The Role of Trublue Laser in Cholesteatoma Surgery.

OBJECTIVE: The retrospective cohort study aimed to determine the safety and efficacy of TruBlue laser application in cholesteatoma surgeries. METHODS: All cholesteatoma surgeries conducted from January 2018 to January 2022 in two tertiary referral hospitals in Hong Kong, with and without use of TruBlue laser, were included. Pure tone audiogram was done pre- and post-operatively to assess hearing. Disease extent was graded with ChOLE score and ChOLE staging. Residual disease was determined clinically, radiologically, or surgically with second look operation. RESULTS: One hundred twenty cholesteatoma cases were identified. There are 39.2% (n = 47) of the cholesteatoma surgeries that utilized TruBlue laser, while 60.8% (n = 73) did not. Overall follow-up duration was 21 ± 12.4 months, ranging from 2 to 47 months. Both groups were similar in demographics, pre-operative hearing and ChOLE staging. The length of stay was comparable in both groups (2 ± 2 days in nonlaser, 1 ± 1 day in laser, p = 0.31). There was no facial nerve injury related to surgery in both groups, and overall complication rates were similar (4.1% in nonlaser, 4.3% in laser, p = 0.97). The postoperative hearing was comparable with good hearing preservation in both groups. Residual cholesteatoma occurred in 17.8% (n = 13) in nonlaser group, and 21.3% (n = 10) in laser group, which was not statistically significant (p = 0.64). Seventy percent of the cholesteatoma residual in laser group occurred at area that TruBlue LASER cannot be applied. CONCLUSION: TruBlue LASER was safe in cholesteatoma surgeries, though no added benefits were shown in reducing cholesteatoma residual rate. A larger controlled study is warranted to discern the true effect of TruBlue LASER. LEVEL OF EVIDENCE: Level 3.

Role of hematological and neurological expressed 1 (HN1) in human cancers.

Hematological and neurological expressed 1 (HN1), also known as Jupiter microtubule associated homolog 1 (JPT1), is a highly conserved protein with widespread expression in various tissues. Ectopic elevation of HN1 has been observed in multiple cancers, highlighting its role in tumorigenesis and progression. Both proteomics and transcriptomics reveal that HN1 is closely associated with severe disease progression, poor prognostic and shorter overall survival. HN1's involvement in cancer cell proliferation and metastasis has been extensively investigated. Overexpression of HN1 is associated with increased tumor growth and disease progression, while its depletion leads to cell cycle arrest and apoptosis. The pivotal role of HN1 in cancer progression, particularly in proliferation, migration, and invasion, underscores its significance in cancer metastasis. Validation of the efficacy and safety of HN1 inhibition, along with the development of diagnostic methods to determine HN1 expression levels in patients, is essential for the translation of HN1-targeted therapies into clinical practice. Overall, HN1 emerges as a valuable prognostic marker and therapeutic target in cancer, and further investigations hold the potential to improve patient outcomes by impeding metastasis and enhancing treatment strategies.

Targeting Nrf2 to treat thyroid cancer.

Oxidative stress (OS) is recognized as a contributing factor in the development and progression of thyroid cancer. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a pivotal transcription factor involved in against OS generated by excessive reactive oxygen species (ROS). It governs the expression of a wide array of genes implicated in detoxification and antioxidant pathways. However, studies have demonstrated that the sustained activation of Nrf2 can contribute to tumor progression and drug resistance in cancers. The expression of Nrf2 was notably elevated in papillary thyroid cancer tissues compared to normal tissues, indicating that Nrf2 may play an oncogenic role in the development of papillary thyroid cancer. Nrf2 and its downstream targets are involved in the progression of thyroid cancer by impacting the prognosis and ferroptosis. Furthermore, the inhibition of Nrf2 can increase the sensitivity of target therapy in thyroid cancer. Therefore, Nrf2 appears to be a potential therapeutic target for the treatment of thyroid cancer. This review summarized current data on Nrf2 expression in thyroid cancer, discussed the function of Nrf2 in thyroid cancer, and analyzed various strategies to inhibit Nrf2.