摘要:

AbstractGranulocyte‐macrophage colony‐stimulating factor (GM‐CSF) has emerged as an important regulation for hematopoietic cell development and function. Within the myeloid lineages, GM‐CSF serves as a growth and developmental factor for intermediate‐stage progenitors between early, interleukin 3‐responsive and late granulocyte colony‐stimulating factor‐responsive precursors. GM‐CSF also serves as an activator of circulating effector cells. The ability of GM‐CSF to induce monocyte expression of tumor necrosis factor, interleukin 1 and other factors, further ties this hormone into a network of cytokines that interact to regulate many hematologic and immunologic responses. The availability of large quantities of recombinant GM‐CSF now provides the opportunity and challenge not only for unraveling the mechanisms regulating hematopoiesis, but also for developing new therapies for enhancement of host defense against infection that were no

ISSN:0737-1454    

DOI:10.1002/stem.5530060602

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

摘要:

AbstractA total of 199 solid human tumors were tested with a rapid thymidine incorporation assay for sensitivity to one of several clinically used multi‐drug combinations and to each agent in the combination separately. Melanomas, lung and breast cancers accounted for the majority of specimens. In 120 specimens, at least one single agent exhibited in vitro activity (80% or greater inhibition of thymidine incorporation), and in 116 of these (96.7%) the drug combination was active in vitro. In the 79 specimens where no single agent was active in vitro, the combination was also inactive in 62 (78.5%). Overall, there was concordance of in vitro activity of the most active single agent and the combination of agents in 89.5% of specimens tested. A lack of significant in vitro synergy was noted in all of the drug combinations and tumor types tested. Of note is the fact that in 141 of the 199 tests (70.9%) either no drug (n = 79) or only 1 drug (n = 62) demonstrated in vitro activity. We conclude that the rapid thymidine incorporation assay can be used to test for in vitro sensitivity to drug combinations, and that sensitivity to a drug combination can be inferred if a tumor is sensitive to any component drug of the combinatio

ISSN:0737-1454    

DOI:10.1002/stem.5530060603

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

摘要:

AbstractTwo assays based on the inhibition of3H‐thymidine incorporation into DNA were used to measure either the antimetabolic or the antiproliferative effects of anticancer drugs. A direct comparison of the two assays was made with cell suspensions obtained from 11 ovarian cancers and 22 malignant melanomas. Drugs with different effects on cell cycle phases were tested by both assays, for a total of 53 drug comparisons. When the sensitivity indices specific for each system was used, a significant association (p<0.01) was noted between the two assays. The agreement of both assays in defining in vitro sensitivity or resistance was 100% for ovarian cancer. For melanoma, 97% of samples resistant to the antimetabolic assay were also resistant to the antiproliferative assay; whereas, only 45% of samples sensitive to the antimetabolic assay were sensitive to the antiproliferative assa

ISSN:0737-1454    

DOI:10.1002/stem.5530060604

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

摘要:

AbstractThe growth of eosinophil progenitors (CFU‐Eo) and its modulation by hydrocortisone (HC), mononuclear cells, interleukin 1 (IL‐1), and interleukin 2 (IL‐2) in three cases of eosinophilia are reported in this paper. One m̈M HC decreased the proportion of CFU‐Eo in each of these three patients, and in each case, the addition of autologous mononuclear cells at a 1:1 ratio abrogated the effect of HC on CFU‐Eo. As studied in two of the three cases, IL‐1 and IL‐2 were able to prevent the effect of HC. Further studies showed no effect of HC when monocyte T cell‐depleted marrow cells were used as the target population. These results suggest that CFU‐Eo production in eosinophilic states is subject to modulation by HC

ISSN:0737-1454    

DOI:10.1002/stem.5530060605

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

摘要:

AbstractThe L‐428 cell line derived from nodular sclerosing Hodgkin's disease was verified to be a human female cell line with surface marker and morphologic characteristics similar to native Hodgkin's cells. Single cells were cloned and subcloned twice to determine the characteristics of the clonogenic L‐428 Hodgkin's cell (resulting in a 10% cloning efficiency). Both mononuclear L‐428 cells and classical Reed‐Sternberg cells arose from solitary cells. The clonogenic cell was the mononuclear Hodgkin's cell, although small abortive colonies sometimes arose from classical binucleate Reed‐Sternberg cells. Cytogenetic and phenotypic analysis supported the clonality of three subclones and indicated, among many findings, consistent abnormalities of the long arm of chromosome 7 (beta‐chain of the T cell receptor) and 14q32 (Ig heavy chain). Distinctive abnormalities of cytogenetics, phenotyping and transforming growth factor‐beta production were exhibited for each clone as well. These observations demonstrate the relationship of the continuum of malignant mononuclear and multinuclear Reed‐Sternberg cells in this cell culture from nodular sclerosing Hodgkin's disease and suggest that a similar relationship exists in native Hodgkin's disease tissue. These observations also support the theory of clonality in Hodgkin's disease and suggest that in vivo contiguous metastasis in the L‐428 Hodgkin's disease patient was most likely accomplished by a Ki‐1 positive sma

ISSN:0737-1454    

DOI:10.1002/stem.5530060606

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

ISSN:0737-1454    

DOI:10.1002/stem.5530060607

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

ISSN:0737-1454    

DOI:10.1002/stem.5530060608

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

ISSN:0737-1454    

DOI:10.1002/stem.5530060609

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

ISSN:0737-1454    

DOI:10.1002/stem.5530060601

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY