Pancreatic cancer is a significant public health concern, with increasing incidence rates and limited treatment options. Recent studies have highlighted the role of the human microbiome, particularly the gut microbiota, in the development and progression of this disease. Microbial dysbiosis, characterized by alterations in the composition and function of the gut microbiota, has been implicated in pancreatic carcinogenesis through mechanisms involving chronic inflammation, immune dysregulation, and metabolic disturbances. Researchers have identified specific microbial signatures associated with pancreatic cancer, offering potential biomarkers for early detection and prognostication. By leveraging advanced sequencing and bioinformatics tools, scientists have delineated differences in the gut microbiota between pancreatic cancer patients and healthy individuals, providing insights into disease pathogenesis and potential diagnostic strategies. Moreover, the microbiome holds promise as a therapeutic target in pancreatic cancer treatment. Interventions aimed at modulating the microbiome, such as probiotics, prebiotics, and fecal microbiota transplantation, have demonstrated potential in enhancing the efficacy of existing cancer therapies, including chemotherapy and immunotherapy. These approaches can influence immune responses, alter tumor microenvironments, and sensitize tumors to treatment, offering new avenues for improving patient outcomes and overcoming therapeutic resistance. Overall, understanding the complex interplay between the microbiome and pancreatic cancer is crucial for advancing our knowledge of disease mechanisms and identifying innovative therapeutic strategies. Here we report phylogenetic analysis of the 16S rDNA microbial sequences of the pancreatic cancer mice microbiome and corresponding age matched healthy mice microbiome. We successfully identified differentially abundant microbiota in pancreatic cancer.

The aryl hydrocarbon receptor (AhR) plays a crucial role in cellular responses to various environmental pollutants, including several known carcinogens. As a ligand-activated transcription factor, AhR activation modulates the expression of genes involved in critical cellular processes, including detoxification pathways, cell proliferation and differentiation, and immune system regulation. The AhR exhibits pleiotropic effects under normal physiological conditions, contributing to the development and function of various organ systems. AhR activity is important in angiogenesis, cardiomyocyte differentiation, oocyte maturation, oculomotor nerve formation, and hematopoietic stem cell maintenance. Additionally, AhR plays a role in regulating immune cell differentiation and function, maintaining the integrity of the intestinal epithelium and its associated immune system, and mediating UVB-induced DNA damage repair responses in the skin. It acts as a critical environmental sensor, mediating cellular responses to various exogenous ligands. Importantly, activation or inhibition of AhR affects distinct signaling pathways depending on the specific ligand and cellular context. Ligands for the AhR are divided into exogenous or endogenous and have agonistic or antagonistic activity. Recently, the AhR role was determined in cancer development. It can exert both tumor-promoting and tumor-suppressive effects depending on factors such as the specific ligand, cell type, and tissue microenvironment. Emerging evidence suggests that AhR may represent a promising target for immunotherapy and serve as a potential biomarker for cervical cancer. AhR interacts with apoptotic pathway, immune checkpoint system, steroid hormones, and immune cell regulation process in cervical cancer. Despite its potential significance, the precise role of AhR in cervical cancer development and progression is still unknown. In this review, we describe significant roles of AhR in gynecological cancers; e.g., in cervical cancer.

Objective: Hepatocellular carcinoma (HCC) incidence has increased dramatically over the previous two decades and is anticipated to rise further in some countries, notably the United States, by 2030. HCC is most widespread in Asia and Africa, where hepatitis B and C are ubiquitous and lead to the development of chronic liver disease and, finally, HCC. In this study, we examined changes in the characteristics and prognosis of HCC patients, as well as the risk of developing HCC after direct-acting antiviral (DAA) medication.
Methods: The study enrolled all individuals who attended the Clinical Oncology and Nuclear Medicine Department, Suez Canal University Hospital, Ismailia, Egypt, with a proven diagnosis of HCC in the period between January 2020 and December 2021. HCC is diagnosed based on radiographic appearance (arterial enhancement phase and delayed washout phase) or compatible histology.
Results: This retrospective cohort included 254 HCC patients, separated into three groups. Kaplan-Meier curves with log-rank analysis revealed that hepatitis C virus (HCV) treatment therapy considerably reduced the time to HCC development following hepatitis diagnosis (p <.001). HCV therapy had a substantial impact on progression-free survival and overall survival in HCC patients (p <.001).
Conclusions: The emergence of DAA medication has greatly altered the management of HCV patients in the context of HCC. DAAs have been shown to be both safe and beneficial in these individuals, particularly in terms of lowering the risk of hepatic decompensation. DAAs have been reported to enhance overall survival in patients with cirrhotic HCV-related HCC, most likely due to decreased hepatic decompensation.

Objective: In many countries, including Russia, breast cancer ranks first in the incidence of cancers in women. The etiology of this disease remains largely unclear, but there is evidence indicating that disturbances in the somatic homeostasis of trace elements may be involved in the process of oncogenesis. Therefore, this study was aimed at identifying changes in the content of trace elements during malignant transformation of breast tissue.
Methods: For this purpose, an effective method of small sample analysis by means of inductively coupled plasma mass spectrometry was developed. The method makes it possible to determine the content of 35 trace elements in microsamples (with mass ≥ 10 mg) of breast tissue obtained by puncture biopsy. With the help of this technique, the samples of cancerous (n = 43) and normal (n = 38) breast tissue were studied.
Results: In malignant breast tissue, the content of Al, As, B, Cd, Co, Cs, Cu, Mg, Mn, Mo, Ni, Rb, Se, Sr, Ti, Tl, U, V, Zn, and Zr was higher, while the content of Ge, Pb, Sb and Th was lower than in healthy gland tissue. All the identified differences were statistically significant.
Conclusions: The significant disruption of somatic homeostasis of trace elements resulting from malignant transformation of breast tissue has been described, but its cause has not been determined, so additional research is required. Further the method we employ, which we have developed and described here, requires tissue samples weighing only a few milligrams, so it is possible to use it with tissue obtained from puncture tissue biopsies.

Objective: Exosome (Exo)-based therapies have attracted considerable interest due to their potential as carriers for therapeutic molecules and their capacity to elicit anti-tumor immune responses. The objective of this study was to engineer TC-1 tumor cell line-derived exosomes with GFP-tagged heat shock protein (Hsp) 27-human papillomavirus (HPV)16 E7 fusion protein and evaluation of cytokine secretion from antigen-presenting cells (APCs: macrophages and dendritic cells) exposed to the engineered exosomes in vitro.
Methods: In this study, different in silico methods were employed to evaluate the Hsp27-E7 and Hsp27-E7-GFP fusion proteins as potential vaccine candidates. Regarding to the in silico data, the Hsp27-E7-GFP fusion gene was subcloned into pCDH lentiviral vector for production of lentivirions harboring the Hsp27-E7-GFP fusion protein in eukaryotic cells. Subsequently, the TC-1 tumor cells were transduced with these lentivirions to isolate the engineered exosomes (i.e., Exo-Hsp27-E7-GFP) using the ExoQuick-TCTM kit and their characterization using physicochemical methods. Finally, the secretion of key cytokines (IFN-γ, TNF-α, and IL-10) was evaluated through incubation of antigen-presenting cells (APCs) with the engineered Exo-Hsp27-E7-GFP using enzyme-linked immunosorbent assay (ELISA).
Results: Our in silico data showed that both the Hsp27-E7 and Hsp27-E7-GFP constructs were soluble and non-allergenic, and exhibited strong interaction with TLR4. Indeed, the linkage of GFP did not affect the physicochemical properties, and interaction of Hsp27-E7 with the immune receptors. Moreover, western blot analysis confirmed the presence of Hsp27-E7-GFP fusion protein in the isolated exosomes. The Exo-Hsp27-E7-GFP could significantly enhance the secretion of TNF-α and IL-10 from APCs compared to Exo and Exo-GFP, as well.
Conclusions: These engineered vesicles derived from tumor cells demonstrate the capacity to induce effective immunity, suggesting their potential as a promising strategy in the development of cell-free vaccine candidates.