Development Of Malignant Tumors Research Articles

An Immunohistochemical Study of MAGE Proteins in Hepatocellular Carcinoma

Hepatocellular carcinoma (HCC) is one the most common primary malignancies with high mortality and morbidity. The melanoma-associated antigen (MAGE) gene family includes several genes that are highly expressed in numerous human cancers, making many of them part of the cancer-testis antigen (CTA) family. MAGE-C1 is expressed in various malignancies but is absent in normal cells, except for the male germ line. Its presence is associated with a worse prognosis, increased tumor aggressiveness, and lymph node invasion. Similarly, MAGE-C2 is linked to the development of various malignant tumors. Despite these associations, the roles and mechanisms of MAGE-C1/MAGE-C2 in HCC remain unclear. This study aimed to evaluate the expression of MAGE-C1 and MAGE-C2 in HCC and correlate it with clinicohistological characteristics. Our findings indicated that MAGE-C1 expression is associated with a higher number of nodules, elevated AFP levels, HBV or HCV positivity, older age, male sex, and lymph node invasion. MAGE-C2 expression was correlated with these characteristics and the presence of cirrhosis. These results align with the limited literature, which suggests a correlation between MAGE expression and older age and HBV infection. Consequently, our study suggests that MAGE-C1 and MAGE-C2 are promising novel biomarkers for prognosis and potential therapeutic targets in HCC.

Aurora-B: a novel biomarker inthe invasion and metastasis of osteosarcoma.

Osteosarcoma (OS), a primary human malignant tumor that affects the bones, mostly arises in children and adolescents. Even though surgical resection followed by radiotherapy and chemotherapy has improved the survival rate up to 60%, the long-term positive effect for most patients with OS is not satisfactory. Hence, elucidating the specific mechanisms involved in the pathogenesis of OS is particularly important. Aurora-B, a serine/threonine kinase, plays a crucial role in centrosome regulation, spindle formation and chromosomal separation during mitosis. It has been found that Aurora-B overexpression is related to the occurrence and development of several malignant tumors, including OS. This article summarizes the role of Aurora-B in the invasion and metastasis of OS.

Relationships of omega-3 and omega-6 polyunsaturated fatty acids with esophageal diseases: a two-sample Mendelian randomization analysis.

Omega-3 polyunsaturated fatty acids (PUFAs) have been widely studied and used as nutritional supplements because of their anti-inflammatory effects. Previous studies have shown an association between polyunsaturated fatty acids such as omega-3 and omega-6 PUFAs with the development of malignant tumors. However, the relationships of omega-3 and omega-6 PUFAs with esophageal diseases have not been characterized. Mendelian randomization (MR) is a statistical method for identifying instrumental variables (IVs) from genome-wide association study (GWAS) data, and is associated with little confounding by environmental or other disease-related factors. We used genome-wide association study (GWAS) data from previously published studies on circulating concentrations of omega-3, omega-6, docosahexaenoic acid (DHA) and linoleic acid (LA), as well as esophageal cancer and other esophageal diseases, which were downloaded from the IEU OpenGwas database (https://gwas.mrcieu.ac.uk/) and the GWAS Catalog database (https://www.ebi.ac.uk/). The inverse variance-weighted approach was used as the principal analysis, and the MR-Egger and weighted median methods were used alongside. A series of sensitivity analyses were used to ensure the robustness of the causality estimates. We found that the circulating omega-3 PUFAs concentration was positively associated with esophageal cancer (p = 8 × 10-4), and circulating DHA concentration (the main component of omega-3 in food), was also positively associated with esophageal cancer (p = 2 × 10-2), but no significant association was found between circulating omega-6 PUFAs and esophageal cancer (p = 0.17), and circulating LA concentration (the main component of omega-6 in food), was also no significant associated with esophageal cancer (p = 0.32). We found no significant relationships of circulating omega-3 and omega-6 PUFAs concentration with four other esophageal diseases. This study indicates that higher levels of circulating omega-3 PUFAs and DHA concentrations may be a risk factor for the development of esophageal cancer. Conversely, an increased omega-6/omega-3 ratio may serve as a protective factor against esophageal cancer. These findings have significant implications for the clinical application of omega-3 PUFAs and the prevention and treatment of esophageal cancer.

FOXM1 transcriptional regulation.

FOXM1 is a key transcriptional regulator involved in various biological processes in mammals, including carbohydrate and lipid metabolism, aging, immune regulation, development, and disease. Early studies have shown that FOXM1 acts as an oncogene by regulating cell proliferation, cell cycle, migration, metastasis, and apoptosis, as well as genes related to diagnosis, treatment, chemotherapy resistance, and prognosis. Researchers are increasingly focusing on FOXM1 functions in tumor microenvironment, epigenetics, and immune infiltration. However, researchers have not comprehensively described FOXM1's involvement in tumor microenvironment shaping, epigenetics, and immune cell infiltration. Here we review the role of FOXM1 in the formation and development of malignant tumors, and we will provide a comprehensive summary of the role of FOXM1 in transcriptional regulation, interacting proteins, tumor microenvironment, epigenetics, and immune infiltration, and suggest areas for further research.

Suppressing SENP1 inhibits esophageal squamous carcinoma cell growth via SIRT6 SUMOylation.

Esophageal squamous cell carcinoma (ESCC) is a prevalent tumor in the gastrointestinal tract, but our understanding of the molecular mechanisms underlying ESCC remains incomplete. Existing studies indicate that SUMO specific peptidase 1 (SENP1) plays a crucial role in the development and progression of various malignant tumors through diverse molecular mechanisms. However, the functional mechanism and clinical implications of SENP1 in the progression of ESCC remain unclear. Bulk RNA-Sequencing (RNA-seq) was used to compare potential genes in the esophageal tissues of mice with ESCC to the control group. The up-regulated SENP1 was selected. The protein level of SENP1 in ESCC patient samples was analyzed by immunohistochemistry and western blot. The potential prognostic value of SENP1 on overall survival of ESCC patients was examined using tissue microarray analysis and the Kaplan-Meier method. The biological function was confirmed through in vitro and in vivo knockdown approaches of SENP1. The role of SENP1 in cell cycle progression and apoptosis of ESCC cells was analyzed by flow cytometry and western blot. The downstream signaling pathways regulated by SENP1 were investigated via using RNA-Seq. SENP1-associated proteins were identified through immunoprecipitation. Overexpression of Sirtuin 6 (SIRT6) wildtype and mutant was performed to investigate the regulatory role of SENP1 in ESCC progression in vitro. Our study discovered that SENP1 was upregulated in ESCC tissues and served as a novel prognostic factor. Moreover, SENP1 enhanced cell proliferation and migration of ESCC cell lines in vitro, as well as promoted tumor growth in vivo. Thymidine kinase 1 (TK1), Geminin (GMNN), cyclin dependent kinase 1(CDK1), and cyclin A2 (CCNA2) were identified as downstream genes of SENP1. Mechanistically, SENP1 deSUMOylated SIRT6 and subsequently inhibited SIRT6-mediated histone 3 lysine 56 (H3K56) deacetylation on those downstream genes. SIRT6 SUMOylation mutant (4KR) rescued the growth inhibition upon SENP1 depletion. SENP1 promotes the malignant progression of ESCC by inhibiting the deacetylase activity of SIRT6 pathway through deSUMOylation. Our findings suggest that SENP1 may serve as a valuable biomarker for prognosis and a target for therapeutic intervention in ESCC.

Development of a prediction model for the association between thyroid dysfunction and breast cancer.

Thyroid dysfunction is associated with the risk of benign and malignant breast tumors, but currently there is a lack of model studies to demonstrate the predictive role of thyroid dysfunction in benign and malignant breast tumors. This study aims to establish a model for predicting the association between thyroid dysfunction and breast cancer. This retrospective study enrolled breast tumor patients from the Affiliated Tumor Hospital of Xinjiang Medical University from 2015 to 2019. Their baseline data and laboratory data were collected. Python was used for data processing and analysis. Data preparation, feature selection, model construction, and model evaluation were conducted. We utilized the classification probabilities generated by the model as scores and further conducted a least absolute shrinkage and selection operator analysis. Analysis of the laboratory data revealed statistically significant differences in thyroid-stimulating hormone, thyroxine, free thyroxine, free triiodothyronine, and thyronine levels between patients with benign and malignant tumors. Based on age, ethnicity, thyroid function, and estrogen levels, the predictive model for breast tumor malignancy indicated that the factors with the greatest importance ranking were age > follicle-stimulating hormone > luteinizing hormone > prolactin > thyroxine > testosterone > ethnicity. The model showed an accuracy rate of 83.70%, precision of 90.69%, sensitivity of 84.74%, and specificity of 81.50%. The area under the receiver operating characteristic curve was 0.9012, close to 1, indicating good predictive performance of the model. The predictive model based on factors such as age, ethnicity, thyroid function, and estrogen levels performs well in predicting the occurrence and development of benign and malignant breast tumors.

Endoscopic ultrasound-guided biliary drainage vs percutaneous transhepatic bile duct drainage in the management of malignant obstructive jaundice.

Malignant obstructive jaundice (MOJ) is a condition characterized by varying degrees of bile duct stenosis and obstruction, accompanied by the progressive development of malignant tumors, leading to high morbidity and mortality rates. Currently, the two most commonly employed methods for its management are percutaneous transhepatic bile duct drainage (PTBD) and endoscopic ultrasound-guided biliary drainage (EUS-BD). While both methods have demonstrated favorable outcomes, additional research needs to be performed to determine their relative efficacy. To compare the therapeutic effectiveness of EUS-BD and PTBD in treating MOJ. This retrospective analysis, conducted between September 2015 and April 2023 at The Third Affiliated Hospital of Soochow University (The First People's Hospital of Changzhou), involved 68 patients with MOJ. The patients were divided into two groups on the basis of surgical procedure received: EUS-BD subgroup (n = 33) and PTBD subgroup (n = 35). Variables such as general data, preoperative and postoperative indices, blood routine, liver function indices, myocardial function indices, operative success rate, clinical effectiveness, and complication rate were analyzed and compared between the subgroups. In the EUS-BD subgroup, hospital stay duration, bile drainage volume, effective catheter time, and clinical effectiveness rate were superior to those in the PTBD subgroup, although the differences were not statistically significant (P > 0.05). The puncture time for the EUS-BD subgroup was shorter than that for the PTBD subgroup (P < 0.05). Postoperative blood routine, liver function index, and myocardial function index in the EUS-BD subgroup were significantly lower than those in the PTBD subgroup (P < 0.05). Additionally, the complication rate in the EUS-BD subgroup was lower than in the PTBD subgroup (P < 0.05). EUS-BD may reduce the number of punctures, improve liver and myocardial functions, alleviate traumatic stress, and decrease complication rates in MOJ treatment.

An osteolytic lesion of the proximal ulna in a patient with Maffucci syndrome: a case report

Maffucci syndrome is a rare, congenital, and nonhereditary syndrome characterized by the occurrence of multiple enchondromas and hemangiomas. According to previous studies, patients diagnosed with Maffucci syndrome have a higher risk of developing malignant tumors, such as ovarian cancer, pancreatic cancer, breast cancer, and central nervous system cancer, in addition to malignant transformations of enchondromas. The authors report a case of a 37-year-old male patient with Maffucci syndrome who presented with multiple enchondromas and hemangiomas. This patient’s presentation and management are discussed, along with a review of the literature. Maffucci syndrome should be expected when encountering a patient with multiple enchondromas and suspected hemangiomas in the limbs. Even if benign lesions such as enchondromas or hemangiomas are diagnosed, regular follow-up is required to monitor for malignant transformations and the development of malignant tumors in other organs.

Dysfunctional adipocytes promote tumor progression through YAP/TAZ-dependent cancer-associated adipocyte transformation

Obesity has emerged as a prominent risk factor for the development of malignant tumors. However, the existing literature on the role of adipocytes in the tumor microenvironment (TME) to elucidate the correlation between obesity and cancer remains insufficient. Here, we aim to investigate the formation of cancer-associated adipocytes (CAAs) and their contribution to tumor growth using mouse models harboring dysfunctional adipocytes. Specifically, we employ adipocyte-specific BECN1 KO (BaKO) mice, which exhibit lipodystrophy due to dysfunctional adipocytes. Our results reveal the activation of YAP/TAZ signaling in both CAAs and BECN1-deficient adipocytes, inducing adipocyte dedifferentiation and formation of a malignant TME. The additional deletion of YAP/TAZ from BaKO mice significantly restores the lipodystrophy and inflammatory phenotypes, leading to tumor regression. Furthermore, mice fed a high-fat diet (HFD) exhibit decreased BECN1 and increased YAP/TAZ expression in their adipose tissues. Treatment with the YAP/TAZ inhibitor, verteporfin, suppresses tumor progression in BaKO and HFD-fed mice, highlighting its efficacy against mice with metabolic dysregulation. Overall, our findings provide insights into the key mediators of CAA and their significance in developing a TME, thereby suggesting a viable approach targeting adipocyte homeostasis to suppress cancer growth.

Phytic acid inhibits RafGOFScrib−/− tumor growth and invasion by suppressing the Yki-mediated JAK/STAT pathway in Drosophila melanogaster

Metastasis is one of the most important factors related to malignant tumor development and therapeutic failure. Phytic acid (PA), a poly-phosphorylated inositol derivative in plant seeds and grains, has been shown to have antitumoral activity. However, the effect of PA on tumor metastasis and the underlying mechanisms remain uncharacterized. In the current study, we aimed to identify the effect of PA on tumor metastasis by employing a Drosophila model of malignant tumor RafGOFScrib−/−. We observed that PA supplementation in food inhibited the invasion and migration of tumors. Further studies indicated that PA drives Yki phosphorylation and inactivation through Lats kinase, which subsequently results in decreased expression of the JAK/STAT pathway ligands unpaired cytokines (Upds). Moreover, the reduced JAK/STAT pathway inhibits the recruitment and proliferation of hemocytes. To summarize, these findings provide valuable pathological and mechanistic insights into the potential application of PA for functional food or natural medicine development.

The Role of Vasodilator-stimulated Phosphoproteins in the Development of Malignant Tumors.

Vasodilator-stimulated phosphoprotein (VASP) is an actin-binding protein that includes three structural domains: Enabled/VASP homolog1 (EVH1), EVH2, and proline-rich (PRR). VASP plays an important role in various cellular behaviors related to cytoskeletal regulation. More importantly, VASP plays a key role in the progression of several malignant tumors and is associated with malignant cell proliferation, invasion, and metastasis. Here, we have summarized current studies on the impact of VASP on the development of several malignant tumors and their mechanisms. This study provides a new theoretical basis for clinical molecular diagnosis and molecular targeted therapy.

Multi-omics pan-cancer study of SPTBN2 and its value as a potential therapeutic target in pancreatic cancer

SPTBN2 is a protein-coding gene that is closely related to the development of malignant tumors. However, its prognostic value and biological function in pan-cancer, especially pancreatic cancer (PAAD), have not been reported. In the present study, a novel exploration of the value and potential mechanism of SPTBN2 in PAAD was conducted using multi-omics in the background of pan-cancer. Via various database analysis, up-regulated expression of SPTBN2 was detected in most of the tumor tissues examined. Overexpression of SPTBN2 in PAAD and kidney renal clear cell cancer patients potentially affected overall survival, disease-specific survival, and progression-free interval. In PAAD, SPTBN2 can be used as an independent factor affecting prognosis. Mutations and amplification of SPTBN2 were detected, with abnormal methylation of SPTBN2 affecting its expression and the survival outcome of PAAD patients. Immunoassay results demonstrate that SPTBN2 was a potential biomarker for predicting therapeutic response in PAAD, and may influence the immunotherapy efficacy of PAAD by regulating levels of CD8 + T cells and neutrophil infiltration. Results from an enrichment analysis indicated that SPTBN2 may regulate the development of PAAD via immune pathways. Thus, SPTBN2 is a potential prognostic biomarker and immunotherapy target based on its crucial role in the development of PAAD.

Exploring a specialized programmed-cell death patterns to predict the prognosis and sensitivity of immunotherapy in cutaneous melanoma via machine learning.

The mortality and therapeutic failure in cutaneous melanoma (CM) are mainly caused by wide metastasis and chemotherapy resistance. Meanwhile, immunotherapy is considered a crucial therapy strategy for CM patients. However, the efficiency of currently available methods and biomarkers in predicting the response of immunotherapy and prognosis of CM is limited. Programmed cell death (PCD) plays a significant role in the occurrence, development, and therapy of various malignant tumors. In this research, we integrated fourteen types of PCD, multi-omics data from TCGA-SKCM and other cohorts in GEO, and clinical CM patients to develop our analysis. Based on significant PCD patterns, two PCD-related CM clusters with different prognosis, tumor microenvironment (TME), and response to immunotherapy were identified. Subsequently, seven PCD-related features, especially CD28, CYP1B1, JAK3, LAMP3, SFN, STAT4, and TRAF1, were utilized to establish the prognostic signature, namely cell death index (CDI). CDI accurately predicted the response to immunotherapy in both CM and other cancers. A nomogram with potential superior predictive ability was constructed, and potential drugs targeting CM patients with specific CDI have also been identified. Given all the above, a novel CDI gene signature was indicated to predict the prognosis and exploit precision therapeutic strategies of CM patients, providing unique opportunities for clinical intelligence and new management methods for the therapy of CM.

Emerging role and function of SPDL1 in human health and diseases.

SPDL1 (spindle apparatus coiled-coil protein 1), also referred to as CCDC99, is a recently identified gene involved in cell cycle regulation. SPDL1 encodes a protein, hSpindly, which plays a critical role in the maintenance of spindle checkpoint silencing during mitosis. hSpindly coordinates microtubule attachment by promoting kinesin recruitment and mitotic checkpoint signaling. Moreover, the protein performs numerous biological functions in vivo and its aberrant expression is closely associated with abnormal neuronal development, pulmonary interstitial fibrosis, and malignant tumor development. In this review, we provide an overview of studies that reveal the characteristics of SPDL1 and of the protein encoded by it, as well as its biological and tumor-promoting functions.

The dual role of LOXL4 in the pathogenesis and development of human malignant tumors: a narrative review.

Lysyl oxidase-like protein 4 (LOXL4) is a secreted copper-dependent amine oxidase involved in the assembly and maintenance of extracellular matrix (ECM), playing a critical role in ECM formation and repair. Tumor-stroma interactions and ECM dysregulation are closely associated with the mechanisms underlying tumor initiation and progression. LOXL4 is the latest identified member of the lysyl oxidase (LOX) protein family. Currently, there is limited and controversial research on the role of LOXL4 in human malignancies. Its specific regulatory pathways, mechanisms, and roles in the occurrence, development, and treatment of malignancies remain incompletely understood. This article aims to illustrate the primary protein structure and the function of LOXL4 protein, and the relationship between LOXL4 protein and the occurrence and development of human malignant tumors to provide a reference for further clinical research. We searched the English literature on LOXL4 in the occurrence and development of various malignant tumors in PubMed and Web of Science. The search keywords include "cancer" "LOXL4" "malignant tumor" "tumorigenesis and development", etc. LOXL4 is up-regulated in human gastric cancer, breast cancer, ovarian cancer, head and neck squamous cell carcinoma, esophageal carcinoma and colorectal cancer, but down-regulated in human bladder cancer and lung cancer and inhibits tumor growth. There are two conflicting reports of both upregulation and downregulation in hepatocellular carcinoma, suggesting that LOXL4 has a bidirectional effect of promoting or inhibiting cancer in different types of human malignant tumors. We further explore the application prospect of LOXL4 protein in the study of malignant tumors, laying a theoretical foundation for the clinical diagnosis, treatment and screening of prognostic markers of malignant tumors. LOXL4 exerts a bidirectional regulatory role, either inhibiting or promoting tumors depending on the type of cancer. We still need more research to further confirm the molecular mechanism of LOXL4 in cancer progression.

A case of testicular cancer in a long‐term hydranencephaly survivor with undescended testes

IntroductionThe development of malignant tumors in patients with hydranencephaly is extremely rare. We describe the first case of testicular cancer that developed in the undescended testes of a long‐term survivor of hydranencephaly.Case presentationA 32‐year‐old man with severe cerebral palsy due to hydranencephaly was referred to our department for the evaluation of a subcutaneous lump in the lower right abdomen. He was a long‐term survivor of hydranencephaly. After confirming the diagnosis of right testicular cancer originating in his undescended testes, surgical resection was performed. Pathological examination revealed a mixed‐type germ cell tumor.ConclusionThe decision‐making process for treating malignant tumors, like testicular cancer, in adults with severe cerebral palsy can be challenging. Clinical ethics consultation could be helpful in avoiding treatment delays.

Brain Tumor Segmentation Using Enhancement Convolved and Deconvolved CNN Model

The brain assumes the role of the primary organ in the human body, serving as the ultimate controller and regulator. Nevertheless, certain instances may give rise to the development of malignant tumors within the brain. At present, a definitive explanation of the etiology of brain cancer has yet to be established. This study develops a model that can accurately identify the presence of a tumor in a given magnetic resonance imaging (MRI) scan and subsequently determine its size within the brain. The proposed methodology comprises a two-step process, namely, tumor extraction and measurement (segmentation), followed by the application of deep learning techniques for the identification and classification of brain tumors. The detection and measurement of a brain tumor involve a series of steps, namely, preprocessing, skull stripping, and tumor segmentation. The overfitting of BTNet-convolutional neural network (CNN) models occurs after a lot of training time because training the model with a large number of images. Moreover, the tuned CNN model shows a better performance for classification step by achieving an accuracy rate of 98%. The performance metrics imply that the BTNet model can reach the optimal classification accuracy for the brain tumor (BraTS 2020) dataset identification. The model analysis segment has a WT specificity of 0.97, a TC specificity of 0.925914, an ET specificity of 0.967717, and Dice scores of 79.73% for ET, 91.64% for WT, and 87.73% for TC.

Uncommon Thigh Mass in Neurofibromatosis Type 1: Unveiling Aggressive Epithelioid Sarcoma.

Patients with neurofibromatosis type I (NF1) have an increased risk of developing soft-tissue sarcomas, particularly those related to the nervous system. Epithelioid sarcoma (ES) is an exceptionally rare subtype of soft-tissue sarcoma, with limited knowledge about its clinical presentation and optimal management in NF1. This report aims to provide insights into the characteristics and outcomes of ES in NF1 patients. A 37-year-old man with a history of NF1 presented with a progressively worsening mass on his right inner thigh. An MRI scan revealed a well-defined tissue mass originating from the adductor magnus muscle, later confirmed as ES through histopathology and immunohistochemistry. Considering poor local and general prognosis, the multidisciplinary team recommended salvage hip disarticulation, however the patient refused and opted for palliative marginal resection to reduce the tumour size. The patient's condition declined rapidly, and he succumbed six days after the surgery. This case highlights the rarity of ES in NF1 patients and underscores the potential for malignant tumour development in this population. Further research is needed to improve our understanding and management of sarcomas in the context of NF1. Patients with neurofibromatosis type 1 or von Recklinghausen's disease have a higher risk than those with other types of neurofibromatosis of developing benign or malignant soft-tissue tumours especially related to the nervous system.Epithelioid sarcoma is an extremely rare subtype of soft-tissue sarcoma and is exceptionally associated with neurofibromatosis type 1.A multidisciplinary approach remains essential in the diagnosis, management, and treatment of soft-tissue sarcomas in patients with neurofibromatosis type 1.

The necroptosis-related signature and tumor microenvironment immune characteristics associated with clinical prognosis and drug sensitivity analysis in stomach adenocarcinoma.

Necroptosis plays an important role in the tumorigenesis, development, metastasis, and drug resistance of malignant tumors. This study explored the new model for assessing stomach adenocarcinoma (STAD) prognosis and immunotherapy by combining long noncoding RNAs associated with necroptosis. Patient clinical data and STAD gene expression profiles were curated from The Cancer Genome Atlas (TCGA). Immune-related genes were sourced from a specialized molecular database. Perl software and R software were used for data processing and analysis. Necroptosis-related lncRNAs in STAD were pinpointed via R's correlation algorithms. These lncRNAs, in conjunction with clinical data, informed the construction of a prognostic lncRNA-associated risk score model using univariate and multivariate Cox regression analyses. The model's prognostic capacity was evaluated by Kaplan-Meier survival curves and validated as an independent prognostic variable. Further, a nomogram incorporating this model with clinical parameters was developed, offering refined individual survival predictions. Subsequent analyses of immune infiltration and chemosensitivity within necroptosis-related lncRNA clusters utilized an arsenal of bioinformatic tools, culminating in RT-PCR validation of lncRNA expression. Through rigorous Cox regression, 21 lncRNAs were implicated in the risk score model. Stratification by median risk scores delineated patients into high- and low-risk cohorts, with the latter demonstrating superior prognostic outcomes. The risk model was corroborated as an independent prognostic indicator for STAD. The integrative nomogram displayed high concordance between predicted and observed survival rates, as evidenced by calibration curves. Differential immune infiltration in risk-defined groups was illuminated by the single sample GSEA (ssGSEA), indicating pronounced immune presence in higher-risk patients. Tumor microenvironment (TME) analysis showed that cluster-C3 had the highest score in the analysis of the three TMEs. Through the differential analysis of immune checkpoints, it was found that almost all immune checkpoint-related genes were expressed differently in various tumor clusters. Among them, CD44 expression was the highest. By comparing all drug sensitivities, we screened out 29 drugs with differences in drug sensitivity across different clusters. Risk score gene expression identification results showed that these lncRNAs were abnormally expressed in gastric cancer cell lines. This investigation provides a robust methodological advance in prognosticating and personalizing immunotherapy for STAD, leveraging quantitatively derived tumor cluster risk scores. It posits the use of necroptosis-related lncRNAs as pivotal molecular beacons for guiding therapeutic strategies and enhancing clinical outcomes in STAD.

Determination of the nutritional and biological value of semi-smoked sausage products made from beef

Sausage products belong to high-calorie products with their own taste and aroma and occupy a significant share in the meat products market of Kazakhstan. In the modern era, one of the most important directions in the creation of technology for meat products is to reduce the content of toxic substances in products and enrich their composition with vitamins, macro - and microelements through natural raw materials. The presented article shows the result of improving the quality indicators of finished products by adding vegetables to them in order to expand the range of semi-smoked beef sausages. Sausage products are meat products made from minced meat and heat – treated, their chemical composition and nutritional value are higher depending on the portion content, i.e. the content of complete proteins, irreplaceable polyunsaturated fatty acids, macro- and microelements and vitamins in the finished product the composition in the sausage recipe depends on the type and size of the portion. In the course of scientific work, it is planned to increase the nutritional and biological value of sausage by reducing the amount of nitrites and spices used in the production of sausages and adding vitamin-rich carrot juice instead. Carrot juice is a real depository of useful vitamins, micro and macroelements, and the antioxidants contained in it are able to prevent the appearance and development of malignant tumors. Especially vitamin A, which is contained in carrots, is characterized by strong antioxidant properties, it is formed from carotene, which enters our body, and it is easily absorbed through squeezed carrot juice. As a result of research, a recipe for new samples of semi-smoked sausages with the addition of carrot juice was created, a production technology was developed, and the nutritional and biological value of the resulting sausage product was determined. Carrot juice contributed to the formation of aroma, taste, color and high-quality characteristics of sausages.