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The review is aimed on the analysis the abilities of noninvasive diagnostics and monitoring of diabetes mellitus (DM) and DM‐associated complications through volatile molecular biomarkers detection in the exhaled breath. The specific biochemical reactions in the body of DM patients and their associations with volatile molecular biomarkers in the breath are considered. The applications of optical spectroscopy methods, including UV, IR, and terahertz spectroscopy for DM‐associated volatile molecular biomarkers measurements, are described. The applications of similar technique combined with machine learning methods in DM diagnostics using the profile of DM‐associated volatile molecular biomarkers in exhaled air or "pattern‐recognition" approach are discussed. [ABSTRACT FROM AUTHOR]

Resistance to cancer therapy continues to be a major limitation for the successful treatment of cancer. There are many published studies on therapy resistance in breast and prostate cancers; however, there are currently no data on molecular markers associated with resistance. The conflicting data were reported regarding the AKT/m-TOR signaling pathway components as markers predicting resistance. The AKT/m-TOR signaling pathway is involved in the development of many human cancers; its activation is related to cell proliferation, angiogenesis, apoptosis, as well as to therapy resistance. Molecular alterations in the AKT/m-TOR signaling pathway provide a platform to identify universal markers associated with the development of resistance to cancer therapy. [ABSTRACT FROM AUTHOR]

The main epidemiological and clinical data on colorectal cancer, as well as the features of molecular pathology, are discussed in the literature review. Efforts are being putto identify promising targets, particularly small non-coding nucleotide sequences, which can lead to new treatments for this disease. The discovery of significant mutations that contribute to the development of colorectal tumors is a major step in the advancement of molecular oncology, as these mutations give rise to heterogeneous tumors that differ in their origin. These mutations play a significant role in the progression of the disease and are now being targeted for treatment. The prognosis for a disease is influenced by the patient's sensitivity to antitumor therapy. However, new approaches to finding effective targets for antitumor treatments face new fundamental challenges due to clinical issues. These issues include the epigenetic regulation of markers of oncogenesis, which allows for the development of new therapeutic strategies. RNA interference, in particular, has been linked to non-copying RNA sequences such as microRNAs. These microRNAs are associated with certain processes that can influence all aspects of oncogenesis. The diversity of microRNAs allows for a differentiated approach when treating tumors in various locations., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

The widespread infectious disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) significantly impacts major human diseases. It is undoubtedly evident that cancer patients are more susceptible to the infection and at a higher risk of severe COVID-19 than the general population. Moreover, the rise in cancers incidence is waiting in the Globe as a long-term effect of post-COVID-19 complications. Multiple mostly unknown mechanisms participate and determine the oncogenic impact of virus-induced transformation. Imbalance in oncogenesis is considered critical in cancer development. Modified immunogenicity and metabolic features emerge as pivotal in COVID-19 pathogenesis and the organism system's response. The molecular mechanisms of the onset of the metabolic disorder have not yet been fully elucidated. The pathology is complicated, multifactorial, and emerging in various processes. Preventive anticancer therapy taking into account the change in metabolic processes, helps them respond better to anti-COVID-19 treatment than relying only on antiviral drugs. The modified therapeutic algorithm was provided to reduce the likelihood of post-acute complications in patients with preexisting pathologies and the onset of other chronic pathologies and cancers.

Objective: The aim of this study was investigation the AKT / mTOR signaling pathway components, transcriptional and growth factors, as well as steroid hormone receptors and nuclear factors Brn-3α and TRIM16 expression in the tissue of the primary thyroid tumor and metastases, depending on the BRAF- V600E status., Material and Methods: The study was enrolled 20 patients with PTCs, who underwent surgical treatment. They were divided into negative BRAF-V600E status (12 people), positive BRAF-V600E status (8 patients). Mutation status was assessed in paired metastatic tissue samples. The molecular marker expression was determined by real-time PCR. The Real-time-PCR-BRAF-V600E reagent kit evaluated the BRAF-V600E mutation., Results: A decrease in the PDK kinase, PTEN, VHL mRNA level in primary cancers was noted, compared with metastases' tissue. An increase in AKT, GSK-3β, mTOR, 70s 6 kinase was revealed in cancers with point mutation compared with the primary tumor without a mutation. Positive mutation status was accompanied by an increase in NF-κB p65, NF-κBp50, VEGF HIF-2 VHL level compared to the primary tumor with negative BRAF-V600E status. In the metastases with the BRAF-V600E point mutation, a decrease in the PDK kinase, HIF-1; VHL; TRIM16, and ERα expression was observed, compared to lymph node metastases (LNMs) without the mutation. The concordance in the BRAF-V600E tumor status and LNMs was observed only in 50% of patients. If the BRAF gene status did not match PTCs and LNMs, an increase in the mTOR, NFkBp65, VHL, and ERα mRNA levels was found in the PTCs. In LNMs, there was an increase in the c-RAF PTEN NFkBp65 VHL expression compared to non-concordant ones., Conclusion: The heterogeneity in the primary tissue's expression profile and metastases was noted. The BRAF-V600E mutation can affect the molecular characteristics both in the primary cancers and metastases. The discrepancy between the mutant status and the molecular factors expression variability in the primary tumor and LNMs determines its progression.

Resistance to cancer therapy continues to be a major limitation for the successful treatment of cancer. There are many published studies on therapy resistance in breast and prostate cancers; however, there are currently no data on molecular markers associated with resistance. The conflicting data were reported regarding the AKT/m-TOR signaling pathway components as markers predicting resistance. The AKT/m-TOR signaling pathway is involved in the development of many human cancers; its activation is related to cell proliferation, angiogenesis, apoptosis, as well as to therapy resistance. Molecular alterations in the AKT/m-TOR signaling pathway provide a platform to identify universal markers associated with the development of resistance to cancer therapy.

Background: The effect of the targeted therapy on cancer molecular markers remains currently unknown. The aim of the study was to investigate the expression and content of transcription, growth factors and components of the AKT/m-TOR signaling pathway in kidney cancer patients before and after targeted therapy with pazopanib. Methods: A total of 157 patients with renal cell carcinoma were enrolled into the study. The level of mRNA expression was investigated by real-time PCR, and the contents of transcription and growth factors, as well as the levels of AKT/m- TOR signaling pathway components were determined by ELISA and Western blotting. Results: Targeted therapy with pazopanib resulted in a 3.1-fold decrease in HIF-2α expression that was accompanied by a reduction in the levels of NF-κB p65 and p50, HIF-1α and CAIX. The levels of GSK-3ß and AKT mRNA were increased; however, the levels of corresponding proteins remained low. The targeted therapy with pazopanib did not influence the level of PTEN phosphatase. A 1.9-fold increase in the level of p70 S6 (S371) was observed after therapy. Conclusion: The efficacy of tyrosine kinase inhibitors is associated with the changes in the angiogenic factors. Molecular characteristics of cancer could determine markers of disease progression as well as potential targets for anticancer therapies, (Creative Commons Attribution License)

Purpose: Tumor cell growth and sensitivity to chemotherapy depend on many factors, among which insulin-like growth factors (IGFs) may play important roles. The aim of the present study was to evaluate the levels of insulin-like growth factors (IGFs) and IGF binding proteins (IGFBPs) in primary tumors and ascites as predictors of response to neoadjuvant chemotherapy in ovarian cancer (OC) patients. Materials and Methods: Tumor tissue samples and ascitic fluid were obtained from 59 patients with advanced OC. The levels of IGF-I, IGF-II, IGFBP-3, IGFBP-4 and PAPP-A were determined using ELISA kits. Taking into account the data on expression of these IGF-related proteins and outcome, logistic regression was performed to identify predictors of response to neoajuvant chemotherapy. Results: Human ovarian tumors expressed IGFs, IGFBP-3, IGFBP-4 and PAPP-A and these proteins were also present in ascites fluid and associated with its volume. IGFs and IGFBPs in ascites and soluble PAPP-A might play a key role in ovarian cancer progression . However, levels of proteins of the IGF system in tumors were not significant predictors of objective clinical response (oCR). Univariate analysis showed that the level of IGF-I in ascites was the only independent predictor for oCR. Conclusion: The level of IGF-I in ascites was shown to be an independent predictor of objective clinical response to chemotherapy for OC patients treated with neoadjuvant chemotherapy and debulking surgery., (Creative Commons Attribution License)

Purpose: To assess IGFBP-6 expression in relation with the presence of the metabolic syndrome, adiponectin receptors (AdipoR1 and AdipoR2) and IGF-IR levels in colorectal adenocarcinoma cases., Materials and Methods: IGFBP-6 mRNA and protein levels were analyzed using real-time quantitative PCR and Western blotting in 46 patients. ELISA and ow cytometry were used for evaluation of AdipoR1, AdipoR2 and IGF-IR., Results: The results showed that IGFBP-6 mRNA expression and the IGFBP-6 content were higher in tumor tissue samples of colorectal cancer patients with and without the metabolic syndrome. In addition, IGFBP-6 mRNA expression was associated with tumor invasion (tumor size) and the IGFBP-6 protein level was associated with nodal status. Positive correlations and positive nonlinear relations were found between the IGFBP-6 level and the AdipoR1 and AdipoR2 contents in colorectal cancer patients., Conclusions: The IGFBP-6 mRNA level and protein level were found to be associated with presence of the metabolic syndrome. Positive correlations indicated probable cross-talk between the IGF-IR-mediated and adiponectin-mediated signaling pathways in colorectal carcinomas. IGFBP-6 may be considered as a potential biomarker associated with lymphogenous metastasis and the metabolic syndrome in colorectal cancer.