Radiotherapeutic treatment of a fighter pilot with nasopharyngeal carcinoma.

BACKGROUND: Radiotherapy is the standard and most effective treatment for nasopharyngeal carcinoma (NPC) in its early stages. However, its application in fighter pilots returning to flying duties with NPC has not been previously reported, presumably due to post-radiotherapeutic complications. CASE REPORT: A 36-yr-old male fighter pilot had a painless mass in the left neck for 5 mo. Pathological diagnosis demonstrated nonkeratinizing squamous cell carcinoma in the left nasopharynx which had metastasized to lymph nodes in the left side of the neck. He was diagnosed and staged with NPC (T1N2M0) before treatment with radiotherapy and adjuvant chemotherapy. The patient suffered from catarrhal otitis media and xerostomia after 3 mo of radiotherapy, but these symptoms resolved. After a total of 8 mo of radiotherapy, he was in remission with no evidence of tumor recurrence or metastasis. He had normal Eustachian tube, hearing, and vestibular function before and after hypobaric chamber testing and passed all flight-related physical examinations. Consequently, he was granted a medical waiver and returned to flying status in two-seat fighter aircraft, flying for 53 h in a 12-mo period. After passing all flight-related tests again, he was then allowed to fly in single-seat aircraft. At the time of submission of this article, he has flown for 147 h and remained on flying status for 26 mo. He will be monitored annually for long-term effects of radiotherapy and/or disease recurrence. CONCLUSIONS: Fighter pilots with NPC may be safely considered for medical waiver with appropriate monitoring after successful treatment.

The epigenetically-regulated miR-34a targeting c-SRC suppresses RAF/MEK/ERK signaling pathway in K-562 cells.

Previous reports show that miR-34a suppressed K-562 cell proliferation and contributed to megakaryocytic differentiation of K-562 cells. Here, we reported that miR-34a, a tumor suppressor gene, is down-regulated in the K-562 cells and chronic myeloid leukemia (CML) patients due to aberrant DNA hypermethylation. c-SRC is a target of miR-34a. Restoring miR-34a expression resulted in down-regulation of c-SRC and phosphorylated (Tyr416) c-SRC protein in K-562 cells, which consequently triggered suppression of the RAF/MEK/ERK signaling pathway to decrease cell proliferation.

Variants in the KCNE1 or KCNE3 gene and risk of Ménière's disease: A meta-analysis.

BACKGROUND: Ménière's disease (MD) is defined as an idiopathic disorder of the inner ear characterized by the triad of tinnitus, vertigo, and sensorineural hearing loss. Although many studies have evaluated the association between variants in the KCNE1 or KCNE3 gene and MD risk, debates still exist. OBJECTIVE: Our aim is to evaluate the association between KCNE gene variants, including KCNE1 rs1805127 and KCNE3 rs2270676, and the risk of MD by a systematic review. METHODS: We searched the literature in PubMed, SCOPUS and EMBASE through May 2015. We calculated pooled odds ratios (OR) and 95% confidence intervals (CIs) using a fixed-effects model or a random-effects model for the risk to MD associated with different KCNE gene variants. The heterogeneity assumption decided the effect model. RESULTS: A total of three relevant studies, with 302 MD cases and 515 controls, were included in this meta-analysis. The results indicated that neither the KCNE1 rs1805127 variant (for G vs. A: OR = 0.724, 95%CI 0.320, 1.638, P= 0.438), nor the KCNE3 rs2270676 variant (for T vs. C: OR = 0.714, 95%CI 0.327, 1.559, P = 0.398) was associated with MD risk. CONCLUSIONS: Based on current evidence from published studies, neither of the two variants from KCNE was significantly associated with the risk of MD. Larger studies with mixed ethnicity subjects and stratified by clinical and sub-clinical characteristics are needed to validate our findings.