Perspectives in Cancer Prevention-Translational Cancer Research
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Being a complex disease that affects millions of people world over, cancer research has assumed great significance. Translational cancer research transforms scientific discoveries in the laboratory or population studies into clinical application to reduce incidence of cancer , morbidity and mortality. It is becoming increasingly evident that cancer is a preventable disease. The IVth International Symposium on Translational Cancer Research held in Udaipur, India in December 2011, discussed various aspects of the biological processes in cancer cells and approaches to cancer prevention. A few contributions from this meeting are presented in this book, providing an in depth analysis of data on cancer prevention and therapeutics. These contributions are either critical reviews or research reports. The topics discussed include evidence-based nutritional recommendations for cancer patients and survivors, risk factors such as stress, enrichment of tumour stem cells by anticancer drug treatment contributing to tumour recurrence and the mechanism of anticancer effects of various natural products. Chemosensitizing effect of curcumin, anti-cancer effect of products from neem, action of sulforaphane and cytotoxic effect of a number of novel synthetic coordination complexes of trace metals have been discussed. Novel molecular targets of angiogenesis and molecular basis of the gender bias to thyroid cancer have also been discussed . This book provides useful information on translational cancer research to clinicians and biomedical scientists.
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in response to paclitaxel contributes to the activation of AP-1 by treating HeLa cells with paclitaxel and/or U0126 (10 M), SP600125 (50 M), and SB203580 (40 M) which are inhibitors of ERK1/2, JNK, and p38, respectively. As expected the inhibitors of all the MAPKs especially that of p38 and JNK significantly inhibited the AP-1 DNA-binding activity induced by the paclitaxel, suggesting the involvement of ERK1/2, JNK, and p38 in the activation of AP-1 induced by paclitaxel (Fig. 3.3e). Hence,
common type of liver cancer and the third leading cause of cancer death worldwide, with 75 % of cases occurring in Southeast Asian countries like China, Hong Kong, Taiwan, Singapore, Korea, and Japan. The etiology of HCC is likely to involve interactions between multiple risk factors. The most commonly reported risk factors are nonspecific cirrhosis (21 %), followed by alcohol-induced liver disease (16 %), HCV infection (10 %), and HBV infection (5 %). In addition, obesity and type II diabetes
play an important role in the mechanisms of cell cycle progression (Sherr 1996; Sherr and Roberts 1999). By binding to Cdk1/2, cyclin B1 can activate Cdk1/2 (cdc2) to facilitate its nuclear accumulation for mitotic initiation in the late G2 phase of mammalian cells. It has been suggested that while SFN-induced cell cycle arrest in the G2/M phase appears to be regulated by cell cycle-related proteins cyclin B1 and Cdk1, the arrest in G1 phase is mediated by the inhibition of cyclin D1 and DNA
Thyroid tissue is responsive to sex steroids as AR and ERs are expressed in normal and cancer thyroid tissues (Marugo et al. 1991; Banu et al. 2001a, b, 2002; Banu and Aruldhas 2002; Thiruvengadam et al. 2003; Stanley et al. 2010, 2012). Though radiation exposure, low iodine diet, family history and previous history of thy- 125 roid goiter and sex chromosomes have been attributed for thyroid cancer incidence, AR and ER genes have emerged as the most significant candidates responsible for the