{"title":"Approaches to investigating growth plate cartilage in the human chondrodysplasias.","authors":"W A Horton","doi":"10.1159/000157100","DOIUrl":"https://doi.org/10.1159/000157100","url":null,"abstract":"","PeriodicalId":77765,"journal":{"name":"Pathology and immunopathology research","volume":"7 1-2","pages":"85-9"},"PeriodicalIF":0.0,"publicationDate":"1988-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000157100","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14198267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Teratomas and allied germ cell tumors: common origin and diverging paths of differentiation.","authors":"C M Pesce, F S Carli","doi":"10.1159/000157117","DOIUrl":"https://doi.org/10.1159/000157117","url":null,"abstract":"","PeriodicalId":77765,"journal":{"name":"Pathology and immunopathology research","volume":"7 3","pages":"208-24"},"PeriodicalIF":0.0,"publicationDate":"1988-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000157117","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13985974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Adoptive therapies: quo vadis?","authors":"J W Clark, D L Longo","doi":"10.1159/000157074","DOIUrl":"https://doi.org/10.1159/000157074","url":null,"abstract":"<p><p>The success of adoptive immunotherapy using interleukin-2 (IL-2) and lymphokine-activated killer (LAK) cells in treating a percentage of patients with melanoma and renal cell carcinoma has provided impetus to research into both how to optimize this treatment as well as approaches into making immunotherapy in general more successful. As the question on how to optimize IL-2 dose, schedule, cell culture conditions, and other specifics of IL-2 plus LAK therapy are addressed in clinical trials, other approaches suggested by data from in vitro, animal, and the clinical studies using IL-2 are emerging into clinical trials. (table; see text) These include two major areas of focus at the present time: (1) the use of IL-2 +/- LAK in combination with a variety of agents which have been shown to be synergistic with it, including other biological response modifiers (such as interferons), agents which may act both as interferon inducers as well as by other mechanisms (poly-IC:LC and flavone-8-acetic acid), and chemotherapeutic agents (especially cyclophosphamide, doxorubicin and agents which have some activity against the disease being treated such as DTIC for melanoma), and (2) various approaches aimed at inducing and expanding tumor-specific immune cells which appear to have greater antitumor activity than LAK cells and which may be major contributors to the antitumor efficacy of IL-2 therapy. These approaches also have the potential benefit of inducing memory cells with a resultant long-term immune antitumor response. Approaches aimed at activating specific antitumor immune cells include the use of IL-2-expanded infiltrating lymphocytes from tumors, exposure of peripheral blood cells cultured in IL-2 to tumor cells to hopefully expand those with a specific antitumor response, and the use of tumor cell vaccines in conjunction with IL-2. In addition to approaches using activated and expanded LAK effectors or specific T cells, the potential role of activated (e.g. by gamma interferon) and expanded (e.g. by macrophage colony stimulating factor) macrophages in the adoptive immunotherapy of cancer remains an area of ongoing exploration both in preclinical studies and clinical trials. As a greater understanding of the antitumor mechanisms of IL-2 and LAK therapy and other forms of adoptive immunotherapy is achieved, therapeutic approaches can be defined which will maximize the ability to mediate the immune destruction of tumor cells.(ABSTRACT TRUNCATED AT 400 WORDS)</p>","PeriodicalId":77765,"journal":{"name":"Pathology and immunopathology research","volume":"7 6","pages":"442-58"},"PeriodicalIF":0.0,"publicationDate":"1988-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000157074","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14202315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Type II collagen deficiency in achondrogenesis (Langer-Saldino).","authors":"D R Eyre","doi":"10.1159/000157101","DOIUrl":"https://doi.org/10.1159/000157101","url":null,"abstract":"","PeriodicalId":77765,"journal":{"name":"Pathology and immunopathology research","volume":"7 1-2","pages":"90-4"},"PeriodicalIF":0.0,"publicationDate":"1988-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000157101","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14349614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
W A Horton, P F Goetinck, S M Sayedin, R R Minor, J Spranger, D L Rimoin, V A McKusick, D H Dayton
{"title":"New perspectives in the human chondrodysplasias.","authors":"W A Horton, P F Goetinck, S M Sayedin, R R Minor, J Spranger, D L Rimoin, V A McKusick, D H Dayton","doi":"10.1159/000157110","DOIUrl":"https://doi.org/10.1159/000157110","url":null,"abstract":"","PeriodicalId":77765,"journal":{"name":"Pathology and immunopathology research","volume":"7 1-2","pages":"146-8"},"PeriodicalIF":0.0,"publicationDate":"1988-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000157110","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14351445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
N R Rose, D A Neumann, A Herskowitz, M D Traystman, K W Beisel
{"title":"Genetics of susceptibility to viral myocarditis in mice.","authors":"N R Rose, D A Neumann, A Herskowitz, M D Traystman, K W Beisel","doi":"10.1159/000157122","DOIUrl":"https://doi.org/10.1159/000157122","url":null,"abstract":"","PeriodicalId":77765,"journal":{"name":"Pathology and immunopathology research","volume":"7 4","pages":"266-78"},"PeriodicalIF":0.0,"publicationDate":"1988-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000157122","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13990964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Immunosuppressive therapy in experimental and clinical myocarditis.","authors":"J B O'Connell, J W Mason","doi":"10.1159/000157124","DOIUrl":"https://doi.org/10.1159/000157124","url":null,"abstract":"","PeriodicalId":77765,"journal":{"name":"Pathology and immunopathology research","volume":"7 4","pages":"292-304"},"PeriodicalIF":0.0,"publicationDate":"1988-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000157124","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14202313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Animal models with chondrodysplasia/osteochondrodysplasia.","authors":"R R Minor, C E Farnum","doi":"10.1159/000157095","DOIUrl":"https://doi.org/10.1159/000157095","url":null,"abstract":"","PeriodicalId":77765,"journal":{"name":"Pathology and immunopathology research","volume":"7 1-2","pages":"62-7"},"PeriodicalIF":0.0,"publicationDate":"1988-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000157095","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14349611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Modulation and reexpression of the chondrocyte phenotype; mediation by cell shape and microfilament modification.","authors":"P D Benya","doi":"10.1159/000157093","DOIUrl":"https://doi.org/10.1159/000157093","url":null,"abstract":"","PeriodicalId":77765,"journal":{"name":"Pathology and immunopathology research","volume":"7 1-2","pages":"51-4"},"PeriodicalIF":0.0,"publicationDate":"1988-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000157093","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14351449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Flow cytometric analysis of normal B lymphoid development.","authors":"M R Loken, V O Shah, Z Hollander, C I Civin","doi":"10.1159/000157129","DOIUrl":"https://doi.org/10.1159/000157129","url":null,"abstract":"<p><p>Identification of the antigens expressed on marrow B lineage cells can be used to develop a model for the sequential acquisition of cell surface antigens during B lymphocyte development. The data suggest that the surface antigen expression is highly controlled during the development of B cells with the coordinated acquisition of multiple cell surface antigens during the maturational process. The developmental scheme in figure 6 is inferred from the expression of cell surface antigens on single samples. Confirmation of the progression from one stage to the next requires the isolation of a particular stage with subsequent induction to the next stage in-vitro. These data suggest that the development of B lymphoid cells may be discrete rather than continuous. The most immature cells identifiable in the bone marrow express CD34+ as well as HLA-DR. The earliest recognizable B lineage cells (CD19+, bright CD10+) also express CD34+. These cells are smaller by forward light scattering when compared to the cells which express only CD34+ (precursor of myeloid cells). Cells within stage I also express TdT in the nucleus and are proliferating. As the cells progress from stage I to stage II, the B lineage cells lose cell surface CD34 and nuclear TdT. At this time the density of HLA-DR and CD45 increases while the amount of CD10 decreases. These changes occur with no detectable change in cell size as assessed by forward light scattering. HLA-DP is first detected on the cells at this time. The progression of cells from stage II to stage III is marked by the acquisition of CD20, HLA-DQ, and sIgM. The amount of CD45 increases further in the transition between stage II and stage III. The acquisition CD21 and CD22 as well as the loss of CD10 distinguishes stage IV from stage III. Once the cellular composition of normal marrow has been defined, perturbations from homeostasis can be identified. Since marrow is the tissue most sensitive to injury by most antineoplastic chemotherapy and radiotherapy regimens, a means of quantifying the changes from the normal state can provide an assessment of the cytotoxic injury produced in individual patients. By monitoring the return to normal, it may be possible to more precisely individualize therapy for each patient. With a clear understanding of normal hematopoiesis, it should also be possible to identify maturational blocks which occur in hypoplastic marrow states. This may provide a means of identifying the regulatory points for each lineage and provide strategies for overcoming the inhibition of development.(ABSTRACT TRUNCATED AT 400 WORDS)</p>","PeriodicalId":77765,"journal":{"name":"Pathology and immunopathology research","volume":"7 5","pages":"357-70"},"PeriodicalIF":0.0,"publicationDate":"1988-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000157129","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14395320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}