRIMARY IMMUNODEFICIENCY

Primary immunodeficiency is one of the reasons for the development of primary multiple malignant tumors.
 The aim of the study is to examine the levels of certain hormones and their receptors in the tissue and peritumoral area of B16/F10 melanoma and Lewis lung carcinoma (LLC) in case of isolated and combined subcutaneous growth in female mice with T-cell immunodeficiency.
 Materials and Methods. BALB/c Nude mice were divided into groups: intact group; 2 control groups (Group 1 with B16/F10 subcutaneous inoculation, Group 2 with LLC subcutaneous inoculation); main group (animals with LLC+B16/F10 inoculation). The ELISA method was used to determine the levels of free testosterone (Tf.), estrone (E1), prolactin (PRL), estrogen receptors (REα and REβ), androgen receptors (RA) and progesterone receptors (RP4) (Cassabio, China). Statistical processing of the obtained results was carried out on a personal computer using STATISTICA 10.0, parametric Student's test and nonparametric Wilcoxon-Mann-Whitney test.
 Results. In the main group, life expectancy reduced due to melanoma growth by 1.8 times and LLC decrease by 2.3 times. In animals with LLC+B16/F10, compared to those with an only one tumor growth variant, estrone level in tumors decreased, but free testosterone level increased. Melanoma growth in animals with LLC+B16/F10 was accompanied by an increase in prolactin level and some sex steroid receptors in the tumor tissue, its peritumoral area, and skin not affected by the malignant process. A decrease of Lewis carcinoma in females of the main group was accompanied by a decrease of all the studied receptors and hormones both in the tumor and its peritumoral area.
 Conclusions. Melanoma growth is probably associated with a high prolactin level and sex steroid receptors in unaffected skin, being a source of melanocytes, the cells from which this tumor develops.

FIGNL1 Expression and its Prognostic Significance in Pan-cancer Analysis.

Fidgetin-like 1 (FIGNL1), a subfamily member of ATPases, is associated with diverse cellular activities (AAA proteins). FIGNL1 is involved in DNA repair. However, the latest study has indicated that FIGNL1 plays a crucial role in the occurrence and development of malignant tumors. FIGNL1 expression was analyzed via Oncomine and GEPIA databases, and its prognostic potential was analyzed using OncoLnc, UALCAN, and GEPIA databases. Moreover, the promoter methylation of FIGNL1 was analyzed through the UALCAN database. FIGNL1-related gene network was found within STRING. Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were investigated across WebGestalt. FIGNL1 correlation with cancer immune infiltrates was estimated using the Tumor Immune Estimation Resource (TIMER) database. We found that FIGNL1 is widely overexpressed in multiple human cancers, and its high expression was correlated with the poor prognosis of patients with kidney renal clear-cell carcinoma (KIRP), low-grade glioma (LGG) of brain and liver hepatocellular carcinoma (LIHC). Additionally, the promoter methylation level of FIGNL1 showed a statistical significance between normal and primary tissues in KIRP and LGG via the UALCAN (P < 0.0001). FIGNL1 expression was highly correlated with the infiltrating levels of CD8+ T and CD4+ T cells, dendritic cells (DCs), macrophages, and neutrophils in LIHC. In this study, the correlation of FIGNL1 expression with the prognosis, promoter methylation, and immune infiltrates in KIRP, LGG, and LIHC was revealed. These findings suggested that FIGNL1 promised to be a prognostic biomarker for KIRP, LGG, and LIHC.

The problem of verification of malignant neoplasms of the stomach in surgical practice

Relevance. Despite numerous efforts made in recent decades, the arsenal of cancer diagnostics is still significantly limited. The purpose of study: to analyze the problem of differential diagnosis of early stage stomach cancer and non-oncological diseases of the abdominal cavity. Materials and methods. In the course of the work, current literary sources of domestic and foreign authors on a given topic were analyzed. Results. The early stages of malignant neoplasms of the stomach are usually asymptomatic or accompanied by nonspecific signs, such as dyspepsia. Symptoms of the development of malignant tumors of the stomach at an early stage may be indistinguishable from the symptoms of benign dyspepsia, while the presence of established "alarming" symptoms may mean a progressive inoperable disease. However, the evidence supporting the use of "alarming" symptoms as selection criteria for endoscopy still remains contradictory, since the presence of "alarming" symptoms in the clinical picture is not always associated with the detection of malignant neoplasms, it is also worth noting that the overall prevalence of these symptoms in the population of patients suffering from dyspeptic disorders is high, while while the number of patients with a history of gastrointestinal cancer is relatively low. Conclusion. Despite the observed trend of decreasing morbidity and mortality, malignant neoplasms of the stomach remain an important part in the structure of oncological diseases. Many of the risk factors remain insufficiently studied and should be the subject of further research to achieve more specific, targeted preventive measures.

Current understanding on the role of CCT3 in cancer research.

Chaperonin containing TCP1 Subunit 3 (CCT3) is an important member of the chaperone protein family, providing a favorable environment for the correct folding of proteins in cell division, proliferation, and apoptosis pathways, which is involved in a variety of biological processes as well as the development and invasion of many malignant tumors. Many malignancies have been extensively examined with CCT3. It is presently used as a possible target for the treatment of many malignancies since it is not only a novel biomarker for the screening and diagnosis of different tumors, but it is also closely associated with tumor progression, prognosis, and survival. Recent studies have shown that the expression of CCT3 is up-regulated in some tumors, such as liver cancer, breast cancer, colon cancer, acute myeloid leukemia, etc. In this paper, we review the role of CCT3 in various tumors.