Cancer Science & Therapy

Introduction: The quality of life of cancer patients is affected by the cancer therapy’s symptoms. Anxiety, stress, and depression all affect cancer patients thus reducing the life style of the patient. The aim of this review was to determine the effects of laughter therapy on anxiety, stress, depression, and quality of life in cancer patients.

Methods: Articles were searched on PubMed and Google Scholar. This review includes randomized controlled trials and case reports from 2000-2015.

Results: 41 studies were found on PubMed and 14,700 studies were found on Google Scholar search. Only two articles met the established review criteria in PubMed and four articles met the established review criteria in Google Scholar. In total, six articles were included in the study.

Conclusion: The results of this study show that laughter therapy may decrease anxiety, stress, and depression and increase the quality of life in cancer patients.

Aflatoxins are mutagenic hepatocarcinogenic fungal metabolites that contribute to chronic hepatitis B and C and viral cirrhosis, which can both evolve into hepatocellular carcinoma.

Objective: To identify and quantify free aflatoxins and AFB1-N7-guanine (AFB1-N7-Gua) adducts (active carcinogen) in the urine of Mexican patients with chronic liver diseases.

Methods: Urine samples from 210 Mexican patients with chronic liver diseases, hepatitis B or C, or viral cirrhosis and four control groups: 1) patients with alcoholic cirrhosis, 2) patients with no hepatic diseases, 3) patients with kidney failure, and 4) healthy persons, were analyzed for free aflatoxins and AFB1-N7-Gua adducts by Inhibitory Indirect ELISA and high performance liquid chromatography, and both methods produced similar results (R2=0.90). A questionnaire regarding foods with high risk of containing aflatoxins was applied to relate diet and disease.

Results: Aflatoxin-positive samples were found from patients in the following groups: hepatitis B (50%), viral cirrhosis (26%), hepatitis C (16.6%), alcoholic cirrhosis (10%), healthy (10%), kidney failure (0.47%), and chronic nonhepatic diseases (0%), with R2=0.95. Risk groups had more AFB1-N7-Gua adducts than controls. High performance liquid chromatography identified free AFB1 (exposure), types M1 and P1 (detoxification metabolites), and Inhibitory Indirect ELISA quantified AFB1-N7-Gua adduct (a DNA repair biomarker).

High-risk foods related (P≤0.001) to hepatic diseases were maize, oil seeds, and dairy products.

Conclusion: Mexican patients with chronic liver diseases exhibited high concentrations of aflatoxins and Aflatoxin-N7-Gua adducts, both of which showed high exposure and the last are significant biomarkers for the risk of liver diseases that predispose patients to liver cancer.

One of the most intriguing scientific mysteries is the origin of cancer. DNA damage plays a potent role in mutagenesis, carcinogenesis and ageing. There has been growing realization in recent years that endogenous substrates or metabolites may be an important source of damage caused to cellular DNA. Further, evidence indicates that endogenous DNA damage occurs at a high frequency as compared to exogenous damage. Such findings have debunked the notion that the genetic material is pristine in the absence of exogenous carcinogens. An in-depth knowledge of the types of endogenous DNA damage is essential for understanding the influence of damage caused by endogenous substrates on the induction of cancer. Therefore, in this review, we have focused on several classes of endogenous metabolites and their putative role in mutagenesis and carcinogenesis from a structural, biological and analytical perspective. The mechanisms by which endogenous substrates may contribute to cancer pathogenesis have also been discussed with the objective that the implications from the findings summarised may pave way for a better understanding of the mechanisms underlying the induction of disease such as cancer. These results, complemented by other data, strongly support one of the theories of carcinogenesis according to which endogenous agents may have a major contribution in spontaneously induced cancer. It is obvious that if an approach could be developed leading to a diminution in endogenous DNA damage, the incidence of diseases such as cancer might be significantly reduced.