NUT Midline Carcinoma of the Nasal Cavity.

Nuclear protein in testis (NUT) midline carcinoma (NMC) is a rare, aggressive, poorly differentiated form of squamous cell carcinoma caused by a chromosomal rearrangement of the NUT gene on chromosome 15. These tumors have a predilection for midline and paramidline structures of the upper aerodigestive tract and mediastinum and can affect patients across a broad age range, including children. In the current example, a 53 year old male presented with a mass originating in the left nasal cavity.

Enhanced Tumor Control with Combination mTOR and PD-L1 Inhibition in Syngeneic Oral Cavity Cancers.

Significant subsets of patients with oral cancer fail to respond to single-agent programmed death (PD) blockade. Syngeneic models of oral cancer were used to determine if blocking oncogenic signaling improved in vivo responses to PD-L1 monoclonal antibody (mAb). Anti-PD-L1 enhanced durable primary tumor control and survival when combined with mTOR (rapamycin), but not in combination with MEK inhibition (PD901) in immunogenic MOC1 tumors.

Pools of programmed death-ligand within the oral cavity tumor microenvironment: Variable alteration by targeted therapies.

Background: Enhanced understanding of programmed death-ligand (PD-L) expression in oral cancer is important for establishing rational combinations of emerging immune checkpoint and molecular targeted therapies.

Methods: We assessed PD-L and interferon (IFN) expression in immunogenic murine oral cancer-1 (MOC1) and poorly immunogenic MOC2 cell models after treatment with mammalian target of rapamycin (mTOR) and MEK1/2 small molecule inhibitors in vitro and in vivo.

Results: PD-L1 but not PD-L2 is expressed on MOC1 and 2 cells and is type I and II IFN-dependent.

mTOR and MEK1/2 inhibition differentially modulate tumor growth and the immune microenvironment in syngeneic models of oral cavity cancer.

We investigated the effects of mTOR and MEK1/2 inhibition on tumor growth and the tumor microenvironment in immunogenic and poorly immunogenic models of murine oral cancer. In vitro, rapamycin and PD901 inhibited signaling through expected downstream targets, but only PD901 reduced viability and altered function of MOC cells. Following transplantation of MOC cells into immune-competent mice, effects on both cancer and infiltrating immune cells were characterized following rapamycin and/or PD901 treatment for 21 days.

Recurrent auricular perichondritis in a child as the initial manifestation of insulin-dependent diabetes mellitus: a case report.

An 8-year-old boy presented to our otolaryngology clinic three times in a 3-month period for treatment of acute auricular perichondritis. At each visit he was treated with an antibiotic, and he responded quickly in each case, with a complete resolution of his infection. The results of standard autoimmune laboratory tests were negative.