bluuebunny/crossref_metadata_2025_split huggingface dataset:
Liver‐to‐lung traffic of cancer cells
Authors: Weiss Leonard , Ward Pamela M. , Holmes Janet C. 
Published: February 2007

AbstractFollowing the injection of B16 melanoma cells into the portal veins of mice, all animals developed liver tumors, but only 16% developed lung tumors. Portal vein injections of radiolabelled B16 and Walker 256 cancer cells into mice and rats, respectively, revealed that all of the cells were temporarily arrested in the liver and most were then slowly released. Bioassays indicated that of 8 × 104 B16 cells released from the liver over 24 h after portal vein injections of 105 cells, only approximately 1% were delivered to the lungs in a viable state. Experiments made with radiolabelled B16 cells showed that transit through either the liver or lungs following portal vein or tail vein injections, respectively, resulted in massive death of cancer cells. It is suggested that the death of most circulating cancer cells passing through the first organ encountered after leaving their primary tumor, serves to severely limit their further direct spread to other organs. It is therefore expected that metastases to these other organs would, to a large extent, be generated by cancer cells from metastases in the “first organs” as distinct from direct seeding from cancer cells released from the primary tumor. If the results of the present experiments have general application, they serve to emphasize the importance of metastasis of metastases in the natural history of the spread of cancer. In a previous publication (Weiss, 1980), studies of lung‐to‐liver traffic of cancer cells in rats revealed that, after tail vein injections, most Walker 256 cells were temporarily arrested in the pulmonary vasculature and then slowly released. A large proportion of the released cancer cells were dead or lethally injured on release from the lungs, and this “first organ processing” apparently accounted for the comparative rarity of extrapulmonary tumors following tail vein injections. In this communication, the concept of “first organ processing” of circulating cancer cells is further examined with respect to the liver‐to‐lung traffic of B16 melanoma and Walker 256 cells injected into the portal veins of mice or rats respectively. Both of these cell types grow well in the lungs following tail‐vein injection.
Alpha‐fetoprotein synthesis in relation to structural peculiarities in postnatal and regenerating mouse liver
Authors: Gleiberman A. S. , Kuprina‐Khramkova N. I. , Rudinskaya‐Beloshapkina T. D. , Abelev G. I. 
Published: February 2007

AbstractThe localization of alpha‐fetoprotein (AFP) and of antigens of liver‐cell plasma membrane (Ag I, Ag II and Ag III) was studied in adult, postnatal and regenerating (CCI4 or paracetamol‐treated mouse liver). Ag I, Ag II and Ag III were solubilized by Triton X‐100 from ghosts of the mouse liver cells. The purification of antigens was performed by gel filtration on Sephadex G‐200 or Ultrogel ACA‐54 with subsequent treatment of antigenic fractions eluted from the column with 5% HCIO4. Ag I and Ag II are common for liver and some other mouse organs, but Ag III is strictly specific for liver. The Ag I is predominantly found in the region of the bile capillaries. Ag II and Ag III are mainly present on membrane adjoining blood sinusoids. The distribution of these three antigens in newborn mouse liver is quite different from that in adult liver and reflects the specific arrangement of hepatocytes at different stages of development — the acinar structure in newborn liver and the plate structure in the adult organ. During regeneration as well as during postnatal development, AFP has been found in areas of marked tissue rearrangement. In both cases, these areas lose the plasma membrane antigens, especially Ag I — the antigen of bile capillary. The reappearance of Ag I on the surface of liver cells coincides with cessation of AFP synthesis and establishment of definitive plate structure. The possible role of liver plate structure in the regulation of AFP synthesis is discussed.
Lymphotoxin amplification of tumor growth inhibition is specific for natural killer cells but not for macrophages
Authors: Ransom Janet H. , Pintus Cristina , Evans Charles H. 
Published: February 2007

AbstractLymphotoxin augments the susceptibility of tumorigenic guinea‐pig cells to natural killer (NK) cell cytolysis in vitro but does not directly stimulate either NK cell or macrophage cytolytic action. The question whether lymphotoxin enhances the susceptibility of tumorigenic guinea‐pig cells to cytolysis or other means of growth inhibition in vivo by syngeneic NK cells or macrophages was, therefore, examined using a modified tumor cell neutralization (Winn) assay. Mineral oil‐, thioglycollateor casein‐induced peritoneal leukocytes, but not the macrophges isolated from the elicited leukocytes obtained from nonimmunized strain 2/N guinea‐pigs, effected enhanced cytolysis of lymphotoxin‐treated guinea‐pig benzo (a)pyrene‐induced 104CI tumor cells in vitro. Neither guinea‐pig splenic NK cells nor oil‐induced peritoneal macrophages alone inhibited the growth of 104CI cells as tumors in vivo when admixed with 104CI cells and injected into guinea‐pigs. However, when the 104CI cells were treated with lymphotoxin before addition of effector cells, NK cells but not macrophages significantly reduced tumor growth in vivo. Therefore, the ability of lymphotoxin to increase the sensitivity of tumor cells to destruction mediated by natural leukocytes is specific for NK cells as compared to macrophages. This form of lymphokine amplification of natural leukocyte cytotoxicity may be one mechanism by which natural and acquired immunity serves or fails to prevent cancer and should be an important consideration in therapeutic approaches to eradicate or control tumor growth.
Coupling of growth and differentiation in normal myeloid precursors and the breakdown of this coupling in leukemia
Authors: Lotem Joseph , Sachs Leo 
Published: February 2007

AbstractNormal myeloid precursors are dependent on the macrophage and granulocyte growth‐inducing protein MGI‐I for cell viability and multiplication. MGI‐I also induces production of the differentiation‐inducing protein MGI‐2, and this induction of a differentiation‐inducing protein by a growth‐inducing protein provides a mechanism for the normal coupling of growth and differentiation. It is shown that this induction of MGI‐2 by MGI‐I occurs in the myeloid precursors and not in some other cells in the normal bone marrow, that the induced MGI‐2 can be detected 6 h after the addition of MGI‐I, and that MGI‐2 can be induced in these cells by purified MGI‐I. There are clones of myeloid leukemic cells that no longer require MGI‐I for cell viability and multiplication, but in which this requirement for MGI‐I can be restored after induction of differentiation by MGI‐2. A similar concentration of MGI‐I was required for the optimum induction of growth in these differentiating leukemic cells and in normal myeloid precursors. In the presence of MGI‐I these differentiating leukemic cells multiplied and then lost their differentiation‐associated properties. In contrast to normal myeloid cells, MGI‐I did not induce MGI‐2 in the MGI‐I requiring differentiating myeloid leukemic cells. This lack of induction of MGI‐2 by MGI‐I occurred in cells cultured in serum‐containing or serum‐free‐medium, and can explain the loss of differentiation‐associated properties. The results indicate that there has been a genetic breakdown of the normal coupling mechanism between growth and differentiation in these leukemic cells so that MGI‐I can no longer induce MGI‐2.
Establishment of a cell line (HCC‐M) from a human hepatocellular carcinoma
Authors: Watanabe Tetsu , Morizane Toshio , Tsuchimoto Kanji , Inagaki Yasutaka , Munakata Yoshio , Nakamura Tatsuya , Kumagai Naoki , Tsuchiya Masaharu 
Published: February 2007

AbstractA continuous human cell line was established from a hepatocellular carcinoma of an HBsAg‐positive Japanese male. The cell line, designated HCC‐M, grows as an adhering monolayer with a doubling time of 24 h in medium RPMI‐1640 supplemented with 10% FCS and grows with 30% clonal efficiency in soft agar. The cells have been shown by light and electron microscopy to be of epithelial type. When they were transplanted sub‐cutaneously into the back of athymic nude mice (BALB/c, nu/nu), tumors developed at the sites of inoculation, which were shown to be hepatocellular carcinoma, similar in morphology to the original tumor from which they were derived. HCC‐M had a chromosome mode of 63 with five identifiable marker chromosomes. HCC‐M produced albumin at the 10th passage but this property was lost by the 30th passage. This cell line has not secreted alpha‐fetoprotein. Hepatitis B viral particles or HBsAg have not been demonstrated in the cells from the primary culture nor in several subsequent subcultures tested.
Flow karyotype analysis and fluorescence‐activated sorting of burkitt‐lymphoma‐associated translocation chromosomes
Authors: Wirschubsky Zvi , Perlmann Catharina , Lindsten Jan , Klein George 
Published: February 2007

AbstractFlow karyotype analysis was performed to assess the feasibility of fluorescence‐activated sorting of Burkitt lymphoma (BL)‐associated translocation chromosomes. The typical 14q+ chromosome in the t(8;14) and the two “variant translations”, the 2q+ in the t(2;8) and the small 22q‐ in the t(8;22), could be identified as single peaks within the flow karyotypes of metaphase chromosomes isolated from several different BL‐lines for each translocation. The translocation chromosomes could be separated with a high degree of purity and in quantities suitable for biochemical analysis. The same analytical and preparative technique was also successfully applied to the identification and sorting of the Philadelphia (Ph1) chromosome in a 9;22 translocation‐carrying CML‐derived line and a familial (11;22) translocation.
Identification by a monoclonal antibody of a glycolipid highly expressed by cells from the human myeloid lineage
Authors: Girardet Christophe , Ladisch Stephan , Heumann Didier , Mach Jean‐Pierre , Carrel Stefan 
Published: February 2007

AbstractA monoclonal antibody4 (MAb) HL‐C5, which bound selectively to cells of the myeloid lineage tested, was derived from a fusion between P3/NS2/I‐AG8 myeloma cells and splenocytes from a mouse immunized with cells of the promyelocytic leukemia line HL‐60. Among a panel of 29 human cell lines derived from either hematopoietic or solid tumors, MAb HL‐C5 was found to react exclusively with cells from the five differentiated acute myeloid leukemia lines, HL‐60, MLI, ML2, ML3, KG‐IB and not with the less differentiated myeloid lines. Fluorescence‐activated cell sorter analysis of normal bone marrow samples confirmed that the reactivity of MAb HL‐C5 was limited to myeloid cells, from the promyelocytic stage of differentiation to the mature granulocytes. Indirect immunoperoxidase staining of cytocentrifuge preparations of normal bone marrow and peripheral blood leukocytes confirmed these results and showed that MAb HL‐C5 stained neutrophils but not eosinophils or basophils. The antigen recognized by HL‐C5 was recovered in the upper phase of chloroform‐methanol‐water lipid extracts prepared from HL‐60 cells. By competitive binding experiments, it was found that MAb HL‐C5 recognizes the same antigenic determinant as MAb WGHS 29‐1, which has been reported to react with glycolipids containing the sugar sequence lacto‐N‐fucopentaose III. Autoradiographs of thin layer chromatograms of HL‐60 glycolipid extracts which were revealed by incubation with MAb HL‐C5 or WGHS 29‐1 followed by the addition of 125l‐labelled rabbit anti‐mouse immunoglobulin antibody confirmed that the two MAbs reacted with the same or structurally very similar glycolipids.
Differential expression of c‐erbB, c‐myc and c‐myb oncogene loci in human lymphomas and leukemias
Authors: Roy‐Burman Pradip , Devi B. Gayathri , Parker John W. 
Published: February 2007

AbstractTotal cellular polyadenylated RNA from a variety of fresh human lymphoma and leukemia cells, characterized by histopathology and certain cell surface markers, was analyzed for the expression of three distinct cellular oncogenes (c‐oncgenes), c‐erbB, c‐myc and c‐myb by dotblot hybridization assays. Probes used were molecularly cloned DNA containing the respective oncogene sequence of avian erythroblastosis virus, myelocytomatosis virus (MC29) and myeloblastosis virus. All lymphoma‐leukemia cells irrespective of B, T or non‐B/non‐T lymphocyte lineage expressed the c‐erbB locus. This gene was also found to be active in normal peripheral blood lymphocytes and lymphocytes from lymph nodes showing reactive hyperplasia. This observation suggested that c‐erbB might be normally involved in cell growth functions since it was not unique to hematopoietic malignancies. In contrast to c‐erbB, elevated expressions of c‐myc or c‐myb were detected in certain neoplasms of B‐lymphocytes and some other lymphoproliferative disorders as compared to the majority of the samples tested which showed either low or undetectable levels of these transcripts. An examination of B‐cell lymphomas and leukemias in which the majority of the cellular populations expressed either Kappa or lambda surface lg light chain molecules revealed variations in the levels of c‐onc transcripts within a morphologic and immunologic subtype. These findings support the notion that, in general, genetic heterogeneity exists in groups of hematopoietic proliferations defined by conventional histopathologic and immunologic criteria. Although with the majority of the specimens there was no obvious correlation between the morphologic cell type of lymphoma/leukemia and the c‐onc RNA levels, interestingly two of the three samples diagnosed as chronic lymphocytic leukemia, B‐cell type, showed considerably increased transcription of the c‐myc gene relative to the other B‐cell neoplasms. Thus a class of differentiated B‐cell leukemia has been identified in which the molecular mechanisms which affect c‐mycgene expression can now be investigated.
Expression of human placental‐type alkaline phosphatase in primary breast cancer
Authors: McDicken I. W. , Stamp G. H. , McLaughlin P. J. , Johnson P. M. 
Published: February 2007

AbstractA monoclonal antibody (H317) with specificity for the heat‐stable placental‐type alkaline phosphatase (Pl‐ALP) isoenzyme has been used to investigate the occurrence of Pl‐ALP in patients with primary breast carcinoma. All pre‐operative plasma samples were negtive for Pl‐ALP in a sensitive solid‐phase enzyme immunoassay with a lower limit of detection of 0.1 U/I. In contrast, using a peroxidase‐anti‐peroxidase staining technique on fixed tissue sections, as well as enzyme immunoassay on fresh tissue extracts, Pl‐ALP could be demonstrated in the carcinomatous tissue of all seven patients investigated.
Variance in resistance to natural and antibody‐dependent cellular cytotoxicity and to complement‐mediated lysis among K562 lines
Authors: Kimber Ian , Moore Michael , Roberts Kevan 
Published: February 2007

AbstractIsolation of sub‐populations of the NK‐sensitive ery‐thro‐leukaemic cell line K562 by limiting dilution techniques has revealed‐marked clonal variation in susceptibility to natural cytotoxicity. Detailed examination of two such lines (E10/P2 and F9/P2) which differed significantly in their susceptibility to both native and activated NK‐cell‐mediated lysis revealed that their differences were stable and independent of culture conditions. The resistant (F9/P2) and sensitive (E10/P2) lines had comparable cold‐inhibitory and effector‐cell adsorption capacities, indicating that differential susceptibility was not attributable to variable expression of NK target structures. F9/P2 was also less susceptible to antibody‐dependent cellular cytotoxicity (ADCC) and complement‐mediated lysis, indicating the existence of variants with a generalized capacity to resist several immunolytic processes.
Genetic control of immune responses to moloney sarcomas in rats: Role of non‐RT‐1 background genes
Authors: Jones Joe M. 
Published: February 2007

AbstractBone marrow chimeras, athymic nude rats and a congeneic strain were utilized to verify and further examine non‐RT‐I linked background genes that influence immune responses of BN and LEW rats to Moloney sarcomas. In transplants that did not involve RT‐I incompatibility, infusion of high‐responder bone marrow into a lethally irradiated low‐responder recipient, or low‐responder bone marrow into a high‐responder recipient, would restore a high antibody response to the gp70 antigen of MuLV. Such transplants did not restore a high response to the p30 antigen. Athymic nude rats did not exhibit a significant response to either p30 or gp70 while euthymic littermates exhibited a significant response to both antigens. Growth of Moloney sarcomas as well as antibody and cellular responses to antigens expressed by such tumors were measured in LEW‐IN rats which carry the RT‐I of BN and the background of LEW. For each of these parameters, LEW‐IN resembled LEW more closely than BN.
Noncarcinogenic chemotherapy with a combination of vincristine, methotrexate and 5‐fluorouracil (VMF) in rats
Authors: Berger M. , Habs M. , Schmähl D. 
Published: February 2007

AbstractThe CMF regimen, which is clinically used in adjuvant therapy of breast cancer, is known to be carcinogenic in rats (Habs and Schmähl, 1981). To examine alternative regimens, a long‐term carcinogenicity study was performed, using the VMF regimen as follows: V (i.v.), M (i.p.) and F (p.o.) at 0.8, 20 and 300 mg/m2, respectively. These doses and a half‐dose regimen (0.5 VMF) were administered every 6 weeks to 80 rats (40 males, 40 females) in each of three groups. Group I served as an untreated control. Groups II, III and IV received 6 × VMF, 18 × 0.5 VMF and 18 × VMF, respectively. Unlike treatment with comparable doses of CMF, the present therapy did not result in an increased tumor rate or a change in tumor type over controls. The chemotherapeutic efficacy of VMF was compared with that of CMF by administering the following doses (mg/m2 i.p.) to groups of 20 rats bearing methylni‐trosourea‐induced primary mammary carcinomas: group I: C (420), 2: V (2.1), 3: M (35) and F (350), 4: C (210), M (21) and F (280), 5: V (1.05), M (21) and F (280), 6: as in 4 except that C was given 24 h prior to M and F, 7: as in 5 except that V was given 24 h prior to M and F, 8: ovariectomy on day 1, 9: control group. Animals bearing a tumor volume of ⩾ 0.8 cm3 were randomly allocated to the individual groups (day 1) and subsequently treated on days 1,8, 15 (V only) 22, and 29. After 5 weeks the following T/C values were recorded: group I: 12.6%, 2:80%, 3:49%, 4: 42.8%, 5: 67%, 6: 49.2%, 7: 26.5%, 8: 45.5%. These results indicate a possible superiority of VMF over CMF, since the former exhibits little or no carcinogenicity at comparable therapeutic activity.
Malignant myeloblastic transformation of murine long‐term bone marrow cultures by F‐MuLV: In vitro reproduction of a long‐term leukemogenesis, and investigation of preleukemic events
Authors: Heard Jean Michel , Fichelson Serge , Sola Brigitte , Martial Marie Antoinette , Berger Roland , Varet Bruno , Levy Jean Paul 
Published: February 2007

AbstractA Friend helper virus I−5(F‐MuLV) which induces my‐eloblastic leukemias in mice after a latency of several months, was used to infect long‐term bone marrow cultures. From 48 to 71 weeks after in vitro infection, 4/14 cultures gave rise to transplantable malignant myeloblas‐tic cells. These cells were shown to genuinely result from an in vitro transformation of virus‐infected normal bone marrow cells. The in vitro transformation reproduced the course of the in vivo disease. It provided unique material for in vitro investigation of the preleukemic stages of long‐term leukemogenesis. Successive cellular events were: (I) freezing of the normal myelomonocytic differentiation process; (2) change from factor‐dependent to an autonomous growth; (3) acquisition of in vivo tumorigenicity.
Incidence and type of tumors induced by DMBA carcinogenesis in H‐2 congenic strains on a B10 background
Authors: Grönberg Alvar , Cochran Alistair J. , Kärre Klas , Klein George , Klein Gunnar O. , Kiessling Rolf 
Published: February 2007

AbstractFive congenic strains on B10 background (B10, B10.S, B10.G, B10.BR and B10.A) were investigated for their susceptibility to tumor induction by 9,10 dimethyl‐1,2 benzanthracene (DMBA). The DMBA was administered via a stomach tube five times at weekly intervals (total 5 mg). Two types of malignancies predominated: diffuse lymphocytic lymphomas with or without thymic involvejent, and epidermal tumors. B10 (H‐2b) was the most resistant strain when total tumor incidences were compared. B10.S (H‐2s) had the highest incidence of both lymphomas and epithelial tumors and B10.G was significantly more susceptible to thymic lymphomas than B10. In B10.S mice thymic lymphomas were more frequent in males than in females, the reverse being true for tumors of epithelial origin. No correlation between tumor incidence and in vitro NK activity was demonstrated.
Histopathological study on N‐ethyl‐N′‐nitro‐N‐nitrosoguanidine‐induced colon cancer in dogs
Authors: Kamano Toshiki , Kishino Hiroshi , Mizukami Ken , Azuma Noboru , Tamura Junji , Katami Atsuo , Kidokoro Tsutomu 
Published: February 2007

AbstractWe prepared a suppository containing 50 mg of N‐ethyl‐N′‐nitro‐N‐nitrosoguanidine (ENNG), and successfully produced experimental colon cancer with good reproducibility by continuous intrarectal insertion of one or two suppositories per day in dogs. The tumors were very similar to human colon cancers, macroscopically and histologically. In one of three dogs subjected to histopathological study, metastases to the lymph nodes, lung, liver and kidney were observed. This animal model produced by a simple procedure will be helpful in investigating treatment of rectal cancer.
Rat AL2, AL3, AL4 and AL5 monoclonal antibodies bind to the common acute lymphoblastic leukaemia antigen (CALLA gp 100)
Authors: Lebacq‐Verheyden Anne‐Marie , Ravoet Anne‐Marie , Bazin Hervé , Sutherland D. Robert , Tidman Nicholas , Greaves Melvyn F. 
Published: February 2007

AbstractFour distinct rat monoclonal antibodies against the common ALL antigen (CALLA, gp 100) were obtained in a single fusion. Rat AL2, AL3, AL4, AL5 and the previously reported mouse J5 monoclonal antibodies identified the same subsets of leukaemic cells. AL2 and AL3 reacted weakly with terminal transferase‐positive cells in normal bone marrow and foetal liver, as well as with a minority of mature granulocytes in blood. Immunoprecipitation experiments and competitive binding assays demonstrated that the four rat antibodies and J5 bound to the same glycoprotein of approximately 100, 000 mol. wt This set of rat monoclonal antibodies directed against CALLA has not only a diagnostic usefulness but may also be of therapeutic value.