To improve traditional Diffuse large B-cell lymphoma (DLBCL) therapy, novel molecular targets will need to be discerned and minimally-toxic drugs that can specifically impact these targets will need to be developed. To this end, the experiments described in this thesis investigated the potential effect(s) of the polyphenolic compound, resveratrol, and the heterocyclic compounds (R)-Roscovitine and CW-313 on the growth and survival of DLBCL in vitro. These drugs were found to target both the PI/3K/AKT and cdk2 pathway, with varying specificity. All drugs induced dose-dependent and time-dependent apoptosis in a number of Germinal Center (GC)-type DLBCL and Activated B Cell (ABC)-type DLBCL cell lines. Resveratrol and (R)-Roscovitine were found to be potent and novel inhibitors of glycoylsis; this process was directly modulated by AKT, involved the reduction of transcript levels of glycolytic enzymes, and resulted in decreased glucose capture as governed by GLUT1 surface receptors and hexokinase protein. Blocking glycolysis independently of these drugs was sufficient to induce apoptosis in DLBCL; rescuing AKT expression was sufficient to inhibit both (R)-Roscovitne- and resveratrol-mediated apoptosis and glycolytic block. In the low response ABC-type DLBCL, the oncogenic transcription factor c-Myc was directly involved in this process. Further, specific depletion of cdk2 by use of CW-313 or introduction of cdk2 siRNA was sufficient to (i) induce apoptosis in DLBCL cell lines and (ii) inhibit Mcl-1 and XIAP expression in a cell type-specific manner. Below, these findings and others are discussed in detail.