A new adhesive bone conduction hearing system as a treatment option for transient hearing loss after middle ear surgery.

OBJECTIVE: The objective of this prospective, single-subject, repeated measures study was to evaluate the audiological benefit and patient satisfaction with an adhesive, pressure-free bone conduction hearing system (ADHEAR; MED-EL, Innsbruck, Austria) in patients who underwent middle ear surgery with transient hearing loss due to auditory canal tamponade. METHODS: Eleven adult subjects suffering from transient conductive hearing loss were enrolled in the study and followed up to 3 weeks after middle ear surgery. Bone and air conduction thresholds were measured pre and postoperatively to evaluate eligibility for enrollment. Postoperative unaided and aided sound-field thresholds, as well as speech tests in quiet and noise were compared to confirm hearing improvement with the hearing system. To determine patient satisfaction, the SSQ12 and a system-specific quality of life questionnaire was administered to all subjects. RESULTS: Speech perception for monosyllables in quiet improved by 46%, with statistical significance for the ADHEAR system compared to the unaided condition after one week. The functional hearing gain improved by 19 dB. Speech perception in noise with the device was - 6.7 dB SNR on average, with a statistically significant improvement of 2.7 dB SNR. The results of the questionnaire showed a high level of patient satisfaction and subjective hearing improvement. No serious skin reactions or other severe complications occurred. CONCLUSION: As long as the auditory canal is blocked due to tamponade, patients benefit from hearing rehabilitation. This adhesive hearing system is a safe and effective device to treat transient conductive hearing loss and may considerably improve treatment for patients even with short-term hearing loss.

Randomized controlled single-blinded clinical trial of functional voice outcome after vascular targeting KTP laser microsurgery of early laryngeal cancer.

BACKGROUND: Local control rate (LCR) of early glottic cancer is high after radiation therapy or transoral laser microsurgery (TLM). The aim of this study was to investigate functional voice outcome after TLM using a microvessel-ablative potassium-titanyl-phosphate (KTP) laser in comparison with a gold standard cutting CO2 laser. METHODS: The primary end point of this prospective, randomized, single-blinded, clinical phase II study with control group was voice outcome during a follow-up of 6 months assayed by Voice Handicap Index (VHI-30)-questionnaires in patients with unilateral high-grade dysplasia, carcinoma in situ or early glottic cancer undergoing TLM-KTP (n = 8) or TLM-CO2 (n = 12). The secondary end point was LCR. RESULTS: Starting from the 9-week-follow-up visit, TLM-KTP yielded significantly reduced VHI scores compared to TLM-CO2 . No relapse occurred after TLM-KTP in contrast to one recurrence after TLM-CO2 within 6 months. CONCLUSION: Multicenter phase II or III studies on voice outcome or local control rate after TLM-KTP in early glottic cancer are warranted enrolling larger patient cohorts.

Antitumoral effect of PLK-1-inhibitor BI2536 in combination with cisplatin and docetaxel in squamous cell carcinoma cell lines of the head and neck.

Inhibition of the polo-like-kinase-1 (PLK-1) has been shown to be effective in several haematological and solid tumor models. In this systemic in vitro study, the antitumor effect of BI2536, a small molecule inhibitor of PLK-1, in combination with cisplatin and docetaxel was examined in nine squamous cell carcinoma cell lines, most of which had a head and neck origin (SCCHN). Dose escalation studies were conducted with nine SCCHN cell lines using BI2536, cisplatin and docetaxel in cell line-specific concentrations. Growth inhibitory and proapoptotic effects were measured quantitatively using cytohistology and a Human Apoptose Array kit. BI2536 in combination with cisplatin and docetaxel showed a markedly higher antiproliferative and apoptotic activity in the SCCHN cell lines investigated (P≤0.008), compared with single agent cisplatin or docetaxel alone. The findings of this study showed that the addition of PLK-1-inhibitor BI2536 to conventional chemotherapeutic drugs led to a statistically higher antiproliferative and apoptotic effect in SCCHN cell lines compared with cisplatin or docetaxel alone. Inaugurating BI2536 in the clinical setting might enhance the antitumoral activity of conventional drugs, possibly leading to less toxic side effects of cancer therapy.

Fighting cancer from different signalling pathways: Effects of the proteasome inhibitor Bortezomib in combination with the polo-like-kinase-1-inhibitor BI2536 in SCCHN.

Inhibition of the proteasome with Bortezomib as well as inhibition of Polo-like-kinase-1 (PLK-1) has been shown to be effective in many solid tumour models and also in squamous cell carcinoma of the head and neck (SCCHN) cell lines. For the first time, we systematically examined the antitumour effect of Bortezomib in combination with BI2536 in SCCHN in an in vitro study. Dose escalation studies were performed with nine SCCHN cell lines using Bortezomib and BI2536 as single agent and combination treatments. Growth-inhibitory and pro-apoptotic effects were measured quantitatively using cytohistology and Human Apoptose Array kit. The combination of Bortezomib and BI2536 showed significant anti-proliferative and apoptotic activity in all SCCHN cell lines investigated (P=0.008) compared to both the untreated control group and Bortezomib alone. A combination treatment regime consisting of the proteasome inhibitor, Bortezomib, and the inhibitor of PLK-1, BI2536, leads to an enhanced anti-proliferative and apoptotic effect in SCCHN cell lines, compared to single agent treatment with Bortezomib alone.

Effects of the Polo-like-kinase-1-inhibitor BI2536 in squamous cell carcinoma cell lines of the head and neck.

Inhibition of the Polo-like-kinase-1 (PLK1) has been shown to be effective in a number of solid tumor models. In this in vitro study, we examined the antitumor effect of BI2536, a small molecule inhibitor of PLK1, in squamous cell carcinoma of the head and neck (SCCHN) cell lines. Dose escalation studies were performed with nine SCCHN cell lines using BI2536. Growth inhibitory and proapoptotic effects were measured quantitatively using cytohistology and a Human Apoptosis Array Kit. BI2536 demonstrated a significant antiproliferative and apoptotic activity in all nine SCCHN cell lines investigated (p<0.009). Our results indicate that inhibition of PLK1 by BI2536 leads to an antiproliferative and apoptotic effect in SCCHN cell lines. In vivo and in the clinical setting, the application of BI2536 may support the antitumoral activity of conventional drugs that are in current use and could decrease the systemic toxicity of these drugs.

Does dexamethasone inhibit anticancer activity of cetuximab in squamous cell carcinoma cell lines of the head and neck?

Glucocorticoids such as dexamethasone are widely used as comedication in the treatment of head and neck cancer, e.g., to improve appetite and decrease weight loss and fatigue in patients with advanced disease or as antiallergic and antiemetic prophylaxis during anti-EGFR therapy. However, the literature suggests that dexamethasone induces resistance to antineoplastic agents in many solid tumor models in vitro and in vivo. Since this phenomenon has never been investigated in head and neck cancer, the present study was conducted to investigate the effect of dexamethasone on the antiproliferative activity of cetuximab in vitro in squamous cell carcinoma of the head and neck (SCCHN) cell lines. The antiproliferative effect of the anti-EGFR agent cetuximab alone and in combination with increasing concentrations of dexamethasone was examined in eight SCCHN cell lines at three different time-points (24, 48 and 72 h). Cell growth inhibition and viability were measured quantitatively using WST and LDH assays. Absolute tumor cell numbers were determined by cell counting in a Rosenthal chamber. Cetuximab alone inhibited the growth of all eight SCCHN cell lines significantly (p=0.008). In some cases the addition of dexamethasone reduced the antiproliferative activity of cetuximab (p