Axillary lymph node recurrence of papillary thyroid microcarcinoma: report of a case.

We report a case of axillary lymph node recurrence of thyroid papillary microcarcinoma (PMC) in a 51-year-old woman who had undergone thyroidectomy with lymph node dissection 5 years earlier. We performed residual thyroid resection with cervical and bilateral axillary lymph node dissection, and pathological examination revealed well-differentiated papillary carcinoma, with partial poor differentiation. Postoperative radioiodine therapy was ineffective, and the patient died of systemic dissemination of the recurrence 8 months after her second operation. The positive cell rates of proliferating cell nuclear antigen and Ki-67 were clearly higher in the recurrent lymph nodes than in the primary thyroid tumor, suggesting increased cell proliferation in the recurrent lymph nodes. Thyroid papillary carcinoma rarely recurs in the axillary lymph nodes, but its possibility must be kept in mind, especially in patients with remarkable cervical lymph node metastasis and those who undergo extensive lymph node dissection.

Immunohistological study of cell cycle-related factors, oncogene expression, and cell proliferation in adenocarcinoma developed in Barrett's esophagus.

In addition to presenting clinicopathological findings in 3 patients with adenocarcinoma developed in Barrett's esophagus, we have investigated the expression of cell cycle-related factors, oncogenes and cell proliferation in normal squamous epithelium, specialized columnar epithelium (SCE) and adenocarcinoma in Barrett's esophagus, using immunohistological techniques. The expression of p21 in adenocarcinoma in Barrett's esophagus tended to be decreased in two mutated p53-strongly-positive patients and to be increased in one mutated p53-weakly-positive patient. Furthermore, mutated p53 was strongly expressed in the deep layer of the cancer, while p21 was expressed in the superficial layer of the cancer. Thus, mutated p53 was inversely correlated with p21 in adenocarcinoma in Barrett's esophagus. The mean positive cell rate (PR) of Ki-67 was 4% in normal squamous epithelium, 24.5% in the SCE, and 41.7% in the adenocarcinoma in Barrett's esophagus. The mean PR of proliferating cell nuclear antigen (PCNA) was 6% in normal squamous epithelium, 29.5% in the SCE, and 55% in the adenocarcinoma in Barrett's esophagus. Thus, the PR of Ki-67 and PCNA were clearly higher in the SCE in Barrett's esophagus than in normal squamous epithelium, indicating increased cell proliferation in the SCE in Barrett's esophagus. In conclusion, mutated p53 was inversely correlated with p21 in adenocarcinoma in Barrett's esophagus. p53 mutation and the expression of oncogenes such as c-erbB-2 and MDM2 were observed in the SCE in Barrett's esophagus, which showed higher cell proliferation than normal squamous epithelium, suggesting a high malignant potential of the SCE in Barrett's esophagus. We considered that it was important to carefully follow-up patients with Barrett's esophagus.