Chronic inflammation drives the growth of colorectal cancer through the dysregulation of molecular pathways within the immune system. Infiltration of immune cells, such as macrophages, into tumoral regions results in the release of proinflammatory cytokines (IL-6; IL-17; TNF-α), fostering tumor proliferation, survival, and invasion. Tumors employ various mechanisms to evade immune surveillance, effectively ‘cloaking’ themselves from detection and subsequent attack. A comprehensive understanding of these intricate molecular interactions is paramount for advancing novel strategies aimed at modulating the immune response against cancer.
7 March 2022 in International Journal of Radiation Biology
The aim of this work is to review the published studies on radiation resistance mechanisms and molecular markers involved in different tumors. The revision has been focused in the last 5 years (201...
9 March 2020 in International Journal of Environmental Health Research
Due to the massive increase in non-ionizing radiation emitting devices, the social concern about the possible malignancy to its exposure has increased the research interest. The International Commission on Non-Ionizing Radiation Protection (ICNIRP) included the radiofrequency electromagnetic field (RF-EMF) of mobile phones on the category 2B as ‘possibly’ carcinogenic to humans. Epidemiological studies noticed a causal association between the exposure to RF-EMF and the incidence of brain neoplasm in different populations, since this is the organ with the highest specific absorption rate. The fact that so many of the ipsilateral tumors found are statistically significant with RF-EMF exposure provides weight suggesting causality. In this way, the higher the exposure (ipsilateral vs contralateral), the longer the cumulative exposure (hours of exposure) and the longer the latency (beyond 10 years); the greater the risk. In addition, considering together all of these parameters suggest a strong causality.
Ageing is a multifactorial degenerative process which causes a decrease in the cellular capacity for repair and adaptation to external stressors. In this way, it is important to maintain the proper balance of the proteome. Heat shock proteins (HSP) will intervene in this balance, which are responsible for the correct assembly, folding and translocation of other proteins when cells are subjected to stressors. This type of protein is overexpressed in human tumor cells, while its deficit, both in function and quantity, contributes to ageing processes. The present work aims to analyze the response of cells from studies carried out in normal and tumor cells that are subjected to stressors. A PubMed search was performed using the keywords "cell ageing, cell longevity, resistance, HSP, heat shock proteins, thermal shock proteins". This search generated 212 articles. Subsequently, a series of inclusion and exclusion criteria were applied to select the articles of interest to be evaluated. Normal cells subjected to external stressors at low doses increase the number of HSP, causing them to become more resistant. In addition, tumor cells expressing high levels of HSP show greater resistance to treatment and increased cell replication. HSP intervene in the cellular resistance of both normal and tumor cells. In the case of normal cells, the increase in HSP levels makes them respond effectively to an external stressor, increasing their resistance and not causing cell death. In the case of tumor cells, there is an increase in resistance to treatment.
Cancer is one of the world’s most significant health problems today. Currently, breast cancer has globally surpassed lung cancer as the most commonly diagnosed cancer in women. In 2020, an estimated 2,261,419 new cases were diagnosed in women worldwide. Therefore, there is a need to understand the processes that can help us better treat this disease. In recent years, research in the fight against cancer has often been based on two treatment modalities. One of them is the use of protein kinase inhibitors, which have been instrumental in the development of new therapeutic strategies. Another crucial route is the use of immunotherapy, which has been touted as a great promise for cancer treatment. Protein kinase alterations can interfere with the effectiveness of other treatments, such as immunotherapy. In this review, we will analyze the role played by protein kinase alterations in breast cancer and their possible impact on the effectiveness of the response to immunotherapy treatments.
24 July 2019 in International Journal of Radiation Biology
Purpose: The aim of this study is to investigate the effects of low frequency and intensity sinusoidal magnetic field (SMF) and pulsed magnetic field (PMF) exposure on the chronological aging and cellular stability of Saccharomyces cerevisiae. Materials and methods: The S. cerevisiae wild type strain (WS8105-1C) was exposed to SMF (2.45 mT, 50 Hz, continuous) and PMF (1.5 mT, 25 Hz, 8 h/day). Chronological aging was evaluated during 40 days. Survival was assayed by clonogenic assay and drop test. Cellular stability was studied by spontaneous mutation count and the index of respiratory competence (IRC). Results: We found that exposure to PMF produces an acceleration of cellular chronological aging, not observed in the groups treated with SMF. A decrease in the spontaneous frequency of mitochondrial mutation during aging was observed in PMF-treated samples. However, no alterations in the IRC during aging were found for both, SMF and PMF, treatments. Conclusions: Exposure to PMF produces the acceleration of aging and an alteration in cellular stability.