bluuebunny/crossref_metadata_2025_split huggingface dataset:
In vivo localization of anti‐osteogenic sarcoma 791T monoclonal antibody in osteogenic sarcoma xenografts
Authors: Pimm M. V. , Embleton M. J. , Perkins A. C. , Price M. R. , Robins R. A. , Robinson G. R. , Baldwin R. W. 
Published: February 2007

AbstractMonoclonal antibody 791T/36, (mouse IgG2b) to the human osteogenic sarcoma 791T was isolated from hybridoma supernatants or ascites fluid and labelled with radioiodine. Following injection into immuno‐deprived CBA mice with subcutaneous xenografts of human osteogenic sarcomas 791T, 788T and 20s, reactive antibody was detectable in the circulation and there was a preferential uptake into tumour tissue compared with muscle, bone or visceral organs. The tumour uptake of radioactivity correlated with the size of the xenograft, up to 20% of the total body counts being within the tumour. Autoradiography of tissue sections showed activity mainly within the subcapsular regions of the xenografts. There was no tumour localization of radio‐labelled normal IgG. Furthermore, with a colon carcinoma and a bladder carcinoma, both unreactive with the 791T/36 antibody, there was no localization of radiolabelled antibody in xenograft growths. With 791T/36 monoclonal antibody labelled with 131I localization into 791T xenografts could be visualized by whole‐body gamma scintigraphy with computerized 99mTc‐pertechnetate or 113mIn‐indium chloride‐labelled blood pool subtraction. These studies demonstrate the potential of monoclonal antibody to a human tumour for in vivo localization both for diagnostic purposes and as a carrier for therapeutic agents.
The characterization of non‐histone proteins whose amounts increase in chromatin from mouse hepatocarcinomas
Authors: Medvedev Zh. A. , Buchanan J. H. , Medvedeva M. N. , Crowne H. M. 
Published: February 2007

AbstractA fraction containing liver‐ and hepatoma‐specific nonhistone proteins has been isolated from the chromatin of mice. Amino acid analysis of this fraction shows that it contains 16 mol of glutamic acid, 10 mol aspartic acid, 7 mol of both arginine and lysine per 100 mol and contains no cysteine or tyrosine. The proteins in this fraction are strongly associated with DNA and are co‐extracted with histones from chromatin with 0.25 M HCI. In chromatin from age‐related hepatomas, the amount of this fraction increased six‐fold. This increase in concentration of these chromatin proteins may be associated with changes of chromatin structure necessary to initiate malignant growth in liver cells.
The role of differentiation in the suppression of tumorigenicity in human cell hybrids
Authors: Peehl Donna M. , Stanbridge Eric J. 
Published: February 2007

AbstractHeLax human keratinocyte hybrid cell populations behave like transformed cells in culture but do not form progressive tumors when inoculated into athymic nude mice. In this respect they behave like HeLa/fibroblast hybrids (Stanbridge et al., 1982). However, the small nodules that do form occasionally have the appearance of moderate to highly differentiated squamous‐cell carcinomas. These observations suggest that differentiation might be the signal suppressing growth of human hybrid cells in vivo. Differentiation occurs rapidly and is not sitespecific. Reconstitution of HeLa/keratinocyte hybrid cells in culture from differentiated nodules gave rise to a line of stem cells, capable of renewed proliferation and differentiation, and a line which lost the ability to differentiate and formed large, progressive tumors when reinjected. These tumors are anaplastic carcinomas that resemble tumors formed both by HeLa and tumorigenic segregant HeLa/fibroblast hybrid cells. Morphological evidence indicates that non‐tumorigenic HeLa/fibroblast hybrid cells also respond to differentiation signals, whereas the tumorigenic segregants do not. Furthermore, the non‐tumorigenic hybrid cells in the nude mouse take on the “phenotypic signature” of the normal parental cell irrespective of the tumorigenic parental cell. Efforts to identify factors in vitro mimicking these differentiation signals have so far failed, but such factors may be important elements in the regulation of proliferation in vivo.
Inhibitory action of BHA on carcinogenesis in F1 and F2 descendants of mice exposed to DMBA during pregnancy
Authors: Rao A. Ramesha 
Published: February 2007

AbstractAdministration of 500 μg of DMBA to female mice during late pregnancy results in the occurrence of tumors in F1 and F2 generation individuals. F1 progeny had a higher percentage of tumor‐bearing individuals than the F2 progeny. All the five litters of F1 females displayed tumor risk but the risk declined progressively in successive litters. Perinatal administration of BHA to the pregnant mice (P generation) receiving 500 μg of DMBA would result in significant reduction in tumor risk among the individuals of F1 generation (p < 0.01) and F2 generation (p < 0.05).
The comparative epidemiology of benign breast lumps and breast cancer in Western Australia
Authors: Fleming N. T. , Armstrong B. K. , Sheiner H. J. 
Published: February 2007

AbstractTotals of 313 patients with breast cancer and 1,283 patients biopsied for benign breast lumps were found in Western Australia in 1978 through review of all histopathological, hospital and cancer registry records. The incidence of breast cancer rose to 146.9 per 100,000 at age 45–54 years and thereafter increased little. The biopsy rate for benign breast lumps rose more sharply to 420.2 per 100,000 at age 45–54 years and then fell. This pattern was mainly due to benign mammary dysplasia (BMD); fibroadenoma showed an earlier peak biopsy rate (30–34 years) and other (mainly non‐neoplastic) benign lumps were biopsied at a relatively constant rate throughout adult life. Rates of breast cancer, BMD and fibroadenoma showed similar relationships to the other descriptive variables studied. The rates of each were higher in single than married women, in residents of the Perth area than residents of other parts of the State and in women employed in professional and related occupations than other employed women. They were lower in migrants from Europe (excluding Great Britain) than native‐born Australians and in women of low socio‐economic status than women of high status. Not all these differences were statistically significant. Rates of other breast lumps did not generally vary in these ways and were conversely related to country of birth, area of residence and socioeconomic status. The parallels in descriptive epidemiology between breast cancer, BMD and fibroadenoma suggest that they may share aetiological factors.
Effects of human γ interferon on cell growth, replication of virus and induction of 2′‐5′oligoadenylate synthetase in three human lymphoblastoid cell lines and K562 cells
Authors: Tomita Yoshimi , Cantell Kari , Kuwata Tsuguo 
Published: February 2007

AbstractHuman α interferon (IFN‐α) and β interferon (IFN‐β) showed antiviral and anticellular effects on human lymphoblastoid Daudi and P3HR‐1 cells, but up to 1,000 units/ ml of γ interferon (IFN‐γ) showed no such effect. Though a fairly high level of dsRNA‐dependent 2′‐5′‐oligoadenylate synthetase (2–5A synthetase) was found in Daudi cells, treatment of these cells with IFN‐α and β enhanced the enzyme level in cells at least four‐fold, but IFN‐γ did not show any such effect. Lymphoblastoid Raji cells were insensitive to the antiviral and anticellular activities of IFN‐α, β and γ, but 2‐5A synthetase was induced in cells by the treatment with IFN‐α and β, though the enzyme level was lower than that found in interferon‐treated Daudi cells. Human leukemic K562 cells were completely insensitive to IFN‐α, β and at the same time to IFN‐γ with regard to the antiviral, anticellular activities and to the induction of 2‐5A synthetase.
Mechanisms of cellular cytotoxicity mediated by effector cells from rats with spontaneous tumors
Authors: Zöller M. , Matzku S. 
Published: February 2007

AbstractWe have previously shown that effector cells from BD X rats bearing spontaneous tumors display increased cytotoxicity towards syngeneic tumor cells compared to effector cells from untreated rats (Zöller and Matzku, 1980a). The increased in vitro cytotoxicity of lymphoid cells from tumor‐bearing (TB) animals was not T‐cell mediated and the question was raised, whether it was due solely to increased natural killer (NK) cell activity, or whether humoral factors could also be involved. We now prove that in a long‐term assay, the presence of B cells is indeed mainly responsible for increased TB cytotoxicity, since: (1) After depletion of surface immunoglobulin positive cells (s‐Ig+), TB cytotoxicity no longer exceeds cytotoxicity of effector cells from untreated rats; (2) Mixtures of s‐Ig+ cells from TB animals with Fc‐receptor positive (Fc‐R+) cells from untreated rats restore the increased TB cytotoxicity; (3) Addition of rabbit Fab' anti rat F(ab')2 reduces TB‐effector cell cytotoxicity. A minor contribution of the increased TB cytotoxicity by activation/numerical increase of NK cells will be discussed.
Demonstration of the tumorigenicity of transformed rat kidney cell‐lines by intravenous allotransplantation in the neonate
Authors: Hard Gordon C. 
Published: February 2007

AbstractThe tumorigenic potential of allogeneic rat kidney cell‐lines transformed in vivo by a carcinogenic dose of dimethylnitrosamine (DMN) was investigated by intravenous injection of single cell suspensions into neonatal outbred rats within 24 h of birth. The cell‐lines tested included mesenchymal populations obtained from DMN‐induced renal mesenchymal tumors (RRMT‐2,‐8,‐9) and transformed mesenchymal (TRKM‐5,‐7,‐8) and epithelial (TRKE‐1) cell‐lines derived from the kidneys of rats treated only hours previously with the carcinogen. Additionally, spontaneous nephroblastoma‐derived embryonal cell‐lines (REN‐1,‐2) were included in the study to extend the potential of the neonatal rat system over a range of differentiation lineages. The transplantation system proved to be a rapid and efficacious assay for demonstrating the malignancy of the mesenchymal and embryonal cell‐lines. The major sites for tumor growth were the lungs, heart and eye, but differences in organ predilection were observed for individual cell‐lines. The transformed epithelial cell‐line (TRKE‐1) proved refractory to the single intravenous inoculation but was transplantation‐positive when a follow‐up subcutaneous dose was administered several days later. The resultant growths produced by the diverse differentiation lineages were histologically characteristic for the tumor tissue affiliate of each cell‐line. The results demonstrate the utility of this transplantation system for testing the malignant potential of morphologically transformed cells across the allogeneic barrier as well as proving that DMN is capable of inducing malignant transformation in both mesenchymal and epithelial cell types of the rat kidney after a very short period of exposure in vivo.
Regulator‐induced suppression of myelomonocytic leukemic cells: Clonal analysis of early cellular events
Authors: Metcalf Donald 
Published: February 2007

AbstractMouse WEHI‐3B myelomonocytic leukemic cells were cloned in semi‐solid agar in the presence of post‐endotoxin serum (ES) or semi‐purified differentiation factor (DF). At the 2‐cell, 4‐cell and 8–32‐cell stage, individual cells were washed and recloned in control cultures to test for clonogenicity and the ability to form differentiating progeny. With increasing clone size, an increasing proportion of treated cells either failed to proliferate or generated differentiating colonies of reduced size. The observed suppression indicated that both ES and DF exert irreversible effects on leukemic stem cell self‐replication within one or two cell cycles. The stem cell suppression observed was markedly asymmetric and most often involved premature differentiation and death of progeny of the affected cells rather than immediate death of the cell. The results are consistent with the possibility that the regulator DF irreversibly modifies one or more of the newly synthesised daughter chromatids of myeloid leukemic cells during the induction of stem cell suppression and differentiation.
Monitoring the effect of anti‐cancer drugs on L1210 cells by a mitochondrial probe, rhodamine‐123
Authors: Bernal Samuel D. , Shapiro Howard M. , Chen Lan Bo 
Published: February 2007

AbstractThe cancer chemotherapeutic agents 1‐β‐D‐arabinofuranosylcytosine (Ara‐C), methotrexate, and 5‐fluorouracil cause a rapid loss of mitochondrial Rh‐123 uptake in L1210 cells, which correlates with the loss of clonogenic ability. The loss of Rh‐123 uptake is irreversible and occurs prior to Trypan Blue staining. Thus, the antimetabolites, unlike freeze‐thawing and detergent treatments, generally cause mitochondrial damage prior to changes in plasma membrane permeability. Since the effect of antimetabolites on Rh‐123 uptake is maximal at 24 h, the Rh‐123 assay may provide a rapid alternative to the clonogenic assay for monitoring the cytotoxic effects of these drugs. Our results also suggest that the inhibition or impairment of mitochondrial function may be an important step in the cytocidal and/or cytostatic action of anti‐cancer drugs.
NK‐patterned binding expressed by non‐NK mouse leukocytes
Authors: Piontek Gerald E. , Grönberg Alvar , Ährlund‐Richter Lars , Kiessling Rolf , Hengartner Hans 
Published: February 2007

AbstractPrevious studies demonstrated that NK‐cell‐enriched spleen cells bind to sensitive but not to resistant mouse lymphoma targets, measured by a single‐cell target binding assay. In the present report we further analyzed this “NK‐patterned” binding using effector cells with high, low or no NK activity. In agreement with previous results, nylon‐wool‐passed spleen cells as well as a cloned cytotoxic cell line with NK activity bound tumor targets largely according to their NK sensitivity; NK‐sensitive tumors had a higher frequency of binders than the more resistant ones. The correlation coefficient relating the percentage target binding cells (TBC) for each tumor with the ability of the same tumor to inhibit lysis in cold target competition assays was consistently higher than that relating percentage TBC with direct NK lysis. A non‐lytic variant of the cloned cytotoxic cell line had a binding pattern identical to that of the lytic line, demonstrating that “NK‐patterned” binding occurred in the absence of lysis. Thymocytes, which are totally devoid of NK activity, also bound preferentially NK‐sensitive targets, and their binding was decreased after trypsin treatment or in the presence of EDTA. Peritoneal macrophages also showed “NK‐patterned” binding, thus demonstrating that this was not restricted to cells in the T‐cell lineage. Variants from a mouse lymphoma selected for decreased NK sensitivity bound a lower frequency of NK‐active (nylon‐wool‐passed spleen cells) and inactive cells (thymocytes, peritoneal macrophages). This study therefore showed that the membrane property conferring NK‐binding selectivity exists on several types of non‐NK leukocytes.
Human interferon inhibits the growth of established human breast tumours in the nude mouse
Authors: Balkwill F. R. , Moodie E. M. , Freedman V. , Fantes K. H. 
Published: February 2007

AbstractIn this paper we describe a model system for looking at the effects of human interferon, IFN, on an established human tumour. Highly purified human IFN derived from lymphoblastoid cells (HuIFNα‐Namalwa) strongly inhibited the growth of a human breast cancer growing as a xenograft in nude mice. The effect was dose‐dependent, required daily treatment for an optimal effect and was time‐dependent, little inhibition being seen before 2 weeks of therapy. With the doses used, however, neither tumour regression nor disappearance were seen and on morphological examination, treated tumours appeared as miniatures of control tumours. The inhibition of the tumour by HuIFNα‐Namalwa appeared to be due to a direct effect on the human cells as this IFN had little effect on the mouse immune system in vitro as measured by NK cells activity. Also HuIFN therapy had no effect on levels of an interferon induced enzyme, 2–5A synthetase, in the mouse spleen cells but stimulated this enzyme in the human tumour.
Role of 3′‐end of viral genome in tumor heteroinduction by the avian sarcoma virus
Authors: Altaner C. , Reinerová M. 
Published: February 2007

AbstractTransformation defective virus was derived by restriction endonuclease cleavage from a clone of the avian sarcoma virus Schmidt‐Ruppin strain, strongly oncogenic for rats. The transfection experiments of chicken cells by digested proviral DNA gave rise to transformation defective virus. The td virus was possible to recover in vivo in chickens. The tumors obtained after a long latent period contained the sarcoma virus which was able to transform chicken cells in vitro and to induce tumors in chickens. All viruses, parental, td‐ and recovered were of D subgroup specificity. The tumor induction experiments in rats have shown that the recovery of viral genome deletion in td mutant by cellular sequences was not enough to regain the oncogenicity for rats. The results stressed the importance of 3‐end sequences of the virus genome, probably the sequences in C region for heteroinduction ability of the avian sarcoma virus.
The human type‐C retrovirus, HTLV, in blacks from the Caribbean region, and relationship to adult T‐cell leukemia/lymphoma
Authors: Blattner William A. , Kalyanaraman V. S. , Robert‐Guroff Marjorie , Lister T. Andrew , Galton David A. G. , Sarin Prem S. , Crawford Michael H. , Catovsky Daniel , Greaves Melvin , Gallo Robert C. 
Published: February 2007

AbstractType‐C RNA tumor viruses have been implicated in the etiology of naturally occurring leukemias and lymphomas of animals. Human T‐cell leukemia/lymphoma virus (HTLV) is the first human virus of this class consistently identified in association with a specific type of human leukemia/lymphoma. The isolation of HTLV was made possible by the ability to grow mature T‐cells in tissue culture usually with T‐cell growth factor (TCGF). We now report a cluster of adult T‐cell leukemia/lymphoma among Blacks from the Caribbean in which all eight cases are positive for HTLV virus and/or antibody. These patients have disease that appears indistinguishable from Japanese adult T‐cell leukemia/lymphoma which, as we have also reported, is associated with HTLV in over 90% of cases. The finding of HTLV antibodies in some of the normal population in the Caribbean and Japan, and the clustering of a specific form of T‐cell leukemia/lymphoma in these virus‐endemic areas, suggest that HTLV infection may be associated with the occurrence of a distinctive clinico‐pathologic entity.
Antigens in an adult T‐cell leukemia virus‐producer cell line: Reactivity with human serum antibodies
Authors: Yamamoto Naoki , Hinuma Yorio 
Published: February 2007

AbstractSera from patients with adult T‐cell leukemia (ATL) or other diseases and from healthy adults, whose titers of antibodies against ATL‐associated antigens (ATLA) had been determined by indirect immunofluorescence, were analysed by a procedure of immunoprecipitation followed by SDS‐polyacrylamide gel electrophoresis. For this an ATL virus (ATLV)‐producer cell line, MT‐2, was labelled with [35S]‐methionine. All 12 anti‐ATLA‐positive sera but none of the eight anti‐ATLA‐negative sera tested reacted specifically with four polypeptides with molecular weights of 70,000, 53,000, 36,000 and 24,000 daltons. Furthermore, enrichment of three polypeptides with molecular weights of 76,000, 43,000 and 28,000 daltons was observed on reaction with anti‐ATLA‐positive sera. In control experiments using ATLA‐negative T‐cell lines, Molt‐4 and HPB‐ALL, none of these seven polypeptides were precipitated by reaction with anti‐ATLA‐positive sera. All six anti‐ATLA‐positive sera tested were shown to react with a polypeptide with a molecular weight of 24,000 of purified ATLV.
Detection of S‐100 protein as an aid to the identification of melanocytic tumors
Authors: Cochran Alistair J. , Wen Duan‐Ren , Herschman Harvey R. , Gaynor Richard B. 
Published: February 2007

AbstractWe sought S‐100 protein in sections prepared from formalin‐fixed paraffin‐embedded tumor and normal tissues by an immunoperoxidase technique with a rabbit antibovine S‐100 protein antiserum as first antibody and aminoethyl carbazole as developer. S‐100 protein was demonstrated in 56 of 56 cutaneous melanomas, regardless or their primary of metastatic status, and in 35 of 35 nevocytic nevi. The amount of S‐100 protein was independent of the degree of melanization of the tumors. Only 1 of 51 non‐neural non‐melanocytic tumors tested contained S‐100 protein. The technique is valuable in confirming the melanocytic nature of primary or metastatic tumors and in detecting small foci of metastatic melanoma in lymph nodes and other tissues. It also seems applicable to research on melanocytic anomalies.
Glutaminase‐free asparaginase from vibrio succinogenes: An antilymphoma enzyme lacking hepatotoxicity
Authors: Distasio John A. , Salazar Ana M. , Nadji Mehrdad , Durden Donald L. 
Published: February 2007

AbstractSuccessful treatment of neoplastic disease has been impeded by the lack of therapeutic agents which specifically destroy tumor cells. Enzymes which selectively deplete substrates required by tumor cells, but not by normal tissue, could improve therapeutic indices dramatically. Presently, microbial asparaginases are used clinically for treating acute lymphocytic leukemia. While these enzymes should destroy neoplastic cells and spare normal tissues, their use is accompanied by many toxic effects and immunosuppression. The administration of Escherichia coli or Erwinia carotovora asparaginase depletes circulating glutamine as well as asparagine. It has been suggested that this glutaminase activity may be responsible for the observed toxicities. We have isolated a glutaminase‐free asparaginase from Vibrio succinogenes with potent antilymphoma activity. Previously, we demonstrated that administration of Vibrio asparaginase does not cause the immunosuppression of humoral or cell‐mediated responses associated with treatment by other microbial enzymes. In the present communication we have evaluated the hepatotoxic effects of different asparaginases since liver damage is the major toxicity associated with treatment by these microbial enzymes. BALB/c mice treated with 50 IU of E. coli asparaginase daily for 4 days exhibited diffuse microfatty infiltration within hepatocytes throughout the liver. Cross‐sections of liver from V. succinogenes asparaginase‐treated mice appeared normal as compared to specimens from control animals. Quantitation of the total amount of extractable lipid from the livers of E. coli asparaginase‐treated animals indicated a 45% and 127% increase in lipid concentration as compared to controls after 4 and 5 days of treatment, respectively. The Vibrio enzyme did not cause a change in extractable lipid concentration as compared to control animals. Plasma antithrombin III activity and albumin, triglyceride and cholesterol concentrations all decreased in E. coli asparaginase‐treated mice, confirming hepatotoxicity. No modifications in plasma proteins were observed in mice treated with asparaginase from V. succinogenes. The plasma lipids did decrease minimally but only the levels of cholesterol were shown to be statistically significant from those of controls. The data strongly support the concept that specific asparagine depletion is not significantly hepatotoxic. More importantly, the asparaginase from V. succinogenes may serve as a potent antileukemic agent without causing damage to normal tissues.