Background We established multiple UM-SCC (University of Michigan Squamous Cell Carcinoma) cell lines. With time, these have been distributed to other labs all over the world. Recent scientific discussions have noted the need to confirm the origin and identity of cell lines in grant proposals and journal articles. We genotyped the UM-SCC cell lines in our collection to confirm their unique identity. Design Early passage UM-SCC cell lines were genotyped and photographed. Results Thus far, 73 unique head and neck UM-SCC cell lines (from 65 donors including 21 lines from 17 females) were genotyped. In 7 cases separate cell lines were established from the same donor. Conclusions These results will be posted on the U of M Head and Neck SPORE Tissue Core website for other investigators to confirm that the UM-SCC cells used in their laboratories have the correct features. Publications using UM-SCC cell lines should confirm the genotype.

In Figure 3B of this article, the VCAP and the control siRNA images are identical. This was the result of a mistake in constructing the figure. The correction to the figure does not affect the conclusion of the paper and the authors would like to apologize for any confusion the error may have caused. The corrected image is printed below.

Objectives The indications for neck dissection concurrent with salvage laryngectomy in the clinically N0 setting remain unclear. Our goals were to determine the prevalence of occult nodal disease, analyze nodal disease distribution patterns, and identify predictors of occult nodal disease in a salvage laryngectomy cohort. Study Design Case series with planned data collection. Setting Tertiary academic center. Subjects Patients with persistent or recurrent laryngeal squamous cell carcinoma after radiation/chemoradiation failure undergoing salvage laryngectomy with neck dissection. Methods We analyzed a single-institution retrospective case series of patients between 1997–2014 and identified those who had clinically N0 necks (n = 203). Clinical and pathologic data, including nodal prevalence and distribution were collected, and statistical analyses were performed. Results Overall, cN0 necks had histologically positive occult nodes in 17% (n=35) of cases. Univariate predictors of occult nodal positivity included recurrent T4 stage (34% T4 vs. 12% non-T4; p=0.0003), and supraglottic subsite (28% supraglottic vs. 10% non-supraglottic; p=0.0006). Histologically positive nodes associated with supraglottic primaries were most frequently positive in ipsilateral level II and III (17% and 16%). Positive nodes for glottic SCC were most frequently positive in the ipsilateral and contralateral paratracheal nodes (11% and 9%). Conclusion Histologically positive occult nodes are identified in 17% of cN0 patients undergoing salvage laryngectomy with neck dissection. Occult nodal disease varies in frequency and distribution based upon tumor subsite. Predictors of high (>20%) occult nodal positivity include T4 tumors and supraglottic subsite. In glottic SCCs, the most frequent sites of occult nodal disease are the paratracheal nodal basins.

Although multifocal tumors and non-invasive/invasive components are commonly encountered in surgical pathology, their genetic relationship is often poorly characterized. We used next generation sequencing (NGS) to characterize somatic alterations in a patient with five spatially distinct, high grade papillary urothelial carcinomas (UC), with one tumor harboring an underlying invasive component. NGS of 409 cancer related genes was performed on DNA isolated from formalin fixed paraffin embedded (FFPE) blocks representing each papillary tumor (n=5), the invasive component of one tumor, and matched normal tissue. We identified 9 unique non-synonymous somatic mutations across the six UC samples, including five present in each carcinoma sample, consistent with clonal origin and limited intertumoral heterogeneity. Copy number and loss of heterogeneity (LOH) profiles were similar in all six carcinomas; however, the invasive carcinoma component uniquely showed focal CDKN2A loss and chromosome 9 LOH, and did not harbor gains of chromosomes 5p or X that were present in the other tumor samples. Phylogenetic analysis supported the invasive component arising from a shared progenitor prior to the outgrowth of cells in the non-invasive tumors. Results were extended to three additional cases of upper tract UC with paired non-invasive/ invasive components, which identified driving alterations exclusive to both non-invasive and invasive components. Lastly, we performed targeted RNAseq using a custom bladder cancer panel, which confirmed gene expression signature differences between paired non-invasive/invasive components. The results and approaches presented here may be useful in understanding the clonal relationships in multifocal cancers or paired non-invasive/invasive components from routine FFPE specimens.