Department of Biological Sciences

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    Black Tea Polyphenols Restrict Benzopyrene-induced Mouse Lung Cancer Progression through Inhibition of Cox-2 and Induction of Caspase-3 Expression
    (APJCP, 2006) Mukherjee, Sudeshna
    Lung cancer is one of the leading causes of cancer related death in most developed and many developing countriesof the world. Due to lack of validated screening methods and poor prognosis, treatment of lung cancer has notimproved significantly over the last two decades. Therefore the risk of the disease needs to be minimized by preventivemeasures. One approach for lung cancer prevention envisages reversal or restriction of precancerous lesions bychemopreventive intervention. It demands a deeper understanding of the pathogenesis of the disease and identificationof the ideal point of intervention. In the present investigation, tea components, epigallocatechin gallate (EGCG) andtheaflavins (TF) were assessed for their chemopreventive potential when administered in the post initiation phase oflung carcinogenesis in an experimental mouse model. Histopathological changes in lungs of mice administeredbenzo(a)pyrene (BP) were followed serially and correlated with the expression of Cox-2, caspase-3 and caspase-7,which play key roles in histopathogenesis of neoplasia. The observations strongly indicate that both EGCG and TFcan influence the expression of these genes to modulate the process of carcinogenesis, resulting in delayed onset andlowered incidence of pre-invasive lung lesions.
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    Tea polyphenols can restrict benzo[a]pyrene-induced lung carcinogenesis by altered expression of p53-associated genes and H-ras, c-myc and cyclin D1
    (Elsiever, 2009-05) Mukherjee, Sudeshna
    The modulatory influence of tea polyphenols (epigallocatechin gallate, epicatechin gallate and theaflavin) on benzo[a]pyrene (B[a]P)-induced lung carcinogenesis in mice was analyzed using histopathological and molecular parameters. Progression of lung lesions was restricted at the hyperplastic stage by tea polyphenols. A significant reduction in cellular proliferative index and an increase in apoptotic index were noted in the restricted lung lesions. High expression of H-ras, c-myc, cyclin D1 and p53 genes was seen at the inflammatory stage (9th week) and in subsequent premalignant lesions, but down-regulation of H-ras at the hyperplastic stage (17th week). Expression of bcl-2 was high in hyperplastic lesions, whereas the expression of mdm2 and bcl-xl increased only at the moderately dysplastic stage (36th week). The tea polyphenols inhibited inflammatory response in the lung lesions on the 9th week, when decreased expression of H-ras and c-myc and increased expression of bax were noted. Prolonged treatment (>9th week) with tea polyphenols resulted in changes in the expression of some additional genes, such as reduced expression of cyclin D1 (from the 17th week), bcl-2 (from the 26th week; mild dysplasia) and p21 (on the 36th week), and high expression of p53 (from the 17th week) and p27 (on the 36th week). These observations indicate that the tea polyphenols can restrict B[a]P-induced lung carcinogenesis by differential modulation of the expression of p53 and its associated genes such as bax, bcl-2, mdm2, p21 and p27, along with H-ras, c-myc and cyclin D1, at different time points.
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    Eugenol restricts DMBA croton oil induced skin carcinogenesis in mice: downregulation of c-Myc and H-ras, and activation of p53 dependent apoptotic pathway.
    (Elsiever, 2010-07-01) Mukherjee, Sudeshna
    Eugenol is the active component of essential oil isolated from clove (Syzigium aromaticum). Eugenol has antimutagenic, antigenotoxic, anti-inflammatory properties. The anticarcinogenic effect of eugenol was evident in different types of cell lines. However, its anticarcinogenic effect in in vivo has not yet been fully explored.