Gastric cancer is the second most common cause of cancer-related deaths in the world, the epidemiology of which has changed within last decades. A trend of steady decline in gastric cancer incidence rates is the effect of the increased standards of hygiene, conscious nutrition, and Helicobacter pylori eradication, which together constitute primary prevention. Avoidance of gastric cancer remains a priority. However, patients with higher risk should be screened for early detection and chemoprevention. Surgical resection enhanced by standardized lymphadenectomy remains the gold standard in gastric cancer therapy. This review briefly summarizes the most important aspects of gastric cancers, which include epidemiology, risk factors, classification, diagnosis, prevention, and treatment. The paper is mostly addressed to physicians who are interested in updating the state of art concerning gastric carcinoma from easily accessible and credible source.
Lycopene is a nutraceutical with health-promoting and anti-cancer activities, but due to a lack of evidence, there are no recommendations regarding its use and dosage. This review aimed to evaluate the benefits of lycopene supplementation in cancer prevention and treatment based on the results of in vivo studies. We identified 72 human and animal studies that were then analysed for endpoints such as cancer incidence, improvement in treatment outcomes, and the mechanisms of lycopene action. We concluded that the results of most of the reviewed in vivo studies confirmed the anti-cancer activities of lycopene. Most of the studies concerned prostate cancer, reflecting the number of in vitro studies. The reported mechanisms of lycopene action in vivo included regulation of oxidative and inflammatory processes, induction of apoptosis, and inhibition of cell division, angiogenesis, and metastasis formation. The predominance of particular mechanisms seemed to depend on tumour organ localisation and the local storage capacity of lycopene. Finally, there is a need to look for predictive factors to identify a population that may benefit from lycopene supplementation. The potential candidates appear to be race, single nucleotide polymorphisms in carotene-cleaving enzymes, some genetic abbreviations, and insulin-like growth factor-dependent and inflammatory diseases.
Distinct molecular subtypes of gastric cancer: from Laurén to molecular pathology Distinct molecular subtypes of gastric cancer: from Laurén to molecular pathology
1 January 2016 in World Journal of Gastroenterology
Currently, gastric cancer (GC) is one of the most frequently diagnosed neoplasms, with a global burden of 723000 deaths in 2012. It is the third leading cause of cancer-related death worldwide. There are numerous possible factors that stimulate the pro-carcinogenic activity of important genes. These factors include genetic susceptibility expressed in a single-nucleotide polymorphism, various acquired mutations (chromosomal instability, microsatellite instability, somatic gene mutations, epigenetic alterations) and environmental circumstances (e.g., Helicobcter pylori infection, EBV infection, diet, and smoking). Most of the aforementioned pathways overlap, and authors agree that a clear-cut pathway for GC may not exist. Thus, the categorization of carcinogenic events is complicated. Lately, it has been claimed that research on early-onset gastric carcinoma (EOGC) and hereditary GC may contribute towards unravelling some part of the mystery of the GC molecular pattern because young patients are less exposed to environmental carcinogens and because carcinogenesis in this setting may be more dependent on genetic factors. The comparison of various aspects that differ and coexist in EOGCs and conventional GCs might enable scientists to: distinguish which features in the pathway of gastric carcinogenesis are modifiable, discover specific GC markers and identify a specific target. This review provides a summary of the data published thus far concerning the molecular characteristics of GC and highlights the outstanding features of EOGC.
Chronic inflammation is a hallmark of cancer cachexia. Polyunsaturated fatty acids (ω-3 PUFAs): eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are known to contribute to the reduction of inflammation, preservation of lean body mass and total body weight, and reduction of cancer-related symptoms, such as anorexia or neuropathy. This systematic review aimed to assess whether the ratio of EPA to DHA used in supplementation in cancer patients matters in the context of the resolution of inflammation and reduction of the risk of cachexia. The analysis included 20 randomized clinical trials with acceptable quality identified from the Pubmed/MEDLINE database. The significant results concerning the resolution of inflammation or improvement in nutritional status were the highest in the case of a low EPA/DHA ratio, i.e., 67%, and decreased, reaching 50% and 36% for the moderate and high ratios, respectively. Most results concerning body weight from high and moderate EPA/DHA ratios showed no benefit or were insignificant. A significant benefit in reducing any reported inflammatory markers was seen in the low EPA/DHA ratio subgroup at 63%, in the moderate at 29%, and in the high ratio subgroup at 11%. The greatest benefit in CRP reduction was obtained by patients during chemotherapy. The review questions the anticachectic and anti-inflammatory effect of ω-3 PUFAs supplementation with doses of EPA higher than DHA. A population that particularly benefits from ω-3 PUFAs supplementation are patients undergoing chemotherapy for advanced cancer.
In colorectal cancer (CRC), pathological factors that correlate with negative prognosis include, among others, overexpression of cyclooxygenase‑2 (COX‑2) and abundant expression of mucin 1 (MUC1). COX‑2 overexpression may therefore be associated with MUC1 overexpression. The aim of the present study was to investigate the possible correlation between COX‑2 and MUC1 expression and to assess the correlation between their individual expression and the clinicopathological features of patients, paying particular attention to survival. The following data was collected from the 170 patients with CRC included in the present study: Age, sex, tumour localization, disease stage and survival. Tumour samples were immunostained with antibodies against COX‑2 and MUC1. Protein expression was scored, relative to reference staining, and correlated with the clinicopathological data of patients. The results revealed no correlation between the expressions of COX‑2 and MUC1, or with any of the studied clinicopathological variables. In addition, the expression of the two proteins were not associated. Neither of the proteins demonstrated prognostic value for survival. The present study did not confirm a direct relationship between the expressions of COX‑2 and MUC1, or between the expression of either protein and the clinicopathological features of patients, including survival.