Initiation Of Carcinogenesis Research Articles

CONTRIBUTION OF BRCA1, BRCA2, CHEK2 GENE MUTATIONS TO THE PATHOGENESIS OF HEREDITARY OVARIAN CANCER IN CRIMEAN FEMALE PATIENTS

Ovarian cancer (OC) is characterized by high heterogeneity of its clinical, morphological and genetic characteristics. A number of genes are identified, the pathology of which leads to the initiation of carcinogenesis, including genes of the DNA damage repair system by homologous recombination. The role of highly penetrant mutations in the BRCA1 and BRCA2 genes has been studied most thoroughly to date.

Chronic exposure to hexavalent chromium induces esophageal tumorigenesis via activating the Notch signaling pathway.

Hexavalent chromium Cr(VI), as a well-established carcinogen, contributes to tumorigenesis for many human cancers, especially respiratory and digestive tumors. However, the potential function and relevant mechanism of Cr(VI) on the initiation of esophageal carcinogenesis are largely unknown. Here, immortalized human esophageal epithelial cells (HEECs) were induced to be malignantly transformed cells, termed HEEC-Cr(VI) cells, via chronic exposure to Cr(VI), which simulates the progress of esophageal tumorigenesis. In vitro and in vivo experiments demonstrated that HEEC-Cr(VI) cells obtain the ability of anchorage-independent growth, greater proliferative capacity, cancer stem cell properties, and the capacity to form subcutaneous xenografts in BALB/c nude mice when compared to their parental cells, HEECs. Additionally, HEEC-Cr(VI) cells exhibited weakened cell motility and enhanced cell adhesion. Interestingly, HEECs with acute exposure to Cr(VI) failed to display those malignant phenotypes of HEEC-Cr(VI) cells, suggesting that Cr(VI)‍-induced malignant transformation, but not Cr(VI) itself, is the cause for the tumor characteristics of HEEC-Cr(VI) cells. Mechanistically, chronic exposure to Cr(VI) induced abnormal activation of Notch signaling, which is crucial to maintaining the capacity for malignant proliferation and stemness of HEEC-Cr(VI) cells. As expected, N-‍[N-‍(3,5-difluorophenacetyl)‍-L-alanyl]‍-S-phenylglycine t-butyl ester (DAPT), an inhibitor for the Notch pathway, drastically attenuated cancerous phenotypes of HEEC-Cr(VI) cells. In conclusion, our study clarified the molecular mechanism underlying Cr(VI)‍-induced esophageal tumorigenesis, which provides novel insights for further basic research and clinical therapeutic strategies about Cr(VI)‍-associated esophageal cancer.

Opening and changing: mammalian SWI/SNF complexes in organ development and carcinogenesis.

The switch/sucrose non-fermentable (SWI/SNF) subfamily are evolutionarily conserved, ATP-dependent chromatin-remodelling complexes that alter nucleosome position and regulate a spectrum of nuclear processes, including gene expression, DNA replication, DNA damage repair, genome stability and tumour suppression. These complexes, through their ATP-dependent chromatin remodelling, contribute to the dynamic regulation of genetic information and the maintenance of cellular processes essential for normal cellular function and overall genomic integrity. Mutations in SWI/SNF subunits are detected in 25% of human malignancies, indicating that efficient functioning of this complex is required to prevent tumourigenesis in diverse tissues. During development, SWI/SNF subunits help establish and maintain gene expression patterns essential for proper cellular identity and function, including maintenance of lineage-specific enhancers. Moreover, specific molecular signatures associated with SWI/SNF mutations, including disruption of SWI/SNF activity at enhancers, evasion of G0 cell cycle arrest, induction of cellular plasticity through pro-oncogene activation and Polycomb group (PcG) complex antagonism, are linked to the initiation and progression of carcinogenesis. Here, we review the molecular insights into the aetiology of human malignancies driven by disruption of the SWI/SNF complex and correlate these mechanisms to their developmental functions. Finally, we discuss the therapeutic potential of targeting SWI/SNF subunits in cancer.

Exploring the Potential of Terpenoids as a Possible Treatment for Cancer: Structure-Activity Relationship and Mechanistic Studies.

Cancer stands as a significant global health challenge due to its mortality rates and the complexities involved in its treatment. Addressing issues, such as metastasis, recurrence, chemoresistance, and treatment-related toxicity, remains pivotal in cancer therapy advancement. Therefore, exploration of novel therapeutic agents has emerged as a priority. As the risk of cancer continues to rise, effective measures must be taken to combat it. One promising approach is to explore natural remedies, such as terpenoids, which have demonstrated anticancer activity. Utilizing terpenoids could aid in the development of potent compounds to fight cancer. By studying the structural makeup of various terpenoid derivatives from previous research, we can identify which structural groups are essential for their anticancer activity. This understanding of the structure-activity relationship is crucial for developing new, effective anticancer agents based on terpenoids. Terpenoids, a diverse class of plant-derived secondary metabolites composed of multiple isoprene units, have garnered attention for their potential anticancer and pharmacological qualities. Some terpenoids exhibit notable anticancer effects by concentrating on several stages of cancer development. They show promise in blocking the initiation of early carcinogenesis by the induction of cell cycle arrest, the inhibition of cancer cell differentiation, and the induction of apoptosis. This study delves into the investigation of specific terpenoids showcasing promising anticancer activity against prevalent malignancies, including breast, colon, ovarian, and lung cancers. The study also explores the relationship between the structure and activity of these compounds, which sheds light on how effective they are against a variety of cancer cell types. The comprehensive discussion centres on elucidating terpenoids with substantial potential for combating diverse cancer types, offering insights into their structural features and promising anticancer mechanisms.

The Aryl Hydrocarbon Receptor and Its Crosstalk: A Chemopreventive Target of Naturally Occurring and Modified Phytochemicals.

The aryl hydrocarbon receptor (AhR) is an environmentally sensitive transcription factor (TF) historically associated with carcinogenesis initiation via the activation of numerous carcinogens. Nowadays, the AhR has been attributed to multiple endogenous functions to maintain cellular homeostasis. Moreover, crosstalk, often reciprocal, has been found between the AhR and several other TFs, particularly estrogen receptors (ERs) and nuclear factor erythroid 2-related factor-2 (Nrf2). Adequate modulation of these signaling pathways seems to be an attractive strategy for cancer chemoprevention. Several naturally occurring and synthetically modified AhR or ER ligands and Nrf2 modulators have been described. Sulfur-containing derivatives of glucosinolates, such as indole-3-carbinol (I3C), and stilbene derivatives are particularly interesting in this context. I3C and its condensation product, 3,3'-diindolylmethane (DIM), are classic examples of blocking agents that increase drug-metabolizing enzyme activity through activation of the AhR. Still, they also affect multiple essential signaling pathways in preventing hormone-dependent cancer. Resveratrol is a competitive antagonist of several classic AhR ligands. Its analogs, with ortho-methoxy substituents, exert stronger antiproliferative and proapoptotic activity. In addition, they modulate AhR activity and estrogen metabolism. Their activity seems related to a number of methoxy groups introduced into the stilbene structure. This review summarizes the data on the chemopreventive potential of these classes of phytochemicals, in the context of AhR and its crosstalk modulation.

Ecosystemic Approach to Understanding Gut Microbiome-Mediated Prevention of Colorectal Cancer.

Humans and their associated microorganisms coexist in complex symbiotic relationships. Continuously advancing research is demonstrating the crucial role of host-associated microbiota in the pathophysiology and etiology of disease and in mediating the prevention thereof. As an exemplar, the gut microbiota, especially colonic bacteria, have been extensively studied in colorectal cancer (CRC), and the growing body of evidence establishes new oncomicrobes and their oncometabolites associated with the initiation and promotion of carcinogenesis. Herein, we discuss the importance of approaching the gut microbiome as an ecosystem rather than an assortment of individual factors, especially in the context of cancer prevention. Furthermore, we argue that a dietary pattern effectively drives multiple nodes of the gut microbial ecosystem toward disease- or health-promoting qualities. In the modern circumstances of excessive consumption of ultraprocessed and animal-based foods and concomitant escalation of chronic disease burden worldwide, we focus on whole food-derived dietary fiber as a key to establishing a health-promoting eubiosis in the gut.

THEORETICAL AND PRACTICAL JUSTIFICATION OF THE SAPROPHYTIC THEORY OF CANCER

The aim of the work was to justify the theoretical and practical aspects of the saprophytic theory of cancer. In the medical section of the book “The Realities of Life”, published in 2009, I described this theory for the first time with some elements of theoretical and practical justification among all the theories of cancer origin. The saprophytic theory of cancer, the theory of the occurrence of cancerous tumors can be of great importance. In this theory the main importance in the initiation of carcinogenesis in the human body have saprophytic bacteria that live with us constantly. The saprophytic theory, as an etiological cause of cancer, may be important in the development of cancerous tumors. There is a significant amount of scientific research and clearly established facts that confirm the infectious origin, whether bacterial or viral, of a cancerous tumor. Cancer can be caused by a type of saprophyte that is practically unaffected by antibiotics. A microorganism that can cause cancerous disease, has the property of reducing the human antifungal immunity, has both the properties of a virus and a bacterium. It is possible that this virus, which settled in bacterium, combined its pathogenic properties for humans. Bacterium at the same time with virus, merging into one organism, into one unit, can contribute to the development of cancer. There is an opinion that the high temperature of the human body sometimes kills cancer cells. Microorganisms are the first step of the oncogenic process, they start it, cause it to appear, and in the future they may not participate in its development. It is likely that only at the first stage of cancer occurrence, we need to kill the microorganisms that are the cause of the cancer. Or we need to find a potential human enemy and create a universal vaccine against it, which will protect the human organism from cancer. Vaccine is not against cancer, but against a microorganism that causes cancer, releasing carcinogenic substances that start the cancer process in organs and tissues.

Correlation of testosterone and ESR2 in prostate cancer

Introduction: Prostate cancer (PCa), as the second most frequent cancer in males, has a significant challenge in determining differential diagnosis and prognosis of aggressive or non-aggressive prostate cancer. For functioning correctly, the prostate needs sex steroid hormones, which are also factors in the initiation and progression of carcinogenesis. Risk and Gleason score upgrading can be predicted by preoperative plasma testosterone levels in men with prostate cancer undergoing radical prostatectomy. Not only testosterone but estrogen also has roles in prostate cancer carcinogenesis. Estrogen Receptor 2 (ESR2) gene has been found to encode ER-β, which has an anti-proliferative effect on prostate tissue. This study aims to look up any correlation between testosterone and ESR2 in prostate cancer. Methods: This is an analytic cross-sectional study. We conducted a quantitative real-time polymerase chain reaction (qPCR) examination involving 15 benign prostate hyperplasia (BPH), 10 non-metastasized PCa, and 21 PCa patients for determining ESR2 expression from formalin-fixed paraffin-embedded (FFPE) prostate cancer tissue with known testosterone level in our institution. Data were analyzed using statistical tests with a significance of p <0.05. Results: The mean testosterone level and ESR2 expression are 785 ng/dl and 236.4 ng/dl 4.6 8.2, respectively, in BPH and PCa. Statistically, there was an inverse correlation between testosterone and ESR2 levels in prostate cancer (p<0.05). Conclusion: This study found lower testosterone correlates with ESR2 modulation.

Metabolic adaption of epithelial cells in asthma: a window to the initiation of carcinogenesis?

Metabolic adaption of epithelial cells in asthma: a window to the initiation of carcinogenesis?

From single DNA adducts measurement to DNA adductomics in molecular epidemiology of cancer.

Environmental carcinogens exert their carcinogenic effects by forming DNA adducts. This type of DNA damage can also be formed endogenously as a result of, e.g., oxidative damage. Unrepaired DNA adducts may induce mutations in critical genes, leading to the initiation of chemical carcinogenesis. Therefore, detection, identification, and quantification of DNA adducts is essential for cancer risk assessment. Over the last 50 years, the major DNA adducts formed by different classes of environmental carcinogens were characterized. With the development of techniques such as 32P-postlabeling, their measurement was implemented into molecular epidemiology. Advances in liquid chromatography-tandem mass spectrometry (LC-MS ) made the measurement of adducts more precise and allowed to gain knowledge about their identity and structures. Therefore, opened the way to DNA adductomics, the "omics" approach investigating DNA adducts comprehensively, similarly to proteomics. This review presents the historical perspective of DNA adducts research and the emerging field of adductomics.

Retroelements in targeted antitumor therapy (review)

Background: Pathological expression of retroelements is determined in most malignant tumors, which reflects the pathogenesis of tumors, since activated retrotransposons cause genomic instability due to a cascade of mutual regulatory influence events between transposons, tumor suppressors and oncogenes. These relationships are reflected in the expression profiles of certain long non-coding RNAs and miRNAs in specific tumor tissues, since retroelements are key sources of non-coding RNAs. Since retroelements serve as drivers for the initiation and progression of carcinogenesis, it is promising to use drugs aimed at inhibiting their expression. The aim of the study: To determine the available methods of influencing retroelements in antitumor therapy, to evaluate the ways of their further improvement for the effective treatment of malignant neoplasms. Materials and methods: The databases Scopus, WoS, PubMed were used to analyze the role of retroelements in the development of tumors, methods of influencing them in the treatment of neoplasms. Results: Reverse transcriptase inhibitors have proven to be effective. Silencing of retrotransposons by acting on histone modifiers can lead to a weakening of the antitumor immune response; therefore, this approach requires RNA guides that direct the formation of heterochromatin in the area where strictly specific retroelements are located. A promising method is viral mimicry aimed at activating the interferon and T-cell response to artificially activated endogenous retroviruses. For this purpose, inhibitors of histone methyltransferases, DNA methyltransferases, and histone deacetylases are used. Their joint use is most effective, especially with PD-1 checkpoint blockers. The arrangement of retroelements in gene introns has become the basis for the development of spliceosomal targeted therapy, which also initiates an antitumor immune response to double-stranded RNA transcripts. We suggest the possibility of using antisense oligonucleotides targeting retroelements in anticancer therapy. Such approach is used to treat age-related macular degeneration, Fukuyama muscular dystrophy, amyotrophic lateral sclerosis. Antisense oligonucleotides targeting microRNAs, proto-oncogenes, and oncosuppressors are used in anticancer therapy and are closely related to retroelements, which could become promising targets for antisense oligonucleotides. Conclusion: In antitumor therapy, it is possible to use two diametrically opposed strategies for influencing retroelements: inhibition and activation. The most promising way is a combination of these methods with specific silencing of retrotransposons using guides (complementary RNAs) and stimulation of the expression of elements not involved in carcinogenesis, but activating the immune response.

The Garlic Compound, Diallyl Trisulfide, Attenuates Benzo[a]Pyrene-Induced Precancerous Effect through Its Antioxidant Effect, AhR Inhibition, and Increased DNA Repair in Human Breast Epithelial Cells.

Exposure to B[a]P, the most characterized polycyclic aromatic hydrocarbon, significantly increases breast cancer risk. Our lab has previously reported that diallyl trisulfide (DATS), a garlic organosulfur compound (OSC) with chemopreventive and cell cycle arrest properties, reduces lipid peroxides and DNA damage in normal breast epithelial (MCF-10A) cells. In this study, we evaluated the ability of DATS to block the B[a]P-induced initiation of carcinogenesis in MCF-10A cells by examining changes in proliferation, clonogenic formation, reactive oxygen species (ROS) formation, 8-hydroxy-2-deoxyguanosine (8-OHdG) levels, and protein expression of ARNT/HIF-1β, CYP1A1, and DNA POLβ. The study results indicate that B[a]P increased proliferation, clonogenic formation, ROS formation, and 8-OHdG levels, as well as increasing the protein expression of ARNT/HIF-1β and CYP1A1 compared to the control. Conversely, DATS/B[a]P co-treatment (CoTx) inhibited cell proliferation, clonogenic formation, ROS formation, and 8-OHdG levels compared to B[a]P alone. Treatment with DATS significantly inhibited (p < 0.0001) AhR expression, implicated in the development and progression of breast cancer. The CoTx also attenuated all the above-mentioned B[a]P-induced changes in protein expression. At the same time, it increased DNA POLβ protein expression, which indicates increased DNA repair, thus causing a chemopreventive effect. These results provide evidence for the chemopreventive effects of DATS in breast cancer prevention.

SALIVARY IL-6 AND IL-8 AS POTENTIAL BIOMARKERS FOR ORAL SQUAMOUS CELL CARCINOMA

Introduction: Early identification of oral squamous cell carcinoma (OSCC) is a crucial factor influencing the disease's prognosis. The elevated levels of IL-6 and IL-8 in saliva are a result of their overproduction in the cancer microenvironment. The production of salivary cytokines, particularly IL-6 and IL-8, has a role in cancer development. These cytokines may also be used as biomarkers. The use of saliva as a biomarker is quite interesting because it is in direct contact with cancer cells, easy to access, non-invasive, and cost-effective. Aim: The aim of this literature review was to assess the potential of salivary IL-6 and IL-8 as biomarkers for OSCC early diagnosis. Review: The initiation of carcinogenesis in the oral cavity is actively repressed by inflammation and cell-mediated immunity. IL-6 and IL-8 are two important molecules involved in stromal-to-cancer cell communication. These cytokines play a major part in the growth, progression, metastasis, and recurrence of OSCC. Several studies have found that OSCC patients have higher levels of salivary IL-6 and IL-8 than healthy people and patients with an oral potentially malignant disorder (OPMD). Conclusion: Salivary IL-6 and IL-8 are very promising potential biomarkers for the early diagnosis of OSCC. Further research is still needed to validate and use these biomarkers clinically.

Deciphering NF-kappaB pathways in smoking-related lung carcinogenesis.

One of the main causes of death worldwide is lung cancer, which is largely caused by cigarette smoking. The crucial transcription factor NF-κB, which controls inflammatory responses and various cellular processes, is a constitutively present cytoplasmic protein strictly regulated by inhibitors like IκB proteins. Upon activation by external stimuli, it undergoes phosphorylation, translocates into the nucleus, and modulates the expression of specific genes. The incontrovertible association between pulmonary malignancy and tobacco consumption underscores and highlights a public health concern. Polycyclic aromatic hydrocarbons and nitrosamines, potent carcinogenic compounds present in the aerosol emitted from combusted tobacco, elicit profound deleterious effects upon inhalation, resulting in severe perturbation of pulmonary tissue integrity. The pathogenesis of smoking-induced lung cancer encompasses an intricate process wherein NF-κB activation plays a pivotal role, triggered by exposure to cigarette smoke through diverse signaling pathways, including those associated with oxidative stress and pro-inflammatory cytokines. Unraveling the participation of NF-κB in smoking-induced lung cancer provides pivotal insights into molecular processes, wherein intricate crosstalk between NF-κB and pathways such as MAPK and PI3K-Akt amplifies the inflammatory response, fostering an environment conducive to the formation of lung cancer. This study reviews the critical function of NF-κB in the complex molecular pathways linked to the initiation and advancement of lung carcinogenesis as well as potential treatment targets. See also the graphical abstract(Fig. 1).

Nrf2, A Target for Precision Oncology in Cancer Prognosis and Treatment.

Activating nuclear factor-erythroid 2-related factor (Nrf2), a master regulator of redox homeostasis, has been shown to suppress initiation of carcinogenesis in normal cells. However, this transcription factor has recently been reported to promote proliferation of some transformed or cancerous cells. In tumor cells, Nrf2 is prone to mutations that result in stabilization and concurrent accumulation of its protein product. A hyperactivated mutant form of Nrf2 could support the cancer cells for enhanced proliferation, invasiveness, and resistance to chemotherapeutic agents and radiotherapy, which are associated with a poor clinical outcome. Hence understanding mutations in Nrf2 would have a significant impact on the prognosis and treatment of cancer in the era of precision medicine. This perspective would provide an insight into the genetic alterations in Nrf2 and suggest the application of small molecules, RNAi, and genome editing technologies, particularly CRISR-Cas9, in therapeutic intervention of cancer in the context of the involvement of Nrf2 mutations.

Efficacy of Two Commercially Available Adsorbents to Reduce the Combined Toxic Effects of Dietary Aflatoxins, Fumonisins, and Zearalenone and Their Residues in the Tissues of Weaned Pigs.

Mycotoxins present a significant health concern within the animal-feed industry, with profound implications for the pig-farming sector. The objective of this study was to evaluate the efficacy of two commercial adsorbents, an organically modified clinoptilolite (OMC) and a multicomponent mycotoxin detoxifying agent (MMDA), to ameliorate the combined adverse effects of dietary aflatoxins (AFs: sum of AFB1, AFB2, AFG1, and AFG2), fumonisins (FBs), and zearalenone (ZEN) at levels of nearly 0.5, 1.0, and 1.0 mg/kg, on a cohort of cross-bred female pigs (N = 24). Pigs were randomly allocated into six experimental groups (control, mycotoxins (MTX) alone, MTX + OMC 1.5 kg/ton, MTX + OMC 3.0 kg/ton, MTX + MMDA 1.5 kg/ton, and MTX + MMDA 3.0 kg/ton), each consisting of four individuals, and subjected to a dietary regimen spanning 42 days. The administration of combined AFs, FBs, and ZEN reduced the body-weight gain and increased the relative weight of the liver, while there was no negative influence observed on the serum biochemistry of animals. The supplementation of OMC and MMDA ameliorated the toxic effects, as observed in organ histology, and provided a notable reduction in residual AFs, FBs, and ZEN levels in the liver and kidneys. Moreover, the OMC supplementation was able to reduce the initiation of liver carcinogenesis without any hepatotoxic side effects. These findings demonstrate that the use of OMC and MMDA effectively mitigated the adverse effects of dietary AFs, FBs, and ZEN in piglets. Further studies should explore the long-term protective effects of the studied adsorbent supplementation to optimize mycotoxin management strategies in pig-farming operations.

Responses of multifunctional immune complement component 1q (C1q) and apoptosis-related genes in Macrophthalmus japonicus tissues and human cells following exposure to environmental pollutants.

Apoptosis is a key defense process for multiple immune system functions, playing a central role in maintaining homeostasis and cell development. The purpose of this study was to evaluate the effects of environmental pollutant exposure on immune-related apoptotic pathways in crab tissues and human cells. To do this, we characterized the multifunctional immune complement component 1q (C1q) gene and analyzed C1q expression in Macrophthalmus japonicus crabs after exposure to di(2-ethylhexyl) phthalate (DEHP) or hexabromocyclododecanes (HBCDs). Moreover, the responses of apoptotic signal-related genes were observed in M. japonicus tissues and human cell lines (HEK293T and HCT116). C1q gene expression was downregulated in the gills and hepatopancreas of M. japonicus after exposure to DEHP or HBCD. Pollutant exposure also increased antioxidant enzyme activities and altered transcription of 15 apoptotic signaling genes in M. japonicus. However, patterns in apoptotic signaling in response to these pollutants differed in human cells. HBCD exposure generated an apoptotic signal (cleaved caspase-3) and inhibited cell growth in both cell lines, whereas DEHP exposure did not produce such a response. These results suggest that exposure to environmental pollutants induced different levels of immune-related apoptosis depending on the cell or tissue type and that this induction of apoptotic signaling may trigger an initiation of carcinogenesis in M. japonicus and in humans as consumers.

Mannose antibody levels in gastric cancer patients (literature review and clinical and experimental study)

Introduction. Glycans play an important role in the pathogenesis of malignant neoplasms, including stomach cancer. In recent years, the attention of many researchers has been drawn to mannose (Man) – hexose, which is an indispensable component of all N-chains of glycoproteins involved in both normal physiological and pathological processes.Aim. To investigate the role of innate immunity factors and ways to influence them through mannose and mannose-containing glycans in gastric cancer patients. Materials and methods. Data on the role of mannose – one of the key monosaccharides in the formation of glycoprotein N-chains – and its binding receptors (mannose receptor, mannose-binding lectin, antibodies) in gastric cancer since 2006 are presented. Levels of anti-glycan antibodies in blood serum samples of 235 gastric cancer patients and 76 healthy donors were evaluated using a glycochip.Results. It has been shown that the level of IgM-class antibodies to Manβ – the core part of N-glycans – in gastric cancer patients is significantly lower compared to the donor group, regardless of age (p = 0.0001). To assess the effect of age on the levels of antiglycan antibodies, patients were divided into two subgroups – before and after 45 years. In the group under 45 years of age, significant differences in the levels of antiglycan antibodies to Manβ persisted, while significant differences in the levels of antiglycan antibodies to Manβ1-4GlcNAcβ were not observed. when comparing groups of patients and donors older than 45 years, the levels of antibodies to Manβ and Manβ1-4GlcNAcβ were significantly higher only in donors. Conclusion. Deficiency of humoral immunity may be one of the key factors in the initiation and progression of carcinogenesis in humans. In our work, in patients with stomach cancer, we revealed a deficiency of antiglycan antibodies to Manβ and to Manβ1-4GlcNAcβ – core fragments of N-chains of glycoproteins, and the deficiency increased with age. The results of the study are a promising platform for further research aimed not only at studying the role of anti-mannose antibodies, but also at developing approaches to adoptive immunoprophylaxis.

63P The impact of disruption of melatonin secretion on the structural-functional changes of the microbiome and the role of the melatonin-microbiome axis in the initiation of carcinogenesis

63P The impact of disruption of melatonin secretion on the structural-functional changes of the microbiome and the role of the melatonin-microbiome axis in the initiation of carcinogenesis

Role of Melatonin-Microbiome Axis in the Initiation of Carcinogenesis: An Investigation on Disruption of Melatonin Secretion and Structural-Functional Changes of the Microbiome

Role of Melatonin-Microbiome Axis in the Initiation of Carcinogenesis: An Investigation on Disruption of Melatonin Secretion and Structural-Functional Changes of the Microbiome