Involvement of ERK activation for cancer cell killing

manojkbhat submitted, created time 1 year 3 months (www.febsletters.org)

In general, the activation of extracellular recognition kinase (ERK) cascade is implicated in exerting tumorigenic effects. Conversely, recent studies suggest that ERK activation may also have role in DNA-damage induced apoptosis. Here we observed an essential requirement of ERK activation in carboplatin induced apoptosis in cervical cancer SiHa and CaSki cells. Under similar treatment conditions p53 was also involved in Carboplatin induced apoptosis in these cells

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MIF coordinates the cell cycle with DNA damage checkpoints. Lessons from knockout mouse models

DanyC submitted, created time 1 year 5 months (www.celldiv.com)

"Macrophage migration inhibitory factor (MIF) is a ubiquitously expressed pro-inflammatory mediator that has also been implicated in the process of oncogenic transformation and tumor progression. They used a genetic approach to show that deletion of the MIF gene in mice has several major consequences for the proliferative and transforming properties of cells. MIF-deficient cells exhibit increased resistance to oncogenic transformation. The transformation defects associated with MIF deficiency can be overcome through concomitant inactivation of the p53 and Rb/E2F tumor suppressor pathways

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Brucella suis urease encoded by ure1 but not ure2 is necessary for intestinal infection of BALB/c mice

crackpot submitted, created time 1 year 6 months (www.biomedcentral.com)

"These findings suggest that the ure1 operon is necessary for optimal growth in culture, urease activity, resistance against low-pH killing, and in vivo persistence of B. suis when inoculated by gavage. The ure2 operon apparently enhances the resistance to low-pH killing in-vitro."

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Roles of DNA topoisomerase II isozymes in chemotherapy and secondary malignancies

cappuccion submitted, created time 1 year 6 months (www.pnas.org)

Drugs that target DNA topoisomerase II (Top2), including etoposide (VP-16), doxorubicin, and mitoxantrone, are among the most effective anticancer drugs in clinical use. However, Top2-based chemotherapy has been associated with higher incidences of secondary malignancies, notably the development of acute myeloid leukemia in VP-16-treated patients. This association is suggestive of a link between carcinogenesis and Top2-mediated DNA damage. We show here that VP-16-induced carcinogenesis involves mainly the {beta} rather than the {alpha} isozyme of Top2.

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