Quantifying smoking exposure, genomic correlates, and related risk of treatment failure in p16 + squamous cell carcinoma of the oropharynx

148 Background: Chemotherapy (CT), radiotherapy (RT), and chemoradiotherapy (CRT) are efficacious treatment options for esophageal squamous cell carcinoma (ESCC). However, local treatment failure remains a major problem. In this study, we applied endoscopic submucosal dissection (ESD) for the treatment of ESCC after local treatment failure with CT, RT, or CRT. The efficacy, safety, and feasibility of salvage ESD were assessed. Methods: Between 2008 and 2014, 611 patients underwent ESD for superficial ESCC in our hospital. Of them, 14 required salvage ESD: 7 for local treatment failure after CT, 4 after CRT, and 3 after RT. Each patient was treated with CT using 5-fluorouracil + cisplatin or RT, which consisted of >50 Gy of irradiation with or without concurrent CT. The following clinical findings were confirmed in all patients: no evidence of lymph node or distant metastasis after treatment, and an endoscopically resectable lesion. Results: The male to female ratio was 11:3 and the mean age was 64.9 (44-81) years. Clinical stages before treatment were T1b/T2/T3/T4 in 10/1/2/1, N0/1 in 7/7, and M0/1 in 13/1, respectively. The mean tumor size was 18.6 mm, and the mean procedure time was 45.7 min. En bloc resection was achieved in 100% of cases, and the R0 resection rate was 78.6%. Histopathological assessment of specimens taken at salvage ESD revealed that 6 lesions (42.9%) had invaded the submucosal layer and had been resected noncuratively because of a positive vertical margin (n = 2) or positive lymphovascular invasion (n = 5). No immediate or delayed complications, including major bleeding or perforation, and no ESD-related deaths occurred. At a mean follow-up period of 26.5 (range, 5–55) months, local recurrence had developed at the treatment site in 2 patient. Overall, 10 patients were still alive. The remaining 4 had developed lymph node metastasis, 2 of whom had died from it. Conclusions: Salvage ESD is an option for ESCC patients with local treatment failure after CT, RT, or CRT.

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Identification of a Prognostic Immune Signature for Esophageal Squamous Cell Carcinoma to Predict Survival and Inflammatory Landscapes

Frontiers in Cell and Developmental Biology ◽

10.3389/fcell.2020.580005 ◽

2020 ◽

Vol 8 ◽

Author(s):

Chaoqi Zhang ◽

Yuejun Luo ◽

Zhen Zhang ◽

Zhihui Zhang ◽

Guochao Zhang ◽

...

Keyword(s):

Squamous Cell Carcinoma ◽

T Cell ◽

Esophageal Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Lung Squamous Cell Carcinoma ◽

Immune Checkpoints ◽

Related Risk ◽

Public Data ◽

Independent Cohort

Immunotherapy has achieved success in the treatment of esophageal squamous cell carcinoma (ESCC). However, studies concerning immune phenotypes within the ESCC microenvironment and their relationship with prognostic outcomes are limited. We constructed and validated an individual immune-related risk signature for patients with ESCC. We collected 196 ESCC cases, including 119 samples from our previous public data (GSE53624) to use as a training set and an independent cohort with 77 quantitative real-time polymerase chain reaction (qRT-PCR) data, which we used for validation. Head and neck squamous cell carcinoma (HNSCC) and lung squamous cell carcinoma (LUSC) cohorts were also collected for validation. A least absolute shrinkage and selection operator (LASSO) model and a stepwise Cox proportional hazards regression model were used to construct the immune-specific signature. The potential mechanism and inflammatory landscapes of the signature were explored using bioinformatics and immunofluorescence assay methods. This signature predicted different prognoses in clinical subgroups and the independent cohort, as well as in patients with HNSCC and LUSC. Further exploration revealed that the signature was associated with specific inflammatory activities (activation of macrophages and T-cell signaling transduction). Additionally, high-risk patients exhibited distinctive immune checkpoints panel and higher regulatory T cell and fibroblast infiltration. This signature served as an independent prognostic factor in ESCC. This was the first applicable immune-related risk signature for ESCC. Our results furnished new hints of immune profiling of ESCC, which may provide some clues to further optimize associated cancer immunotherapies.

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