Upper aerodigestive tract squamous cell carcinoma: distribution of extracapsular spread and soft tissue deposits in the neck.

OBJECTIVE: Extracapsular spread (ECS) and soft tissue deposits (STD) of squamous cell carcinoma (SCC) in the neck of patients with metastatic SCC of the upper aerodigestive tract have been shown to adversely affect actuarial and disease-free survival. No studies to date have detailed the distribution of ECS and STD within the neck. MATERIAL AND METHODS: A total of 215 neck dissections from 155 patients were prospectively collected and analysed for the presence of both STD and ECS. As no classification for STD exists, their distribution was classified according to the nodal levels used for classification of cervical lymph nodes as described by the Memorial Sloan-Kettering Cancer Center. RESULTS: A total of 81 neck dissections from 59 patients were found to have either metastatic lymph nodes with ECS, STD or both. The distribution of lymph node metastasis, ECS and STD was very similar. Level II was most frequently affected, with Levels III and IV being affected less frequently. There were very few lymph node metastases to Level V, and this level contained no evidence of either ECS or STD. CONCLUSION: The method of pathological assessment of neck dissection specimens and reporting on the presence of ECS and STD has not been formalized. By analysing neck dissection specimens in the manner described we can report on the presence or absence of ECS and STD with increased accuracy. This has considerable implications for patient management.

Lymphodepletion in the ApcMin/+ mouse model of intestinal tumorigenesis.

Germ line mutations in the Adenomatous polyposis coli tumor suppressor gene cause a hereditary form of intestinal tumorigenesis in both mice and man. Here we show that in Apc(Min/+) mice, which carry a heterozygous germ line mutation at codon 850 of Apc, there is progressive loss of immature and mature thymocytes from approximately 80 days of age with complete regression of the thymus by 120 days. In addition, Apc(Min/+) mice show parallel depletion of splenic natural killer (NK) cells, immature B cells, and B progenitor cells in bone marrow due to complete loss of interleukin 7 (IL-7)-dependent B-cell progenitors. Using bone marrow transplantation experiments into wild-type recipients, we have shown that the capacity of transplanted Apc(Min/+) bone marrow cells for T- and B-cell development appears normal. In contrast, although the Apc(Min/+) bone marrow microenvironment supported short-term reconstitution with wild-type bone marrow, Apc(Min/+) animals that received transplants subsequently underwent lymphodepletion. Fibroblast colony-forming unit (CFU-F) colony assays revealed a significant reduction in colony-forming mesenchymal progenitor cells in the bone marrow of Apc(Min/+) mice compared with wild-type animals prior to the onset of lymphodepletion. This suggests that an altered bone marrow microenvironment may account for the selective lymphocyte depletion observed in this model of familial adenomatous polyposis.