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Biomedical subjects

B Drewinko

Publications and source records attributed to B Drewinko.

At least 127 records · Page 7Linked to original sources
PubMed1977

Tumor growth patterns in multiple myeloma.

Serial changes in tumor mass were evaluated in 61 patients with multiple myeloma who had received intermittent courses of melphalan-prednisone until death. The variations in the kinetics of tumor reduction and relapse could be explained by a mathematical model based on two cell populations, one sensitive to and one resistant to chemotherapy. For all responding patients, the median tumor halving-time was 1.3 months and the median doubling time was 2.9 months. The duration of a constant tumor mass during remission was brief in most patients. A larger fraction of resistant cells prior to therapy was associated with a slower tumor doubling-time during relapse. With a constant fractional reduction of sensitive cells and a tumor halving-time of one month or less, all cells sensitive to alkylating agents would be eliminated with 3 years of uninterrupted intermittent therapy.

Cell Division↗
PubMed1977

Computerized hematology: operation of a high-volume hematology laboratory.

Operation of automated hematology testing, on-line to a laboratory-dedicated computer, is described. The computer stores, retrieves and monitors the results of two Model S Sr. Coulter Counters, three Technicon platelet counters, one Electra 600-D, and six leukocyte differential consoles, which are interphased to the computer. All other hematology tests are batch-entered via the keyboard of cathode-ray tubes. The computer generates specimen labels, worksheets, and lists of incomplete tests, monitors all on-line instruments, and performs all the calculations used in the procedures of quality control. Results are available instantaneously on cathod-ray tubes strategically located in patient-related areas throughout the institution. These can be obtained as all of the results for a given day or as cumulative summaries or histogram-type plots of results for a given day.

Autoanalysis↗
PubMed1977

Growth kinetics of plasma cell myeloma.

The plasma cell labeling index(ex) (LI) of 128 patients with multiple myeloma at various stages of disease was compared as a function of tumor mass load and length of treatment. No significant differences in LI were noted for patients with various degrees of tumor reduction. Patients observed during the first 3 months of treatment had significantly higher LI than did untreated patients and those studied after longer intervals. In vivo cell-cycle analysis of myeloma cells by the halving time of the grain-count method failed to establish the length of the cell cycle but defined the length of S+G2 phases as being longer than 60 hours. Similar studies conducted in vitro defined a shorter combined length of S+G2 phase. In 2 patients in whom continuous infusion with [3H] thymidine was performed, the generation time was established as 8 days. Both patients had similar initial LI (5.7 and 6.6) but different growth fractions (19 and 47%). The measured tumor mass doubling time was much longer than the calculated one, suggesting the presence of considerable intrinsic cell loss (83 and 47%). These observations were summarized by a hypothetical two-compartment model for the growth kinetics of multiple myeloma.

Bone Marrow↗
PubMed1977

Correlation of DNA distribution abnormalities with cytogenetic findings in human adult leukemia and lymphoma.

Pulse cytophotometric analysis of bone marrow cells from 175 patients with leukemia or lymphoma showed abnormalities of cellular DNA distribution in 29 patients for an overall incidence of 16.6 percent. Comparative standard cytogenetic examination indicated that high-degree chromosomal aberrations (less than or equal to 44, greater than or equal to 53 chromosomes) can generally be detected on DNA histograms, whereas patients with diploid, pseudodiploid, 45-hypodiploid, and 47-hyperdiploid abnormalities usually escape recognition by this technique. There were 11 patients with normal diploid or near-diploid karyotypes exhibiting marked DNA deviations; this discrepancy may reflect lack of proliferation of some leukemic clones which is a prerequisite for cytogenetic identification.

Adult↗
PubMed1977

Cellular response to treatment with 4-(3-(2-chloroethyl)-3-nitrosoureido)-cis-cyclohexanecarboxylic acid, a water-soluble nitrosourea derivative.

The lethal effects of 4-(3-(2-chloroethyl)-3-nitrosoureido)-cis-cyclohexanecarboxylic acid (cis-acid), a water-soluble nitrosourea derivative, were investigated on a human lymphoma cell line. The survival of asynchronous cells exposed to increasing concentrations of the drug was characterized by a threshold exponential curve (Do = 20 microgram/ml; Dq = 20 microgram/ml, 1 hour) similar to that of other nitrosourea derivatives. cis-Acid exerted its main killing effect on cells in early S and in late G2 phase. Cells in mid S and early G1 phase were tenfold more resistant. Changes in survival response as a function of cell cycle stage were reflected primarily by changes in the extent of the shoulder region of the survival curve. In contrast to other nitrosoureas, the lethal effectiveness of cis-acid in solution was stable and the drug could sterilize large numbers of cells in short periods of time. Another important major difference observed for cis-acid with respect to classic nitrosourea derivatives was the capacity of treated cells to recover from sublethal and potentially lethal damage. Our studies have shown that cis-acid is as effective in killing cultured human lymphoma cells as other nitrosoureas, but possibly with a mechanism different from that of these compounds. The major shortcoming noted for cis-acid, namely the capacity of treated cells to recover from drug-induced damage, is offset by the relatively long stability of its killing effect. This, and the fact that cis-acid can be administered in an aqueous solution, make this agent an appealing compound for clinical trials.

Antineoplastic Agents↗
PubMed1976

Identification and subcellular localization of a sarcoma-associated antigen(s) in a human cell line.

The present investigation was designed to demonstrate and identify the subcellular localization of sarcoma-associated antigen(s) (TAA) in an established human neurogenic sarcoma line (T cell line). Indirect immunofluorescence was used to screen sera from patients with sarcoma, nonsarcoma neoplasias, and from presumably normal blood bank donors. The positive sera were submitted to a series of absorptions to remove possible nonspecific cross-reacting antibodies. The target cells were then studied with electron microscopy, utilizing the indirect immunoperoxidase technique to determine the subcellular localization of the sarcoma-associated antigen(s). Findings indicate that sarcoma-bearing patients have circulating antisarcoma antibodies directed to antigen(s) localized at the surface membrane of T cells. These antibodies pertain to the IgM or IgG immunoglobulin class. The exact nature of the sarcoma-associated antigen(s) identified in this study is not known at the present time. However, the results obtained strongly suggest that these substances may represent a new type of tumor-associated antigen(s).

Antibodies, Neoplasm↗
PubMed1976

Inhibition of human lymphoma cell-line colony formation by lymphocytes from patients with lymphoma and cancer hospital employees.

Inhibition of human lymphoma cell-line colony formation (ICF) was induced by peripheral blood lymphocytes (PBL) from patients with lymphoma and apparently healthy cancer hospital personnel. PBL from patients with non-lymphoma neoplasms and from normal blood bank donors did not elicit ICF. ICF was most marked when PBL were cocultivated for 24 hours in a ratio of 1000:I with target lymphoma cells that had been cultured for 24 hours before exposure. No significant ICF was observed when target cells consisted of human neurogenic sarcoma, melanoma, colon adenocarcinoma, or Chinese hamster cells. It is possible that ICF is elicited by PBL sensitized to a cross-reacting antigen present on the membrane of cultured lymphoma cells. This antigen may be synthesized by a transmissible etiologic factor.

Adenocarcinoma↗
PubMed1976

Uptake of 1-beta-D-arabinofuranosylcytosine and prednisolone by synchronized human lymphoma cells.

The cytotoxicity of many antitumor agents exhibits cell-cycle phase specificity. Using a human lymphoma cell line synchronized by thymidine block, we have investigated the differential uptake of radioactive 1-beta-D-arabinofuranosylcytosine (ara-C) and prednisolone in various phases of the cycle. Uptake of ara-C is highest during early S and declines steadily throughout the rest of the cycle. In comparison, prednisolone demonstrates no significant age-dependent difference in uptake although its cytotoxicity is cell cycle sensitive.

Cell Division↗
PubMed1976

Comparison of the efficacies of closed trephine needle biopsy, aspirated paraffin-embedded clot section, and smear preparation in the diagnosis of bone-marrow involvement by lymphoma.

Bone marrow aspirates totaling 1,024 and trephine biopsies totaling 386 were obtained from 234 patients with various diagnoses of lymphoma. The study analyzed the morphologic patterns of bone-marrow involvement by each entity and compared the sensitivity of aspiration versus biopsy for detecting lymphomatous involvement of bone marrow. Lymphoma may appear in one of three forms: nodular, diffuse (packed bone marrow), and diffusely infiltrative. Trephine biopsy was superior to aspiration in most instances, especially for the nodular form. In some cases, however, examination of paraffin-embedded clot sections and smears was diagnostic of lymphoma whereas the biopsy section appeared negative.

Biopsy, Needle↗
PubMed1976

Survival and cycle-progression delay of human lymphoma cells in vitro exposed to VP-16-213.

The lethal and kinetic effects of VP-16-213 were analyzed in a human lymphoid cell line (T1 cells) in vitro. When asynchronous T1 cells were exposed to increasing concentrations of VP-16-213 for 1 hour, an exponential survival curve with a Do (mean lethal dose equal to the concentration required to reduce survival by 63% on the exponential part of the survival curve) of 3 mug/ml was obtained. Increasing exposure time also reduced survival exponentially. Synchronized cells showed age-dependent sensitivity to VP-16-213 with the greatest lethal damage experienced by cells treated in S and G2 phase. The major kinetic response of the T1 cells to VP-16-213 was a delay in G2 phase, the extent and duration of which was a function of drug concentration, exposure time, and cell cycle stage of drug addition; thus, cells in S phase were most effectively blocked in the subsequent G2 phase. Continuous treatment with concentrations of VP-16-213 (greater than 0.5 mug/ml for greater than 3 hours) caused a retardation of S-phase transit with prompt recovery after drug release. Treatment with 10.0 mug/ml for greater than 3 hours resulted in a "frozen state" of the whole life cycle, inducing only minor compartment changes. DNA synthesis was inhibited in the majority of cells with an S-phase DNA content. There was no correlation between the extent of perturbation and lethal effects after treatment with VP-16-213.

Cell Division↗
PubMed1976

Combination chemotherapy in vitro with cis-dichlorodiammineplatinum(II).

Cis-dichlorodiammineplatinum(II) (DDP) was paired with 11 other chemotherapeutic drugs in a search for possible synergistic pairs. Cell lethality was investigated by the colony-formation technique utilizing a long-term culture of human lymphoma cells. Synergistic effects were noted for pair combinations with all alkylating agents, bleomycin, adriamycin, camptothecin, and cytosine arabinoside. Additive effects were recorded for combinations with prednisolone and VP-16-213, while DDP reduced the capacity of cells to absorb sublethal damage induced by alkylating agents.

Alkylating Agents↗