Predict oral cancer recurrence from blood and saliva

It's good news for a substantial number of patients that scientists have developed blood and saliva tests that help accurately predict returns of HPV-linked oral cancers. As known, the tests screen for DNA fragments of the human papillomavirus (HPV) shed from cancer cells lingering in the mouth or other parts of the body.

Patients with such cancers are generally examined every one to three months in the first year after diagnosis. Recurrences are often found when patients experience ulcers, pain or lumps in the neck. However imaging tests are unreliable in detecting cancer recurrence earlier, and the location of oropharyngeal cancers make it difficult for physicians to spot budding lesions.

A investigator says, "There is a window of opportunity in the year after initial therapy to take an aggressive approach to spotting recurrences and intensively addressing them while they are still highly treatable. Until now, there has been no reliable biological way to identify which patients are at higher risk for recurrence, so these tests should greatly help do so."

High predictive value for recurrence

For the study, investigators analyzed blood and saliva samples from 93 oropharyngeal cancer patients including 81 patients with HPV-positive tumors, and found that Hpv DNA detected in both blood and saliva samples after treatment was predictive for recurrence nearly 70% of the time in a subset of the patients.

Scientists are seeking other genomic biomarkers that would increase the specificity of HPV DNA testing in blood and saliva. Meanwhile, What is alarming is that the research is too small to link test results to the severity of recurrence.

As reflected in the updated Hanahan and Weinberg review, the past decade has witnessed increasing acknowledgment that the tumor microenvironment provides the context for carcinogenesis. We now recognize that the key to malignant cells successfully seeding cancer is proper amendment of the soil during neoplastic progression, and that for cancer to evolve from early dysplastic lesions into invasive cancer, malignant cells must continue to modify the tissue in an organ-specific manner to facilitate survival. Thus, the acquisition of mutations, such as activation of oncogenic signaling pathways, by early cancer cells not only promotes cancer cell growth but may also act on the surrounding tissue to recruit and activate stromal cells and reprogram the microenvironment. Therapeutically targeting the tumor microenvironment is now attractive because, compared with the variable routes taken by cells to become cancers, the response of tissues to cancer is relatively consistent. This idea raises the possibility that controlling and eliminating cancer may be more readily achieved indirectly via the tissue microenvironment.

Cancer-associated fibroblasts (Caf) are biologically distinct from resident tissue fibroblasts and are functionally polar opposites. Normal stroma can actively suppress tumor growth, but a shift of programming converts quiescent fibroblasts into CAFs, whose action promotes tumorigenesis. Intriguingly, senescent fibroblasts, which accumulate with age, also display protumorigenic activity. Comparison of the secretory phenotype of CAFs and senescent fibroblasts revealed an overlap in expression of secreted factors referred to as senescence-associated secretory phenotype (SASP) factors. These observations raise the question of how this common secretory phenotype is regulated and whether it provides a therapeutic opportunity.

Numerologist Warda is hooked on OG-L002 fishing, collecting. And lastly her encouragement comes from socializing along with her companions.