Journal of Cancer Prevention最新文献

Herein, an instrument free facile acid-base titrimetric methodology is reported for lysophosphatidic acid (LPA) measurement in serum and plasma samples for ovarian cancer detection. The concept is based on the titrimetric method in which alkaline solution was titrated with free fatty acid. Free fatty acid is generated due to action of the lysophospholipase to LPA. A phospholipid derivative known as LPA can function as a signaling molecule. A glycerol backbone serves as the foundation for phosphatidic acid, which also has bonds to an unsaturated fatty acid at carbon-1, a hydroxyl group at carbon-2, and a phosphate molecule at carbon-3. Free fatty acid and glycerol-3-phosphate are formed when LPA reacts with lysophospholipase. The formation of free fatty acid depends on the concentration of LPA. The standard graph of known concentrations of LPA, LPA spiked serum and LPA spiked plasma was plotted. The concentration of LPA in unknown serum and plasma were calculated from the standard graph. The limit of detection of LPA in spiked serum and plasma samples via titrimetric assay was calculated as 0.156 μmol/L. A patient's chance of survival may be outweighed by an early diagnosis of ovarian cancer.

[This corrects the article on p. 199 in vol. 27, PMID: 36713944.].

In the present study, we investigated the effects of exhaustive exercise and recovery on inflammatory, pro-apoptotic, and anti-oxidative responses in human peripheral blood mononuclear cells (PBMCs). Sixteen volunteers participated in a guided physical activity program in which they were subjected to progressive exercise on the treadmill until they were exhausted followed by an 1-hour recovery period. Isolated human PBMCs were collected before exercise, immediately after exercise, and after 1-hour recovery. Exhaustive exercise induced expression of heme oxygenase-1 and glutamate cysteine ligase catalytic subunit and activation of NF-κB and NF-E2 related factor 2 (Nrf2). Apoptosis, as measured by activity and cleavage of caspase-3 and its substrate PARP also significantly increased. However, induction of redox signaling and the pro-apoptotic response fully returned to the baseline level during the 1-hour recovery period. On the other hand, COX-2 expression was continuously elevated after exercise cessation throughout the 1-hour recovery period. Taking all these findings into account, we conclude that exhaustive exercise transiently induces Nrf2-mediated antioxidant gene expression and eliminates damaged cells through apoptosis as part of an adaptive cytoprotective response against oxidative and inflammatory stress.

Advances in omics and immunology over the past 20 years have revolutionized the approach to cancer prevention, with the goal now focused on identifying populations at higher risk for developing cancer in their lifetime as a result of either extensive exposure to environmental carcinogens or harboring precancer lesions or inherited genetic mutations that predispose them to specific types of cancer(s). Thus, the naïve idea that cancer could be "prevented" in the general population has evolved to a more practical approach based on the understanding that the target population for preventive agents will be individuals who already have alterations, in gene pathways, whether inherited or environmentally caused, and the goal will be to "intercept" these lesions at the earliest stages in the path from an initial genetic lesion to full-blown cancer. The Division of Cancer Prevention of the National Cancer Institute and the Office of Disease Prevention at the National Institutes of Health recently sponsored the second biennial "Translational Advances in Cancer Preventive Agent Development Meeting," held virtually from September 7-9th. In this Meeting Report, we highlight the scientific sessions of this meeting that covered the most recent advances in preventive agent development that also highlighted these rapidly emerging trends in this research area.

Chronic exposure to inorganic arsenic (iAs) elevates reactive oxygen species (ROS) generation and up-regulates TGF-β signalling. This promotes induction of epithelial to mesenchymal transition (EMT) and causes the development of squamous cell carcinoma (SCC) of skin. Black tea is a popular beverage worldwide and an effective antioxidant. Chemopreventive potential of black tea extract (BTE) against iAs induced carcinogenicity has been explored here. The study aims to investigate the role of BTE in prevention of iAs-induced SCC of skin in Swiss albino mice via the modulation of TGF-β signalling and EMT. Mice were divided into (1) control, (2) iAs, (3) iAs+BTE, and (4) BTE groups and were administered iAs and BTE alone, or in combination for 330 days. Histological studies were performed to assess development of SCC. ROS generation was estimated by flowcytometry. Expression of TGF-β and downstream proteins belonging to suppressor of mothers against decapentaplegic (Smad), phosphoinositide-3-kinase (PI3K)-protein kinase B (AKT) and mitogen-activated protein kinase (MAPK) pathways was assessed by immunoblotting. Expression of EMT markers was evaluated by immunoblotting, immunohistochemistry and semi-quantitative reverse transcriptase-PCR. After 330 days of iAs treatment, development of invasive SCC of skin probably due to excess ROS generation, elevation of TGF-β, downregulation of the Smad pathway, upregulation of PI3K-AKT and MAPK signalling molecules and induction of EMT was observed. All these modulations were found to be reversed by BTE, which inhibits iAs induced SCC of skin by quenching excess ROS, promoting Smad mediated TGF-β signalling, downregulating signalling intermediates of PI3K-AKT and MAPK pathways and inhibiting EMT.

As a principal component of solar radiation, ultraviolet B (UVB) exposure can be harmful depending on the duration and intensity because the human body can easily be exposed to it. Many studies have demonstrated that UVB causes a series of inflammatory and other skin disorders. UVB has been classified as the Group 1 carcinogen by the International Agency for Research on Cancer. Diverse studies have focused on UVB exposure but the complex perspective of acute and chronic UVB exposure is still lacking. This review presents the differences between acute and chronic exposure to UVB and summarizes public information in terms of toxicogenomic characteristics. We also demonstrated the differences between adverse effects of acute and chronic UVB exposure on the skin system. From the published literatures, we compared the biological pathways predict of the adverse effects caused by each UVB exposure type. Furthermore, our review not only clarifies the differences in each UVB exposure network but also suggests major hub genes related to cellular mechanisms and diseases that are thought to be affected by acute and chronic UVB exposure.

Cedrol, a sesquiterpene alcohol, isolated from Juniperus chinensis has been reported to inhibit minichromosome maintenance (MCM) proteins as cancer biomarkers in human lung cancer in vitro. In the present study, we investigated the anti-cancer activity of cedrol in vitro and in vivo using human colorectal cancer HT29 cells and a human colorectal tumor xenograft model. Cedrol inhibited MCM protein expression and cell growth in HT29 cells, which are associated with G1 arrest and the induction of apoptosis. We demonstrated that cedrol effectively reduced HT29 tumor growth without apparent weight loss in a human tumor xenograft model. Compared with vehicle- and adriamycin-treated tumor tissues, cedrol induced changes in the tumor tissue structure, resulting in a reduced cell density within the tumor parenchyma and reduced vascularization. Moreover, the expression of MCM7, an important subunit of MCM helicase, was significantly suppressed by cedrol in tumor tissue. Collectively, these results suggest that cedrol may act as a potential anti-cancer agent for colorectal cancer by inhibiting MCM protein expression and tumor growth.

Since ancient times, honey has been used in traditional medicine owing to its pharmacological effects. It possesses anticancer properties. However, the therapeutic implications of Sangju honey in cancer remains unknown. Therefore, we aimed to demonstrate the potential anticancer effects of Sangju honey on human oral squamous cell carcinoma (OSCC), particularly focusing on epithelial-mesenchymal transition (EMT) and apoptotic and mitogen-activated protein kinase (MAPK) signaling pathways. Ca9-22 and YD-10B human OSCC cells were treated with 0.25% or 0.5% Sangju honey, and the cell viability was examined using the Cell Counting Kit-8 assay. Cell morphology studies were conducted to observe morphological changes, and the wound-healing assay was performed to evaluate the proliferation of honey-treated OSCC cells. Western blot analysis was conducted to investigate protein expression related to EMT and apoptotic and MAPK signaling pathways. Sangju honey reduced cell viability, induced morphological changes, and significantly suppressed the proliferation and migration of Ca9-22 and YD-10B cells. The expression of E-cadherin and N-cadherin was increased and decreased, respectively, in both OSCC cell lines. Moreover, Sangju honey stimulated apoptosis by increasing the expression of p21, p53, cleaved caspase 3, and caspase 9. Furthermore, it downregulated the expression of phospho (p)-extracellular signal-regulated kinases 1 and 2, p-c-Jun amino-terminal kinase, and p-p38 in Ca9-22 and YD-10B cells. Sangju honey inhibits Ca9-22 and YD-10B cell proliferation by regulating EMT, inducing apoptosis, and suppressing the MAPK signaling pathway. Thus, it is a potential anticancer agent for human OSCC.

Individual dietary patterns may be influenced by diet-related behaviours, which may eventually play a significant role in contributing to colorectal cancer risk. As nearly half of colorectal cancer cases can be prevented through diet and lifestyle modification, in this study, we aimed to present an overview of the literature on diet-related behaviour and its effect on colorectal cancer risk among adults. Articles published from 2011 until July 2021 were selected. Out of the 1,198 articles retrieved, 25 were analyzed. There were 16 case-control studies, and nine of them were cohort studies. As a finding, the instruments used in this review were food frequency questionnaires (n = 23), followed by a semi-structured interview (n = 1), and diet records (n = 1). We demonstrated that unhealthy diet-related behaviours are linked to an increased risk of colorectal cancer in adults and those food frequency questionnaires or food records are common instruments used to collect diet-related behaviours. This article imparts the research trends and directions of colorectal cancer risk factors and shows that diet-related behaviour varies and changes over time.