Endovascular Treatment for Primary Tumor Hemorrhage in Oropharyngeal Carcinoma: A Report of Two Cases.

Acute arterial hemorrhage is a damaging and sometimes lethal complication that occurs in patients with head and neck cancer. However, achieving hemostasis can be challenging because of the difficulty in applying pressure in the throat and oral cavity. In this context, endovascular treatment (ET) has been performed in recent years. This report aims to describe the benefits of ET for acute bleeding. Additionally, our findings emphasize the importance of early diagnosis and treatment of tumor-related bleeding, not only for immediate life-saving benefits but also for the potential resumption of irradiation and chemotherapy, which can lead to favorable long-term prognoses in some instances. We describe two cases of primary tumor bleeding where treatment was successful with ET. Neurosurgeons performed these treatments, and effective hemostasis was achieved in both cases. No complications or rebleeding were observed. ET is a better option for hemorrhage from oropharyngeal tumors than for hemorrhage from the main trunk of the carotid artery. The efficacy of ET is dependent on the vessels involved, and early identification of the culprit artery can predict the prognosis. ET should be considered an option for acute arterial hemorrhage in head and neck cancer.

Preoperative simulation using three-dimensional printer in four temporal bone surgeries.

Preoperative simulation using a three-dimensional printer is effective to perform safe surgery by knowing the range limit of drilling in the temporal bone. Moreover, simulations using models are thought to be useful for education of young surgeon.

CD69 Imposes Tumor-Specific CD8+ T-cell Fate in Tumor-Draining Lymph Nodes.

Tumor-specific CD8+ T cells play a pivotal role in antitumor immunity and are a key target of immunotherapeutic approaches. Intratumoral CD8+ T cells are heterogeneous; Tcf1+ stemlike CD8+ T cells give rise to their cytotoxic progeny-Tim-3+ terminally differentiated CD8+ T cells. However, where and how this differentiation process occurs has not been elucidated. We herein show that terminally differentiated CD8+ T cells can be generated within tumor-draining lymph nodes (TDLN) and that CD69 expression on tumor-specific CD8+ T cells controls its differentiation process through regulating the expression of the transcription factor TOX. In TDLNs, CD69 deficiency diminished TOX expression in tumor-specific CD8+ T cells, and consequently promoted generation of functional terminally differentiated CD8+ T cells. Anti-CD69 administration promoted the generation of terminally differentiated CD8+ T cells, and the combined use of anti-CD69 and anti-programmed cell death protein 1 (PD-1) showed an efficient antitumor effect. Thus, CD69 is an attractive target for cancer immunotherapy that synergizes with immune checkpoint blockade.

A case of jugular bulb diverticulum causing pulsatile tinnitus.

If you suspect pulsatile tinnitus from a medical interview, you should check for jugular bulb diverticulum and cortical bone defects on temporal bone CT, in addition to thorough physical examination and contrast-enhanced imaging.

Toxic epidermal necrolysis associated with nivolumab treatment for head and neck cancer.

This report is the first to document TEN caused by nivolumab treatment in head and neck cancer. We believe this article can contribute significantly in understanding the principles of nivolumab treatment in patients with head and neck cancer.

CD69 prevents PLZFhi innate precursors from prematurely exiting the thymus and aborting NKT2 cell differentiation.

While CD69 may regulate thymocyte egress by inhibiting S1P1 expression, CD69 expression is not thought to be required for normal thymocyte development. Here we show that CD69 is in fact specifically required for the differentiation of mature NKT2 cells, which do not themselves express CD69. Mechanistically, CD69 expression is required on CD24+ PLZFhi innate precursors for their retention in the thymus and completion of their differentiation into mature NKT2 cells. By contrast, CD69-deficient CD24+ PLZFhi innate precursors express S1P1 and prematurely exit the thymus, while S1P1 inhibitor treatment of CD69-deficient mice retains CD24+ PLZFhi innate precursors in the thymus and restores NKT2 cell differentiation. Thus, CD69 prevents S1P1 expression on CD24+ PLZFhi innate precursor cells from aborting NKT2 differentiation in the thymus. This study reveals the importance of CD69 to prolong the thymic residency time of developing immature precursors for proper differentiation of a T cell subset.

Crucial role of CD69 in anti-tumor immunity through regulating the exhaustion of tumor-infiltrating T cells.

The introduction of immune checkpoint inhibitors in cancer treatment highlights the negative regulation of anti-tumor immunity, such as effector T-cell exhaustion in the tumor microenvironment. However, the mechanisms underlying the induction and prevention of T-cell exhaustion remain largely unknown. We found that CD69, a type II glycoprotein known to regulate inflammation through T-cell migration and retention in tissues, plays an important role in inducing the exhaustion of tumor-infiltrating T cells. Cd69-/- mice showed reduced tumor growth and metastasis in a 4T1-luc2 murine breast cancer model, in which increased numbers of tumor-infiltrating lymphocytes, relatively little T-cell exhaustion, and enhanced IFNγ production were observed. Anti-CD69 monoclonal antibody treatment attenuated the T-cell exhaustion and tumor progression in tumor-bearing mice. These findings highlight a novel role of CD69 in controlling the tumor immune escape mediated by T-cell exhaustion and indicate that CD69 is a novel target for cancer immunotherapy.