Estrogen receptor (ER) signaling is a critical regulator of cell proliferation, differentiation, and survival in breast cancer (BC) and other hormone-sensitive cancers. In this review, we explore the mechanism of ER-dependent downstream signaling in BC and the role of estrogens as growth factors necessary for cancer invasion and dissemination. The significance of the clinical implications of ER signaling in BC, including the potential of endocrine therapies that target estrogens’ synthesis and ER-dependent signal transmission, such as aromatase inhibitors or selective estrogen receptor modulators, is discussed. As a consequence, the challenges associated with the resistance to these therapies resulting from acquired ER mutations and potential strategies to overcome them are the critical point for the new treatment strategies’ development.

Lung cancer is a disease that in recent years has become one of the greatest threats to modern society. Every year there are more and more new cases and the percentage of deaths caused by this type of cancer increases. Despite many studies, scientists are still looking for answers regarding the mechanisms of lung cancer development and progression, with particular emphasis on the role of the immune system. The aim of this literature review was to present the importance of disorders of the immune system and the accompanying changes at the level of cell signaling in the pathogenesis of lung cancer. The collected results showed that in the process of immunopathogenesis of almost all subtypes of lung cancer, changes in the tumor microenvironment, deregulation of immune checkpoints and abnormalities in cell signaling pathways are involved, which contribute to the multistage and multifaceted carcinogenesis of this type of cancer. We, therefore, suggest that in future studies, researchers should focus on a detailed analysis of tumor microenvironmental immune checkpoints, and to validate their validity, perform genetic polymorphism analyses in a wide range of patients and healthy individuals to determine the genetic susceptibility to lung cancer development. In addition, further research related to the analysis of the tumor microenvironment; immune system disorders, with a particular emphasis on immunological checkpoints and genetic differences may contribute to the development of new personalized therapies that improve the prognosis of patients.

Using Fourier Transform Infrared spectroscopy (FTIR), it is possible to show chemical composition of materials and / or profile chemical changes occurring in tissues, cells, and body fluids during onset and progression of diseases. For diagnostic application, the use of blood would be the most appropriate in biospectroscopy studies since, (i) it is easily accessible and, (ii) enables frequent analyses of biochemical changes occurring in pathological states. At present, different studies have investigated potential of serum, plasma and sputum being alternative biofluids for lung cancer detection using FTIR. However, until now, it has not been shown which biofluid; among serum and plasma, that can serve as the best material medium for detecting lung cancer with highest levels of accuracy. In this study, plasma and serum isolated from blood consenting participants without lung cancer symptoms (controls) and lung cancer patients. The samples were measured using FTIR and subsequently analyzed by machine learning (ML) algorithms in order to show which fluids (serum or plasma) would better enhance detection of lung cancer. Higher absorbances values of PO²⁻, CH₂, CH₃ and amides vibrations in FTIR spectra of both serum and plasma samples, collected from lung cancer patients were observed in comparison to individuals without lung cancer symptoms (controls). Principal component analysis (PCA) of FTIR spectra showed plasma and serum samples collected from lung cancer patients and individuals without lung cancer symptoms were better differentiated in fingerprinting region (from 800 to 1800 cm^− 1) when compared to lipid region (2800–3000 cm^− 1). Moreover, also sensitivity specificity and accuracy calculated by logistic regression (LR) and receive operating characteristic (ROC) showed higher values for fingerprint range (800–1800 cm^− 1) in comparison with lipids (2800–3000 cm^− 1) one for both, serum and plasma. However, using these methods differences between serum and plasma were not existed. From the all obtained results, it was visible, that both fluids could be used in detected lung cancer using FTIR. Moreover, it was also showed that fingerprint range gave a better distinction between the studied patient groups than the lipid range. This was noticeable for both serum and plasma.

Background: Non-small-cell lung cancer (NSCLC) is one of the most frequently diagnosed diseases among all types of lung cancer. Infectious diseases contribute to morbidity and mortality by delaying appropriate anti-cancer therapy in patients with NSCLC. Methods: The study aimed to evaluate the effectiveness of vaccination with the 13-valent pneumococcal conjugate vaccine (PCV13) in 288 newly diagnosed NSCLC patients. The analysis of the post-vaccination response was performed after vaccination by assessing the frequency of plasmablasts via flow cytometry and by assessing the concentration of specific anti-pneumococcal antibodies using enzyme-linked immunosorbent assays. Results: The results of the study showed that NSCLC patients responded to the vaccine with an increase in the frequencies of plasmablasts and antibodies but to a lesser extent than healthy controls. The immune system response to PCV13 vaccination was better in patients with lower-stage NSCLC. We found higher antibody levels after vaccination in NSCLC patients who survived 5 years of follow-up. Conclusions: We hope that our research will contribute to increasing patients′ and physicians′ awareness of the importance of including PCV13 vaccinations in the standard of oncological care, which will extend the survival time of patients and improve their quality of life.

Infection with Epstein-Barr virus (EBV) worsens the prognosis in chronic lymphocytic leukemia (CLL), but the underlying mechanisms are not yet established. We intended to assess whether EBV affects the course of CLL by the deregulation of the CTLA-4/CD86 signaling pathway. We used polymerase chain reaction to measure the load of EBV DNA in the blood of 110 newly diagnosed patients with CLL. The expression of CTLA-4 and CD86 antigen on lymphocytes was assessed with flow cytometry. Additionally, CTLA-4 and CD86 serum concentrations were measured through enzyme-linked immunosorbent assays. Fifty-four percent of the patients had detectable EBV DNA [EBV(+)]. In EBV(+) patients the CTLA-4 and CD86 serum concentrations and their expressions on investigated cell populations were significantly higher than in EBV(−) patients. EBV load correlated positively with unfavorable prognostic markers of CLL and the expression of CTLA-4 on CD3+ lymphocytes (r = 0.5339; p = 0.027) and CD86 on CD19+ cells (r = 0.6950; p < 0.001). During a median follow-up period of 32 months EBV(+) patients were more likely to require treatment or have lymphocyte doubling (p < 0.001). Among EBV(+) but not EBV(−) patients, increased expressions of CTLA-4 lymphocytes were associated with elevated risks of progression. We propose that EBV coinfection may worsen prognosis in CLL patients, partly due to EBV-induced up-regulation of CTLA-4 expression.