B-cell populations are expanded in breast cancer patients compared with healthy controls.

BACKGROUND: Historically, humoral immunity was considered unimportant in anti-tumor immunity, and the differentiation and anti-tumor activity of B cells in breast cancer are poorly understood. However, it was recently discovered that B cells participate in tumor immunity through both antibody production and immunosuppressive mechanisms. We analyzed the expression of B-cell differentiation markers in detail using fluorescence-activated cell sorting to investigate the relationship between B-cell subsets and breast cancer etiology. METHODS: Blood samples were taken from breast cancer patients and healthy donors, and peripheral blood mononuclear cells were collected. B cells at various stages of differentiation were identified by the expression of combinations of the cell surface markers CD5, CD19, CD21, CD24, CD27, CD38, CD45, and IgD. Statistical analysis of the proportions of each B-cell subtype in the different patient groups was then performed. RESULTS: Twenty-seven breast cancer patients and 12 controls were considered. The proportion of total B cells was significantly higher in cancer patients than in controls (11.51 ± 2.059 vs 8.905 ± 0.379%, respectively; p = 0.001). Breast cancer patients were then classified as High-B or Low-B for further analysis. A significantly higher proportion of memory B cells was found in the High-B group than in the Low-B or control groups (p = 0.003 and p = 0.043, respectively). CONCLUSIONS: Breast cancer patients generally have a higher proportion of B cells than healthy controls, but this is highly variable. Analysis of the major B-cell surface markers indicates that memory B cells in particular are significantly expanded, or more robust, in breast cancer patients.

Small Intestinal Metastasis from Esophageal Squamous Cell Carcinoma Presenting with Perforated Peritonitis.

Metastatic tumors of the small intestinal tract from extra-abdominal sites are rare. We report herein a rare case of small intestinal metastasis from esophageal carcinoma that presented with perforated peritonitis. A 71-year-old man with dysphagia was referred to our hospital for further examination and treatment, and was diagnosed with type 3 advanced esophageal squamous cell carcinoma of the lower thoracic esophagus. Based on a diagnosis of Stage II cancer, a radical esophagectomy with three-field lymph node dissection was performed after neoadjuvant chemotherapy composed of 5-fluorouracil plus cisplatin. Pathological examination of the resected specimen revealed a moderately differentiated squamous cell carcinoma, extending into the adventitia with lymph node metastasis (T3, N2, M0, Stage III). During postoperative adjuvant chemotherapy, the patient complained of abdominal pain and was found to have perforated peritonitis. Emergency laparotomy was performed. A jejunal perforation with a submucosal nodule approximately 80 cm distal from the ligament of Treitz was detected, and completely resected by jejunal partial resection. Histopathology of the specimen showed a perforation of the small intestine due to metastasis of esophageal squamous cell carcinoma with mesenteric lymph node metastasis. The patient died of cancer 9 months after surgery. An extremely rare case of small intestinal metastasis from esophageal carcinoma presenting with perforated peritonitis was described.

Antitumor effect of new HER2 peptide vaccination based on B cell epitope.

BACKGROUND: While the benefit of passive immunotherapy is commonly accepted, active immunization may have advantages for the patient's quality of life. We identified a new epitope of Mab CH401 against Her-2/neu extracellular domain (N: 167-175), and evaluated the effect of active immunization of the 20mer peptide containing the epitope (CH401 peptide). MATERIALS AND METHODS: Epitope-mapping was performed using ELISA with Her-2/neu-related multiple antigen peptides (MAP). BALB/c mice were transplanted with Her-2/neu-expressing lymphoma cell line and immunized with the peptides. For monitoring the condition, ELISA and flow cytometry was performed. RESULTS: CH401 peptide induced Her-2/neu-specific IgG antibody. Tumor growth in immunized mice was suppressed and tumor-infiltrating lymphocytes comprised more CD8(+) T-cells, which secreted larger amounts of interleukin-2 after the peptide re-stimulation. CONCLUSION: The new Her-2/neu peptide contained epitopes for CD4(+) and CD8(+) T-cells, which contributes to the suppressive effect on Her-2/neu-expressing tumor cell growth.