Peptides derived from viral or bacterial antigens or mutant oncogene or tumor suppressor gene products may be applied towards this method. For example, using this method, a synthetic peptide which corresponds to the site of the mutation in the tumor suppressor gene product p53 can be used to induce a CTL response which kills tumor cells endogenously expressing the mutant p53 gene. Phosphotyrosyl residues in signalling proteins, which appear to act as molecular switches in phosphotyrosyl-dependent cellular signal transduction pathways, are potential targets for therapeutic agents. Peptides containing OMT residues are therefore potential therapeutic agents for disease states with altered cellular signaling including cancer. The method is based on detecting high levels of the mRNA for ERCC1 which includes exon VIII or concurrent expression of ERCC1 and XPAC mRNAs in fresh tumor tissues.
DAG is released from membrane phospholipids in response to the binding of a variety of agonists.
PK-C, when activated, is capable of phosphorlyating a variety of other proteins involved in cellular processes including growth, differentiation, inflammation, nerve function, tumor promotion, and ocogenic expression. Given the global action of PK-C, molecules that can activate or inactivate this enzyme would be very useful. The claims of this invention describe a series of a diaclyglycerol analogues, which act as potent pharmacological agonists of PK-C and can be easily synthesized. A major complication in treating tumors is that many of the known treatments, such as surgery, radiation or chemotherapy, have serious side effects. Other types of cancers are not amenable to conventional therapies due to the fact that the exact mechanism by which the disease develops is unknown.