bluuebunny/crossref_metadata_2025_split huggingface dataset:
A sub‐site‐specific analysis of the relationship between colorectal cancer and parity in complete male and female norwegian birth cohorts
Authors: Kravdal Øystein , Glattre Eystein , Kvåle Gunnar , Tretli Steinar 
Published: February 2007

AbstractRegister and census data for complete cohorts of Norwegian men and women born between 1935 and 1969 have been used to examine the relationship between reproductive factors and the incidence of colorectal cancer. Among 1.1 million men and 1.1 million women under observation, 491 male and 859 female cases of colorectal cancer were diagnosed during the period of follow‐up. Our hazard model estimates clearly show that in these young cohorts, women with 2 or more children run a lower risk of having a malignant tumor in the cecum or ascending colon than do other women of the same age and in the same birth cohort. No association with parity is found with respect to cancer in the transverse or descending colon, whereas a downward trend in the effect estimates, followed by an upturn, appears for the rectum, sigmoid colon and rectosigmoid junction. Such correlations, which also hold when we control for education and place of residence, are not found for men. The observed relationship between parity and cancer incidence is not likely to be exclusively explained by life‐style differentials. Presumably, there is a biological effect of the number of pregnancies and deliveries, net of age at first birth and other reproductive factors, on the development of colorectal cancer.
Interferon‐γ modulates retinoblastoma gene mrna in monocytoid cells
Authors: Mistchenko Alicia S. , Diez Roberto A. , Romquin Nicole , Sancéau Josiane , Wietzerbin Juana 
Published: February 2007

AbstractTo study the effect of interferon gamma (IFN‐γ) on the expression of the retinoblastoma (RB) susceptibility gene, we performed Northern‐blot analysis on RNA extracted from Wish, HEL and monocytoid cell lines U‐937 and THP‐I treated with 1,000 IU/ml of recombinant IFN‐γ. In U‐937 and THP‐I cells, IFN‐γ increased the abundance of RB mRNA. In Wish and HEL cells, co‐treatment with cycloheximide was required for IFN‐γ to increase the level of RB mRNA. Pre‐treatment THP‐I cells with cycloheximide prior to IFN‐y treatment augmented the effects of IFN‐γ on RB gene expression. The effect of IFN‐γ in THP‐I cells was observed after 3 hr treatment, being more pronounced after 6 hr and persisting until at least 18 hr, although at a lower level. These results suggest that IFN‐γ regulates the level of RB mRNA by different mechanisms in the different cell types. This cytokine increases the abundance of RB mRNA in monocytoid cell lines, reinforced by prior treatment with cycloheximide. Inhibition of protein synthesis is required in Wish and HEL cell lines before IFN‐γ has an effect on RB gene expression.
Induction of apoptosis in human leukemic cells by the ether lipid 1‐octadecyl‐2‐methyl‐RAC‐glycero‐3‐ phosphocholine. A possible basis for its selective action
Authors: Diomede Luisa , Colotta Francesco , Piovani Bianca , Re Fabio , Modest Edward J. , Salmona Mario 
Published: February 2007

AbstractEther‐linked glycerophospholipids (ether lipids, EL) are membrane‐interactive drugs selectively cytotoxic toward neoplastic cells compared with normal cells. No conclusive explanation has yet been provided for this selectivity. We now present data indicating that the drug 1‐octadecyl‐2‐methyl‐rac‐glycero‐3‐phosphocholine (ET‐18‐OMe) induces apoptosis, or programmed cell death, in human leukemic cells. Apoptotic death is induced selectively by ET‐18‐OMe in HL60 cells, which are sensitive to the drug's cytotoxic action, but not in the resistant K562 cell line. Enrichment of HL60 cells with cholesterol (HWO‐CHOL cells) significantly protects the cells from the cytotoxic effect and from the induction of apoptosis by ET‐18‐OMe; the percentage of fragmented DNA is only 17% for HL60‐CHOL, compared with 50% in native HL60 cells after exposure to 20 μ ET‐18‐OMe for 24 hr. Our study provides a possible explanation for differences in sensitivity to EL among different cell types and illustrates an indirect interaction of EL with cellular DNA.
Production and characterization of a mouse/human chimeric antibody directed against human neuroblastoma
Authors: Amstutz H. , Rytz Ch. , Novak‐Hofer I. , Spycher M. , Schubiger P. A. , Blaser K. , Morgenthaler J.‐J. 
Published: February 2007

AbstractHybridoma CE7 produces a murine antibody (yl/k) which binds to a 190‐kDa cell‐surface glycoprotein of human neuroblas‐toma. Because of its tumor specificity, it has been used routinely in clinical pathology to confirm diagnosis of neuroblastoma. We have Isolated the gene segments coding for the variable regions of the immunoglobulin Hand L chain of this hybridoma. These V genes were used to construct mouse/human chimeric H and L chain genes (yl/K) which were then expressed in SP2/0 cells. A cell‐blnding inhibition assay showed that the specificity of the chimeric CE7 antibody (chCE7) is identical to that of the original CE7. Radioiodinated chCE7 binds to approximately 43,000 sites per neuroblastoma cell with an affinity of IOIO M‐I. In neuroblastoma‐bearing nude mice, biodistribution studies with [I25I]ch‐CE7 were performed and tumor accumulations of up to 32% of injected dose/g tissue together with low blood and organ uptake were found.
Effects of EGF, BFGF, NGF and PDGF(bb) on cell proliferative, migratory and invasive capacities of human brain‐tumour biopsies In Vitro
Authors: Engebraaten Olav , Bjerkvig Rolf , Pedersen Paal‐Henning , Laerum Ole Didrik 
Published: February 2007

AbstractSpheroids initiated directly from human primary gliomas were used to investigate the effects of EGF, bFGF, NGF and PDGF(bb) on cell proliferation, migration and invasion into foetal rat brain tissue. EGF increased tumour spheroid volume in 10 of 13 glioblastomas studied, whereas 5 of 11 tumours responded to bFGF. NGF increased the spheroid volume in 2 of 5 tumours. In 8 tumours, PDGF(bb) had no effect on tumour spheroid volume. An increase in BUdR‐labelling indices confirmed that cell proliferation was responsible for the volume increase observed in stimulated spheroids. EGF stimulated cell migration in 5 and bFGF in 3 of 8 tumours studied. NGF stimulated cell migration in 1 of 5 glioblastomas, whereas 1 of 3 glioblastomas responded to PDGF(bb). The effects of growth factors on the invasion of spheroids prepared from the glioblastoma biopsy specimens were also studied in vitro using foetal rat brain aggregates as target tissue. EGF stimulated invasion in 7 of 8 glioblastomas studied, whereas bFGF stimulated invasion in 2 of these tumours. NGF or PDGF(bb) did not increase the invasiveness of the glioblastoma tissue. Our results represent the net effect of the growth factors on a complex tumour‐cell population. We conclude that exogenously administered growth factors, EGF in particular, increase the cell proliferation as well as migratory and invasive capacities of cultured primary brain tumour biopsies in vitro.
Long‐term impact of reproductive factors on cancer risk
Authors: La Vecchia Carlo , Negri Eva , Franceschi Silvia , Parazzini Fabio 
Published: February 2007

AbstractThe relationship between reproductive variables (parity, age at first birth, number of induced and spontaneous abortions) and cancer risk has been analysed using data from an integrated series of case‐control studies conducted in northern Italy between 1983 and 1992. The overall data‐set included women below age 75 with histologically confirmed cancers of the following sites: oesophagus, 58; stomach, 280; colon, 405; rectum, 210; liver, 82; gall‐bladder, 29; pancreas, 129; breast, 3,415; cervix, 742; endometrium, 725; ovary, 953; bladder, 68; kidney, 56; thyroid, 180; lymphomas, 80; myelomas, 57; and a total of 5,619 controls admitted to hospital for acute non‐neoplastic, non‐gynaecological, non‐hormone‐related conditions. Multivariate odds ratios, as estimators of relative risks (RR), were obtained after allowance for age, education, use of oral contraceptives and oestrogen replacement treatments, plus various reproductive factors. Direct significant trends with parity were observed for cancer of the liver (RR for women with ≥4 births vs. nulliparae = 3.3) and cervix uteri (RR = 4.1). The risk of gall‐bladder cancer was also elevated for multiparae (RR = 1.9). No significant inverse trend in risk emerged. However, the RRs in multiparae were significantly below unity for breast (RR = 0.8), endometrium (RR = 0.7), and ovary (RR = 0.8). With reference to age at first birth, a significant trend in risk was observed for breast cancer (RR = 1.4 for 25 to 29 and 1.5 for ≥30 vs. ≤ 25 years). In contrast, the risk of cervical cancer was inversely related to age at first birth. For spontaneous abortions, the only significant inverse trend was for ovarian cancer (RR = 0.7 for ≥2 vs. 0 abortions), but also the point estimate for endometrial cancer in women with ≥2 abortions was below unity. For induced abortions, there was a strong inverse trend in risk for endometrial cancer (RR = 0.5), and the RRs were below unity also for colon and breast cancer. In contrast, cervical cancer was directly associated with the number of spontaneous abortions. Although the underlying aetiological interpretations are different for various cancer sites, this study provides, in a large and uniform data‐set, quantitative information on the long‐term impact of reproductive factors on cancer risk.
Sinonasal cancer and occupational exposure to formaldehyde and other substances
Authors: Luce Danièle , Gérin Michel , Leclerc Annette , Morcet Jean‐François , Brugère Jacques , Goldberg Marcel 
Published: February 2007

AbstractA case‐control study of cancer of the nose and paranasal sinuses was conducted in France to determine whether occupational exposure to formaldehyde was associated with an Increased risk of sinonasal cancer. Exposures to 14 other substances or groups of substances were also studied (wood dust, leather dust, textile dust, flour dust, sugar dust, coal/coke dust, nickel compounds, chromium compounds, chromium VI, welding fumes, soldering fumes, cutting oils, paints and lacquers, glues and adhesives). Cases (n = 207) and controls (n = 409) were interviewed to obtain detailed information on job history and other potential risk factors for sinonasal cancer. In addition, a questionnaire specially designed for this study was used to help assess exposures to formaldehyde and other substances of interest. The questionnaires were translated into history of occupational exposure by an expert in industrial hygiene, without knowledge of case‐control status. Several exposure variables (lifetime average level, duration, cumulative level) were used to describe the risks related to exposure to formaldehyde. Potential confounding factors (occupational and non occupational) were examined and adjusted for when necessary.No significant association was found between exposure to formaldehyde and squamous‐cell carcinomas of the sinonasal cavities.Because of the strong association between exposure to wood dust and nasal adenocarcinoma, it was not possible to assess an independent effect of formaldehyde on this type of cancer. However, among males exposed to medium or high levels of wood dust, the risk of adenocarcinoma associated with formaldehyde was significantly elevated for the highest exposure categories for average level (OR = 5.3, 95% confidence interval = 1.3‐22.2), cumulative level (OR = 6.9, 95% CI = 1.7‐ 28.2) and duration of exposure (OR = 6.9,95% CI = 1.7‐27.8).Although a residual confounding effect of wood dust could not be excluded, this study suggests that exposure to both formaldehyde and wood dust may increase the risk of nasal adenocarcinoma, by comparison with the risk due to wood dust alone.This study also indicated an increased risk among males who had been exposed to glues and adhesives, for all histologic types, which was not explained by a confounding effect of paints and lacquers, wood dust or formaldehyde. No other significant association was observed.
Characteristic patterns of hox gene expression in different types of human leukemia
Authors: Celetti Angela , Barba Pasquale , Cillo Clemente , Rotoli Bruno , Boncinelli Edoardo , Magli Maria Cristina 
Published: February 2007

AbstractHomeobox‐containing genes are a network of genes encoding DNA‐binding proteins highly conserved throughout evolution. They are involved in the control of normal development as well as in the regulation of gene expression in adult differentiating systems, including hematopoiesis. Aberrant expression of homeobox‐containing genes has recently been related to leukemic phenotype. Human homeobox‐containing genes of the HOX family are organized into 4 large clusters. We have analyzed the expression of HOX genes in different types of human leukemia to investigate whether the physical organization of HOX loci reflects a regulatory hierarchy involved in the differentiation of hematopoietic cells or whether HOX gene expression might contribute to the leukemic phenotype. Our results show that HOX genes are coordinately regulated in blocks in myeloid cells whereas they appear to function as isolated genes in lymphoid cells. Six contiguous genes of the HOX2 locus, highly expressed in acute non‐lymphocytic leukemia, are switched off in chronic myelogenous leukemia, suggesting that down‐regulation of HOX2 genes might be required for cell maturation of the myeloid lineages. In contrast, a few scattered genes are active in lymphoid populations. These observations suggest that hematopoietic cells express a repertoire of HOX genes characteristic of a particular cell lineage at a specific stage of differentiation. The characteristic patterns of HOX gene expression may reflect the potentially important role that these genes play in cell lineage determination during both normal and leukemic hematopoiesis.
Cancer‐cell traffic in the liver. II. Arrest, transit and death of B16F10 and M5076 cells in the sinusoids
Authors: Barbera‐Guillem Emilio , Smith Isabel , Weiss Leonard 
Published: February 2007

AbstractFluorescent probes were used to detect BUdR‐labelled B16F10 and M5076 cancer cells delivered to the livers of mice via intrasplenic injection. In liver sections stained for succinic dehydrogenase, which permits the periportal, acinar zone I to be distinguished from the pericentral zone 3, counts were made the zonal distribution of fluorescent, intact cancer cells and, by default, the numbers of “lost” cells. Very few intact cancer cells leave the liver from the single bolus of the intrasplenic injection, and even fewer of these generate pulmonary lesions; therefore, within the time limits of these experiments, the liver virtually a closed system. A dynamic view of intrahepatic cancer‐cell traffic with respect to zones I (periportal) and 3 (pericentral) was obtained from static measurements of cell densities at different times after intrasplenic injection, by means of Markov chain probability analysis. This indicated that, during the first hour after arrival in zone I of the liver sinusoids, there is 10% probability of a B16F10 cell remaining intact in zone 1, an 89% probability of cell death in zone 1 and only a 1% probability of the cell passing into zone 3. During the same period, there is a 77% probability of an M5076 cell remaining intact in zone 1, 21% probability of death, and a 2% probability of relocation to zone 3. In both cell types, very few cells were lost from zone 3. Further proportional death in zone 1 diminished over the next 23 hr, concomitant with an increased proportion of cell death in zone 3. Our results indicate that, although there is considerable variation between the 2 cell types studied here, most (B16) or many (M5076) of these cancer cells entering the liver via the portal vein die within 1 hr in zone 1 of liver lobules. In addition, very few of the cells delivered to zone 1 travel along the sinusoids to zone 3, and few of these reach the lungs in a viable state.
Carcinogen‐induced accumulation of adeno‐associated parvovirus dna is transient as a result of two antagonistic activities that both require De Novo protein synthesis
Authors: Bantel‐Schaal Ursula 
Published: February 2007

AbstractHelper‐independent synthesis of adeno‐associated parvovirus type 5 (AAV‐5) DNA in SV40‐transformed Syrian hamster cells is induced by chemical carcinogens, UV light and other stress treatments and has previously been shown to be transient. To gain some insight into the underlying mechanism, the influence of inhibitors of protein synthesis on AAV DNA accumulation was investigated. It is shown that transience is the result of 2 antagonistic activities‐synthesis and decomposition. Both depend on de novo protein synthesis and are in part overlapping. The 2 activities are influenced by the amount of AAV uptake and/or by cell density. In less dense cultures, calculated initial amount of AAV DNA and relative accumulation per cell are higher. The effect may be due to the activity of transiently synthesized AAV‐encoded regulatory proteins that increase replication and have inhibitory effects on DNA decomposition, or to the influence on cellular adhesion.
Loss of heterozygosity at the short arm of chromosome 3 in renal‐cell cancer correlates with the cytological tumour type
Authors: Van Hout A. H. Der , Van Berg E. Den , Van Vlies P. Der , Dijkhuizen T. , Störkel S. , Oosterhuis J. W. , De Jong B. , Buys C. H. C. M. 
Published: February 2007

AbstractA majority of renal‐cell tumours retain heterozygosity at the short arm of chromosome 3. To investigate possible histopathological differences between tumours with and without such losses, we compared loss of heterozygosity data from 51 tumours with 1 histological and 2 different cytological classifications of renal‐cell tumour. Using the cytological classification of Thoenes et al., we only found tumours with loss of heterozygosity in these authors' clear‐cell category. Possibly, only these tumours arise by a mechanism of double loss of a tumour‐suppressor gene on 3p, non‐clear‐cell renal tumours having a different genetic background. Alternatively, deletions may occur in all subtypes, in which case those subtypes in which no LOH is found may also contain deletions too small to be detected with the set of 3p probes we used. A cytogenetic analysis was carried out on 30 of the tumours. Results of molecular and microscopic cytogenetic analyses did not seem to be in agreement in 12 cases. In 6 of these we found allelic losses in tumours showing morphologically normal copies of chromosome 3. Mitotic recombination or loss of one chromosome 3 homologue followed by duplication of the remaining homologue is a likely explanation. The other 6 cases showed microscopic abnormalities of chromosome 3 which were not reflected, or only partly reflected, as allelic losses. These discrepancies are caused either by the limitations of microscopic analysis in exactly determining a breakpoint or tracing a translocated part of a chromosome, or by the failure of molecular analysis to demonstrate LOH if this occurs in only a minority of cells.
Comparative cytogenetic and dna flow cytometric analysis of 150 bone and soft‐tissue tumors
Authors: Mandahl Nils , Baldetorp Bo , Fernö Mårten , Åkerman Måns , Rydholm Anders , Heim Sverre , Willén Helena , Killander Dick , Mitelman Felix 
Published: February 2007

AbstractSamples from 48 benign and 102 malignant bone and soft‐tissue tumors were analyzed cytogenetically and by DNA flow cytometry. Clonal chromosome abnormalities were found in 82 tumors and normal karyotypes in 68; 61 tumors were DNA‐non‐diploid and 89 were diploid. The cytogenetically abnormal tumors were used for comparison between the 2 types of investigation; 45 of these tumors were DNA‐diploid and 37 were DNA‐non‐diploid. There was, with few exceptions, good correspondence between the quantitative estimates of genomic changes by the 2 methods, indicating that the cells cytogenetically analyzed from short‐term cultures are representative of the in vivo cell populations. Discrepancies were primarily found in cases with indexes above 1.5, in which the DNA index was higher than the chromosome index. The chromosome analysis suggested that skewed stemline (G0/G1) peaks in the diploid region in DNA histograms indicate the presence of cell populations with small net quantitative genomic changes, although not all such populations were detected by DNA flow cytometric analysis. The view that one of the peaks in bimodal stemline DNA histograms with narrow peaks represents a non‐diploid cell population was also corroborated. On average, the cell populations giving rise to double stemlines in DNA histograms showed quantitatively larger genomic changes than those that gave rise to broad or skewed diploid G0/G1 peaks. The findings indicate that these histogram profiles are not artifactual but reflect chromosomal changes in the tumor parenchyma.
Over‐expression of p53 nuclear oncoprotein in transitional‐cell bladder cancer and its prognostic value
Authors: Lipponen Pertti K. 
Published: February 2007

AbstractTwo hundred and twelve archival bladder‐cancer biopsy specimens were analyzed immunohistochemically to detect over‐expression of p53 protein. The results of immunohistochemical analysis were correlated to established histological and quantitative prognostic factors and survival of patients during a mean follow‐up period of more than 10 years. Twentynine percent of tumours were positive for p53 protein, and over‐expression was associated with high histological grade, non‐papillary growth architecture, dense inflammatory cell reaction, DNA aneuploidy, high S‐phase fraction, high mitotic frequency and high SD of nuclear area. Progression in T, N and M categories was significantly related to over‐expression of p53 protein. In univariate survival analysis, over‐expression of p53 predicted poor outcome in the entire cohort, in papillary tumours and in muscle‐invasive tumours but not in superficial tumours. In a multivariate survival analysis, over‐expression of p53 oncoprotein had no independent prognostic value over clinical stage and mitotic index. The results confirm that p53 is involved in the growth regulation of bladder cancer and is certainly a subject for detailed analysis of specific mutations.
Differential regulation of gelatinase b and tissue‐type plasminogen activator expression in human bowes melanoma cells
Authors: Houde Michel , De Bruyne Georges , Bracke Marc , Ingelman‐sundberg Magnus , Skoglund GÓRan , Masure Stefan , Van Damme Jo , Opdenakker Ghislain 
Published: February 2007

AbstractA comparison of the production of tissue‐type plasminogen activator (t‐PA) and gelatinases A and B was made at the mRNA and protein levels in human Bowes melanoma cells treated with phorbol myristate acetate (PMA). Immunocytochemical analysis confirmed previous quantitative data on PMA‐mediated induction of t‐PA. It also showed that t‐PA immunoreactivity can be restrained to the local environment of the producing cell, most probably by interaction with extracellular matrix components. Zymographical analysis showed that gelatinase B protein was induced by PMA, whereas gelatinase A remained at the constitutive level. Protein kinase C (PKC) appeared to be involved in this regulation since, after PMA treatment (I) the PKC activity was found to be translocated from the cytosol to the particulate fraction of the cells and (2) addition of staurosporine and H‐7 blocked the gelatinase B increase. Northern‐blot hybridization showed a transient rise in t‐PA and gelatinase B mRNA levels whereas gelatinase A mRNA levels remained unchanged. When c‐fos and c‐jun mRNAs were investigated, only that of c‐fos was affected by PMA. Activation by PMA can be kinetically ordered as follows: translocation of PKC to the membrane fraction, transcription of the c‐fos gene and eclipsing of gelatinase B mRNA, increase in steady‐state mRNA levels of t‐PA and gelatinase B and, finally, secretion of t‐PA and gelatinase B glycoproteins. Our data also suggest that various proteases that are known to cooperate in the remodeling of the extracellular matrix can be differently regulated in one tumor‐cell type.