bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hormone sensitivity in vitro and in vivo of v‐ras‐transfected mcf‐7 cell derivatives
Authors: Van Roy F. , Mareel M. , Vleminckx K. , Beyaert R. , Fiers W. , Devleeschouwer N. , Muquardt C. , Legros N. , Bracke M. , Leclercq G. 
Published: February 2007

AbstractHuman mammary carcinoma cell lines (MCF‐7) were analysed for their hormone sensitivity before and after transfection with a v‐Ha‐ras oncogene or with a neomycin‐resistance gene followed by selection in vitro or in vivo. Our aim was to test how the expression of the ras oncogene would influence the estradiol sensitivity of MCF‐7 cells. In culture, MCF‐7 cells expressing the viral p21 oncogene product, as compared to parental MCF‐7 cells and their control derivatives, showed lower levels of a 67‐kDa estrogen receptor. Progesterone receptors, however, remained sensitive to up‐regulation by estrogens. The oncogene‐expressing cells were less sensitive than all controls to stimulation of proliferation by 10‐8M estradiol or to inhibition of proliferation by 2‐CH3‐4‐OH tamoxifen, and this was not dependent upon the type of culture medium used. After s. c. or i. p. injection into female athymic nude mice, ovariectomized or left intact, the growth of MCF‐7 cells expressing the ras oncogene product and of all control cells was sensitive to stimulation by estrogen supplementation. Conversely, cell lines derived from tumors generated with long latency in untreated athymic nude mice by v‐ras‐expressing MCF‐7 cells showed efficient formation of quickly growing tumors in the absence of estrogen supplementation. No differences were observed in invasion and metastasis of the different MCF‐7 cell types injected into athymic nude mice that were supplemented with estrogens or not.
Inflammation and anti‐tumor resistance. V. Production of a cytostatic factor following cooperation of elicited polymorphonuclear leukocytes and macrophages
Authors: Hevin Marie‐Brigitte , Friguet Bertrand , Fauve Robert M. 
Published: February 2007

AbstractWhen Lewis tumor cells (3LL) included in a gel of polyacrylamide microbeads are injected into mice and recovered I day later, incorporation of 125I‐UdR is strongly reduced. In contrast, no reduction is observed in irradiated mice. The cytostatic effect is non‐existent in 6 hr‐old granuloma (granulocytes 909%, macrophages 10%), but is maximal in 48 hr‐old granuloma (granulocytes 50%, macrophages 50%). When 6 hr‐old granuloma cells (which are not cytostatic) are incubated with bone‐marrow‐derived macrophages (BMs) (which are slightly cytostatic), considerable cytostasis against 3LL is observed, such an effect being strongly reduced if the 2 cell populations are separated. This suggests that close contact of live polymorphs with macrophages is necessary for full expression of cytostasis. No increase in cytostasis of bonemarrow macrophages is observed when BMs are incubated with a cell‐free extract of freeze‐thawed 6‐hr‐old granuloma cells. Cell contact is not necessary between granuloma cells and 3LL since the cytostatic activity is found in the supernatant of incubated phagocytic cells. Cytostasis is also observed with B16, P815, J774 cells and normal mouse bone‐marrow cells. An active cytostatic fraction has been purified from the supernatant of 48‐hr‐old granuloma cells following molecular filtration and HPLC. The cytostatic factor has a low molecular weight (400–500 daltons), is not a peptide and presents maximum absorption at 267 nm.
The use of clonogenic assays in assessing the response of human lung cancer cell lines to α and γ interferons alone or in combination with adriamycin
Authors: Jabbar S. A. B. , Twentyman P. R. 
Published: February 2007

AbstractThe antiproliferative and cytotoxic effects of purified IFN‐α and recombinant IFN‐γ were investigated using both direct cell counting and a clonogenic assay on a panel of 5 established human lung cancer cell lines and for 2 of them also on their multidrug‐resistant counterparts. There was considerable heterogeneity in the response of the cell lines to the IFNs in terms of growth inhibition. Clonogenic assay of IFN‐treated cells indicated that, where a cell line had responded markedly to an IFN, only a small fraction of the cells remaining after IFN treatment were clonogenically viable. When cells were placed into the clonogenic assay in the presence of IFNs, the time course of colony formation was different from that seen in the control cultures for most of the cell lines. The measured “surviving fraction” was greatly dependent upon the time of colony counting. When the effects of IFNs in combination with ADM were studied, conclusions regarding the interaction of the effects of the agents also depended upon the time at which colonies were counted.
Specific chromosomal mutagenesis observed in stimulated lymphocytes from patients with S‐ANLL
Authors: Mamuris Zissis , Dumont Jeanine , Dutrillaux Bernard , Aurias Alain 
Published: February 2007

AbstractAn analysis of R‐banded PHA‐stimulated lymphocytes from 13 patients with secondary acute non‐lymphocytic leukemia (S‐ANLL) following breast cancer or lymphoma, and treatment by alkylating agents and/or radiotherapy, is reported. We found that chromosomes 5, 7, 11 and 17 are over‐involved in structural rearrangements. These anomalies are similar to those observed in the same categories of patients without S‐ANLL, and after in vitro treatment of normal lymphocytes by the alkylating agent melphalan. These anomalies are thus likely to be induced by treatment, independently of S‐ANLL. However, the same chromosomes (5, 7, 11 and 17) are recurrently deficient in leukemic S‐ANLL clones. In spite of these similarities, it remains unlikely that the deficiencies observed in leukemic clones were directly induced at the time of treatment. Probably, treatment of primary cancers induces nonrandom mutations of recessive genes located on these chromosomes as also indicated by chromosomal lesions. Various rearrangements including deletions of the homologous normal counterparts may then occur, unmasking mutated recessive genes. The latter stage would be concomitant with the leukemogenic process.
Gastrin‐releasing peptide in normal and neoplastic human lung: Measurement and biochemical characterization
Authors: McKillop Jane M. , McCann John P. , Gibbons John R. P. , Johnston Colin F. , Buchanan Keith D. 
Published: February 2007

AbstractLevels of gastrin‐releasing peptide (GRP) were determined by radioimmunoassay in human normal main and lobar bronchus and parenchymal lung tissue extracts. It was found that the level of GRP differed significantly between all 3 areas. The concentration of GRP was statistically higher in main bronchus (median 6.74 ng/g) compared to both lobar bronchus (median 4.79 ng/g) and parenchymal lung (median 1.73 ng/g), and also statistically higher in lobar bronchus compared to parenchymal lung. Chromatographically, GRP‐immunoreactivity in both main and lobar bronchial extracts corresponded to GRP1‐27 and GRP18‐27, while in lung tissue only one major species was identified which corresponded in retention time to GRP18‐27. No significant difference was detected when the levels of GRP in normal lobar bronchus and normal lung tissue were compared to the levels in lobar bronchus and lung taken from patients with lung carcinoma, at a site adjacent to the carcinoma. However, a significant difference was observed between the GRP content of normal main bronchus compared to main bronchus from patients with carcinoma. GRP was measured in 26/56 lung carcinomas examined. The levels ranged from 42,000 ng/g in a carcinoid tumour to 0.18 ng/g in a squamous‐cell carcinoma, though only in 6 tumours were the levels outside the range determined for normal pulmonary tissue. Chromatography of selected tumour extracts of different histopathologies showed that there were differences in the GRP products present.
Age at first birth, parity and risk of breast cancer: A meta‐analysis of 8 studies from the nordic countries
Authors: Ewertz Marianne , Duffy Stephen W. , Adami Hans‐Olov , Kvåle Gunnar , Lund Eiliv , Meirik Olav , Mellemgaard Anders , Soini Irma , Tulinius Hrafn 
Published: February 2007

AbstractSeveral large epidemiological studies in the Nordic countries have failed to confirm an association between age at first birth and breast cancer independent of parity. To assess whether lack of power or heterogeneity between the countries could explain this, a meta‐analysis was performed of 8 population‐based studies (3 cohort and 5 case‐control) of breast cancer and reproductive variables in the Nordic countries, including a total of 5,568 cases. It confirmed that low parity and late age at first birth are significant and independent determinants of breast‐cancer risk. Nulliparity was assoclated with a 30% increase in risk compared with parous women, and for every 2 births, the risk was reduced by about 16%. There was a significant trend of increasing risk with increasing age at first birth, women giving first birth after the age of 35 years having a 40% increased risk compared to those with a first birth before the age of 20 years. Tests for heterogeneity between studies were not significant for any of the examined variables. In the absence of bias, this suggests that several individual Nordic studies may have had too little power to detect the weak effect of age at first birth observed in the meta‐analysis.
Western blot analysis of serological responses following immunization with vaccinia viral lysates of melanoma cells
Authors: Hersey P. , Werkman H. , Edwards A. E. 
Published: February 2007

AbstractWestern blot analysis was used to characterize the antibody response of melanoma patients during immunization with vaccinia‐virus‐induced melanoma cell lysates (VMCL). Strong antibody responses were detectable within 4 weeks from commencement of immunization against different fractions (from 3 to 10) in blots of VMCL. The approximate MW of the main fractions identified were 100, 91, 85, 77, 64‐66, 49, 46, 43 and 34‐36 kDa. Comparison of the reactivity of the sera with extracts of vaccinia virus suggested that the reactivity against VMCL was not against viral antigens in the lysates. Studies on autologous extracts from 7 patients immunized with VMCL indicated that the majority of the fractions identified in extracts of VMCL were also identified in autologous extracts of melanoma cells. This indicated vaccine‐induced responses against the patients' tumor cells and not merely against alloantigens in the vaccine. Sera from the immunized patients appeared to identify a number of fractions of similar MW in extracts of colon and glioma cells, suggesting that the responses were not specific for melanoma. Possible exceptions were reactivity against melanoma fractions of 85, 64‐66 and 36 kDa. Our studies provide evidence for the effectiveness of VMCL in inducing antibody responses against autologous melanoma cells and form a basis for subsequent biochemical and genetic analysis of the antigens identified by antibody responses in immunized patients.
Induction of macrophage procoagulant expression by cisplatin, daunorubicin and doxorubicin
Authors: Wheeler Helen R. , Geczy Carolyn L. 
Published: February 2007

AbstractCisplatin, doxorubicin and daunorubicin (drugs which intercalate with DNA) influenced the membrane‐bound procoagulant potential of murine thioglycollate‐induced peritoneal exudate (TG‐PEC) macrophages and the monocytoid cell line WEHI 265, whereas the antimetabolites 5‐fluorouracil and methotrexate had no effect. Enhanced procoagulant was not caused by non‐specific toxicity of these agents. Cisplatin directly increased the procoagulant expressed on WEHI 265 cells, whereas MPCA on TG‐PEC was enhanced only when cisplatin was combined with a second stimulant, either bacterial lipopolysaccharide (LPS) or interferon (IFNγ). WEHI 265 cells failed to respond to the anthracycline drugs, either alone or in combination with LPS, whereas they enhanced the IFNγ response. Doxorubicin and daunorubicin increased the LPS response of TG‐PEC by approximately 4‐fold and the IFNγ response by approximately 10‐fold. Pulsing experiments suggested that the anthracyclines enhanced procoagulant expression by a mechanism different from cisplatin. Daunorubicin primed TG‐PEC within 4 hr to respond to low levels of LPS, whereas either LPS or cisplatin primed these cells to respond to cisplatin or LPS respectively. Furthermore, the procoagulant expressed by TG‐PEC stimulated by LPS/cisplatin had properties of tissue factor (TF: 50% total activity) and Factor VIIa (50% total procoagulant)‐like activities, whereas the predominant procoagulant on LPS/anthracycline activated TG‐PEC was TF‐like (70% total activity) with weak Factor VIIa and prothrombinase‐like properties.
Effect of plasma gangliosides on the growth of ehrlich ascites tumor
Authors: Saha Sandip , Ghosh Asit 
Published: February 2007

AbstractTotal plasma gangliosides of Ehrlich ascltes tumor‐bearing mice enhanced tumor growth when adoptively transferred with the same tumor cells in mice. However, individual gangliosides acted differently. Out of 6 gangliosides separated from plasma, 2 components enhanced tumor growth, whereas the remaining 4 inhibited tumor growth, Neither of the 2 enhancing components in various combinations with the 4 inhibitory components could restore the enhancing effect. The enhancing effect was restored only when both the enhancing components were mixed with the remaining 4 ganglioside components, i. e., with full/complete reconstitution.
Hyperplasia of mouse duodenal crypts and its control by NK cells during the initial phase of DMH carcinogenesis
Authors: Altmann G. G. , Parhar R. S. , Lala P. K. 
Published: February 2007

AbstractThe possible regulatory role of NK cells on early events in chemical carcinogenesis remains undefined. The present study examined whether NK cells control 1, 2‐dimethylhydrazine (DMH)‐induced hyperplasia of the duodenal crypt in CD, mice. Mice receiving chronic DMH treatment showed a dose‐dependent hyperplasia confined to the proliferative zone, with a parallel increase in mitotic and 3H‐TdR‐labelled cells and significant suppression of splenic NK activity. Complete ablation of splenic NK activity with anti‐asialo GM‐1 antibody (αAGM‐1) treatment slightly enhanced hyperplasia. Halving of the DMH dose for 2 weeks led to regression of hyperplasia, which was totally prevented by αAGM‐1 treatment. The αAGM‐1 treatment alone did not influence crypt size in normal mice. Finally, a stimulation of NK activity with Poly I:C treatment in DMH‐treated mice caused regression of the DMH‐induced hyperplasia. Our results suggest that hyperplastic cells with possible genetic alterations induced by the carcinogen express target structures for NK cells, but that simultaneous carcinogen‐induced suppression of NK activity hampers their containment, allowing progression of hyperplasia to neoplasia, possibly owing to additional genetic changes.
Detection of ebv gene expression in reed‐sternberg cells of Hodgkin's disease
Authors: Wu Tzyy‐Choou , Mann Risa B. , Charache Patricia , Hayward S. Diane , Staal Steve , Lambe Beverly C. , Ambinder Richard F. 
Published: February 2007

AbstractEBV DNA has been detected by Southern blot hybridization in 20‐25% of Hodgkin's disease tumor specimens and localized to the Reed‐Sternberg cells by in situ hybridization. In the present investigation we used a 3H‐labelled EBER I anti‐sense RNA for in situ hybridization of archival formalinfixed paraffin‐embedded Hodgkin's disease specimens previ ously shown by Southern Blot hybridization to be EBV‐positive. In 6 of 8 specimens neoplastic cells showed an intense signal in virtually all of the tumor cells. The background lym phocytes, eosinophils, plasma cells and histiocytes did not demonstrate significant hybridization. In each case hybridiza tion tended to spare the nucleoli. Hybridization was detected in specimens with histologies of mixed cellularity and nodular sclerosis. The intensity of signal relative to background is bet ter than that in previous studies utilizing 35S‐labelled large internal repeat probes for EBV in Reed‐Sternberg cells. The exposure time is one week in contrast to the 4‐5 weeks reported by others for detection of EBV in Hodgkin's disease. Both increased relative intensity and shorter exposure re quirements may be attributed to the very high number of EBER transcripts in the target cells. The demonstration that EBER I is expressed is consistent with a role for EBV in growth regulation of Reed‐Sternberg cells and suggests that the virus is not merely a silent passenger in Hodgkin's disease.
Chromosome aberrations induced by etoposide (VP‐16) are not random
Authors: Maraschin Joëlle , Dutrillaux Bernard , Aurias Alain 
Published: February 2007

AbstractThe clastogenic effect of etoposide, an anti‐cancer chemotherapeutic drug, was investigated in vitro on lymphocytes of 5 healthy donors. The analysis of the first division metaphases arising after mutagenesis in G1, phase shows that chromosome‐type aberrations are much more frequent than chromatid‐type lesions. The distribution in relation to chromosome lengths of the 439 breakpoints that were accurately identified is not random: chromosomes I, II and 17 are most frequently involved, while chromosomes 4, 5 and × are seldom affected. This non‐random distribution may be related to chromosome structure, since R‐band‐rich chromosomes are significantly more affected than G‐band‐rich chromosomes.
Survival of breast‐cancer patients and body size indicators
Authors: Kyogoku Shinji , Hirohata Tomio , Takeshita Setsuko , Nomura Yasuo , Shigematsu Takao , Horie Akio 
Published: February 2007

AbstractThe association of breast‐cancer survival with various risk factors was investigated using data of 213 breast‐cancer patients who underwent surgical operation between 1975 and 1978. They were followed‐up until 1987, and a total of 64 deaths including 47 breast‐cancer deaths were certified. The 5‐year and 10‐year relative survival rates were 78.5% and 75.3% respectively. Of the various factors investigated, some anthropometric indicators revealed interesting results; i. e., body weight, Quetelet index, and body surface area at the time of operation turned out to be strong predictors of survival with a statistically significant trend towards lower survival with larger body structure even after adjustment for confounding factors (e. g., clinical stage) using a proportionalhazard model. The estimated survival probability for women with Quetelet index of 20 was about 12% higher than that with Quetelet index of 24 over a 10‐year or more follow‐up period. Other variables exhibiting prognostic importance were clinical stage, TNM classification, and some histological findings, while height and reproductive life indicators were, as a rule, not significantly related to survival.
Quantitation of endogenous lectin expression in 3LL tumors, growing subcutaneously and in the kidneys of mice
Authors: Vidal‐Vanaclocha F. , Barbera‐Guillem E. , Weiss L. , Glaves D. , Gabius H‐J. 
Published: February 2007

AbstractBy means of microdensitometry and image analysis, quantitative measurements were compared of endogenous lectin expression in tissue sections from 3LL carcinomas growing in the subcutis and kidneys of mice following the direct injection of cancer cells. The lectins were visualized by means of a modification of the ABC‐peroxidase technique. In comparison with the subjective, visual inspection of similar materials reported previously, these quantitative techniques not only confirmed, but also provided additional information on siteassociated changes in 3LL cell populations. Previously, 2 classes of cancer cells were recognized within the tumors on the basis of staining intensity, compared with 3 classes in the present study and, in addition, the relative areas occupied by these 3 densitometric classes were determined by imageanalysis. Both “low” and “high” integrated intensities were significantly greater in the kidney tumors in 11 of 24 cases, and in 6 of 24 cases of s. c. tumors. The areas occupied by “high” and “low” intensity cells were significantly higher in 14 of 24 kidney tumors, and in 2 of 24 s. c. tumors. The results indicate often marked differences in endogenous lectin expression, between 3LL cancer cells from a common source, after direct delivery and growth in 2 different anatomic sites. These results indicate the necessity of taking into account analogous changes, when comparing these and other properties of cancer cell populations in metastases with those in primary tumors, with respect to both the generation of siteassociated differences and their possible site‐associated abrogation.
Physical activity and colon cancer: A case‐referent study in Stockholm
Authors: De Verdier Maria Gerhardsson , Steineck Gunnar , Hagman Ulla , Rieger Åke , Norell Staffan E. 
Published: February 2007

AbstractA population‐based case‐referent study on physical activity (during working and recreational hours) and colon cancer was performed in Stockholm in 1986‐1988. The study included 1,081 subjects. Low physical activity was associated with an excess risk of colon (but not rectum) cancer for both men and women, showing a dose‐response relationship with decreasing levels of physical activity. The effect was seen in the left colon (relative risk = 3.2, 95% confidence interval = 1.5–7.0) rather than in the right colon (relative risk =1.1, 0.5–2.5). These results persisted after adjustment for year of birth, gender, body mass, intake of total energy, protein, total fat, dietary fibre, and browned meat surface.
Type of alcoholic beverage and cancer of the oral cavity, pharynx and oesophagus in an Italian area with high wine consumption
Authors: Barra Salvatore , Franceschi Silvia , Negri Eva , Talamini Renato , La Vecchia Carlo 
Published: February 2007

AbstractThe role of different types of alcoholic beverage on cancer of the upper digestive tract was investigated in a case‐control study conducted in the northern part of Italy on 305 male cases of cancer of the oral cavity and pharynx, 288 of oesophageal cancer and 1621 controls admitted to hospital for acute, non‐neoplastic conditions, unrelated to alcohol intake. Similar significant trends of risk increase with increasing alcohol intake were seen for cancers of the oral cavity, pharynx and oesophagus independent of type (or types) of beverage consumed. Among the heaviest drinkers (i. e. ≥84 drinks/week) odds ratios (ORs) of cancer of the oral cavity and pharynx for wine only, wine and spirits, and combination of wine, spirits, and beer were 11.2, 9.9 and 4.1, respectively. Corresponding oesophageal cancer ORs were 15.0, 10.0 and 6.0. This study from an area with high wine consumption confirms that wine per se can greatly enhance the risk of cancer of the upper digestive tract and suggests that the most frequently used alcoholic beverage in each study appears to be the most important determinant of these tumours.