Predictive value of nodal maximum standardized uptake value of pretreatment [18F]fluorodeoxyglucose positron emission tomography imaging in patients with esophageal cancer.

We retrospectively reviewed 102 patients with esophageal cancer (97.1% squamous cell carcinoma, 96.1% stage III) received FDG-PET staging and were treated by chemoradiotherapy with or without resection to assess whether the pretreatment [18F]fluorodeoxyglucose positron emission tomography (FDG-PET) maximum standardized uptake value (SUVmax) of the primary tumor and metastatic lymph nodes can predict the prognosis of patients with esophageal cancer. Receiver operating characteristic analysis was performed to find the cutoff values for primary tumor SUVmax and nodal SUVmax. The influence of clinical factors including primary tumor SUVmax and nodal SUVmax on local progression-free survival, nodal progression-free survival (NPFS), distant metastases-free survival (DMFS), and overall survival (OS) were evaluated using univariate and multivariate analyses. A total of 40 patients received esophagectomy after neoadjuvant chemoradiotherapy (trimodality), while 62 patients received definitive chemoradiotherapy (dCRT). The median follow-up was 26.4 months. The SUVmax of primary tumor had no significant predictive value on all outcomes, while the SUVmax of metastatic lymph nodes had predictive value on several outcomes. High nodal SUVmax (≥7) predicted for worse outcomes than low nodal SUVmax (<7) in the patients who received dCRT (two-year DMFS, 17% vs. 92%, P < 0.001; NPFS, 14% vs. 81%, P = 0.001; OS, 21% vs. 50%, P = 0.003), but not in those received trimodality. On multivariate analysis of patients receiving dCRT, nodal SUVmax was the strongest independent predictor on DMFS (hazard ratio [HR] 13.93, P < 0.001), NPFS (HR 3.99, P = 0.026), PFS (HR 2.90, P = 0.003), and OS (HR 3.80, P = 0.001). High pretreatment nodal SUVmax predicts worse treatment outcomes for the patients treated with dCRT.

Prediction of marrow graft rejection by the lymphocyte-mediated cytotoxicity and antibody-dependent cell-mediated cytotoxicity assays.

We previously reported on 26 patients with severe aplastic anemia who were studied using the lymphocyte-mediated cytotoxicity (LMC) and antibody-dependent cell-mediated cytotoxicity (ADCC) assays. Eighty-one additional patients have now been studied. Overall, lymphocytes of 47% of the patients in LMC and sera of 30% in ADCC were reactive against the lymphocytes of HLA-identical siblings. LMC reactivity was more frequent in patients studied less than 1 month after diagnosis, but the frequency of ADCC reactivity was unrelated to time after diagnosis. In patients receiving the basic cyclophosphamide (CY) regimen, LMC results correlated with rejection in patients receiving transplants greater than or equal to 1 month after diagnosis but not in patients receiving transplants less than 1 month after diagnosis. Reactivity in ADCC correlated with graft rejection regardless of the time between diagnosis and study. No correlation between results of either assay and graft outcome was found in patients who received conditioning regimens aimed at abrogating rejection including total body irradiation or addition of donor buffy coat cells to the marrow inoculum. The finding of reactivity in the LMC assay early after diagnosis and in 8 or 15 untransfused patients indicates that mechanisms in addition to transfusion-induced sensitization must be involved in LMC reactivity. This LMC reactivity may be an epiphenomenon secondary to the stem cell defect of aplastic anemia. Alternatively, this LMC reactivity may be involved in the etiology of aplastic anemia.

Autoimmune and alloimmune phenomena in patients with aplastic anemia: cytotoxicity against autologous lymphocytes and lymphocytes from HLA identical siblings.

We have studied peripheral blood lymphocytes of 117 patients with severe aplastic anemia and 237 healthy individuals for reactivity against autologous lymphocytes and/or lymphocytes from HLA-identical siblings using a 51Cr release assay. Lymphocytes from 29% of the patients exhibited reactivity against their own lymphocytes, while only 3% of lymphocytes from normal individuals showed such reactivity. Lymphocytes from 49% of the patients showed reactivity against lymphocytes from their HLA-identical siblings compared to 4% of normal individuals. Correlation existed between allogeneic and autologous reactivities (p < 0.001), suggesting a common pathway for cytotoxicity. Both reactivities showed an association with extremely low granulocyte counts (p < 0.01) and an inability of the patient's mononulcear cells to stimulate in allogeneic mixed leukocyte culture (p < 0.05) as well as an inverse correlation with time from diagnosis (p < 0.001). At least two explanations exist for the transfusion-independent autologous and allogeneic cytotoxicities: (1) they could be epiphenomena secondary to the stem cell defect, such as the loss of a cell that suppresses (or regulates) naturally occurring cytotoxic cells, or (2) they may be involved in the cause of the disease.