bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of a hepatocyte membrane antigen during hepatocarcinogenesis and in the developing liver of the rat
Authors: Matsumoto Masahiro , Tamakoshi Katsutoshi , Kanai Koichi , Kako Makoto , Fukumoto Tetsuo 
Published: February 2007

AbstractChanges in the expression of a cell membrane antigen during hepatocarcinogenesis and in the developing liver were analyzed by HAM.4, a monoclonal antibody (MAb) against a membrane glycoprotein of normal rat hepatocyte. Of the precancerous lesions observed during hepatocarcinogenesis induced by diethylnitrosamine, 2‐acetylaminofluorene and partial hepatectomy, early neoplastic foci were uniformly stained by HAM.4. In contrast, some cells in the neoplastic nodules at the late stage did not express HAM.4 antigen on the cell surface. Of the cancer tissues, well‐differentiated hepatocellular carcinomas were stained by HAM.4 whereas poorly differentiated carcinomas did not bind HAM.4. In developing rat liver, HAM.4 antigen was first expressed on fetal hepatocytes at the 18th day of gestation. It gradually increased until 4 weeks after birth when the intensity of the stain was almost the same as in adult rat liver. These results suggest that the expression of a membrane antigen defined by HAM.4 is closely associated with the differentiation of bile canalicular face and that HAM.4 might be useful in characterizing differentiation of cells during malignant transformation of hepatocytes.
Development of in vivo models for studies of brain metastasis
Authors: Schackert G. , Fidler I. J. 
Published: February 2007

AbstractTo develop an in vivo model for studies of brain metastasis, varying doses of K‐1735 tumor cells with differing metastatic potentials were injected into the carotid arteries of anesthetized mice. Direct intracerebral administration of cells produced tumors in the brain parenchyma, and all tumor cells produced melanotic lesions at these sites. Studies with radio‐actively‐labelled tumor cells confirmed that tumor cells reached the meninges and extracerebral organs. Distant metastases were found in the lungs and hearts of mice which received K‐1735 cells into the carotid artery, but not in animals which received tumorigenic non‐metastatic cells. Regardless of the type of cells injected, no growths were found in the meninges. The high degree of reproducibility recommends this model for studies designed to investigate the biology and therapy of cancer metastasis to the brain.
An atypical t(12;15) translocation of chromosomes found in murine plasmacytomas and activation of the c‐myc oncogene
Authors: Ohno Shinsuke , Takahashi Rei , Mihara Koh‐Ichiro , Chen Hui‐Ling , Migita Shunsuke , Sugiyama Taketoshi 
Published: February 2007

AbstractCells from murine plasmacytomas (MPC) consistently exhibit either the 12;15 or the 6;15 translocation. Recently, we found that cells from 2 MPC (ABPC 45 and ABPC 26) did not exhibit any known translocation. However, these MPC contained one chromosome 15 (15q‐) that was shorter than its normal homologue and one 12 (12q+) that was longer than its normal 12 counterpart. Chromosome 15q‐ contained only one thin D band, corresponding in size to either D1 or D3 band. A minor light band D2 was apparently deleted. Chromosome 12q+ contained a light F1 band that was longer than the normal 12F1. In ABPC 45, the c‐myc gene was assigned by in situ hybridization to the F1 region of 12q+ as well as to its original site of 15D2. Moreover, the in situ hybridization experiment assigned the Sα gene to the F1 regions of both chromosomes 12 and 12q+. These findings indicate that a minor light band D2 of chromosome 15 carrying the c‐myc gene was translocated into the major light band F1 of 12, resulting in a longer chromosome 12q+ and a correspondingly shorter chromosome 15q‐. This type of chromosomal translocation suggests that ABPC 45 developed through a cytogenetic mechanism different from that of MPC with the typical t(12;15) translocation.
Target‐cell specificity of hematopoietic regulatory proteins for different clones of myeloid leukemic cells: Two regulators secreted by krebs carcinoma cells
Authors: Shabo Yosef , Lotem Joseph , Sachs Leo 
Published: February 2007

AbstractThe normal myeloid hematopoietic regulatory proteins include one class of proteins that induces viability and multiplication of normal myeloid precursor cells to form colonies (called MGI‐1=CSF or IL‐3) and another class (called MGI‐2=DF) that induces differentiation of normal myeloid precursors without inducing cell multiplication. Different clones of myeloid leukemia cells can differ in their response to these regulatory proteins. The present experiments characterize proteins secreted by Krebs ascites carcinoma cells that induce differentiation of 2 different types of myeloid leukemic cell clones (clones II and 7‐M12). The results indicate the following: (1) Krebs cells produce 2 distinct and separable proteins, each inducing differentiation in one of the leukemic clones. (2) One protein induced differentiation of clone‐II myeloid leukemic cells and of normal myeloid precursor cells was free of any colony‐inducing (MGI‐1=CSF or IL‐3) activity, bound to double‐stranded mammalian DNA, and was thus a differentiation‐inducing protein MGI‐2, This MGI‐2 protein (MGI‐2A) was purified to a single silver‐stained band on an SDS polyacrylamide gel. (3) The other protein induced differentiation of clone 7‐M12 myeloid leukemic cells, did not bind to doublestranded DNA and could not be separated from the myeloid growth‐inducing protein MGI‐IGM (GM‐CSF) after 6 steps of purification including high‐pressure liquid chromatography. The use of specific antisera confirmed that the protein which induced differentiation of clone 7‐M12 leukemic cells was MGI‐IGM. The results show that Krebs ascites tumor cells produce 2 different myeloid hematopoietic regulatory proteins that differ in their target specificity for different clones of myeloid leukemic cells.
Autologous mixed lymphocyte‐tumor reaction and autologous mixed lymphocyte reaction. II. Generation of specific and non‐specific killer T cells capable of lysing autologous tumor
Authors: Uchida Atsushi , Moore Michael , Klein Eva 
Published: February 2007

AbstractThe specific and non‐specific nature of autotumor cytotoxicity induced in autologous mixed lymphocyte‐tumor culture (AMLTC) and autologous mixed lymphocyte culture (AMLC) was studied in patients with carcinomatous pleural effusions. Small‐ and medium‐sized blood lymphocytes that were isolated by centrifugation on discontinuous Percoll gradients did not lyse autologous, freshly isolated effusion tumor cells. In vitro activation of the small lymphocytes, but not of the medium lymphocytes, with autologous tumor cells generated cytotoxic potential restricted to autologous tumor. When stimulated with autologous non‐malignant non‐T cells, the medium lymphocytes, but not small lymphocytes, were triggered to cytotoxicity that acted not only on autologous tumor cells but also on allogenek tumor cells, T blasts, and tumor cell lines. Experiments using monoclonal antibodies (MAb) and complement (C) showed that both types of killer cells were CD2+CD3+CD16‐ T cells. Autotumor cytotoxicity developed in AMLTC was mediated by the CD4+CD8+ T cell subset in 6 of 9 cases and the CD4+ CD8‐ subset in the other 3 cases. In contrast, cytotoxicity induced in AMLC was exerted exclusively by the CD8+ subset. The enrichment of blasts from cultured T cells on discontinuous density gradients enhanced autotumor killing activity, with no reactivity recorded for blast depleted, resting T cells. Addition of mito‐mycin‐C‐treated large granular lymphocytes (LGL) to AMLTC abolished the induction of autotumor killer cells, whereas non‐specific killer cells were generated in AMLC irrespective of the pretence of LGL. These results indicate that stimulation of autoreactive T cells in AMLTC and in AMLC could induce 2 distinct types of autotumor killer cells.
Frequency of gallbladder cancer in chile, A high‐risk area
Authors: Nervi Flavio , Duarte Ignacio , Gómez Guillermo , Rodríguez Germán , Pino Guido Del , Ferrerio Osvaldo , Covarrubias Carmen , Valdivieso Vicente , Torres María Isabel , Urzúa Alejandro 
Published: February 2007

AbstractWe report an autopsy study of gallbladder cancer prevalence in Chile, where the risk of this disease is among the highest reported world‐wide. In 14,768 autopsy protocols obtained from 3 university hospitals, 45% of women and 20% of men older than 20 years had gallstone disease (the major known risk factor for gallbladder cancer). The prevalence of gallbladder cancer in Chileans was compared to that found in a Swedish‐Chechoslovakian autopsy study previously published. These countries were chosen because of their high frequency of gallstone disease. The comparison was performed by using logistic regression models adjusting for possible differences in the age‐sex structure or the true incidence of gallstones in both populations. We found that the most important single risk factor for gallbladder cancer in Chile was gallstone disease, with an estimated effect on the logistic scale meaning that the cancer risk for subjects with gallstones is seven times higher than for those without the disease. Second in importance was the risk for sex, women being 2.8 times higher than for men. The estimated difference in the sex composition and the incidence of gallstones resulted in 17.9% higher odds of cancer in Chile than in Sweden and Czechoslovakia. However, this difference was not significant. This study suggests that the major etiologic factors of gallbladder cancer in Chileans, Swedes and Czechoslovakians are primarily related to gallstone disease.
Epidemiologic evidence of an association between body iron stores and risk of cancer
Authors: Selby Joseph V. , Friedman Gary D. 
Published: February 2007

AbstractBiologic evidence suggests that high body iron stores could promote development of cancer. Because a previous study had shown an association between prescribed iron medication and lung cancer risk in men, we examined recent iron use as well as 2 additional indirect measures of body iron stores, anemia and the total iron‐binding capacity (TIBC) of plasma, in relation to subsequent risk of cancer in a larger cohort of 174,507 persons. Women, but not men, who reported recent iron use had a lower risk of lung cancer Chan those who did not [RR = 0.60, 95% confidence limits (CL) 0.37, 0.97] after adjustment for age and cigarette smoking. Women who had used iron appeared to remain relatively iron‐depleted. Risk for other cancers was slightly, but not significantly, lower in women who used iron. Anemia (hemoglobin < 12 g) was also associated with lower risk of lung cancer in women (RR = 0.61, 95% CL 0.61, 0.98), but not in men. TIBC, which is inversely related to body iron stores, was inversely related to risk of lung cancer in women in a graded fashion (RR = 0.41, 95% CL 0.23, 0.73 comparing highest with lowest quartile). In men, a protective effect of higher TIBC against lung cancer was suggested, but did not reach statistical significance. These indirect measures of body iron stores appeared to reflect iron stores better in women than in men, probably because variability in iron stores is greater in women and iron deficiency more prevalent. A possible alternative explanation for our findings is incomplete adjustment for the confounding effects of cigarette smoking. This could apply to iron use and hemoglobin level which were related to smoking, but not to TIBC, which was nat. These data, which indicate lower risk of cancer in iron‐depleted women, lend epidemiologic support to the hypothesis that high iron stores may increase cancer risk, at least for lung cancer.
Ectopic expression of the Y (Ley) antigen defined by monoclonal antibody 12‐4LE in distal colonic adenocarcinomas
Authors: Bara Jacques , Mollicone Rosella , Herrero‐Zabaleta Eugenie , Gautier Rodolphe , Daher Nagib , Oriol Rafael 
Published: February 2007

AbstractMonoclonal antibody (MAb) 12‐4LE reacts specifically with the αFuc(1‐2)βGal(1‐4)[αFuc(1‐3)]GlcNAc‐R synthetic oligosaccharide and consequently characterizes the Y (Ley) antigen. In normal individuals, this MAb reacts more strongly on samples from blood group O persons, indicating that the Y structure is better recognized when terminal A or B sugars are not added to the Y structure. In fetal and normal adult gastrointestinal tract, this antibody reacts with the epithelium of stomach, small intestine and proximal colon, but not of distal colon. In the adult, cells from the surface epithelium of the gastric, small intestinal and cecal mucosae express the Y antigen according to the secretor phenotype of each individual, thus characterizing the so‐called “upward differentiation” pattern. In contrast, mucus cells of the pylorus and duodenal Brünner glands, as well as Paneth cells, always express the Y antigen irrespective of secretor phenotype, thereby characterizing the so‐called “downward differentiation” pattern. Proximal fetal colonic mucosa has the same genetic control as the downward differentiation pattern of the adult. Distal fetal colonic mucosa is negative with anti‐Y, as in the adult. Y antigen was not expressed in hyperplastic (10 cases), juvenile (5 cases) or adenomatous (42 cases) polyps, except for some spreading villous adenomas in which rare Y‐positive foci could be observed but which were not specifically associated with dysplastic glands. Polyps from familiar polyposis did not express this antigen. In adenocarcinomas, the Y antigen was expressed in 41/45 (91%) of distal tumors and 15/35 (43%) of cecal tumors, independently of ABO phenotype. The ectopic expression of this Y antigen on distal colon adenocarcinomas may be a useful tool in the detection of distal colonic carcinomas.
Syngeneic in vivo passage of the murine BW 5147 lymphoma results in the expression of a stable metastatic phenotype
Authors: De Baetselier Patrick , Roos Ed , van Hecke Dominique , Verschaeve Luc , Brys Lea , Verschueren Hendrik 
Published: February 2007

AbstractBW 5147 lymphoma tells are non‐invasive tumor cells which do not generate experimental m etas Cases following i.v. inoculation. In contrast, s.c. and intra‐splenic (i.s.) growth of BW cells resulted in widespread colonization of liver and spleen. Cells derived from either s.c. tumors or metastatic lesions did generate metastases after i.v. administration. The capacity of these tumor‐derived BW cells to disseminate via blood‐borne cells was irreversible and stable, indicating that one in vivo passage of BW cells results in the generation of new, metastatic BW variants. Concomitantly, these variants exhibited an inherent invasive potential as manifested by their capacity to infiltrate in vitro monolayers of hepatocytes and fibro‐blasts. The BW variants expressed new membrane markers such as H‐2 antigens, the Lyt 1,2 T‐cell differentiation antigen and the MTH antigen (a newly defined membrane antigen, expressed predominantly on murine metastatic T‐cell lymphomas and mature T lymphocytes). This phenomenon was observed with both cloned and uncloned BW populations, suggesting that an inductive rather than a selective mechanism accounts for the transition of BW cells towards a more malignant phenotype. These observations confirm the concept that local factors at the growth site of a tumor might influence the metastatic behavior of that tumor, possibly via induction of silent differentiation programs.
Albumin‐negative hepatocytes in sprague‐dawley x analbuminemic F1 rats treated with hepatic carcinogens
Authors: Ogawa Katsuhiro , Yokota Kin‐Ichi , Sonoda Tomoko , Piao Zhi Si , Mori Michio , Nagase Sumi 
Published: February 2007

AbstractAnalbuminemic rats (NAR) are a mutant breed with an inherent inability to synthesize albumin. However, heterozygous rats born of a pair of NAR and Sprague‐Dawley (SD) rats can synthesize albumin. Immunohistochemical staining for albumin shows that, although the majority of hepatocytes of SD x NAR F1 (female SD x male NAR) rats are positive for albumin, a small number of hepatocytes are negative. These albumin‐negative hepatocytes are frequently found in the form of clusters which appear cytologically normal. When the rats were given a dietary regimen of 2‐acetyl‐aminofluorene (2‐AAF), there was a significant increase in the number of albumin‐negative hepatocytes. On the other hand, diethylni‐trosamine (DEN) or 5‐azacytidine did not increase the number of albumin‐negative hepatocytes. 2‐AAF and DEN also induced enzyme‐altered hepatocytes but the albumin‐negative hepatocytes were of a completely different class from the enzyme‐altered hepatocytes. The results of this study indicate that some kind(s) of carcinogens induce mutated hepatocytes which are probably not involved in carcinogenesis.
Both N‐ras and c‐myc are activated in the shac human stomach fibrosarcoma cell line
Authors: Andeol Y. , Nakdeux P. C. , Daya‐Grosjean L. , Brison O. , Cebrian J. , Suarez H. 
Published: February 2007

AbstractA transforming N‐ras gene was isolated from the SHAC human stomach fibrosarcoma cell line. A single‐point mutation resulting in the substitution of histidine for glutamine at codon 61 was found in the SHAC transforming allele. The N‐ras gene is overexpressed in the tumor cells and transformant cells. The N‐ras p21 product was studied by immunoprecipi‐tation and showed no alteration in mobility as compared to the normal p31 protein. The c‐myc gene is amplified and overexpressed in these cells. This report gives evidence that an amplified c‐myc and a mutated N‐ras gene are both present in this tumor cell line and provides support for the idea that co‐operation of at least 2 activated cellular oncogenes is required for carcinogenesis.
Three epstein‐barr virus (EBV)‐determined nuclear antigens induced by the BamHI E region of EBV DNA
Authors: Shimizu Norio , Yamaki Mitsuo , Sakuma Sadatoshi , Ono Yasushi , Takada Kenzo 
Published: February 2007

AbstractIn our previous study (Takada et al., 1986a), we showed that the BamHI E fragment of Epstein‐Barr virus (EBV) DNA induces a nuclear antigen that is detected by human antisera against EBV‐determined nuclear antigen (EBNA), when transfected into baby hamster kidney (BHK) cells. The present study shows that the sub‐fragment containing the central open reading frame BERF2b of the BamHI E fragment (Baer et al., 1984) is responsible for nuclear antigen induction. In addition, 2 fragments corresponding to 2 other open reading frames of the BamHI E, BERF1 and BERF4 also induce nuclear antigens upon transfection into BHK cells. These 3 antigens, designated RF2b, RF1 and RF4 antigens, were serologically classified as EBNA and andgenically distinct. In immunoblotting analysis of latently EBV‐infected BJ‐B95‐8 cells, 3 high‐molecular‐weight polypeptides (136, 142 and 147 kDa) ware identified by anti‐EBNA sera. Immunoblotting analysis of transfected BHK cells indicated that the RF2b antigen is 145 kDa in its native form and antigenically related to the 147‐kDa protein of BJ‐B95‐B cells. Although RF1 and RF4 antigens were not detected by immunoblotting, reactivities of sera with RF1 and RF4 antigens in the immunofluorescence test were correlated with those of sera with the 136‐ and 142‐kDa polypeptides of BJ‐B95‐8 cells, respectively. The results suggest that 3 high‐molecular‐weight proteins of latently EBV‐infected cells are encoded by 3 open reading frames of the BamHI E DNA fragment.
Variants of amphotropic type‐C retrovirus isolated from cultures of moloney‐ and rauscher‐MuLV‐induced tumors
Authors: Chang Kenneth S. S. , Wang Lai‐Che , Gao Changlie 
Published: February 2007

AbstractWe isolated and characterized 2 strains of type‐C retrovirus, R5NX and YACNX, from established lymphoid cell cultures derived from Rauscher‐MuLV‐induced lymphoma (RBL‐5) in a C57BL/6 mouse, and Moloney‐MuLV‐induced lymphoma (YAC) in an A‐strain mouse, respectively. The RSNX and YACNX viruses were compared with the prototype 4070A strain of amphotropic virus isolated from feral mice in California, and were found to belong to the same amphotropic virus class on the basis of viral interference, neutralization tests, and other biological properties. However, they were not quite identical with respect to viral neutralization antigens and restriction enzyme cleavage patterns of the proviral DNA. The possibility that these viruses may have been present in the original tumor together with the R‐MuLV or M‐MuLV as “exogenous” viruses rather than as contaminants of cell cultures by the 4070A virus is discussed. Although these 1 new isolates were not pathogenic when inoculated into newborn C3H/HE mice, they could establish persistent infections in these mice.
Enzymatic elimination of O6‐ethylguanine from the DNA of ethylnitrosourea‐exposed normal and malignant rat brain cells grown under cell culture versus in vivo conditions
Authors: Huh Nam‐Ho , Rajewsky Manfred F. 
Published: February 2007

AbstractThe developing rat brain exhibits a pronounced susceptibility to the tumorigenic effect of ethylnitrosourea (EtNU) and an extremely low repair activity for the DNA alkylation product O6‐ethylguanine (O6‐EtGuar‐). We have recently found that a collection of malignant neural cell lines originating from prenatal BDIX‐rat brain cells were all highly O6‐EtGua repair‐proficient (O6‐EtGuar+). Subcloned lines showed considerable variability of the repair capacity, suggesting instability of the O6‐EtGua repair phenotype. Using one of the subcloned lines (BT3Caf) as a model, we show here that BT3Caf cells grown in monolayer culture repair O6‐EtGua much more rapidly than those grown in the form of s.c. tumors in BDIX‐rats (whereas O6‐ethylthymine is not repaired under either condition). Furthermore, normal prenatal BDIX‐rat brain cells (O6‐EtGuar‐ in vivo) gradually acquire an O6‐EtGuar‐ phenotype upon transfer to long‐term monolayer culture. The cellular capacity for enzymatic DNA repair is of particular relevance in relation to both the malignant transformation of normal cells and the therapeutic inactivatton of cancer cells by DNA‐reactive drugs. Further analyses are thus required of the molecular mechanisms controlling the expression of DNA repair enzymes as a function of cell differentiation, in terms of the cellular response to altered microenv iron mental conditions, and in search for possibilities to reduce the repair capacity of cancer cells.
High tumour prolactin receptor content and lack of increase in serum prolactin levels as predictors of good response to endocrine therapy in rat mammary cancer
Authors: di Carlo F. , Muccioli G. , Bellussi G. , Conti G. , Racca S. 
Published: February 2007

AbstractCorrelations between anti‐neoplastic activity of medroxy‐progesterone acetate (MPA), on the one hand, and serum prolactin (PRL) levels as well as tumour PRL and insulin receptor content, on the other, were investigated in female rats bearing dimethylbenzanthracene (DMBA)‐induced mammary tumours. Changes in liver PRL receptor concentrations were also studied. MPA was injected for 15 days. Regression was observed in 16 out of 50 (32%) tumours from rats treated with MPA. Twenty‐seven out of 50 (54%) continued to grow regardless of treatment. Stasis was seen in the remaining 7 tumours (14%). Serum PRL levels increased significantly in rats with tumours which were non‐responsive to MPA. Concentration of PRL receptors in the liver of all animals was reduced by MPA treatment. A remarkable increase occurred only in those mammary tumours which responded to therapy. The concentrations of PRL receptors in the tumours non‐responsive to MPA were similar to those detected in control tumours. Unlike PRL receptors, tumour insulin receptor levels were not modified by MPA treatment, five out of 14 tumours (35.7%), previously growing in spite of MPA administration, regressed when bromocriptine was added to MPA. A significant reduction in serum PRL levels occurred in all rats undergoing the latter treatment. No difference was observed between responsive and non‐responsive animals; on the contrary, the PRL receptor content of responsive tumours increased significantly in comparison with that of non‐responsive tumours.