bluuebunny/crossref_metadata_2025_split huggingface dataset:
Xenografts in pharmacologically immunosuppressed mice as a model to test the chemotherapeutic sensitivity of human tumors
Authors: Floersheim G. L. , Bieri A. , Chiodetti Nicole 
Published: February 2007

AbstractA human tumor xenograft model using pharmacologically immunosuppressed mice was assessed for its suitability to test preclinically the sensitivity of colorectal carcinomas, bone sarcomas and melanomas against anticancer agents. Besides ionizing radiation, 14 cytotoxic drugs including 5‐fluorouracil (5‐FU), dimethylmyleran (DMM), cytosine arabinoside, cyclophosphamide, melphalan, BCNU, mitomycin C, adriamycin, bleomycin, etoposide, vinblastine, cisplatin, procarbazine and DTIC were assayed. Ionizing radiation, 5‐FU and DMM were also applied at lethal doses followed by bone‐marrow rescue heavy therapy. Four colon carcinomas responded poorly to most of the agents but one tumor displayed marked sensitivity to BCNU. Lethal doses of radiation, 5‐FU and DMM could also show considerable activity. High sensitivity was shown by a Ewing sarcoma to DMM and cyclophosphamide and by an osteosarcoma to the latter drug. No strong effects were seen against melanomas. Lethal doses of DMM induced the best regression of one colon carcinoma. In general, the superiority of heavy therapy for solid human tumors compared to maximally tolerated doses was demonstrated. Individual carcinomas of the same type displayed different drug sensitivity.
Acquired resistance towards immune defense during metastatic progression represents a secondary phenomenon
Authors: Zöller M. 
Published: February 2007

AbstractThe role of natural immune defense in the control of metastatic spread of tumor cells was evaluated by adapting an s.c.‐grown, antigenic, but non‐immunogenic rat fibrosarcoma (Bsp6S) to ascitic growth (BSp6A) in the strain of origin (BDX), where peritoneal cells display a high level of NK and macrophage activity. Parallel tests were performed to determine whether tumor cells can selectively adapt to non‐specific immune defense, i.e. whether antigenicity of the non‐immunogenic tumor remains unaltered, and whether this is accompanied by metastatic progression. During adaptation to ascitic growth the tumor line gradually lost susceptibility to NK cells and macrophages. This was due to the appearance of an increasing number of resistant clones (BSp6S, none; BSp6A, 50% of clones), which had lost binding structures for NK cells and macrophages. No alteration could be observed in antigenicity of the BSp6A variant as revealed by clonal analysis using LD of CTL. Neither BSp6S nor BSp6A cells metastasized. When the ascitic variant was retransplanted s.c. (BSp6AS), susceptibility to NK cells and macrophages was further decreased, in the sense that all clones of the BSp6AS variant became resistant. Furthermore, the BSp6AS variant had lost some of the tumor‐associated antigens (TAAs) found on BSp6S and A variants. More important, upon s.c. transplantation BSp6AS regularly metastasized to the draining LN, contrary to BSp6S and BSp6A. When locally growing tumors were excised, rats implanted with BSp6AS frequently died with metastatic tumor burdens in LNs and lung, while other animals survived after excision of BSp6S or BSp6A. The data indicate a correlation between resistance to lysis, morphology and metastatic capacity. But the initial loss of susceptibility to NK cells and macrophages during adaptation to ascitic growth, which can be considered as an escape mechanism, was not accompanied by increased metastatic capacity. Hence, we suppose that with respect to metastatic progression of the BSp6AS variant, resistance to lysis by loss of binding structures represents only a secondary, but not a causative, element.
Actin filaments and tumorigenicity in a fischer rat embryo fibroblast cell line (3Y1) transformed by ultraviolet‐irradiated HSV
Authors: Tsuchie H. , Katsumoto T. , Hama S. , Hattori N. , Morimoto H. , Kamahora T. , Kurimura T. 
Published: February 2007

AbstractThe characteristics of the cytoskeleton of a Fischer rat embryo fibroblast cell line (3Y1) transformed by ultraviolet (UV)‐irradiated HSV were studied by indirect immunofluorescence using anti‐actin IgG. Parental 3Y1 cells possessed well‐developed actin filaments, while 3Y1 cells transformed by UV‐irradiated HSV also retained well‐developed actin filaments. Transformed cells were divided into 2 groups according to tumorigenicity in newborn Fischer rats; one had a strongly tumorigenic potential and the other a weakly tumorigenic potential. Tumor‐derived cell lines exhibited a highly tumorigenic potential, and were also divided into 2 groups, one with well‐developed actin filaments and the other without well‐developed actin filaments. Our results suggested that transformation or tumor formation by HSV is a multi‐step process and that morphological loss of actin filaments in the cells is not essential to the tumorigenic potential of the cells transformed by HSV.
Altered growth properties and cell surface changes in ras transformed mouse bladder epithelium
Authors: Summerhayes I. C. , Malone P. , Visvanathan K. 
Published: February 2007

AbstractTransfection of the c‐Ha‐ras‐1 oncogene, cloned from EJ/T24 cells, into different mouse bladder epithelial cell lines resulted in the acquisition of tumorigenic potential and, in all but one cell line (MB331), anchorage‐independent growth. Sera from syngeneic mice bearing tumours immunoprecipitated an 18 kDa protein from ras‐transfected urothelial cells which was not detectable in their parental counterparts. Screening of a limited panel of mouse cell lines showed this protein to be urothelium‐specific and associated with the expression of an activated ras gene. Polyoma middle T and v‐myc‐transfected bladder epithelial cells did not express this 18kDa protein. Localization of this protein to the cell surface was demonstrated by immunofluorescence and absorption studies.
Production and characterization of monoclonal antibodies against human neuroblastoma
Authors: Schönmann S. M. , Iyer J. , Laeng H. , Gerber H. A. , Käser H. , Blaser K. 
Published: February 2007

AbstractMAb were derived from mice immunized with cells of the human neuroblastoma line IMR‐32. Five hybridomas were selected according to their selective binding to human cell lines, tumors and normal tissues. One of them, CE7, reacted with all sympatho‐adreno‐medullary cells (neuroblastoma, ganglioneuroblastoma, ganglioneuroma, pheochromocytoma, adrenal medulla, sympathetic ganglion cells). Weak cross‐reactivities were observed with melanocytes and with some human melanoma and glioma cell lines. The antigen recognized by CE7 was markedly expressed on neuroblastoma tumors of all histological grades, independently of the adrenergic or cholinergic nature of these cells. MAb derived from clones AD2, BCI, BC4 and CB10 bound variably to some, but not to all, neuroblastoma cells. By using these MAb, 3 phenotypes of neuroblastoma lines could be distinguished. The binding profiles of these types, however, showed no correlation with origin of the cell lines or stage of the disease.
Transmission of human T‐cell leukemia virus (HTLV‐I) by blood transfusion: Demonstration of proviral DNA in recipients' blood lymphocytes
Authors: Sato Hiroyuki , Okochi Kazuo 
Published: February 2007

AbstractHuman T‐cell clones bearing antigens encoded by human T‐cell leukemia/lymphoma virus (HTLV‐I) were isolated from 6 patients who produced antibodies against HTLV‐I after having received anti‐HTLV‐I‐positive blood units containing cell components. On the other hand, it was not possible to isolate clonal cells carrying viral antigens from the recipients who did not produce antibodies. The clonal cell lines had the same surface markers as neoplastic cells of adult T‐cell leukemia and had the HLA phenotype of the recipients themselves. Proviral DNA of HTLV‐I was demonstrated in each of the clonal cell lines. The site of integration was different in each case even if the clones were derived from the same recipient. These results indicate that blood transfusion can cause persistent HTLV‐I infection.
The role of prostaglandin E1 in ornithine decarboxylase induction by tumor promoters
Authors: Ordman Alfred B. , Simsiman R. C. , Cleaveland Jeffrey S. , Boutwell R. K. 
Published: February 2007

AbstractThe effect of topical application of PGE on induction of ODC in mouse epidermis was measured. When direct induction of ODC by TPA was blocked by also applying indomethacin, maximum ODC activity occurred only when PGE was applied simultaneously with TPA 41/2 hr before killing of the mice. If either TPA or PGE was applied at other times, ODC activity decreased substantially. Induction of ODC by mezerein was blocked by indomethacin but restored by PGE, as was observed with TPA, but induction by ethyl phenylpropiolate was not affected by indomethacin or PGE. DMBA did not cause a consistent increase in ODC activity, nor was its inductive action affected by indomethacin or PGE. However, another weak inducer, acetic acid, exhibited elevated ODC activity when PGE was also applied. Inhibition by topical retinoic acid of ODC induction by TPA was partially overcome in a dose‐response fashion by PGE. The results indicate that at least 2 events, elevation of PGE and another independent event, are required for induction of ODC activity. It appears that TPA causes at least 4 independent events essential for tumor promotion. A model for the events in the 2‐stage tumor promotion model is proposed.
Presence of human papillomavirus type‐16 and type‐18 DNA sequences and their expression in cervical cancers and cell lines from japanese patients
Authors: Tsunokawa Youko , Takebe Naoko , Nozawa Shiro , Kasamatsu Tatsuhiro , Gissmann Lutz , Hausen Harald Zur , Terada Masaaki , Sugimura Takashi 
Published: February 2007

AbstractSouthern blot analyses of surgical specimens of cervical carcinoma from Japanese patients showed that 3/9 samples contained human papillomavirus (HPV) type‐16 DNA sequences, and 2 contained HPV type‐18 DNA sequences. By Northern blot analyses, RNA transcripts of HPV DNA sequences were demon‐trated in some of the tissues containing HPV type‐16 or HPV type‐18 DNA sequences. Two cell lines established from cervical cancers of Japanese patients also contained HPV type‐18 genomes and these cell lines contained HPV type‐18 transcripts. Two other cervical cancer cell lines from a Japanese patient were found to contain HPV type‐16 DNA sequences and their RNA transcripts.
Virus production and surface marker expression in human lymphocytes immortalized following dual infection with human T‐cell leukemia virus and Epstein‐Barr virus
Authors: Mochizuki Shigenobu , Kawamura Kiyoko , Maruyama Koshi 
Published: February 2007

AbstractBy co‐cultivating peripheral blood lymphocytes from normal male donors with cells from a line designated Lma‐66VP, established from a female donor and simultaneously producing both HTLV‐I and EBV, 2 continuous culture lines were obtained. Normal male lymphocytes were considered to be immortalized by co‐cultivation because they were of male karyotype and lacked the 3q + chromosome that was observed in all Lma‐66VP cells. These immortalized cultures were designated Co‐culture I and Co‐culture 2. After prolonged cultivation, chromosome abnormalities characteristic of each co‐culture line were observed in all cells examined, indicating their clonal origin. Immortalized cells initially produced both HTLV‐I and EBV. Although production of EBV was not seen in the co‐culture lines after prolonged cultivation when all cells examined had the characteristic chromosomal abnormality indicating their clonality, EBNA+ cells persisted. Thus, clonal cells were doubly infected by HTLV‐I and EBV. While the majority of clonal cells in Lma‐66VP, Co‐culture I, and Co‐culture 2 lines expressed a surface marker of B‐cells, small numbers of cells expressed a T‐cell surface marker. These findings demonstrate that human lymphocytes immortalized following dual infection by HTLV‐I and EBV exhibit chromosome rearrangement, resulting in expression of surface markers inconsistent with their differentiation lineage.
Modulation of protein kinase C and Ca2+ lipid‐independent protein kinase in lymphoma induced by moloney murine leukemia virus in BALB/c mice
Authors: Wolfson M. , Aboud M. , Ofir R. , Weinstein Y. , Segal S. 
Published: February 2007

AbstractWe investigated the possible role of protein kinase C (PKC) in the progression of Moloney murine leukemia virus (Mo‐MuLV)‐induced lymphoma in BALB/c mice. Mice injected with Mo‐MuLV on the first day after birth developed lymphoma within 1 1/2 3 months. The development of lymphoma was characterized by a gradual increase in the number of spleen cells. However, no analogous changes could be detected in the thymuses of these mice, although cells of both organs were found to be virus producers as early as 3‐4 weeks after inoculation. PKC activity, which was assayed in extracts of spleen and thymus cells, declined gradually during the development of lymphoma. Concomitantly with this decline, a progressive appearance of Ca2+/ lipid‐independent protein kinase activity was observed. TPA treatment of intact cells from normal mice reduced the level of soluble PKC activity, while inducing Ca2+/lipid‐independent phosphorylation. By contrast, TPA had no effect on these enzymatic activities in cells derived from leukemic mice. Spleen enlargement caused by injection of a non‐leukemogenic inflammatory agent such as mineral oil was ineffective in this respect, suggesting that the PKC‐Ca2+ /lipid‐independent protein kinase modulation is associated with the virally induced leukemogenesis.
Phenotypes of placental‐type alkaline phosphatase in seminoma sera as defined by monoclonal antibodies
Authors: Wahren B. , Hinkula J. , Stigbrand T. , Jeppsson A. , Andersson L. , Esposti P. L. , Edsmyr F. , Millán J. L. 
Published: February 2007

AbstractPLAP‐like enzymes could be detected in serum of patients with primary testicular tumors, in particular seminomas. The use of a panel of monoclonal antibodies (MAbs) permitted typing into 6 different testicular serum phenotypes, of which one appeared similar to a placental type (II) and 2 have not been previously described. Most tumor sera belonged to type I, as described for seminoma tissues. With a more advanced tumor the mean serum PLAP‐like levels increased. After operation, after radiotherapy or with no evidence of disease lower or non‐detectable enzyme levels were found. In typing the tissue PLAP‐like antigen in serum of the same patient or sera from recurrences of a seminoma in the same patient, the same phenotypes of PLAP‐like antigen were usually but not always found. None of the 6 phenotypes appeared to confer a poorer prognosis. We conclude that the expression of PLAP‐like antigen is eutopic and is enhanced by testicular malignancy, especially in seminoma cells.
Mode of transmission of human T‐cell leukemia virus type I (HTLV I) in a human promyelocytic leukemia HL60 cell
Authors: Hiramatsu K. , Masuda M. , Yoshikura H. 
Published: February 2007

AbstractHTLV‐I propagated in IMR90 human diploid fibroblasts was transmitted to human myeloid leukemia HL60 cells at a low efficiency. After co‐cultivation for 3 months, the viral genome was detected in 14/48 HL60 cell clones. Among the 14 HTLV‐I‐infected clones, 8 contained subgenomic fragments alone or in addition to the complete HTLV‐I genome. The frequency of deleted proviruses (9/24 total proviruses) was unexpectedly high. Hirt's supernatant of some of the clones harboring complete HTLV‐I genome(s) in the chromosome contained both linear and circular HTLV‐I proviral DNAs. The circular DNAs were composed of one LTR and 2 LTR closed circular proviruses. These clones produced infectious HTLV‐I constitutively, which was proved by transmission of the viral genome into fresh IMR90 cells by co‐cultivation. However, in these clones, re‐integration of extrachromosomal provirus into their own chromosomes was not observed.
Potential carcinogenicity of Aza‐aromatic hydrocarbons: Azabenz(A)anthracenes
Authors: Miao R. M. , Tanga M. J. , Suk W. A. , Miller A. , Reist E. J. 
Published: February 2007

AbstractThe potential carcinogenicity of 3 azabenz(a)‐anthracenes was determined in vitro. The 3 compounds tested were 1‐, 2‐, and 9‐azabenz(a)‐anthracene. The initial assay was chemical carcinogen‐induced enhancement of anchorage‐independent survival of Rauscher leukemia virus‐infected Fischer rat embryo cells, 2FR450 (2FR4). Cells treated with 2‐ and 9‐azabenz(a)anthracene showed dose‐dependent increased survival. After continued subculturing, the surviving cells from 2‐ and 9‐azabenz(a)anthracenetreated cultures displayed morphological transformation and ability to grow in semi‐solid medium. Mocktreated controls and I‐azabenz(a)anthracene‐treated cultures did not show either of these properties. These data suggest that certain azabenz(a)anthracenes are potential carcinogens.
Fecal bile acids and neutral sterols in rats with spontaneous colon cancer
Authors: Hayashi Eijiro , Amuro Yoshiki , Endo Tomoichiro , Yamamoto Hideo , Miyamoto Makoto , Kishimoto Susumu 
Published: February 2007

AbstractFecal bile acids and neutral sterols of spontaneous colon cancer‐bearing Wistar‐Furth strain rats were examined and compared with those of control rats of the same strain by gas chromatography and gas chromatography‐mass spectrometry. The amount of total fecal bile acids and the percentage of fecal lithocholic acid were almost similar in both groups, but the percentage of fecal deoxycholic acid was significantly higher in the colon cancer group than in the controls. The amount of total fecal neutral sterols and the percentage of fecal coprostanol were also markedly higher in the colon cancer group than in the controls. The percentage of cholesterol and the amount of β‐sitosterol were, however, almost similar in the two groups. These results indicate that fecal deoxycholic acid and fecal coprostanol are notably higher in rats with colon cancer than in controls.
A radioimmunoassay for the detection of a human tumor‐associated glycoprotein (tag‐72) using monoclonal antibody B72.3
Authors: Paterson Andrew J. , Schlom Jeffrey , Sears Henry F. , Bennett Jeffrey , Colcher David 
Published: February 2007

AbstractMonoclonal antibody (MAb) B72.3 was generated against a carcinoma metastasis and has been shown to bind with a high degree of selectivity to a tumor‐associated glycoprotein (TAG‐72) found in human colon and breast carcinomas, while showing minimal reactivity to any normal adult tissues. Competition radioimmunoassays have been developed for the detection of TAG‐72 in tumors and sera from both athymic mice bearing human carcinoma xenografts and patients with colon, breast and other carcinomas. The distribution of TAG‐72 in human tumor xenografts was restricted to tumors originating from the LS‐174T human colon carcinoma, with no significant reactivity being detected in human tumor xenografts from a different colon carcinoma, a human breast carcinoma, or a human melanoma. The levels of TAG‐72 in clinical material obtained from surgery were examined; high levels were found in colon carcinomas and to a lesser extent in breast carcinomas, while no detectable levels were found in normal tissues. Sera from apparently normal patients contained a mean level of 2.2 units per ml of TAG‐72. A level of 3 standard deviations above the mean level of TAG‐72 found in normals was employed as a cut‐off value to indicate a positive test result in subsequent studies. No patient with inflammatory disease or other benign colon disease exhibited elevated levels of TAG‐72. Seven out of 20 advanced colon cancer patients and 7 out of 20 patients with other carcinomas had elevated serum levels of TAG‐72. The serum TAG‐72 levels were compared with the serum levels of antigens recognized by the MAbs currently used to screen sera of carcinoma patients (CEA, GICA, and OC125). It was clearly demonstrated that TAG‐72 is different from these antigens and can be found in some sera in which no antigen is detected by otherwise available MAb RIAs.
Immunohistologic expression of blood‐group antigens in normal human gastrointestinal tract and colonic carcinoma
Authors: Cordon‐Cardo Carlos , Lloyd Kenneth O. , Sakamoto Junichi , McGroarty Mary Ellen , Old Lloyd J. , Melamed Myron R. 
Published: February 2007

AbstractA panel of 7 mouse monoclonal antibodies and the lectin from Ulex europeus, detecting blood‐group‐related antigens of the ABH and Lewis systems, have been used to define the distribution of these antigenic structures within the human gastrointestinal tract, and to characterize their expression and modulation in colorectal carcinomas. The reagents employed detect the following blood‐group specificities: A (all variants), B. H (type 2), Lewisa, Lewisb, × (Lewisx), Y (Lewisy) and type I precursor chain. Immunohistochemical studies demonstrate that these antigens are differentially expressed in various cell types and developmental stages of the human gastrointestinal tract. ABH expression undergoes developmental modulation in the human colorectal tract from positive to negative during embryogenesis, and is lost in adult cells. Colorectal tumors exhibit neosynthesis of ABH specificities that appear in tumor cells, and accumulation of the precursor antigens. They also show increased expression of Lewis antigens, especially Y determinant, which has a restricted pattern of distribution in normal tissues and is not found in normal colonic mucosa. Enhancement of the Lewis antigens is observed in all colorectal tumors analyzed, regardless of blood‐group type and secretory status of the individuals studied. Tumor modulation of these antigens may be related to activation of suppressed genes and enhancement of fucosyltransferases.
Human‐human hybridomas for the study of anti‐tumor immune response in patients with colorectal cancer
Authors: Borup‐Christensen P. , Erb Karin , Jensenius J. C. , Nielsen B. , Svehag S.‐E. 
Published: February 2007

AbstractHuman‐human hybridoma technology was evaluated for the study of humoral immune reactions of colorectal cancer patients against their own tumors. Six fusions were carried out with lymphocytes from mesenteric lymph nodes from patients with colorectal cancer, using the human B‐lymphoma cell line LICR‐LON‐HMy‐2 as fusion partner. A total of 294 wells with cell growth were obtained. Supernatants from 26 of these reacted in enzyme‐linked immuno‐sorbent assay (ELISA) with one or more colon cancer cell lines. Cells from only one of these wells (D 4213) could be cloned. The clone was shown to produce antibody which by immunocytochemical analysis reacted with a panel of colon cancer cell lines and melanoma cell lines but not with several other cancer cell lines or normal human leukocytes. By immunohistochemical analysis on formalin‐fixed paraffin‐embedded tissue this antibody reacted strongly with antigen expressed by autologous and allogeneic colorectal cancers. Faint staining could occasionally be observed on normal colon epithelium. D4213 is a hybrid cell line since it is setraploid and produces kappa and lambda light chains as well as gamma and mu chains, whereas HMy‐2 produces only kappa and gamma chains. The study suggests that patients may possess B cells producing antibody reactive with their own malignant cells.