Abstract:A prospective study was performed during a 2-year-period. A total of 127 patients presenting with a squamous cell carcinoma of the head, neck and upper aerodigestive tract were entered into the study. Patients were classified according to the primary site, namely: larynx (n = 44), oropharynx (n = 28), hypopharynx (n = 17) and oral cavity (n = 19) and others (n = 19). Patients were staged according to the UICC TNM classification (1987) and the nature and duration of their symptoms were recorded. Sixty-one per c… Show more
“…The final fully adjusted model shows how delay in diagnosis negatively affects prognosis, by increasing both recurrence and oral cancer mortality rates. Several previous studies report on the importance of early diagnosis in the prognosis of oral cancer patients 8,15,21 . Other studies have reported no association between diagnosis delay and oral cancer survival 8,15 .…”
“…The final fully adjusted model shows how delay in diagnosis negatively affects prognosis, by increasing both recurrence and oral cancer mortality rates. Several previous studies report on the importance of early diagnosis in the prognosis of oral cancer patients 8,15,21 . Other studies have reported no association between diagnosis delay and oral cancer survival 8,15 .…”
“…More than 60% of head and neck squamous cell carcinoma (HNSCC) patients present with advanced-staged disease, which is associated with a high mortality rate [1]. The current treatment for advanced-stage HNSCC is cisplatin and radiation for patients with good performance status; patients with limited performance status receive high-dose cisplatin alone [2]–[4].…”
Cisplatin resistance in head and neck squamous cell carcinoma (HNSCC) reduces survival. In this study we hypothesized that methylation of key genes mediates cisplatin resistance. We determined whether a demethylating drug, decitabine, could augment the anti-proliferative and apoptotic effects of cisplatin on SCC-25/CP, a cisplatin-resistant tongue SCC cell line. We showed that decitabine treatment restored cisplatin sensitivity in SCC-25/CP and significantly reduced the cisplatin dose required to induce apoptosis. We then created a xenograft model with SCC-25/CP and determined that decitabine and cisplatin combination treatment resulted in significantly reduced tumor growth and mechanical allodynia compared to control. To establish a gene classifier we quantified methylation in cancer tissue of cisplatin-sensitive and cisplatin-resistant HNSCC patients. Cisplatin-sensitive and cisplatin-resistant patient tumors had distinct methylation profiles. When we quantified methylation and expression of genes in the classifier in HNSCC cells in vitro, we showed that decitabine treatment of cisplatin-resistant HNSCC cells reversed methylation and gene expression toward a cisplatin-sensitive profile. The study provides direct evidence that decitabine restores cisplatin sensitivity in in vitro and in vivo models of HNSCC. Combination treatment of cisplatin and decitabine significantly reduces HNSCC growth and HNSCC pain. Furthermore, gene methylation could be used as a biomarker of cisplatin-resistance.
“…About one third of the patients present with early-stage disease (stages I and II; see Table 1), whereas two thirds of the patients present with advanced-stage disease (stages III and IV; ref. 2). Initial therapy of HNSCC is surgery and/or radiotherapy.…”
Purpose: Despite improvements in locoregional treatment of head and neck squamous cell carcinoma (HNSCC), local and distant failure rates remain high. The strongest prognostic indicator of HNSCC is the presence of lymph node metastases in the neck, but the value of this indicator has limitations when using for the individual patient. The presence of micrometastatic cells in bone marrow has been shown to be a putative prognostic indicator in HNSCC and other epithelial malignancies, which might allow more accurate staging and selection of patients for whom adjuvant or experimental therapy is recommended. The gene encoding the E48 antigen is selectively expressed by HNSCC, and the detection of E48 transcripts in bone marrow by reverse transcription-polymerase chain reaction (RT-PCR) presumably represents the presence of micrometastatic cells. The purpose of this study was to determine the association between the presence of micrometastatic cells in bone marrow of HNSCC patients and clinical outcome.Experimental Design: A total of 162 patients treated surgically for primary HNSCC underwent a single bone marrow aspiration from the upper iliac crest for detection of micrometastatic cells using E48 RT-PCR. In total, 139 patients were evaluable. The primary statistical endpoints were disease-free survival and distant metastasis-free survival. In addition, bone marrow samples of 30 noncancer controls were evaluated.Results: E48 RT-PCR indicated the presence of micrometastatic cells in the bone marrow in 56 of 139 (40%) of the HNSCC patients and 0 of 30 of the noncancer controls (P < 0.0001). The presence of micrometastatic cells had no significant influence on disease-free survival or distant metastasis-free survival for the whole group of HNSCC patients (P ؍ 0.1460 and P ؍ 0.2912, respectively). For patients with >2 lymph node metastases, however, the presence of micrometastatic cells was associated with a poor distant metastasisfree survival (P ؍ 0.0210).Conclusions: The presence of micrometastatic cells in bone marrow of HNSCC patients with >2 lymph node metastases is correlated with a poor distant metastasis-free survival. In this subgroup of HNSCC patients, E48 RT-PCR seems to be a valuable tool to identify patients who are at increased risk for development of distant metastases and therefore might benefit from experimental adjuvant systemic therapy.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.