Biomedical subjects
Publications and source records attributed to E Perlin.
Considerable morbidity and mortality occur among the elderly every year in the United States as a result of falls. Assessing the risk of falling with use of thorough history taking, physical examination, and special tests of balance and gait allows physicians to make specific safety recommendations.
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Osteogenic sarcoma of the mandible is a rare tumor, comprising less than 0.5% of all head and neck tumors, and, even in large institutions, the experience in management of such tumors is limited. Current therapy for osteogenic sarcoma of the long bones is based on a more extensive experience in large centers and includes a major role for chemotherapy. We report two cases of osteogenic sarcoma of the mandible that were treated by combined chemotherapy, radiation therapy, and surgery. The expected disease-free survival of patients with this disease, treated by surgery alone, would have been less then 50% in the first year. The survival of these two consecutive patients for more than one year, free of disease, is significant and encourages further use of this type of treatment.
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A prospective randomized trial was conducted comparing the clinical response of 78 previously untreated patients with advanced metastatic breast cancer to a combination of cyclophosphamide, methotrexate, and 5-fluorouracil (CMF) or to a combination of cyclophosphamide, adriamycin, and 5-fluorouracil (CAF). Sixty-two percent of the patients receiving CMF responded to treatment compared to an 82% response rate for the patients receiving CAF. Although within acceptable limits, hematologic and GI toxicity was greater with CAF. There was no significant difference in the duration of response to the two regimens. Therefore, the therapeutic difference between the two therapies is a higher initial response rate to the adriamycin containing regimen.
Acute lymphoblastic leukemia was observed in a 22-year-old white female patient and was manifested by normal palelet counts, 50--60% hand mirror cells (HMC) in the bone marrow, and prolonged survival without treatment. The characteristic neoplastic cell had a nucleus within the "mirror" portion and a cytoplasmic uropod forming the "handle" portion. The presence of acid phosphatase and beta-glucuronidase activity suggested that the cell was a T cell lymphoblast. However, extensive immunologic surface marker studies indicated the cells were non-T, non-B. Terminal transferase activity further supported the lymphoid nature of the cell. The hand mirrow cells were considered a real phenomenon since they were demonstrated on phase contrast microscopy, scanning electron microscopy, and transmission electron microscopy. The cells did not grow in tissue culture and cytogenetics revealed a normal female karyotype. From the above observations, the HMC is a lymphoblast with morphological, cytochemical, and immunological features which may differentiate it from the usual cell in acute lymphoblastic leukemia. Therefore, cases involving increased numbers of hand mirror cells in the bone marrow and acute lymphoblastic leukemia require further investigation to elucidate the full importance of this cell. This study represents the first attempt to investigate this cell in detail.
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The leukocyte adherence inhibition (LAI) assay was utilized as a test for cellular immunity to Epstein-Barr virus (EBV) antigens in 22 patients with infectious mononucleosis (IM), 47 patients with lymphoma, 101 carcinoma patients, and 84 subjects without cancer. Response to EB virion ("v") antigen was generally present at the time of diagnosis in the IM patients but the response to EB soluble ("S") antigen was delayed. An increased CMI response to "v" antigen was found in patients with IM, Hodgkin's disease and non-Hodgkin's lymphoma as compared to controls with and without cancer. Patients with Hodgkin's disease had depressed responses to the EBV-associated "S" antigen. The finding of increased LAI responses to "v" antigen in Hodgkin's disease patients with high EBV antibody titers conflicts with previous reports attributing high antibody responses against EBV to a generalized depressed cell-mediated immunity.
The use of antineoplastic agents is rapidly increasing. A general classification of these drugs and their mechanisms of action is presented. Many of the drugs have an adverse effect on oral tissue, and the practicing dentist today must be well acquainted with these effects. A discussion of the features of these reactions and their management is presented.
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Lymphocyte proliferation assays with autologous tumor material in mixed leukocyte-tumor interactions (MLTI) were employed to monitor tumor-associated cell-mediated immune responses of peripheral blood lymphocytes from patients with carcinoma of the breast. In addition, leukocyte migration inhibition (LMI) assays were employed to compare reactivity to autologous breast-tumor extracts versus allogeneic breast-tumor extracts. Positive lymphoproliferative responses to tumor-associated antigens (TAA) were observed in the MLTI assay with the use of either intact autologous tumor cells or crude extracts (in mug and ng quantities) in 12 of 34 (35%) breast cancer patients studied. Positive reactivity to tumor, but not to normal tissue of reactive patients, was observed in repeated assays. Finally, patients demonstrating positive MLTI responses to autologous tumor extracts likewise responded in LMI assays to these same autologus extracts as well as to allogeneic breast-tumor extracts, but not to non-breast-tumor extracts. Thus breast tumors appeared to possess common TAA among both male and female patients.
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A phase 1 to 2 evaluation of a combination of adriamycin (ADR) and dibromodulcitol (DBD) was performed in patients with progressive, metastatic breast carcinoma. All but one patient had been treated previously with chemotherapy. ADR was given on Day 1 or Days 1 and 8, and DBD was given on Days 1 to 10 of each 21- to 28-day treatment cycle. Side effects were evaluable in 54 patients, and 50 patients were evaluable for therapeutic response. The dose-limiting toxicities were leukopenia and thrombocytopenia. The severity of both toxicities increased as both the ADR and DBD doses increased; however, the effect of increases in DBD dose was much more profound. The mean white blood cell count and platelet nadirs occurred, respectively, on Days 15.3 and 15.9; both nadirs were delayed for 0.6 day by each 30-mg/sq m/day increase in the DBD dose and delayed for 1.7 to 3.9 days using the Day 1, 8 rather than the Day 1 ADR schedule Recovery of the peripheral counts by Day 29 was prolonged by the Day 1, 8 ADR schedule and by increasing the DBD dose. A tolerable dose schedule for previously treated patients was considered to be ADR, 40 mg/sq m on Day 1, and DBD, 135 mg/sq m on Days 1 to 10 repeated every 28 days. Responses were observed in 46% (23 of 50) of the patients. There were 1 complete remission, 19 partial remissions, and 3 improvements. Thirteen patients showed no change and 14 developed progressive disease. There were responses in 13 of 37 (36%) with visceral dominant disease as compared to 7 of 8 (87%) with osseous and 3 of 5 (60%) with soft tissue-dominant disease. There were 22 of 48 (46%) responses in patients previously exposed to alkylating agent therapy. Twnety-two patients had responded and 19 had failed to respond to prior alkylating agent-containing regimens; the response rates to DBD in these groups were respectively, 45 and 42%. The median time to remission was 29 days. The median time to therapeutic failure was 5.1 months for responders, 2.3 months for patients with no change, and 29 days for progressors. The combination of ADR and DBD appears to be an active and well-tolerated program in patients with previously treated metastatic breast carcinoma.
One hundred and seven patients with carcinoma of the lung underwent immunologic testing, and 62 of these patients were randomized to an immunotherapy protocol comparing the effects of Pasteur strain BCG, either alone or combined with allogeneic tumor cells, to the effects of no immunotherapy. Patients with residual disease left at the time of surgery or with metastatic disease at the time of diagnosis showed no increase in survival as a result of this form of immunotherapy. An insufficient number of patients with less advanced disease, in whom we would expect the most beneficial effect, have been entered in this study. In general, we were unable to document substantial effects of immunotherapy on the immunologic parameters tested. Only in recall antigen skin testing was there a statistically significant increase in reactivity in the immunotherapy groups. Tests of general immune status appeared to have a predictive value in monitoring lung cancer patients. Anergic patients had a poorer prognosis than did patients who demonstrated skin test reactivity. Patients with normal percentages of lymphocytes (T cells) forming rosettes with sheep erythrocytes at 29 degrees C were generally normal in other tests of immune competence. In serial studies of rosette formation, all patients who developed recurrent disease had a pattern of depressed or falling rosette values, and these abnormalities occurred an average of 3.1 months prior to clinical detection of recurrence. Patients with large-cell anaplastic carcinoma were found to have a significantly higher incidence of depressed rosette levels than the other histologic types. Both large and small-cell anaplastic patients had significantly depressed lymphocyte proliferation by mitogens and allogeneic cells. Although lung cancer patients have been described as immunologically depressed, they are capable of recognizing tumor-associated antigens. When tested in leukocyte migration inhibition assays with tumor-associated antigens, the majority of the patients in our study were found to be reactive. The use of a 3 M KCl extract of pleural effusion cells from a patient with pulmonary adenocarcinoma has given good reactivity and specificity in lung cancer patients of all histologic types. In addition, these patients have been shown to respond in a mixed lymphocyte/tumor interaction to tumor-associated antigens (Dean, 1976b).
Quantitative serial serum measurements of human chorionic gonadotropin (hCG) and alpha-fetoprotein (AFP) levels using sensitive double-antibody radioimmunoassays were performed in nine patients with germinal cell tumors before and during treatment. The sera of eight of the nine were found to have a hCG marker and five of the nine an AFP marker. The sera of four patients were found to have both. Serial serum levels of hCG, of AFP, or both were useful for monitoring disease activity during therapy in all nine patients. In two patients tumor masses failed to diminish during chemotherapy, but the tumor markers fell appropriately. At surgery one patient had a mature teratoma, the other a mature teratoma with a microscopic focus of an embryonal cell tumor. In one patient tumor reactivation was reflected by the emergence of only one of two previously elevated tumor markers. One patient had a rise in hCG, another a rise in both markers coincident with recurrence of tumor. Serial measurements of AFP and hCG are useful for following the response to therapy of germinal tumors, and can assist in making therapeutic decisions.
Receptor sites for a group of four steroid hormones were estimated by competitive binding assay of a biopsy specimen of carcinoma from a male breast. The results indicate that the tissue contained a significant number of binding sites for 17beta estradiol, and probably for dihydrotestosterone and progesterone, but not for testosterone. These preliminary data suggest that, as in the female, certain mammary carcinomas in the male may be under the influence of steroid hormones. Correlation of such data with responses to therapy may help to establish a more rational approach to the treatment of carcinoma of the male breast.