bluuebunny/crossref_metadata_2025_split huggingface dataset:
Risk factors of breast cancer in burma
Authors: Thein‐Hlaing  , Thein‐Maung‐Myint  
Published: February 2007

AbstractA hospital‐based case‐control study of breast cancer was undertaken in Rangoon. The age‐standardized incidence rate, 25.1 per 100,000 woman‐years and the shape of the age‐incidence curve show that Rangoon women have an intermediate level of breast cancer risk compared to women of other countries in the world. The analysis is based on 193 cases and 400 controls. Breast cancer risk was found to be directly related to educational attainment. There was an increased risk associated with early menarche and late menopause. The most striking finding was the strong inverse relationship between risk and parity; women who had six or more children have only one‐third the breast cancer risk of married women who had less than four children. This association is not confounded by case‐control differences in age at birth of first child. The association of breast cancer risk with age at first birth was not striking; only women with a first birth after age 30 were at increased risk. Breast cancer risk was unrelated to lactation. Overall, the epidemiology of breast cancer in Burma is similar to that in most other countries. However, the possibility of an unusual relationship of risk to parity and age at first parturition warrants further exploration.
Melphalan‐induced chromosome damage in sensitive and resistant human melanoma cell lines
Authors: Parsons P. G. , Morrison Leanne 
Published: February 2007

AbstractTwelve consecutive treatments of a human melanoma cell line (MM253) with melphalan gave a subline (MM253‐12M) which was five times more resistant to melphalan with respect to survival. In contrast to mustard‐resistant rodent cells, the MM253‐12M line had a higher stemline number than the parent line while growth rate and cell and colony morphology were unchanged. A further melphalan treatment following attempted mutagenesis with UV did not increase resistance. In a comparison of these two lines with two melanoma lines derived from other patients and the rat XC line, resistance was correlated with lower frequency of melphalan‐induced chromosome aberrations, determined 48 h after a 4‐h exposure to melphalan(3 μg/ml). In the two cell lines studied, aberration‐free metaphase cells from treated culture had fewer chromosomes than untreated cells. DNA synthesis studied in the 4‐ to 72‐h period after treatment was inhibited to the same extent in MM253 and MM253‐12M cells at 4 μg/ml but to a greater extent in the sensitive line at 0.1‐1.5 μg/ml. During the first hour of treatment at 0.1‐1.5 μg/ml, DNA synthesis in MM253 appeared to be enhanced.
Genetic transmission of mammary tumour virus in the DBAf mouse strain
Authors: Verstraeten A. A. , Van Nie R. 
Published: February 2007

AbstractMTV antigens were demonstrable by radio‐immunoassay in milk samples from individual DBAf mice, and in samples from (♀B́LB/c × ♂DBAf) F1 mice. Although some samples collected during the first lactation periods of these mice were virus‐negative, all samples of later lactation periods were virus‐positive. From 75 mice of the [♀(♂BALB/c× ♂ BALB/c× DBAf)]Bc I population, milk samples were collected during one or more lactation periods and tested for the presence of viral antigens; the samples of 42 mice were virus‐positive. In the {([BALB/c ×(BALB/c × DBAf)]) × BALB/c}Bc II population two groups were distinguished. In the first group, the progeny of virus‐positive Bc I mothers, 37 out of 62 mice had detectable levels of viral antigen in the milk. None of the 43 samples from mice of the second group, derived from MTV‐negative Bc I females, were virus‐positive. These data suggest that the presence of viral antigens in the milk of DBAf mice is controlled by a single dominant gene; evidence for linkage of this gene and the albino locus was obtained (recombination percentage: 20).
Mammary leukaemia (ML) antigen isolated from L1210 leukaemia cells
Authors: Zak‐Nejmark Teresa , Steuden Jadwiga , Radzikowski Czesławs 
Published: February 2007

AbstractCrude 3 M KCI extracts from L 1210 cells and purified ML antigen were characterized and the presence of ML antigens was verified by various anti‐ML sera, as well as by antisera to disrupted MMTV B particles. Selected ML‐positive fractions from preparative polyacrylamide electrophoresis and purified ML antigen isolated by affinity chromatography were analyzed by polyacrylamide disc electrophoresis. With both procedures the same sharp band was obtained. The molecular weight of both preparations was found to be 73,500 as estimated. The relationship between ML antigen, MMTV antigenic products and cell‐associated viral proteins is discussed.
Specificity of acquired clonal chromosome abnormalities in new zealand black mice
Authors: Fialkow Philip J. , Bryant Jean I. , Friedman Jan M. 
Published: February 2007

AbstractNew Zealand Black (NZB) mice, an inbred strain characterized by immunological dysfunction and lymphoreticular malignancy, also develop populations of aneuploid spleen cells. In detailed cytogenetic analyses performed on 10 NZBs, the chromosomally abnormal cells were found to be clonally related within each mouse. Moreover, the karyotypic changes observed were highly non‐random, usually involving the 15 (10/10 mice), 2 (8/10 mice), 16 or 17 (9/10 mice), and sex (6/10 mice) chromosomes. These observations suggest an important relationship between chromosomal alterations and tumorigenesis in NZB mice and emphasize the role of chromosome 15 in murine abnormal lymphoreticular proliferations.
Relationship between epstein‐barr virus (EBV)‐production and the loss of the ebv receptor/complement receptor complex in a series of sublines derived from the same original burkitt's lymphoma
Authors: Klein George , Yefeno Eitan , Falk Kerstin , Westman Anitha 
Published: February 2007

AbstractVirus production, EBV (P3HR‐1 substrain) superinfectability, IdUrd inducibility, EBV receptor and complement (C3) receptor expression were assessed in two independently maintained Jijoye lines, the derived P3HR‐1 clone that releases a growth inhibitory and cytopathic, non‐transforming viral mutant, and in non‐producer sublines derived from the P3HR‐1 line by the spontaneous cessation of virus production. Both Jijoye lines were superinfectable, inducible, and carried EBV and C3 receptors. Virus‐producing P3HR‐1 cells and recently derived non‐producer sublines lacked EBV‐receptors and C3 receptors, could not be superinfected, but were IdUrd inducible. Two long‐passaged non‐producer sublines of P3HR‐1 reexpressed EBV and C3 receptors to an equal degree (different in the two sublines). EBV‐superinfectability became partially reestablished in the subline with the higher expression of EBV and C3 receptors. These findings support the hypothesis that the EBV‐receptor/C3 receptor negativity of the producer P3HR‐1 sublines and their recent non‐producer derivatives is due to negative selection by the growth‐inhibitory, cytopathic P3HR‐1 virus variant. The closely linked disappearance and reappearance of EBV‐receptors and complement receptors gives further support to the idea that these two receptors are either identical or closely linked constituents of the cell membrane.
Failure to relate the anti‐tumour action of cyclophosphamide with the immunogenicity of two murine fibrosarcomas
Authors: Evans R. 
Published: February 2007

AbstractA single intraperitoneal injection of cyclophos‐phamide (CY) had a stronger anti‐tumour effect upon two syngeneic mouse fibrosarcomas when given within a few days of tumour implantation than when given 7‐20 days after. CY was more active against the fast‐growing, relatively non‐immunogenic CBA fibrosarcoma, FS13, inducing a higher proportion of permanent regressions, than the slower‐growing, highly immunogenic C57BL fibrosarcoma, FS6, at all comparable stages of tumour growth. Whole‐body irradiation, which suppressed concomitant immunity in FS6‐tumour‐bearing mice, had no effect on the anti‐tumour action of CY. A study of the cellular composition of the tumour masses over a 4‐day period immediately after CY injection showed that there was a decrease in total cell yields, involving mainly a decrease in neoplastic cells, although normal cells, Fc‐receptor‐positive and ‐negative, were also affected to a lesser degree. The overall findings indicated a lack of correlation between the anti‐tumour effects of CY and tumour immunogenicity. Moreover, it was apparent that the anti‐tumour action of CY was mediated by a direct effect of its metabolites on neoplastic cells rather than by host anti‐tumour effector mechanisms.
Genetic control of sensitivity to moloney‐virus‐induced leukemias in mice. I. Demonstration of multigenic control
Authors: Gisselbrecht S. , Pozo F. , Debré P. , Hurot M. A. , Lacombe M. J. , Levy J. P. 
Published: February 2007

AbstractThe appearance of hematopoietic malignancies and the level of viremia were studied in mice of different inbred strains and their F1 or F2 hybrids inoculated with the Moloney leukemia virus (MLV) The viremia was regularly measured in individual mice by radioimmunoassay of the major internal virion component p30. A complex genetic control was found. (1) The level of circulating virus was controlled by at least two genes. An H‐2 linked gene, tentatively called Rmv‐1, displayed a dominant sensitivity. Alleles for resistance existed in H‐2b and H‐2r haplotypes and alleles for sensitivity in H‐2a, H‐2d and H‐2f. Another gene with dominant resistance mapped outside the H‐2 complex and probably interacted with Rmv‐1. (2) A good correlation existed between viremia and the appearance of leukemias, the most viremic strains being also the most leukemic. (3) Nevertheless, additional genes which were not involved in the viremia control could be determinant in the induction of malignancies. One of them with a resistant allele in DBA/2 mice seemed to inhibit the appearance of leukemia despite a high level of viremia. Another gene controlled the spleen involvement resulting in generalized leukemias in sensitive lines contrasting with mainly thymus‐localized tumors in resistant animals.
Murine rous‐sarcoma‐specific immunity detected by leukocyte adherence inhibition: Inhibitory effect of normal serum
Authors: Wikstrand Carol J. , Proctor Jude O. , Hartsell Stephen C. , Haughton Geoffrey 
Published: February 2007

AbstractThe standard one‐stage lymphocyte adherence inhibition (LAI) assay was used to investigate cellular and humoral immune responses within the murine Rous sarcoma system. Significant specific cellular reactivity to Rous sarcoma antigen extracts was detected when the responder peritoneal exudate cells (PEC) were obtained from mice bearing or immunized against primary or transplanted Rous sarcomas; no cellular reactivity to control methylcholanthrene (MC)‐induced tumor antigen extracts was observed. Similarly, specific cell‐mediated recognition of MC tumor antigen extract was demonstrated. Initial experiments designed to assess the role of serum components in the LAI assay demonstrated that normal mouse serum of C57BL/10ScSn, B10.D2, or A/WySn origin, either fresh or frozen, obtained from old (over 7 months) or young (under 6 weeks) mice non‐specifically abrogated the specific loss of PEC adherence.
EBV antigens in lymphocytes of patients with exudative tonsillitis, infectious mononucleosis and hodgkin's disease
Authors: Veltri Robert W. , McClung James E. , Sprinkle Philip M. 
Published: February 2007

AbstractA protocol utilizing isokinetic gradients to isolate human lymphocytes is combined with another that purifies the C3 receptor‐bearing B lymphocyte subpopulation, thus enriching the EB virus genome‐carrying population. Also, rabbit antisera were prepared to the Epstein‐Barr virus nuclear antigen (EBNA) and the early antigen (EA) and utilized in an indirect immunofluorescence test (IIT) to detect these antigens in human lymphocytes isolated from various disease states. Using these methods we demonstrated excellent correlation between standard methods previously employed to detect EB virus‐coded antigens and our IIT employing xenogenic antisera. Such tests were done on lymphoblastoid cell lines as well as lymphocytes isolated directly from patients with EB vims lymphoproliferative diseases. Human palatine tonsil‐derived lymphocytes from children with exudative tonsillitis and peripheral blood lymphocytes of infectious mononucleosis contained only EBNA in C3 receptor‐bearing B lymphocytes. However, patients with lymphoproliferative disorders, including Hodgkin's disease, harbored in their spleens and lymph nodes lymphocytes producing both EBNA and EA.
Initial tumor cell arrest in animals of defined coagulative status
Authors: Glaves D. , Weiss L. 
Published: February 2007

AbstractExperiments were made to evaluate the potential role played by thrombogenic factors on the hematogenous arrest of circulating tumor cells in mice with demonstrable coagulopathies associated with the presence of a primary tumor, by administration of “therapeutic” doses of anticoagulants. The effects of warfarin, aspirin and heparin administration on the early arrest patterns of 125IdUrd‐labelled TA3 carcinoma and Gardner lympho‐sarcoma cells injected intravenously into tumor‐bearing mice were examined. Several hematologic parameters of carcinoma‐ and lymphosarcoma‐bearing animals were measured prior to anti‐coagulation experiments and the results indicated that mice had coagulopathies similar to those found in cancer patients with disseminated intra‐vascular coagulation syndrome, i.e., thrombocyto‐penia and elevated fibrinogen levels. Despite the presence of coagulation abnormalities and effective anticoagulation in recipient animals, all three agents were without effect on localization patterns of both tumor types. It was concluded that the proposed involvement of thrombogenesis in metastasis was probably not due to any role played by those clotting factors inhibited by aspirin, warfarin and heparin in early intravascular tumor cell arrest.
The specificity of neutralizing antibodies to feline leukaemia viruses
Authors: Russell Peter H. , Jarrett Oswald 
Published: February 2007

AbstractFeline leukaemia viruses (FeLV) of subgroups A (FeLV‐A), B (FeLV‐B) and C (FeLV‐C) were examined by neutralization. The FeLV‐A isolates were monotypic. By contrast, there was antigenic variation within subgroups B and C. There was also considerable cross‐reactivity between subgroups. Thus, FeLV‐A viruses showed weak cross‐reactivity to the standard FeLV‐C isolate; four of the subgroup B viruses were identical and cross‐reacted with the standard FeLV‐C, but not with FeLV‐A or the fifth FeLV‐B, and this latter virus weakly cross‐reacted with FeLV‐A but not with the FeLV‐C; within subgroup C, one virus was indistinguishable from the standard FeLV‐C strain but the other two were very similar to FeLV‐A. Therefore, subgroup classification based on interference did not altogether correspond with neutralizing behaviour for subgroups B and C.
Effects of corynebacterium parvum and cortisone on the primary lewis tumour and its metastases
Authors: Jones P. D. E. , Sadler T. E. , Castro J. E. 
Published: February 2007

AbstractThe effects of Corynebacterinm parvum and cortisone acetate (CA) on the primary Lewis lung carcinoma and its pulmonary metastases were investigated. C. parvum given IV either on the same day or 7 days after tumour inoculation, reduced primary tumour growth, while 2.5 mg CA (high‐dose) given SC 4 and 11 days after tumour, alone or in combination with C. parvum, administered on day 0, reduced primary tumour growth to the same extent as C. parvum alone. High‐dose CA given on days 2 and 6 had no effect on primary tumour growth or the action of C. parvum, administered on day 7, while 0.05 mg CA (low‐dose) given on days 4 and 11 did not alter tumour growth or the action of C. parvum, given at the same time as tumour. High‐dose CA given 4 and 11 days after tumour caused a significant enhancement in metastases. C. parvum given to these mice on the same day as tumour significantly reduced the pulmonary nodules but only to the level found in control, saline‐treated mice. In mice given C. parvum alone, metastases were significantly reduced when compared with controls. Similarly, high‐dose CA given on days 2 and 6 significantly enhanced metastases, and C. parvum on day 7 reduced their level to that found in control mice. Low‐dose CA had no effect on the number of metastases or the antimetastatic action of C. parvum. The relevance of these results to the clinical situation is discussed.
Infectious mononucleosis and Hodgkin's disease
Authors: Muñoz N. , Davidson R. J. L. , Witthoff B. , Ericsson J. E. , De‐Thé G. 
Published: February 2007

AbstractA cohort of 9,454 patients with infectious mono‐nucleosis, serologically confirmed, was followed up to determine their risk of developing lymphopro‐liferative diseases. A total of 1,759 patients was identified in Scotland from 1959 to 1971 and 7,695 in Sweden from 1952 to 1970. The cancer cases were identified by matching the list of patients with infectious mononucleosis against a list of patients with lymphoma, nasopharyngeal and colon carcinomas registered through 1972 in Sweden and through 1973 in Scotland. A four‐fold increase in risk was found for Hodgkin's disease based on 7 cases observed against 1.8 expected. Most of the excess cases of Hodgkin's disease occurred within three years of the diagnosis of infectious mononucleosis and among females. These results are similar to those of four other cohort studies and it is concluded that a positive association exists between infectious mononucleosis and Hodgkin's disease. Several explanations of this association were evaluated. Firstly, it may be that a very small proportion of persons who are in the course of developing Hodgkin's disease are temporarily misdiagnosed as having infectious mononucleosis. Secondly, infectious mononucleosis may increase the susceptibility to a factor which causes or promotes the development of Hodgkin's disease. Thirdly, infectious mononucleosis and Hodgkin's disease may share a common aetiology. Arguments in favour of, or against, each of these explanations are presented.
Chromosome 14 translocations in non‐burkitt lymphomas
Authors: Fukuhara Shirou , Rowley Janet D. 
Published: February 2007

AbstractChromosome studies were performed on malignant cells obtained from 27 patients with non‐Burkitt lymphomas. A marker chromosome affecting the long arm of No. 14 (14q+) was the single most frequent abnormality and was noted in 17 of these patients. The frequency of the 14q+ marker varied with the type of lymphoma. For patients with malignant lymphoma, histiocytic, the frequency was 5 of 8; for mixed‐cell type, 1 of 3; for poorly differentiated lymphocytic, 8 of 8; for well‐differentiated lymphocytic, 0 of 3; for lymphoblastic, 0 of 1; for Hodgkin's disease, 2 of 3; and for mycosis fungoides, 1 of 1. The donor chromosome involved in the 14q translocation was identified in 12 cases; certain chromosomes appeared to be affected more frequently than others. Although the break point was band 14q32 in most cases, the exact location of the receptor site on 14q was not always consistent. The distal part of 14q24 was also involved as a receptor site in at least one translocation. These findings suggest that, in some types of lymphoid malignancy, cells with a 14q translocation have a proliferative advantage over cells with other chromosome re‐arrangements. The presence of the 14q translocation may be important in the future for the distinction among morphologically different, but functionally comparable, subgroups of lymphoid malignancies.
Regional differences in tumor growth: Studies of the vascular system
Authors: Auerbach Robert , Morrissey Lawrence W. , Kubai Louis , Sidky Younan A. 
Published: February 2007

AbstractWe have previously shown that tumor cells inoculated into the thoracic region of the trunk grow much more rapidly and with a higher frequency than do an equivalent number of cells injected more posteriorly. We thought that these results might have been a reflection of an underlying difference in the vascular system supplying these regions of the trunk. The present experiments which were undertaken to characterize various aspects of the vascular system associated with the transplantation sites used in these studies include measurements of rates of diffusion of salt solutions, of protein clearance, and of the retention of radio‐labelled cells and cellular debris. We have examined local differences in temperatures and studied the effect of change of ambient temperature on those local differences as well as on tumor growth. More directly, we have measured blood flow to the capillaries by intracardiac administration of radioactive microspheres, and assessed the ability of inoculated tumor cells to induce angiogenesis. We have been unable to detect any major differences in the parameters of the vascular system that we have analyzed. Thus we cannot offer any satisfactory explanation for the observed four‐fold differences in tumor growth in anterior vs posterior inoculation sites. The results are discussed in terms of underlying developmental gradients which can be invoked to provide a basis for further experimentation.
A portion of the feline leukaemia virus genome is not endogenous in cat cells
Authors: Okabe H. , Dubuy J. , Gilden R. V. , Gardner M. B. 
Published: February 2007

AbstractAlthough viral sequences closely related to feline leukaemia virus are represented in multiple copies in cellular DNA of all domestic cats, a specific fraction was present only in the virus‐infected cells. This fraction was detected by viral cDNA enriched by a prior absorption of a total complementary DNA (cDNA) transcript with normal cat liver DNA. The recycled cDNA hybridized well with the cellular DNA of virus‐infected cells, but to a lesser extent with DNA from uninfected cat cells. The probe was used to differentiate virus‐positive from virus‐negative tumour tissues of cats. The same approach with cDNA of another endogenous feline virus, RD114, failed to show any difference between a virus‐infected cell line and normal cells, including both virus‐inducible and non‐inducible lines.
Relationship of tumor‐specific transplantation antigens to the histocompatibility complex: Dissociation of in vitro alloantigen expression and in vivo alloimmunity from tumor‐specific transplantation antigen strength
Authors: Chauvenet P. H. , Smith R. T. 
Published: February 2007

AbstractThe studies reported here explore the relationship between tumor‐specific transplantation antigens (TSTA) and (1) the expression of serologically defined specificities, and (2) the immunogenicity of H‐2K‐ or H‐2D‐determined alloantigens on methylcholanthrene (MCA)‐induced murine fibro‐sarcomas. Expression of H‐2K and H‐2D serologically‐detected private specificities on groups of tumors raised in B10.A, B10.BR or B10.D2 strains varied greatly among tumors. No regular reciprocal or direct relationship to tumor TSTA strength was found. Each tumor, however, expressed H‐2K or H‐2D alloantigens stably as determined by direct cytotoxicity or absorption techniques. Even those tumors expressing little or no detectable alloantigen by serologic analysis were immunogenic in H‐2K or H‐2D incompatible congeneic hosts. This was assayed in terms of capacity to evoke primary or secondary tumor resistance, and to induce allo‐antibody toward private H‐2K or H‐2D end specificities. An exception was that B10.BR tumors failed to induce anti‐H‐2Dk antibody despite strong surface alloantigen expression. While TSTA strength did not correlate with serologically detected alloantigen expression, TSTA strength did tend to correlate inversely with capacity to resist primary growth in the H‐2K different host, and directly with resistance in the H‐2D different host.