Proteomic and genomic technologies have been developed that can simultaneously detect large panels of cancer biomarkers in body fluids such as serum, plasma, sputum, saliva or urine. These approaches provide great promise for the early detection of cancer, but have thrust the field into the era of diagnostic multianalyte-based cancer tests with few, if any, models for the implementation of such tests. These multianalyte tests may be based on the detection of serum antibodies to tumor antigens, the presence of cancer-related proteins in serum or the presence of tumor-specific genomic changes that appear in plasma as free DNA. The application of noninvasive diagnostic approaches to detect early stage cancer will provide the physician with greater presymptomatic periods for clinical intervention, but it is uncertain how the various forces will impact their implementation in a patient care setting. Utilization will be balanced by medical follow-up pathways, commercial/reimbursement factors and regulatory issues that influence implementation of new devices in the marketplace.

The concentration of testosterone in whole saliva is significantly increased (by 9%) after toothbrushing. In ultrafiltrates of saliva collected at the same time as the whole saliva, testosterone concentrations after tooth-brushing were unchanged. In 88% of the 162 whole-saliva specimens, but not in the ultrafiltrates, we also measured higher hemoglobin concentrations after toothbrushing. We conclude that the increase of testosterone in whole saliva after toothbrushing can be attributed to a protein-bound fraction. For analytes that are bound to serum proteins, salivary measurements can give spurious results. This problem can be avoided by using as a diagnostic medium an ultrafiltrate of saliva collected directly in the mouth.

Background. We have developed a device for the simplified collection of a prepurified sample of saliva in the mouth.

Fifteen sulfur-containing compounds were examined for their ability to both protect normal hematopoietic stem cells (NCFU) from the cytotoxic effect of nitrogen mustard (HN2), and potentiate the cytotoxicity of HN2 to AKR leukemia cells (LCFU). All except four agents demonstrated some protection of NCFU with WR-2721 being most active. Five of the agents were also protective for LCFU with cysteine and glutathione being most active. However, a number of agents potentiated the cytotoxicity of HN2 to LCFU, the most active being disulfiram and AET followed by cysteamine, DMSO, WR-638, and WR-3689. The dose-response relationship for the potentiation was defined for DMSO. A second leukemia model, L1210, was also studied for potentiation of HN2 cytotoxicity by four of the most active agents--WR-2721, AET, DMSO, and disulfiram. The first two agents showed no effect (either protection or potentiation) when given either 15 min or 6 hr before HN2 administration. The last two agents, however, potentiated the cytotoxicity to a level similar to that found with the AKR leukemia.