Results: Patients with SCCHN had significantly lower absolute numbers of CD3؉ CD4؉, and CD8؉ T cells than normal controls. However, no differences in the percentages of T-cell subsets between patients and normal controls were observed. Patients with active disease had significantly lower CD3؉ and CD4؉ T-cell counts than those with NED. Patients who had NED after surgery and radiotherapy had the lowest T-cell counts among the NED cohort. Patients who had NED for >2 years did not recover their T-cell counts, and the T-cell imbalance was evident many years after curative surgery. The tumor-node-metastasis (TNM) stage or site of the disease was not related to the absolute T-cell count. Patients with recurrent disease at the time of blood draw tended to have the lowest CD4؉ T-cell counts. Conclusions:Patients with SCCHN have altered lymphocyte homeostasis, which persists for months or years after curative therapies.

This study has validated a multidimensional BVFL nomenclature paradigm. This vocal fold nomenclature paradigm includes nine distinct vocal fold lesions: vocal fold nodules, vocal fold polyp, pseudocyst, vocal fold cyst (subepithelial or ligament), nonspecific vocal fold lesion, vocal fold fibrous mass (subepithelial or ligament), and reactive lesion.

Multiplexed serum cytokine profiles may be applicable to early detection, for screening those at high risk for SCCHN, and as clinically predictive biomarkers of disease status in successfully treated patients.

C-4.

Apoptosis of circulating CD8+T cells seen in patients with squamous cell carcinoma of the head and neck (HNSCC) suggests a possibility of lymphocyte imbalance. Therefore, absolute numbers and percentages of T lymphocyte subsets were examined in the peripheral blood of patients with HNSCC and age-matched controls. Venous blood was obtained from 148 patients with HNSCC and 54 normal volunteers. Absolute numbers of CD3+, CD4+ and CD8+ T lymphocytes were determined using fluorobeads in a flow-cytometry-based technique. Percentages of T lymphocyte subsets were also evaluated by flow cytometry. The patients were grouped, at the time of blood draw (active vs. no evident disease, NED), type of therapy administered and the length of follow-up. Patients with HNSCC were found to have significantly lower absolute numbers of CD3+, CD4+and CD8+T cells than normal controls (NC). However, no differences in the percentages of T cell subsets between patients and NC were observed. Patients with active disease had significantly lower CD3+ and CD4+ T cell counts than those with NED. Patients with NED after surgery and radiotherapy had lower T cell counts than those treated by surgery alone. Patients who remained without evident disease for more than 2 years did not recover their T cell counts, and the T cell imbalance was evident many years after curative surgery. Patients with recurrent disease at the time of blood draw tended to have the lowest CD4+T cell counts. The TNM stage or site of the disease were not related to the absolute T cell count. Our data indicate that patients with HNSCC have altered lymphocyte homeostasis, which persists for months or years after curative therapies.