bluuebunny/crossref_metadata_2025_split huggingface dataset:
Chromosomal banding patterns in human large bowel cancer
Authors: Reichmann Amelia , Martin Paulette , Levin Bernard 
Published: February 2007

AbstractCytogenetic banding studies were performed on direct preparations from 31 large bowel tumors. Twenty‐eight of these were from primary sites and three from metastases. Some distinctive patterns were observed. The 31 tumors were separable into four groups: (1) Tumors with normal karyotypes (three cases); (2) tumors with simple gains of chromosomes (three cases); (3) tumors with gains, losses and structural aberrations (ten cases). Groups 1, 2 and 3 were all in the diploid range; and (4) tumors with hypotriploid‐hypotetraploid karyotypes (15 cases). Non‐random gains of several chromosomes, especially No. 8 and non‐random losses of No. 17 were seen in this series. Thirteen cases had sex chromosome abnormalities. The most prominent structural abnormalities involved chomosomes No. 1 and No. 5. Marker chromosomes were sometimes absent, but when present ranged from simple translocations to the most complex rearrangements. Doubling of chromosome and/or marker chromosomes were prominent in Group 4. Double minutes were seen in all three metastatic tumors and three primary cancers. Premature chromosome condensation was observed in three cases in the hypotriploid‐hypotetraploid group.
Kaposi's sarcoma. IV. Detection of CMV DNA, CMV RNA and CMNA in tumor biopsies
Authors: Boldogh I. , Beth E. , Huang E.‐S. , Kyalwazi S. K. , Giraldo G. 
Published: February 2007

AbstractIn order to determine whether human cytomegalovirus‐ (CMV) DNA homologous sequences as well as CMV‐specific RNA(s) and antigen(s) exist in tumor biopsies of Kaposi's sarcoma (KS) DNA‐DNA reassociation, RNA‐DNA in situ cytohybridization and anticomplement immunofluorescence test (ACIF) tests were applied. Three of 10 DNAs extracted from Kaposi sarcoma biopsies contained DNA sequences homologous to radioactively labelled human CMV DNA probe. The amount of CMV DNA in these sarcoma tissues was calculated to range from 0.7 to 1 genome equivalent per diploid cell. The presence of virus‐specific RNA was also demonstrated in sections from five of 10 tumor biopsies. CMV‐determined nuclear antigen(s) (CMNA) present in variable degrees were also demonstrated. In contrast, we could not detect any herpes simple virus type II (HSV‐2) or Epstein‐Barr virus (EBV) DNA sequences in DNA of these tumor biopsies. Furthermore, there were no detectable HSV‐2 or EBV‐specific RNA or virus‐specific antigens in sections of these biopsies. These results provide new lines of evidence for the relationship between CMV and Kaposi's sarcoma.
Increased cancer incidence in the progeny of male rats exposed to ethylnitrosourea before mating
Authors: Tomatis L. , Cabral J. R. P. , Likhachev A. J. , Ponomarkov V. 
Published: February 2007

AbstractResults from previous experiments have indicated the persistence of an increased cancer risk in subsequent generations following prenatal exposure to a chemical carcinogen. In the present experiment, the possible role of prezygotic events in determining cancer risk was investigated in the progeny of male rats treated with ethylnitrosourea (ENU) before mating with untreated females. Eight BDVI male rats were given a single i.p. dose of 80 mg/kg bw ENU and each rat was then caged at weeks 1, 2, 3 and 4 after treatment with three untreated females. Fertility was lower and preweaning mortality higher in the experimental group, as compared to controls, particularly at the 4th‐week mating. Survival rates after weaning were similar in the progeny of treated males and controls, as was the total incidence of tumours. However, analysis of tumour incidence at the various organ sites showed an increased incidence of neurogenic tumours in the progeny of ENU‐treated males, as compared to that of controls.
Embryo‐derived teratocarcinoma. III. Development of tumors from teratocarcinoma‐permissive and non‐permissive strain embryos transplanted to F1 hybrids
Authors: Solter Davor , Dominis Mara , Damjanov Ivan 
Published: February 2007

AbstractSeven‐day‐old mouse embryos of two teratocarcinoma‐permissive (C3H and BALB/c) and two teratocarcinoma‐non‐permissive (C57BL/6 and AKR) strains were transplanted to their F1 hybrids to determine the role of the genetic background of the recipient animals in controlling embryo‐derived teratocarcinogenesis. The yield of teratocarcinomas in F1 hybrid recipients of embryonic grafts was either identical with the yield in syngeneic recipients or increased or decreased, depending on the strain of the embryo and the F1 hybrid combination. In certain hybrids, the yield of malignant tumors remained the same as in the syngeneic recipients but the F1 hybrids exerted a stimulatory effect on tumor growth and the tumors weighed more than those in syngeneic recipients. A matroclinous effect was also seen in certain hybrids. These data indicate that embryo‐derived teratocarcinogenesis in histocompatible F1 mice depends on the genetic background of adult recipients. The teratocarcinogenic potential of non‐permissive and permissive strain mouse embryos can be modified by choosing appropriate F1 hybrids for embryonic transplantations.
Correlation of glycosphingolipids and sialic acid in YAC‐1 lymphoma variants with their sensitivity to natural killer‐cell‐mediated lysis
Authors: Yogeeswaran G. , Gronberg A. , Hansson M. , Dalianis T. , Kiessling R. , Welsh R. M. 
Published: February 2007

AbstractSialoglycoconjugates and glycosphingolipids were quantitated in a series of variants derived from the YAC‐1 lymphoma, known to be highly sensitive to natural killer (NK)‐cell‐mediated lysis. The variants, which had widely diverging sensitivities to NK cells, were obtained by a number of methods, including selection in the presence of NK cells, antibody to H‐2, or antibody to the murine leukemia‐virus‐induced antigen, and by fusion of sensitive cells with an NK‐resistant cell line, A9HT. The sensitivities of these cells to NK‐cell‐mediated lysis did not correlate with their sensitivities to anti‐H‐2a cytotoxic T cells. While no correlation could be made between the NK‐sensitivity of these variants and their total cellular sialic acid, a statistically significant inverse correlation was observed between the levels of percentage neuraminidase releasable surface sialic acid of total labelled sialyl components and sensitivity to NK cells. This correlation with cell surface sialic acid was observed with either endogenous or lymphocytic choriomeningitis virus‐induced activated NK cells as effectors. Neuraminidase treatment of insensitive target cells caused a moderate increase in sensitivity but failed to render the resistant targets as sensitive as YAC‐1. Analysis of glycosphingolipids among the variants revealed a strong positive correlation between the total cell neutral glycolipid with chromatographic migration of asialo‐GM2 and sensitivity to endogenous or activated NK‐cell‐mediated lysis. Significant correlations were not found with any other neutral glycolipids. However, ganglioside homologues with chromatographic mobility of GM1, GD1a, GD1b, and GT also showed a positive correlation with both endogenous and activated NK‐cell‐mediated lysis. The ratio of asialo‐GM2 to GM2 had a highly significant positive correlation with sensitivity. These correlative results suggest that asialo‐GM2 and certain gangliosides could be involved in binding or lytic events in NK cell:target cell interactions, and that high levels of sialic acid and sialylation on the cell surface may inhibit and/or modify such interactions. Further studies with these YAC variants should be useful for examining the biochemical bases of target cell‐effector cell interactions in the NK‐system.
Liver cell dysplasia in association with hepatocellular carcinoma, cirrhosis and hepatitis b surface antigen in Hong Kong
Authors: Ho Joana C. I. , Wu Piu‐Chee , Mak Tak‐Kwan 
Published: February 2007

AbstractLiver‐cell dysplasia was identified in 60% of 558 cases of cirrhosis with and without hepatocellular carcinoma (HCC) in Chinese coming to necropsy in Hong Kong from 1963 to 1978. A significant correlation was found between liver‐cell dysplasia and the identification of hepatitis B surface antigen (HBsAg) in the livers, suggesting that dysplasia may be causally related to hepatitis B virus (HBV). Applying Bayes' theorem to our series of male deaths, we calculated that for Chinese male non‐cirrhotics showing liver‐cell dysplasia at necropsy, compared with male non‐cirrhotics showing no liver‐cell dysplasia, the approximate risk factor for HCC is 13:1, whereas for male cirrhotics with liver‐cell dysplasia, compared with male cirrhotics without liver cell dysplasia, the risk factor for HCC is approximately 2:1. In the presence of dysplasia, the risk for HCC is increased two‐fold in males who are also HBsAg‐positive. Thus, the presence of liver‐cell dysplasia in cirrhotic or non‐cirrhotic livers accompanies a significantly higher risk of developing HCC, especially in the presence of HBsAg.
Phenotypic changes of human neuroblastoma cells in culture induced by 12‐O‐tetradecanoyl‐phorbol‐13‐acetate
Authors: Påhlman Sven , Odelstad Lena , Larsson Erik , Grotte Gunnar , Nilsson Kenneth 
Published: February 2007

AbstractSK‐N‐SH and SH‐SYSY human neuroblastoma cells treated by 12‐O‐tetradecanoyl‐phorbol‐13‐acetate (TPA) express morphological and biochemical changes, which indicate that differentiation towards more mature cells has occurred. The most prominent morphological changes were the development in 40–60% of the cells of cell‐surface projections longer than 50 μm and cytoplasmic neurosecretory granules demonstrated by electron microscopy. At the biochemical level, TPA induced a two‐fold increase in the relative activity of neuron‐specific enolase and 30‐ to 40‐fold increase in noradrenaline and adrenaline concentrations. A decrease in proliferation rate of TPA‐treated cells was observed. The biological effects of TPA were slightly potentiated by nerve growth factor.
A single‐dose protocol for azaserine initiation of pancreatic carcinogenesis in the rat
Authors: Yager James D. , Roebuck Bill D. , Zurlo Joanne , Longnecker Daniel S. , Weselcouch Edward O. , Wilpone Seri A. 
Published: February 2007

AbstractPreviously, the induction of pancreatic carcinogenesis in the rat using azaserine has involved a multiple‐dose treatment protocol. The objective of the present study was to determine the effect of multiple azaserine treatments on pancreatic DNA synthesis and to develop a protocol for a single‐dose initiation of pancreatic carcinogenesis by azaserine in the rat. Pancreatic DNA synthesis in young rats, which was determined by measuring the amount of [3H]‐thymidine incorporation into DNA, was found to be elevated at 4.3 weeks of age and to decrease to a baseline level by 6.3 weeks. Treatment of 4‐week‐old rats with azaserine resulted in a dose‐dependent inhibition of [3H]‐thymidine incorporation into both pancreatic and liver DNA. Maximum inhibition was seen at 10 mg/kg body weight. This inhibition was followed by a gradual return of incorporation to normal values over a 48 h period. One week following pretreatment with four weekly injections of azaserine at 30 mg/kg, [3H]‐thymidine incorporation into pancreatic and liver DNA was significantly elevated, suggesting that multiple injection protocols cause enhanced DNA synthesis which could have a co‐carcinogenic and/or promotional effect. Single‐doses of azaserine (10, 30 and 60 mg/kg) given at 7 weeks of age caused the appearance of more atypical acinar cell nodules (AACN) than when given at 5 weeks of age. The most effective dose was 30 mg/kg. Using alkaline elution, we determined that this response was due to the occurrence of more DNA damage in the 7‐week‐old animals. Thus, these results demonstrate a rationale for the use of single‐dose initiation protocols in the pancreas. An effective single‐dose protocol for induction of AACN in azaserine‐treated rats fed semi‐synthetic diet is presented.
Incidence of ovarian cancer in relation to the use of oral contraceptives
Authors: Weiss Noel S. , Lyon Joseph L. , Liff Jonathan M. , Vollmer William M. , Daling Janet R. 
Published: February 2007

AbstractFemale residents of six counties in Washington and Utah in whom a diagnosis of ovarian cancer was made during 1975–79 were interviewed concerning prior use of oral contraceptives. Interviews with a random sample of women drawn from these same counties were obtained for comparison. A smaller proportion of women with epithelial ovarian tumors had taken oral contraceptives than had controls: the estimated risk of ovarian cancer in uses relative to that in non‐users was 0.57 (p = 0.04). The magnitude of the decreased risk depended on the duration over which oral contraceptives had been taken, as the negative association was present only after 4 or more years of use. In many ways, the use of oral contraceptives mimics the physiologic effects of pregnancy. The results of the present investigation, when interpreted together with those from other epidemiologic studies and from experiments in animals, suggest that, like pregnancy, the use of oral contraceptives has a protective effect against the development of ovarian cancer.
Dietary factors and breast cancer risk
Authors: Lubin Jay H. , Burns Patricia E. , Blot William J. , Ziegler Regina G. , Lees Alan W. , Fraumeni Joseph F. 
Published: February 2007

AbstractAs part of a case‐control study in northern Alberta, Canada, 577 women aged 30–80 with breast cancer diagnosed during 1976–77 and a population‐based agestratified random sample of 826 disease‐free female controls were questioned about certain aspects of their diet. Computing relative risks (RRs) by tertiles, significant increasing trends were found with more frequent consumption of beef (RRs of 1.0, 2.3, 1.5; test for trend, p <0.001), pork (RRs of 1.0, 1.6, 2.2; test for trend, p <0.001), and sweet desserts (RRs of 1.0, 1.3, 1.5; test for trend, p = 0.01). Elevated risks were also noted for use of butter at the table and for frying with butter or margarine, as opposed to vegetable oils. The association of total beef and pork consumption with breast cancer was not materially affected by controlling for age at first birth, family history of breast cancer, previous benign breast biopsy or socioeconomic status. Nor was the association reduced by controlling for ages of menarche and menopause, even though within the control series the intake of beef and pork reported in adult life was higher among those with a lower age at menarche or a older age at natural menopause.
Is testicular cancer incidence related to marital status?
Authors: Davies Joan M. 
Published: February 2007

AbstractIn Western countries there has been a striking rise in the incidence of testicular cancer among young men, but little is known about the aetiology of the disease. Epidemiological studies in the USA have yielded conflicting findings on a possible relationship between marital status and testicular cancer. National analyses of 1957‐61 deaths in England and Wales by marital status were published in 1964, and showed that under the age of 65 single men had higher death rates from this cause than married men. Possible interpretations of these findings are discussed.
Phenotypic drift of metastatic and cell‐surface properties of mammary adenocarcinoma cell clones during growth in vitro
Authors: Neri Anthony , Nicolson Garth L. 
Published: February 2007

AbstractWe have examined cell clones obtained from a 13762 mammary adenocarcinoma tumor and its spontaneous lung metastasis for phenotypic stability during serial culture passage in vitro. Two clones that varied markedly in their metastatic properties were chosen for further examination. One of these clones (MTC) obtained from the parental transplanted tumor initially failed to metastasize within 23 days post‐injection s.c. but gained the ability to form spontaneous pulmonary metastases after several serial passages in vitro. Another clone (MTLn3) derived from a spontaneous lung metastasis was initially highly metastatic after short‐term culture, but lost the potential to form large numbers of spontaneous lung metastases with long‐term culture. In contrast to MTA, clone MTLn3 displayed lymph‐node metastasis, and the frequency of lymph‐node involvement increased when late‐passage cultures of MTLn3 cells were assayed in vivo. Both clones from late‐passage cultures produced larger tumor sizes at the primary (mammary fat pad) injection sites compared to early passage cells. The morphologies of MTC cells changed with serial tissue culture passage, while the morphologies of MTLn3 cells did not change. The display of fibronectin on MTC cells by immunofluorescence did not change with culture passage; fibronectin was not detected in cultures of clone MTLn3. Fibronectin was also found on MTC cells by cell surface labelling using lactoperoxidase‐catalyzed iodination‐sodium dodecylsulfate polyacrylamide gel electrophoresis‐autoradio‐graphy. lodination of fibronectin on MTC cells did not vary with culture passage, and as in immunofluorescence experiments it was not detected on MTLn3 cells. There was a decrease in exposure of certain cell surface proteins on MTC cells with culture passage, but we did not detect modifications with this procedure that correlated with culture passage of MTLn3 cells. We conclude that prolonged culture in vitro can result in modifications of metastatic and cell‐surface properties of tumor cell clones.
Incidence and type of tumors induced in C57BL bg/bg mice and +/bg littermates by oral administration of DMBA
Authors: Argov Shmuel , Cochran Alistair J. , Kärre Klas , Klein Gunnar O. , Klein George 
Published: February 2007

AbstractAs an attempt to study the effect of the beige (bg) mutation on chemical carcinogenesis, 64 C57Bl/bg/bg mice and 83 +/bglittermate controls received DMBA in five weekly intragastric doses. The incidence of tumors of different histological types was monitored through observation periods ranging between 165 and 500 days. By 165 days after the first DMBA feeding, 18% of the +/bg and 31% of the bg/bg mice had developed tumors. The beige mice had a higher incidence of epithelial and non‐epithelial tumors arising in cutaneous or subcutaneous sites than the controls. The total incidence of lymphomas was similar in the two groups. However, lymphomas appeared somewhat earlier in beige than in control mice. Altogether 33 +/bg and 27 bg/bg mice were followed for 500 days. By this time, 73% of the +/bg and 78% of the bg/bg mice had developed tumors. The beige group showed a higher incidence of non‐thymic lymphomas than the controls. In contrast, the incidence of thymic lymphoma, cutaneous epithelial tumors and bile‐duct adenomas was similar in the two groups or higher in +/bg than in bg/bg mice. The results suggest that the bg mutation causes a certain defect in a mechanism that may prevent or delay the onset of nonthymic lymphomas and of epithelial and non‐epithelial cutaneous tumors in DMBA‐treated mice. The differences between the two groups were smaller than those previously reported in relation to the increased susceptibility of beige mice to certain transplanted tumors, attributed to the known defect in natural killer (NK) activity in the beige mice. The reduced differential in the DMBA system may be due to the partial reduction of NK activity, induced by the carcinogen, as reported previously (Ehrlich et al., 1980) and confirmed in the present study.
Quantitative studies of natural immunity to solid tumours in rats. NK activity in animals with primary or transplanted spontaneous tumours
Authors: Flannery Graham R. , Brooks Colin G. 
Published: February 2007

AbstractNatural killer (NK) cell activity was measured in a quantitative 6 h chromium release assay using sarcoma Mc7 cells as targets. The total NK lytic activity present in the spleen and blood of tumour‐bearing animals was compared with the corresponding values for age/sex/ parity‐matched animals. Rats with primary spontaneous tumours in the breast or subcutaneous sites showed normal levels of NK activity, while rats with primary spontaneous kidney tumours had elevated NK activity, the degree of augmentation being greater with increasing tumour size. A similar elevation of NK activity was generally found in animals with large, transplanted, spontaneous or chemically‐induced tumours. This augmentation could only be detected when total lytic activity was considered: when NK activity was measured merely on a cell‐for‐cell basis, it often appeared to be depressed in such animals, in agreement with previous reports. However, with one rapidly metastasizing spontaneous tumour, a real depression of both spleen and blood NK activity was found. Small inocula of cells from non‐immunogenic spontaneous mammary tumours or from other non‐immunogenic spontaneous tumours caused no early increase in systemic NK activity when injected into the mammary pad, a site where spontaneous tumours frequently arise. However, cells from one immunogenic spontaneous tumour and 2/3 immunogenic chemically‐induced tumours did occasionally stimulate significant early increases in NK activity when placed at this site. Early changes in peritoneal exudate NK activity were also investigated using small inocula of these tumours injected intraperitoneally. Augmentation of NK activity occurred with a 3‐fold greater frequency following inoculation with immunogenic tumour cells than with non‐immunogenic cells in this system. It can be concluded from these studies that: (1) spontaneous tumours do not selectively arise in members of an inbred strain with subnormal NK activity; (2) most large tumours in rats stimulate rather than depress NK activity; (3) early boosting of NK activity by small inocula of tumour cells placed in the mammary pad does not occur with non‐immunogenic spontaneous tumours; (4) early boosting of NK activity in the peritoneal site does occur with non‐immunogenic tumours, but with a very low frequency. The latter findings suggest that developing spontaneous tumours are unlikely to stimulate the NK system, and emphasize the importance of using syngeneic, spontaneous tumours for studying tumour‐host relationships in animals.
Heterotransplantation of small‐cell carcinoma of the lung into nude mice: Comparison of intracranial and subcutaneous routes
Authors: Gazdar Adi F. , Carney Desmond N. , Sims Harvie L. , Simmons Alfreda 
Published: February 2007

AbstractWe compared and contrasted intracranial (i.c.) and subcutaneous (s.c.) heterotransplantation of small‐cell carcinoma of the lung (SCCL) into athymic nude mice. Fresh human SCCL tumor specimens, tumor colonies grown in soft agarose and continuous cell lines were used. Tumors induced by the three types of specimens were similar, but s.c. and i.c. transplants differed. S.c. tumors had longer latent times, were non‐invasive and non‐lethal. l.c. tumors had shorter latent periods, invariably grew in the meninges, frequently invaded and destroyed the underlying brain, and were lethal. The tumor‐inducing dose for i.c. transplantation was 10 to 1,000 times lower than for s.c. transplantation. Pooled colonies of SCCL tumor specimens grown in soft agarose were inoculated i.c. While they contained relatively small numbers of cells (400–10,000), 83% of these colony specimens induced tumors after 58–243 days, confirming the «stem‐cell» origin of the colonies. l.c. and s.c. transplants retained the characteristic morphology of SCCL, and, with one exception, did not metastasize to distant organs. Continous cell lines could be established readily from both types of transplants, and they retained the characteristic cytology, growth and biochemical properties of the original SCCL tumors. l.c. heterotransplantation of SCCL is a useful tool, especially when small numbers of tumor cells are available, and may provide a model to study the biology and therapy of meningeal carcinomatosis.