Intrinsic or acquired resistance to chemotherapeutic agents is a common phenomenon and a major challenge in the treatment of cancer patients. Chemoresistance is defined by a complex network of factors including multi-drug resistance proteins, reduced cellular uptake of the drug, enhanced DNA repair, intracellular drug inactivation, and evasion of apoptosis. Pre-clinical models have demonstrated that many chemotherapy drugs, such as platinum-based agents, antracyclines, and taxanes, promote the activation of the NF-κB pathway. NF-κB is a key transcription factor, playing a role in the development and progression of cancer and chemoresistance through the activation of a multitude of mediators including anti-apoptotic genes. Consequently, NF-κB has emerged as a promising anti-cancer target. Here, we describe the role of NF-κB in cancer and in the development of resistance, particularly cisplatin. Additionally, the potential benefits and disadvantages of targeting NF-κB signaling by pharmacological intervention will be addressed.

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Background: Stathmin 1 is a cytosolic phosphoprotein that plays a crucial role in the control of cellular division and proliferation by regulating microtubule dynamics. In addition, Stathmin1 is associated with tumor growth and progression. Our study aimed to determine differences in overall (OS) and disease free survival (DFS) in patients with non-small lung cancer (NSCLC) stratified by STMN1 tumor expression.

matory drugs may exert tumoricidal effects in the colon,4 thus accounting for the reduced risk of cancer of the colon with regular use of these drugs. Large scale therapeutic trials of non-steroidal antiinflammatory drugs in established cancers of the colon and chemopreventive trials in high risk patients would therefore be appropriate since the risk of potential side effects in such cohorts would be justified. Initial reports of such studies are encouraging.5