Project Summary

 

Burkitt's lymphoma (BL) is a highly aggressive non-Hodgkin B-cell lymphoma that is common in Sub-Saharan Africa. Although 90% of children with BL are cured in first world countries, this disease still remains fatal in developing countries. The major reason for this disproportionality is that African governments cannot afford elaborate regimens used to treat BL. Thus, developing BL treatment that is both effective and cheap is crucial.

Tamoxifen, a selective estrogen receptor modulator (SERM), is a widely used breast cancer drug currently only used to treat cancers that have estrogen receptors (ER+). There are a few studies reporting that Tamoxifen is able to induce apoptosis (programmed cell death) in cancer cells that do not have estrogen receptors (ER-) by inhibiting protein kinase C (PKC). PKC triggers PI3k/Akt pathway, activating mTOR, a protein that promotes cell growth. Elucidating Tamoxifen's mechanism of action is essential to exploit its ER independent phenomenon.

This study examines the effect of Tamoxifen on ER- BL cell line, Ramos, which has been never tested with Tamoxifen before, and investigates its mechanism of action on this ER- cancer cell. It was hypothesized that Tamoxifen will decrease Ramos cell viability by disrupting the PKC/ PI3k/Akt pathway, which is constitutively activated in Ramos, and hence inhibit mTOR activity.

This project is split into two phases: first phase focuses on whether Tamoxifen actually decreases the cell viability of Ramos cells and second phase focuses on suggesting Tamoxifen's mechanism of action on ER- Ramos cells.

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