No abstract

Imaging surveillance after treatment for head and neck cancer is challenging because of complicated resection and reconstruction surgery, in addition to posttreatment changes from radiation and chemotherapy. The posttreatment neck is often a source of anxiety for diagnostic radiologists, leading to suboptimal reporting and no standardized guidance for next management steps. Nevertheless, imaging is critical for detecting submucosal recurrences in a timely manner, so that patients remain candidates for salvage surgery. In 2016, the ACR convened the Neck Imaging Reporting and Data Systems (NI-RADS) Committee with the goals to (1) provide recommendations for surveillance imaging; (2) produce a lexicon to distinguish between benign posttreatment change and residual or recurrent tumor in the posttreatment neck; and (3) propose a NI-RADS template for reporting on the basis of this lexicon with defined levels of suspicion and management recommendations. In this article, the authors present the ACR NI-RADS Committee's recommendations, which provide guidance regarding the management of patients after treatment for head and neck cancer.

The goal of this study was to characterize the molecular mechanisms underlying cetuximab-mediated upregulation of HLA class I antigen-processing machinery components in head and neck cancer (HNC) cells and to determine the clinical significance of these changes in cetuximab-treated HNC patients. Flow cytometry, signaling studies and chromatin immunoprecipitation (ChIP) assays were performed using HNC cells treated with cetuximab alone or with Fcγ receptor (FcγR)-bearing lymphocytes to establish the mechanism of EGFR-dependent regulation of HLA APM expression. A prospective phase II clinical trial of neoadjuvant cetuximab was utilized to correlate HLA class I expression with clinical response in HNC patients. EGFR blockade triggered STAT1 activation and HLA upregulation, in a src homology-containing protein (SHP)-2-dependent fashion, more prominently in HLA-B/C than in HLA-A alleles. EGFR signaling blockade also enhanced IFNγ receptor 1 (IFNAR) expression, augmenting induction of HLA class I and TAP1/2 expression by IFNγ, which was abrogated in STAT1−/− cells. Cetuximab enhanced HNC cell recognition by EGFR853–861-specific CTLs, and notably enhanced surface presentation of a non-EGFR peptide (MAGE-3271–279). HLA class I upregulation was significantly associated with clinical response in cetuximab-treated HNC patients. EGFR induces HLA downregulation through SHP-2/STAT1 suppression. Reversal of HLA class I downregulation was more prominent in clinical responders to cetuximab therapy, supporting an important role for adaptive immunity in cetuximab antitumor activity. Abrogating EGFR-induced immune escape mechanisms and restoring STAT1 signaling to reverse HLA downregulation using cetuximab should be combined with strategies to enhance adaptive cellular immunity.

The proposed sphenoid sinus pneumatization classification in the coronal plane is simple and reproducible. It predicts the distance between vidian and maxillary nerve, determines the size of the surgical window to access the middle cranial fossa transnasally, and instructs on the potential risk to neurovascular structures during surgery.

Bowel injuries are challenging to diagnose on CT. Radiologists with various levels of experience and expertise can achieve accurate and reproducible results using a variety of CT criteria.

No abstract

Imaging combined with clinical information is critical to correctly identify patients who are candidates for microvascular decompression. The purpose of this article is to review trigeminal nerve anatomy and to provide strategies for radiologists to recognize important MRI findings in patients with trigeminal neuralgia.

CT is not a reliable method for determining the presence of ECS in p16-positive HNSCC patients.