bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of age, birth cohort and period of death on Swiss cancer mortality, 1951–1984
Authors: Levi Fabio , La Vecchia Carlo , Decarli Adriano , Randriamiharisoa Alex 
Published: February 2007

AbstractSwiss death certification data over the period 1951–1984 for total cancer mortality and 30 major cancer sites in the population aged 25 to 74 years were analysed using a log‐linear Poisson model with arbitrary constraints on the parameters to isolate the effects of birth cohort, calendar period of death and age. The overall pattern of total cancer mortality in males was stable for period values and showed some moderate decreases in cohort values restricted to the generations born after 1930. Cancer mortality trends were more favourable in females, with steady, though moderate, declines in both cohort and period values. According to the estimates from the model, the worst affected generation for male lung cancer was that born around 1910, and a flattening of trends or some moderate decline was observed for more recent cohorts, although this decline was considerably more limited than in other European countries. There were decreases in cohort and period values for stomach, intestine and oesophageal cancer in both sexes and (cervix) uteri in females. Increases were observed in both cohort and period trends for pancreas and liver in males and for several other neoplasms, including prostate, brain, leukaemias and lymphomas, restricted, however, for the latter sites, to the earlier cohorts and hence partly attributable to improved diagnosis and certification in the elderly. Although age values for lung cancer in females were around 10‐times lower than in males, upward trends in female lung cancer cohort values were observed in subsequent cohorts and for period values from the late 1960's onwards. Therefore, future trends in female lung cancer mortality should continue to be monitored. The application of these age/period/cohort models thus provides a summary guide for the reading and interpretation of cancer mortality trends, although it cannot replace careful inspection of single age‐specific rates.
Case‐control study of human papillomaviruses and cervical cancer in Latin America
Authors: Reeves William C. , Caussy Deoraj , Brinton Louise A. , Brenes Maria M. , Montalvan Patricia , Gomez Basilio , De Britton Rosa C. , Morice Eugenio , Gattan Eduardo , De Lao Suzanne Loo , Rawls William E. 
Published: February 2007

AbstractHuman papillomavirus (HPV) types 16 and 18 have been implicated as risk factors for cervical dysplasla and neoplasia. However, most studies have been observational, uncontrolled and conducted in populations at low risk for invasive cancer. We r sport a pilot case‐control study of incident invasive cervical cancer in Panama, Costa Rica and Bogota, Colombia. Between July and September 1985 we enrolled 46 consecutive newly diagnosed invasive cervical cancer cases and 51 age‐matted control women. Subjects were interviewed and samples collected for HPV DNA assays. HPV infection was defined by a filter in situ DNA hybidization technique under non‐stringent and stringent conditions against HPV‐6/11, 16 and 18 DNA probes. More cases (91 %) than controls (63%) had HPV DNA detected (non‐stringent) and more cases than controls had HPV‐16 or 18 DNA (67% vs. 43%, p = 0.02). Age at first intercourse was the most significant risk factor for HPV 16/18 Infection in all subjects. Smoking was significantly associated with cervical cancer (52% of cases vs. 27% controls) but was not associated with HPV infection.
Cellular and humoral immune responses to synthetic peptides deduced from the amino‐acid sequences of Epstein‐Barr virus‐encoded proteins in EBV‐transformed cells
Authors: Dillner Joakim , Szigeti Robert , Henle Werner , Henle Gertrude , Lerner Richard A. , Klein George 
Published: February 2007

AbstractTen synthetic peptides containing 18–22 residues deduced from the amino‐acid sequences of the EBV‐encoded latent‐infection‐associated membrane protein (LMP) and the 2 principal nuclear antigens, EBNA‐1 and EBNA‐2, were tested for their ability to induce lymphokine release from sensitized T‐cells of EBV‐seropositive donors, as measured by the leukocyte migration inhibition assay (LMI). Only one of the 10 free peptides induced EBV‐speeific LMI. After Sepharose‐coupling, 4 additional peptides were regularly active. In parallel, the sera of the same and other donors were screened for synthetic peptide‐blnding antibodies, as measured by an ELISA assay. Antibodies to 9 of the 10 peptides were detected in 25–80% of EBV‐antibody‐positive, but not in EBV‐antibody‐negative sera. A comparison of the two responses indicates that the humoral immune system tends to react with more epitopes on a given protein than the cellular immune system. Furthermore, the antibody reactivity pattern to different epitopes is more variable from individual to individual than the T‐cell response. Also, the epitopes detected by antibodies and sensitized T‐cells are often not identical.
Specific abnormalities of chromosome 14 in patients with acute type of adult T‐cell leukemia/lymphoma
Authors: Miyamoto Kanji , Tomita Noriko , Ishn Akio , Miyamoto Naoaki , Nonaka Hiroshi , Kondo Toshifumi , Sugihara Takashi , Yawata Yoshihito , Tada Shinya , Tsubota Teruhiko , Kitajima Koichi , Kimura Ikuro 
Published: February 2007

AbstractChromosome analysis was performed on I patient with diffuse lymphoma of mixed type by histologic diagnosis and on 7 patients with the acute type of adult T‐cell leukemia (ATL). Specific abnormalities in chromosome 14 at break band q11 with the assigned locus of the α‐chain gene of the T‐cell antigen receptor were identified in 6 of 8 patients. Inv(l4) (q11q32) was found in 2 patients and translocation of chromosome 14 at break band q 11 was observed in 4. Donor chromosomes involved in translocation of the 14q11 varied, i.e., chromosomes 3, 7 or X, with the exception of one patient whose donor chromosome origin could not be determined. The breakpoint in chromosome 3 was in band p25, a region reported to include the locus of the c‐raf‐l oncogene. In chromosome 7, it was in band p11, a region reported to include the locus of the c‐erb‐B oncogene, and in the sex chromosome X, it was in band q11. One patient also had a chromosome 14 aberration at break band q32. Of the 2 remaining patients, one had lost chromosome 14 and the other had an isochro‐mosome 14q. Our observation and other reported findings suggest that the rearrangement of chromosome 14 at break band q11 is specific for lymphoma‐type or acute‐type ATL patients, and aberrations of proto‐oncogene expression or the coding sequence by recombination involving a T‐cell antigen receptor gene due to chromosome inversion or chromosome translocation may play an important role in T‐cell neoplasia including ATL.
Methylxanthines and breast cancer
Authors: Schairer Catherine , Brinton Louise A. , Hoover Robert N. 
Published: February 2007

AbstractWe investigated the relationship between methylxanthine consumption and breast cancer using data from a case‐control study which included 1,510 cases and 1,882 controls identified through a nation‐wide breast cancer screening program. There was no evidence of a positive association between methylxanthine consumption and risk of breast cancer. In fact, there was some suggestion of a negative association, particularly in women diagnosed after age 50. In addition, there was no evidence of increased risk with past or recent methylxanthine consumption, or with the consumption, of caffeine or specific beverages, most notably brewed or instant caffeinated coffee and tea.
Lack of correlation between rare Ha‐ras alleles and urothelial cancer in Japan
Authors: Ishikawa Jiro , Maeda Sakan , Takahashi Rei , Kamidono Sadao , Sugiyama Taketoshi 
Published: February 2007

AbstractRestriction fragment length polymorphism (RFLP) of Haras gene was surveyed by Southern blot analysis in leukocyte DNA from 55 normal individuals and 58 urothelial cancer patients in Japan. Three common alleles and 4 rare alleles were classified. The frequency of common alleles in normal Japanese individuals differed from that in Caucasians previously reported; a 7.2–7.5‐kb Bam HI fragment of common al‐lele wits not observed in Japanese individuals. No significant increase in frequency of the rare Ha‐ras allele was observed in the group of cancer patients. Moreover, no significant different in frequency was observed for the 3 common alleles. Tumor DNA was compared with leukocyte DNA in 30 urothelial cancer patients: in 3 of 8 cases with heterozygous Haras locus, decreased intensity of one band, indicating partial loss of one allele in tumor DNA, was observed. In 3 tumors with either deletion of one Ha‐ras allele or a rare Ha‐ras allele, expression of Ha‐ras gene was examined by Northern blot aralysis. Such genetic alterations did not always result in a marked increase in Ha‐ras expression. These data suggest that tl‐ese genetic alterations are not directly related to Haras expression, and that RFLP of Ha‐ras gene is not a useful genetic marker for urothelial cancer. On the other hand, deletion of one Ha‐ras allele was observed in 1 of 5 cases of bladde‐ cancer and in 2 of 3 cases of renal pelvic cancer, suggesting that that deletion may be important in the development of urothelial cancer.
Interleukin‐2‐stimulated natural killer activity against malignant and benign endometrium
Authors: Timonen Tuomo , Lehtovirta Pentti , Saksela Eero 
Published: February 2007

AbstractNatural cell‐mediated immunity against autologous tumor cells, autologous endometrial epithelium, and allogeneic epi‐dermoid carcinoma cell line HeLa was tested in 8 patients with endometrial carcinoma and one patient with endome‐irial stromal sarcoma. The average cytotoxicity of unstimu‐lated peripheral blood lymphocytes against autologous tumor and HeLa cells was weak but significant. Pretreatment of effector cells for 3–5 days with 300 U/ml recombinant inter‐leukin‐2 (rIL‐2) resulted in increased cytotoxicity against malignant target cells in 7 out of 9 cases. The 2 patients' effector cells which were refractory to rIL‐2 could be stimulated to; ppreciable lytic activity against the malignant target cells with a recently described cytokine which induces morphological differentiation of natural killer cells. Benign endometrial cells were weakly sensitive to rIL‐2‐activated lysis in 2 cases. The precursors of the rIL‐2‐activated killer cells were mostly CD16‐positive and CD3‐negative, and co‐sedimented with endogenous natural killer cells in discontinuous density gradient centrifugations. These results indicate the rIL‐2‐activated killer cells have a capacity to distinguish between normal and malignant endometrial cells, and that the precursors of the lytic cells in this system belong to the same subpopulation of lym‐phocytes as endogenous natural killer cells. In addition, rIL‐2 alone may not in all cases be sufficient for optimal generation of cytotoxicity against malignant cells.
A case‐control study of diet and gastric cancer in Northern Italy
Authors: La Vecchia Carlo , Negri Eva , Decarli Adriano , D'Avanzo Barbara , Franceschi Silvia 
Published: February 2007

AbstractDietary factors in the aetiology of stomach cancer were investigated using data from a case‐control study conducted in Northern Italy on 206 histologically confirmed carcinomas and 474 control subjects in hospital for acute, non‐digestive conditions, unrelated to any of the potential risk factors for giistric cancer. Dietary histories concerned the frequency of consumption per week of 29 selected food Items (including ttie major sources of starches, proteins, fats, fibres, vitamins A and C, nitrates and nitrites in the Italian diet) and subjective stores for condiments and salt intake. Pasta and rice (the rajor sources of starch), polenta (a porridge made of maize) and ham were positively related with gastric cancer risk, whereas green vegetables and fresh fruit as a whole (and specifically citrus fruit) and selected fibre‐rich aliments (such aii whole‐grain bread or pasta) showed protective effects on giistric cancer risk. Allowance for major identified potential distorting factors (chiefly indicators of socio‐economic status) reduced the positive association with pasta or rice consumption, but did not appreciably modify any of the other risk estimates. When a single logistic model was fitted including all food items significant in univariate analysis, the 3 items remaining statistically significant were green vegetables (rel‐acive risk, RR = 0.27 for upper vs. lower tertile), polenta (f;R = 2.32) and ham (RR = 1.60). Indices of beta‐carotene and ascorbate intake were negatively and strongly related with giistric cancer risk, but the association with these micronu‐trients was no longer evident after simultaneous allowance for various food items. An approximately 7‐fold difference in risk was found between extreme quintiles of a scale measuring major positive and negative associations.
Phenotypic and functional analysis of human CD3 + and CD3− clones with “lymphokine‐activated killer” (LAK) activity. Frequent occurrence of CD3 + LAK clones which produce interleukin‐2
Authors: Mingari M. C. , Ferrini S. , Pende D. , Bottino C. , Prigione I. , Moretta A. , Moretta L. 
Published: February 2007

AbstractClones capable of lysing fresh, uncultured tumor cells (“lym‐phokine‐activated killer”: “LAK” activity) were selected from microcultures derived from either E‐rosette‐positive or E‐ rosette‐negative cell populations. All the selected clones displayed a strong cytolytic activity against the NK‐sensitive K562 cell line. Two major phenotypic groups of clones could be identified: a first group expressed the CD3 differentiation antigen, present exclusively on mature T lymphocytes; however, in contrast to typical cytolytic T lymphocytes, the majority of these clones expressed the unusual CD4‐ CD8‐ phenotype, whereas the remainder were CD4‐ CD8 +. A second group was represented by CD3 ‐ clones which, in most instances, expressed the T‐cell‐lineage‐specific CD2 antigen. Following stimulation with phytohemagglutinin (PHA), most of the CD3 + LAK clones produced lnterleukin‐2 (1L‐2) and interferon‐γ (1FN‐γ) whereas those expressing the CD3 ‐ phenotype did not. Since previous studies indicated that PHA may be inefficient in inducing lymphokine production by T‐ cell variants lacking the CD3/T cell receptor complex (TCR), CD3 ‐ clones were further stimulated with the calcium iono‐phore A23187 plus phorbol 12‐myristate 13‐acetate (PMA). Only 2/11 CD3 ‐ LAK clones produced small amounts of IL‐2, whereas the majority released 1FN‐γ. Given the peculiar phenotypic and functional properties of many CD3 + LAK clones, we suggest that they may belong to a T‐cell subset distinct from typical CTLs.
Cell‐surface laminin‐like molecules and α‐D‐galactopyranosyl end‐groups of cloned strongly and weakly metastatic murine fibrosarcoma cells
Authors: Grimstad Ivar Amund , Bosnes Vidar 
Published: February 2007

AbstractIndications from previous work that cancer cell‐surface laminin‐like molecules and α‐D‐galactopyranosyl end‐groups may contribute to spontaneous metastasis were further investigated. Both moieties are known to mediate cell attachment to various foreign surfaces. Five strongly metastatic and 5 weakly metastatic cell clones from a murine fibrosarcoma were examined for the occurrence of both cell‐surface moieties by immunofluorescence flow cytometry and micros‐ copy. None of these clones was rich in laminin‐like molecules, Which were least strongly expressed by the highly metastatic Clones. The α‐D‐galactopyranosyl end‐groups were strongly expressed by all strongly metastatic clones and by 2 weakly metastatic clones, but were only weakly expressed by the other weakly metastatic clones. These results indicate that the laminin‐like cell‐surface molecules are not necessary for spontaneous metastasis formation. However, the α‐D‐galactopyranosyl end‐groups may be necessary, but are not sufficient for the cancer cells to form metastases. These carbohydrates are known to occur on the laminin‐like molecules. The present results show that they must also exist on other cell‐surface molecules.
Evidence that sulphated polysaccharides inhibit tumour metastasis by blocking tumour‐cell‐derived heparanases
Authors: Parish Christopher R. , Coombe Deirdre R. , Jakobsen Karen B. , Bennett Francis A. , Underwood P. Anne 
Published: February 2007

AbstractRecent studies in this laboratory demonstrated that several sulphated polysaccharides can inhibit metastasis of the rat mammary adenocarcinoma 13762 MAT, probably by preventing the passage of tumour cells through the walls of blood vessels. In order to directly test this possibility, 13762 MAT cells were cultured with (35S)O4=‐labelled subendothelial extracellular matrices (ECM) and ECM degradation was monitored in either the presence or absence of different sulphated polysaccharides. Degradation products were detected by sodium dodecyl sulphate polyacrylamide gel electrophoresis and subsequent autoradiography. The 5 sulphated polysaccharides that had previously been shown to possess anti‐metastatic activity were potent inhibitors of the degradation of subendothelial ECM by 13762 MAT cells. In contrast, of the 4 polysaccharides tested that failed to inhibit metastasis, 3 had no effect on ECM breakdown and one (carrageenan‐kappa) was substantially less effective at inhibiting ECM degradation than the anti‐metastatic preparations. It was also shown that 13762 MAT cells produce a heparan sulphate‐specific glycosidase (heparanase) that degrades the heparan sulphate side‐chains of the ECM, the action of this enzyme rather than that of other ECM‐solubilizing enzymes being inhibited by the anti‐metastatic sulphated polysaccharides. Additional experiments indicated that the anti‐coagulant activity of the polysaccharides probably plays a minor role In their anti‐metastatic effects since heparin, almost completely depleted (98–99.5%) of heparin molecules with anti‐coagulant activity by passage over an anti‐thrombin III column, retained its ability to inhibit 13762 MAT heparanases and was almost as effective as unfractionated heparin at inhibiting tumour‐cell metastasis. Collectively, these data suggest that sulphated polysaccharides inhibit the metastasis of 13762 MAT cells by inhibiting tumour‐cell‐derived heparanases involved in the penetration of the vascular endothelium and Its underlying basement membrane by tumour cells.
Adhesion of human breast cancer cell line MCF‐7 to human vascular endothelial cells in culture. enhancement by activated platelets
Authors: Abecassis Joseph , Millon‐Collard RéGine , Klein‐Soyer Claude , Nicora Francesca , Fricker Jean‐Pierre , Beretz Alain , Eber Michel , Muller Danièle , Cazenave Jean‐Pierre 
Published: February 2007

AbstractThe interactions of MCF‐7 tumor cells with human vascular endothelial cells (EC) and subendothelial extracellular matrices (ECM) were morphologically observed by electron microscopy and quantitatively evaluated by labelling tumor cells with 111Indium‐oxine. MCF‐7 tumor cells adhered more rapidly to ECM than to the apical surface of a confluent monolayer of EC. The affinity of MCF‐7 cells for type‐IV collagen was greater than for fibronectin, suggesting that type‐IV collagen contributes to the higher rate of adhesion of MCF‐7 cells to the subendothelial ECM. Otherwise, the attachment of tumor cells to EC was increased in the presence of both washed platelets and 0.1% citrated platelet‐poor plasma (cPPP), a condition accelerating platelet aggregation by tumor cells. The enhancement of MCF‐7 adhesion to EC in the presence of platelets and cPPP was completely blocked by the addition of prostacyclin, or hirudin, a specific thrombin inhibitor. In ultrastructural studies, MCF‐7 initiated EC retraction, and firm attachment and flattening occurred on exposed ECM. When MCF‐7 cells were incubated with platelets and cPPP, most of the tumor cells adhering to the EC and inducing disruption of endothelial monolayer were closely packed and associated with platelet aggregates. MCF‐7 cells appeared to adhere more efficiently to exposed subendothelial ECM when they were associated into multicellular aggregates containing platelets and trapped in a fibrin thrombus. Thus, this homologous human system of cultured vascular EC and breast carcinoma line MCF‐7 cells may be used to assess anti‐aggregant compounds for their ability to alter tumor‐cell implantation on EC‐lined surfaces.
The role of chromosome 15 in murine leukemogenesis. II. Relationship between tumorigenicity and the dosage of lymphoma vs. normal‐parent‐derived chromosomes 15 in somatic cell hybrids
Authors: Uno Masatsune , Wirschubsky Zvi , Babonits Magda , Wiener Francis , Sümegi Janos , Klein George 
Published: February 2007

AbstractSomatic cell hybrids were generated between an MCF‐vi‐rus‐induced 15‐trisomic T‐cell lymphoma of AKR origin with a proviral insertion near the c‐myc locus, and normal diploid fibroblasts or lymphocytes of CBAT6T6 origin. Three lymphoma/fibroblast fusions were performed. Six independently‐derived clones from 2 fusions were tested for tumorigenicity. Three of the 6 clones were weakly malignant (take incidence 20% below), and 3 were strongly malignant (take incidence over 80%). All 3 lymphoma/lymphocyte hybrids and 6 derived clones were strongly malignant. All hybrids contained a nearly complete chromosomal complement of both parental cells. This was confirmed at the molecular level by determining the ratio of germ‐line (G) vs. rearranged (R) myc‐carrying Eco RI fragments that showed the expected 1.9–2.7:1 proportion. Malignant segregants selected from the weakly malignant lymphoma/fibroblast hybrids by in vivo inoculation showed changed 15‐chromosome ratios. Four out of the 6 clones showed amplification of the lymphoma‐derived 15‐chromosome that carries the R‐myc fragment and a concomitant decrease in the average number of the G‐myc‐carrying chromosomes. This was deduced from the fact that the G:R ratio was between 2 and 3:1 in the in vitro hybrids but became inverted (1:2–3) in the tumors. Two tumors showed no amplification of R‐myc. C‐myc was decreased. One of these tumors showed a change in the G:R ratio from 2.5:1.0 to 1.2:1.0, while the other was essentially unchanged (1.9:1.0 in the in vitro clone and 2.2:1.0 in the derived tumor). These findings support the notion that both the amplification of the lymphoma‐derived 15‐chromosome with the retro virally rearranged c‐myc carrying fragment and/or the loss of the G‐myc‐carrying 15‐chr can contribute to the tumorigenic potential of the hybrids.