bluuebunny/crossref_metadata_2025_split huggingface dataset:
Metastasis: Reticuloendothelial system and organ retention of disseminated malignant cells
Authors: Glaves Dorothy 
Published: February 2007

AbstractThe lung retention patterns of B16 melanoma cells were determined after intravenous injection of [125l]dUrd‐labelled tumor cells into B16 melanomabearing mice. Experiments were performed with mice undergoing acute or chronic reactions to bacterial endotoxin or zymosan, both of which were shown to modify the activity of the reticuloendothelial system as assessed by carbon clearance assays. On the one hand, the release of arrested melanoma cells from the lungs was retarded in mice with both endotoxin‐ and zymosaninduced acute inflammation. There was a parallel increase in the numbers of pulmonary tumor nodules which developed after injection of non‐radiolabelled melanoma cells into similarly treated groups of mice. On the other hand, fewer tumor cells were retained in the lungs of mice undergoing chronic responses to endotoxin, and fewer pulmonary tumor nodules subsequently arose after injection of unlabelled cells. However, in mice pre‐treated with zymosan, retention of melanoma cells was not different from that in controls and greatly increased numbers of pulmonary nodules grew in zymosan pre‐treated mice receiving nonradiolabelled cells. These experiments were discussed in terms of the contribution of the reticuloendothelial system to the release of arrested cancer cells from the pulmonary vasculature.
Establishment of a cell line (NPC/HK1) from a differentiated squamous carcinoma of the nasopharynx
Authors: Huang D. P. , Ho J. H. C. , Poon Y. F. , Chew E. C. , Saw D. , Lui M. , Li C. L. , Mak L. S. , Lai S. H. , Lau W. H. 
Published: February 2007

AbstractA long‐term cell culture epithelioid cell line was established from a recurrent squamous carcinoma of the nasopharynx of a Chinese male 17 1/2 years after radiation therapy. The cell line, designated NPC/HKI, has been passaged 72 times over a period of 1 year. The cells have been shown by light and electron microscopies to be of the squamous epithelial type. When they were transplanted subcutaneously into the back of athymic nude BALB/c (nu/nu) mice, tumors developed at the sites of inoculation, which on histological examination were shown to be well‐differentiated squamous carcinomas, similar in morphology to the recurrent human tumor from which they were derived. Karyotypic analysis of cells from the cell line demonstrates an aneuploid human type with a modal chromosome number of 74 with both numerical and structural aberrations. Viral particles or Epstein‐Barr viral nuclear antigen (EBNA) has not been demonstrated in the cells from the primary culture or several of the subcultures tested. The presence of EBNA in touch smears prepared from the biopsy tissue was inconclusive. Infection of the subcultured cells with EBV from P3HR1 and B95‐8 cells was unsuccessful.
Multiple cases of Burkitt's lymphoma and other neoplasms in families in the north mara district of Tanzania
Authors: Brubaker G. , Levin A. G. , Steel C. M. , Creasey G. , Cameron H. M. , Linsell C. A. , Smith P. G. 
Published: February 2007

AbstractIn an area of Tanzania in which Burkitt's lymphoma (BL) is endemic, five families are described in which multiple cases of BL were found or BL occurred with other neoplasms. The patients include two brothers and one half‐brother with BL, two brothers with BL, a woman with nasopharyngeal carcinoma (NPC) whose daughter had BL, a boy with BL whose sister developed chronic myelogenous leukaemia (CML), and a man with CML whose son developed BL. The two full‐sib pairs with BL is significantly more than would be expected to have arisen by chance and the association of BL with NPC and CML among close relatives is remarkable in view of the rarity of the last two neoplasms in the study area. It is suggested that genetic factors may be important in determining susceptibility to the three malignancies in this population, but the possibility that the clustering of cases within families may be due to local environmental factors cannot be excluded.
Membrane‐associated antigens on tumor cells from transitional‐cell carcinoma of the human urinary bladder. I. Immunological characterization by xenogeneic antisera
Authors: Schneider Michael U. , Troye Marita , Paulie Staffan , Perlmann Peter 
Published: February 2007

AbstractAn antiserum was raised in rabbits by immunization with a human tumor cell line, T‐24, derived from transitional cell carcinoma (TCC) of the urinary bladder. The specificity of the IgG fraction was assessed by antibody‐dependent cellular cytotoxicity (ADCC), using purified blood lymphocytes from healthy human donors as effector cells and seven human cell lines as target cells (T‐24 and two additional TCC‐lines, two normal urothelial lines, one colon carcinoma and one malignant melanoma). The IgG induced strong lysis of all seven target cell types. However, lysis of the five urothelial lines was significantly stronger than that of the control tumors. Conversely, antisera to either of the control tumors induced a significantly stronger lysis of the homologous tumors than of the urothelial cells. All antisera contained antibodies to fetal bovine serum but removal of these by absorption did not change the specificity of the ADCC reactions. When the anti T‐24 serum was exhaustively absorbed with glutaraldehyde‐fixed spleen homogenate, the cytotoxicity to the control tumor targets was abolished. Although absorption reduced the antibody titer of the IgG preparation, ADCC to the TCC targets remained at a high level. There was no difference in the degree of lysis of the three TCC targets. Lysis of the two target lines from normal urothelium was slightly lower than that of the tumor cells. The results indicate that the anti‐TCC serum contained antibodies to one or several antigens shared by five urothelial cell lines but not by the control tumors. Whether or not it also contained antibodies to TCC‐associated antigens remains to be established. The molecular basis for these findings will be given in the accompanying paper.
Plasma membrane‐associated antigens on tumor cells derived from transitional‐cell carcinoma of the human urinary bladder. II. Identification at the molecular level of plasma membrane‐associated antigens
Authors: Schneider Michael U. , Paulie Staffan , Troye Marita , Perlmann Peter 
Published: February 2007

AbstractThe surface proteins of seven human cell lines (three bladder carcinomas (TCC), two normal urothelial lines, one colon carcinoma, and one malignant melanoma) were labelled with 125I by the glucose oxidase‐lactoperoxidase technique. Plasma membranes of the cells were isolated and analysed by sodium dodecyl sulphate electrophoresis (SDS‐PAGE). When analysed under reducing conditions by staining with protein stain, ˜45 distinct membrane polypeptides were detected in all membrane preparations. Although the banding patterns for all cell lines were very similar, a 23 K and a 110 K band were only seen in the five unrothelial lines. When the same gels were analysed by autoradiography, between 13 and 17 bands were detected for each of the cell lines. However, in this case, analysis revealed individual and stable banding profiles for each. One 180 K band and one 100 K band were only seen in the auto‐radiographs of the two normal lines but not in those of the tumor membranes. Analysis under non‐reducing conditions gave similar results. The antigenicity of these surface components was analysed by incubating detergent extracts of surface‐iodinated cells with IgG from a rabbit anti‐TCC serum, absorbed with fetal bovine serum and bound to protein A (from Staphylococcus aureus) on a matrix of Sepharose 4B. Analysis of the eluates by autoradiography after SDS‐PAGE under reducing conditions showed that many of the labelled polypeptides were antigenic and shared by all seven cell lines. Analysis of eluates from IgG preparations, exhaustively absorbed with human spleen, revealed the presence of at least one antigenic 110 K polypeptide confined to the membrane of the urothelial cells. Preparation of a rabbit antiserum to this 110 K component, isolated from one of the TCC‐lines and tested by ADCC, indicated that this polypeptide constitutes an important surface antigen, present on urothelial cells of both TCC‐and normal origin but absent from the colon carcinoma and malignant melanoma used for control.
Long‐term experience with burkitt's lymphoma in uganda
Authors: Olweny Charles L. M. , Katongole‐Mbidde Edward , Otim David , Lwanga Stephen K. , Magrath Ian T. , Ziegler John L. 
Published: February 2007

AbstractThe cumulative results and long‐term follow‐up of all patients with Burkitt's lymphoma treated at the Uganda cancer Institute Kampala are reported. The annual admission rate is 29. The tumor patients commonly present with jaw swelling (72%), abdominal swelling (56%) and central nervous system involvement (30%). Complete response rate is achieved in a high proportion of patients (81 %). About 50% of these relapse, equal numbers relapsing before and after 3 months. The most important factor influencing remission duration and survival is disease stage. Other important factors are treatment protocols and, to a lesser extent, the type of relapse. Central nervous system relapse does not necessarily augur poor prognosis as second remissions and long‐term survival can be achieved with appropriate therapy. Presently 25% of all treated patients have survived free of disease well beyond 5 years.
NATURAL CELLULAR REACTIVITIES MEDIATED BY SPLENOCYTES FROM MICE BEARING THREE TYPES OF PRIMARY TUMOR
Authors: Ehrlich Rachel , Efrati Margalit , Bar‐Eyal Aviva , Wollberg Miriam , Schiby Ginette , Ran Maya , Wrrz Issac P. 
Published: February 2007

AbstractThe ability of splenocytes from mice bearing three types of primary tumor to lyse YAC‐l target cells (NK activity) and to inhibit [125l]dUrd incorporation ([125l]dUrd l‐l = cytostasis) into B16‐F10 target cells was compared to the ability of normal splenocytes to perform such activities. The tumor systems used were urethane‐induced lung adenomas in BALB/c mice, di‐methylbenzanthracene (DMBA)‐induced tumors in hormonally‐stimulated BALB/c mice and mammary tumors in force‐bred C3HeB mice. The two types of natural cellular reactivity in lung adenoma‐bearing mice were unaffected. The NK activity of mice bearing DMBA and forced‐breeding‐induced tumors was suppressed. The cytostatic ability of splenocytes from mice bearing DMBA‐induced tumors was significantly elevated. The spleens of mice bearing primary DMBA‐induced tumors contained cells able to suppress NK activity or to compete against target cells for NK cells.
Plasminogen activator synthesis accompanying chemical carcinogen‐induced in vitro transformation of syrian hamster and guinea‐pig fetal cells
Authors: Slsskin Enid E. , Weinstein I. Bernard , Evans Charles H. , Dipaolo Joseph A. 
Published: February 2007

AbstractThe production of the extracellular protease, plas‐minogen activator, in relationship to growth in semi‐solid medium and tumorigenicity has been studied in Syrian hamster embryo and strain 2 guinea‐pig embryo cell culture models of chemical carcinogenesis. Whereas normal hamster and guinea‐pig embryo cells had negligible levels of plasminogen activator, neoplastically transformed cells derived from cultures exposed to chemical carcinogens had high levels of plasminogen activator and grew as progressively enlarging colonies in soft agar. The development of plasminogen activator secretion in relation to neoplastic transformation was further studied in the guinea‐pig cells where the latent period between carcinogen exposure and neoplastic transformation ranged from 4 months to more than one year. The production of plasminogen activator in this system also exhibited a long latent period, and acquisition of extracellular plasminogen activator correlated temporally with growth in agar and tumorigenicity. Plasminogen activator and growth in semi‐solid agar in concert are useful markers for identification of neoplastic cells transformed in culture following exposure to a chemical carcinogen.
Induction of the EBV cycle in B‐lymphocyte‐derived lines is accompanied by increased natural killer (NK) sensitivity and the expression of EBV‐related antigen(s) detected by the ADCC reaction
Authors: Patarroyo Manuel , Blazar Beverly , Pearson Gary , Klein Eva , Klein George 
Published: February 2007

AbstractHuman B‐lymphocyte‐derived lines were forced to enter the EBV‐cycle by superinfection with the P3HR‐l substrain of EBV or sodium butyrate treatment. The induced cells were used as targets for natural killing (NK) and EBV‐specific, antibody‐dependent cellular cytotoxicity (ADCC). Two Burkitt lymphoma lines, Raji and Daudi, and one normal adult derived lymphoblastoid cell line, NAD‐7, were comparable in their ADCC‐sensitivity after induction, but only the Burkitt lymphoma‐derived lines showed a major increase in NK‐sensitivity. The superinfection‐induced membrane change, responsible for both NK and ADCC sensitivity, is an early function of the viral cycle, correlated with the appearance of early antigens (EA). Indirect evidence indicates that the NK and ADCC target sites are different but this problem requires further investigation. Sodium butyrate induced an increased NK sensitivity and EBV‐related ADCC sensitivity in the Burkitt lymphoma‐derived P3HR‐l line. Lymphocyte effectors from different donors showed great differences in their NK and ADCC activity. Optimal ADCC could be demonstrated with effectors that were intermediate in their NK‐activity.
Evidence of separate pathways for viral and chemical carcinogenesis in c3h/stwi mouse mammary glands
Authors: Smith Gilbert H. , Arthur Larry A. , Medina Daniel 
Published: February 2007

AbstractMammary tumors in mice may arise as the result of exogenous infection with the mouse mammary tumor virus [MMTV(S)], usually via the milk; by the action of endogenous MMTV genes which are transmitted genetically and are sometimes expressed as infectious virus [MMTV(L)]; or by the action of chemical carcinogens. We have examined the etiological relationship between chemical and virus in the induction of mammary cancer in C3H/StWi mice. Mammary tumors were induced with 7.12‐dimethylbenz(a)anthracene (DMBA) in virgin C3H/StWi mice infected with exogenous mouse mammary tumor virus (C3H/StMTV) and in uninfected C3H/StWi females. The percent tumor risk in females whose glands were infected with exogenous mouse mammary tumor virus [MMTV(S)] was not different from that of MMTV(S)‐negative, C3H/StWi mice following treatment with DMBA. This result suggested that there was no synergistic effect between the two carcinogens, exogenous MMTV and Dmba. All the tumors arising in DMBA‐treated C3H/StMTV virgins were positive for MMTV env gene product, gp52 and MMTV gag gene product, p27 by radioimmune competition assay. MMTV(S)‐induced hyperplastic alveolar nodules (HAN) were observed in 62 % of the untreated C3H/StMTV glands at 8 months of age. Therefore, MMTV(S) was present and active in the mammary gland during the experimental period but had no enhancing influence on the sensitivity of the gland to carcinogenesis by DMBA. Tumors appearing in DMBA‐treated C3H/StWi virgin females were also tested for MMTV gp52 and p27 antigens to determine the presence of endogenous MMTV gene activity. Only occasional C3H/StWi tumors were positive and in most of these, p27, but not gp52 was detected, suggesting non‐coordinate expression of these endogenous MMTV gene products. Both alveolar (HAN) and ductal hyperplasia (DH) were found in DMBA‐treated C3H/StMTV glands, whereas only DH were found in DMBA‐treated C3H/StWi mice. Nevertheless, the DMBA‐induced C3H/StMTV tumor histopathology was remarkably indistinguishable from that in tumors produced by DMBA in C3H/StWi mice, implying that in both groups, tumors arose primarily from the chemically‐induced mammary dysplasias. These data taken together appear to support the conclusion that DMBA and Mmtv follow separate pathways to the induction of cancer in the mouse mammary gland.
Regulation of natural killer activity in vivo. II. The effect of alcohol consumption on human peripheral blood natural killer activity
Authors: Saxena Queen B. , Mezey Esteban , Adler William H. 
Published: February 2007

AbstractNatural killer (NK) activity of human peripheral blood lymphocytes (HPBL) was studied in 32 alcoholics and 15 control subjects in a 4‐h chromium release assay using K562 tumor target cells. The natural killer activity of human peripheral blood lymphocytes in alcoholics was significantly higher than the level found in the control group. NK activity of PBL from alcoholics was still higher than that of similarly treated PBL from control subjects after carbonyl iron and magnet treatment, or after passage through a nylon wool column or after removal of cells rosetting with sheep erythrocytes. Changes in T cell, B cell or macrophage populations, therefore, are not the mechanism for increased NK activity in alcoholics.
Transformed and neoplastic phenotype: Reversibility during culture by cell density and cell shape
Authors: Brouty‐boye Danièle , Tucker Robert W. , Folkman Tudah 
Published: February 2007

AbstractThe ability of parental and transformed mouse C3H (10T1/2) cells to grow when held at a graded series of cell shapes (flat to round) was studied using substrata of decreasing adhesivity. The parental cells showed a decrease in growth when they reached the most rounded configurations. In contrast, transformed cells proliferated at the same rate regardless of cell shape. In addition, when transformed cells were serially passaged at low density on highly adhesive plastic, which maintained cells in a flat configuration, a reversion from the transformed phenotype to a non‐transformed phenotype occurred with the concomitant return of growth control by cell shape. However, when transformed cells were passaged at low density on a substratum which prevented cell spreading, the reversion to the parental phenotype did not occur and the cells escaped the growth control of cell shape and remained tumorigenic. Thus, in this cell system it appears that a change in cell configuration can dictate whether or not the transformed and neoplastic phenotype will be expressed.
Chromosome analyses of lymphoid cell lines derived from patients with chronic lymphocytic leukemia
Authors: Najfeld V. , Fialkow P. J. , Karande A. , Nilsson K. , Klein G. , Penfold G. 
Published: February 2007

AbstractTo study chromosome complements of chronic lymphocytic leukemia cells, six Epstein‐Barr virus‐transformed lymphoid lines were established from two patients with this disease who were heterozygous for the X‐chromosome‐linked enzyme glucose‐6‐phosphate de‐hydrogenase (G6PD). Immunoglobulin and G6PD were used as markers of the leukemic versus normal cell origin of the cell lines. The two lines, derived from putative normal cells, had no chromosomal changes. In contrast, chomosome abnormalities were found in each of the four cell lines of presumed leukemic cell origin. Although the chromosome aberrations are not as specific as the Philadelphia chromosome, there appears to be non‐random involvement in chronic lymphocytic leukemia of some chomosomes, such as the No. 12.
Cytotoxicity to tumor cells of monocytes from normal individuals and cancer patients
Authors: Gerrard Theresa L. , Terz Jose J. , Kaplan Alan M. 
Published: February 2007

AbstractThis study was aimed at characterizing the parameters which regulate human monocyte‐mediated cytotoxicity to tumor cells as well as characterizing the target cell specificity, kinetics, etc., of the cytotoxic mechanism. Normal human peripheral blood monocytes were cytotoxic to tumor cells in an in vitro assay, measuring release of [3H]thymidine from human target cells. Monocyte cytolysis was observed with several adherent tumor lines including T24, a bladder cancer line; LR, a melanoma line; and an SV40‐transformed W138 fibroblast line, with maximal cytolysis observed at 72 h. Lymphokines were not required to induce and only infrequently enhanced monocyte cytotoxicity. Prolonged exposure of monocytes to lymphokines or in vitro culturing of monocytes prior to lymphokine exposure did not alter the monocytes' response to lymphokine signals with respect to cytotoxicity. Lymphokines induced monocytes to exhibit enhanced spreading, suggesting that monocytes were susceptible to lymphokine signals but that the development of cytolytic function was independent of lymphokines. In contrast to the cytolysis of adherent tumor cells, monocytes were less effective in killing the non‐adherent lymphoid target cells K562, Raji, and CEM. Monocytes were selectively cytotoxic to tumor cells and generally did not kill normal human fibroblast cell lines or PHA‐stimulated lymphocytes. Monocytes from cancer patients exhibited normal cytotoxicity to several human tumor lines. Plasmas from some cancer patients were inhibitory to cytotoxicity mediated by both autologous monocytes and normal monocytes.
Non‐random duplication of chromosome 15 in murine T‐cell leukemias: Further studies on translocation heterozygotes
Authors: Wiener F. , Spira J. , Babonits M. , Haran‐Ghera N. , Klein G. 
Published: February 2007

AbstractFour combinations of translocation heterozygotes with cytogenetically distinct chromosomes 15 were used to investigate whether the T‐cell leukemia‐associated duplication of chromosome 15 is a non‐random or a random event. In leukemias of AKR X CBAT6T6 F1 (Group I) and C57BL X CBAT6T6 F1 (Group IV) crosses the duplication was non‐random, affecting the AKR‐derived chromosome 15 (Group I) and CBAT6T6‐derived T (14;15) 6 chromosome (Group IV), respectively. In contrast, in leukemias induced in CBA X CBA T6T6 F1 combinations (Group III) ‐ where both chromosomes 15 (normal and translocated) were CBA‐derived ‐ the duplication was random. Similarly, in the Rb6;15 X CBAT6T6 F1 cross (group II) the duplication of chromosome 15 appeared to be random. The results supported the hypothesis that the genetic content of chromosome 15 rather than its translocated state is decisive for the preferential duplication of this chromosome in T‐cell leukemogenesis. However, the genetic background of the strain from which chromosome 15 is derived may also influence the duplication pattern of individual tumors.
Inhibition of murine tumor growth and prostaglandin synthesis by indomethacin
Authors: Fulton Amy M. , Levy Julia G. 
Published: February 2007

AbstractInhibition of the growth of a transplantable methylcholanthrene‐induced tumor was achieved in mice by administering indomethacin or aspirin in the drinking water, these drugs having in common the ability to inhibit prostaglandin synthesis. Indomethacin was able to reduce the levels of prostaglandin E (PGE) in the tumor tissue. When tumors from these animals were cultured in vitro, the culture supernatant fluid from drug‐treated animals showed lower levels of PGE released into the media, but after several days in culture, tumor cells from indomethacin‐treated animals fully recovered their ability to produce PGE. The relative size of tumors in untreated animals was directly related to the amount of PGE activity present in these tumors.