bluuebunny/crossref_metadata_2025_split huggingface dataset:
Early indicators of efficacy of breast cancer screening programmes. Results of the florence district programme
Authors: Paci Eugenio , Ciatto Stefano , Buiatti Eva , Cecchini Silvia , Palli Domenico , Turco Marco Rosselli Del 
Published: February 2007

AbstractA mammographic breast cancer screening programme has been ongoing in the Florence District (Italy) since 1970 and a favourable impact of screening on breast cancer mortality of women aged 50‐70 has been shown by means of a casecontrol study. Two hundred and eleven screen‐ and 116 interval‐detected cancers in the period 1975‐1986 have been identified, and detection rates calculated, for first and repeated screening test (2nd to 7th). Overall, 22,980 subjects were screened and 44,988 repeated tests performed. The observed number of interval cancers has been compared with the expected incident cancers and their ratio (O/E) studied at different time intervals since last test. The O/E ratio at the third year since the last test was 0.98 for the age‐group 40–49 0.50 (95% CI: 0.23‐0.95) and 0.39 (95% CI: 0.26‐0.94) for the 50‐59 and 60‐69 groups, respectively. The prevalence/incidence ratio (P/I) was then calculated as an early indicator of efficacy. For the 40‐49 age‐group the P/I ratio at first test was 1.09, suggesting poor anticipation of diagnosis. In contrast, for women 50‐59 and 60‐69 results suggest quite a good diagnosis anticipation (P/I: 3.14; 4.82), confirming the result of the previous case‐control study on mortality reduction. The proportion of advanced carcinomas (stage II or worse) and 5‐year survival have been analysed and discussed. The study confirms the opportunity of using early indicators of screening efficacy for monitoring of screening services.
Immune status as a determinant of human papillomavirus detection and its association with anal epithelial abnormalities
Authors: Melbye Mads , Palefsky Joel , Gonzales John , Ryder Lars P. , Nielsen Henrik , Bergman Olav , Pindborg Jens , Biggar Robert J. 
Published: February 2007

AbstractOne hundred and twenty Danish homosexual men were enrolled to characterize risk factors for anal type‐specific human papillomavirus (HPV) expression and to examine its association with anal epithelial atypia. Detection of HPV strongly correlated with immunosuppression measured by Tlymphocyte subset markers and rose nearly linearly from 7.3% among subjects with CD4/CD8 ratios above 1.0 to 35.3% among those with a ratio below 0.4 (p trend = 0.003). No association was found between presence of HPV and a wide range of lifestyle factors including number of sex partners/year, smoking, alcohol consumption and illegal drug intake. However, self‐reported history of anal condyloma in the past year was correlated with HPV (p < 0.001). Simultaneous testing for presence of HPV in the oral cavity showed evidence of HPV 16, 18 and 31, 33, 35. Anal smears were abnormal in 19.5% of the men and correlated strongly with presence of HPV (OR = 601, p < 0.0001). Type‐specific associations were found with HPV 31/33/35 (OR = 8.5) and HPV 16/18 (OR = 3.1) only. The association remained significant after adjusting for immune status. Overall, HPV was detected in 50% of the cases with abnormal smears. However, HPV was found in all subjects with abnormal smears and a CD4/CD8 ratio below 0.4, compared to only 3 of 14 subjects with abnormal smears and a ratio ± 1.3. In conclusion, (I) HPV may be missed in a substantial number of infected subjects with a normal immune system. This may have an impact on studies trying to describe risk factors for HPV transmission and its correlation with cancer development. (2) The finding of HPV 16,18 and 31,33,35 in the oral cavity makes oral‐genital sexual activity at least a hypothetical route of transmission for these HPV types. (3) HPV appears to play a central role in the development of anal epithelial abnormality.
A model‐based analysis of the hip project for breast cancer screening
Authors: Van Oortmarssen G. J. , Habbema J. D. F. , Lubbe J. T. H. N. , Van Der Maas P. J. 
Published: February 2007

AbstractA computer simulation approach is used to test assumptions about sensitivity of mammography and physical examination, and about the duration of preclinical screendetectable breast cancer. Values between 50% and 80% for the combined sensitivity of the 2 tests give a good explanation of the results of the HIP randomized trial of breast cancer screening. The mean duration of the preclinical stage can vary from 1.6 years for high sensitivity values to 2.7 years for low values. In comparison with previous analyses of the HIP data, our estimate for the sensitivity is lower, and the mean duration of the preclinical stage is longer. This is a consequence of the use of a more detailed model in our analysis, allowing for a more complete use of the HIP data in testing model assumptions. Similar analyses of data from recent screening projects in The Netherlands resulted in compatible estimates for the duration of preclinical breast cancer.
Cancer incidence in migrants to new south wales
Authors: McCredie Margaret , Coates Marylon S. , Ford Joyce M. 
Published: February 2007

AbstractCancer incidence in migrants to New South Wales (NSW) from the British Isles, north‐central, eastern and southern Europe, the Middle East and Asia has been compared with that in Australian‐born residents using data from the NSW Central Cancer Registry for 1972‐84. Indirectly standardized incidence ratios (SIRS) were low in migrants from all 6 regions for melanoma of skin and cancers of lip and, except in men from eastern Europe, colon. Oesophageal, rectal and prostatic cancers also tended to be relatively less common. Cancers which were more common than in the Australian‐born were those of the stomach and, for men, bladder (except in the Asian‐born). Migrants from different regions showed variations from the cancer pattern of the Australian‐born population which, for the most part, were predictable from the known incidence of cancer in the countries within the region of origin. Exceptions were the high relative incidence of nasopharyngeal cancer in migrants from southern Europe and bladder cancer in men from all regions other than Asia.
Cancer in migrants to uruguay
Authors: De Stefani E. , Parkin D. M. , Khlat M. , Vassallo A. , Abella M. 
Published: February 2007

AbstractMortality rates from different cancers in the principal groups of migrants to Uruguay are compared with those in their countries of origin (Argentina, Brazil, Italy and Spain) and in the Uruguay‐born population. Oesophageal cancer is very common in Uruguay and European‐born populations, initially at low risk, appear to acquire rather higher rates after migration. For most migrants, the mortality from cancers of the breast, colon‐rectum, corpus uteri and prostate is closer to the moderately elevated rates of Uruguay than those in their countries of origin. The results suggest that migrants to Uruguay undergo changes in some important environmental exposures, probably dietary, which give rise to substantial alterations in cancer risk within their lifespan.
Enhanced invasiveness and metastatic potential of epithelial cell lines cultured in the presence of dimethyl sulphoxide
Authors: Bentel Jacqueline M. , Rhodes Gregory C. , Markus Irit , Smith Garry J. 
Published: February 2007

AbstractSeveral passage cycles of poorly metastatic malignant epithelial cells through immunosuppressed mice failed to induce enhanced metastasis‐forming ability of cells derived from either the primary subcutaneous tumours or the resultant lung metastases. In vitro treatment of cultured malignant cells with dimethyl sulphoxide (DMSO) induced a reversible change in phenotype towards increased invasiveness but did not significantly increase metastasis formation. A cloned‐cell line from a spontaneous in vitro transformant in the presence of DMSO was highly invasive and highly metastatic. In vitro treatment of cultured cells with 2% (v/v) DMSO produced alterations in morphology with decreased growth rate of all cell lines and decreased anchorage‐independent colony formation in several malignant cell lines. All in vitro and in vivo effects were reversible following both short‐ and long‐term (1 year) culture of cells in the presence of DMSO, suggesting epigenetic effects. These data support the concept of independent genetic controls for the invasiveness of tumours and the ability to form metastases.
Immunolocalization of phosphoprotein B23 in proliferating and non‐proliferating hela cells
Authors: Yung Benjamin Y‐M. , Bor Amy M‐s. , Yang Y. H. 
Published: February 2007

AbstractLocalization of protein B23 in HeLa cells under different growth conditions was studied using indirect immunofluorescence. Bright nucleolar fluorescence was observed in exponentially growing cells. After 3 to 4 days, the initial cell inocula entered a phase of stationary growth as defined by no increments in cell number. The nucleolar fluorescence was then diminished and a general nuclear immunofluorexence was observed. This change in localization of fluorescence indicated that protein B23 had migrated out of the nucleoli during the suboptimal growth conditions. Relocation of protein B23 in nucleoli was observed in cells of stationary growth after treatment with adriamycin or daunomycin at their subtoxic concentrations (10−10 M). Adriamycin and daunomycin, at their toxic concentrations (>5.0. ± 10−7 M), on the other hand, inhibited cell growth and induced B23 translocation from nucleoli to nucleoplasm in growing cells. These results indicate that both adriamycin and daunomycin exhibit biphasic effects on the proliferation of cells by either stimulation or inhibition depending on the drug concentrations and the growth conditions. B23 translocation, as observed by immunofluorescence may be a simple and rapid method for assessing inhibition‐stimulation growth response to anti‐tumor therapy.
Heterogeneity of the motility responses in malignant tumor cells: A biological basis for the diversity and homing of metastatic cells
Authors: Kohn Elise C. , Francis Elizabeth A. , Liotta Lance A. , Schiffmann Elliott 
Published: February 2007

AbstractTumor metastasis requires highly motile cells that can respond to appropriate stimuli. A2058 human melanoma cells were shown previously to secrete a highly potent autocrine motility factor (AMF) that stimulates chemokinetic movement. We have shown that the insulin polypeptides (IPS; insulin‐like growth factors I and II [IGF‐I, ‐II] and insulin) stimulated A2058 cell chemotaxis and chemokinesis. We now report that the IPs and AMF stimulate locomotion in other human malignant cell lines. Insulin (100 nm) induced motility of up to 50% of the magnitude of the AMF response in human carcinoma lines MDA‐231 (breast), T24 (bladder), and OVCAR3 (ovarian). The tumorigenic and metastatic SR Ha‐ras‐transfected rat embryo fibroblast cell line responded to insulin with both chemotaxis and chemokinesis and was 100% of that seen for AMF. The ED50 for IGF‐I in the carcinoma cell lines was in the order of I nm, but the magnitude of the responses at this concentration was 40% of the AMF‐stimulated response, with the exception of the A2058 cells, which were maximally stimulated at I nn. IGF‐II induced maximal motility of 75 to 130% of the AMF‐stimulated response in the carcinoma lines with ED50, of <10 nM. IGF‐II‐stimulated motility in the carcinoma lines was predominantly chemotactic by modified checkerboard analysis. Cell pretreatment with pertussis toxin inhibited 90‐100% of AMF‐induced motility, whereas migration to the IPS was not pertussis toxinsusceptible. In growth studies, IGF‐I induced mitogenesis up to 140% of basal media control growth. In general, maximal growth stimulation was seen at 100 nn IGF‐I, and optimal migration was seen at 10 nM IGF‐I. The IGFs are secreted by normal stroma in a number of organs that are common sites for primary and metastatic disease. Therefore, we suggest that IPS may be important homing and mitogenic signals for tumor cells in the process of invasion and metastasis and that the differential motility stimulation and respective mechanisms of action by these physiologically important agents may underlie the diversity of the metastatic process.
Tumour‐induced host stromal‐cell transformation: Induction of mouse spindle‐cell fibrosarcoma not mediated by gene transfer
Authors: Russell Pamela J. , Brown Joanne , Grimmond Sean , Stapleton Paula , Russell Peter , Raghavan Derek , Symonds Geoff 
Published: February 2007

AbstractTumour‐induced host‐cell transformation has been addressed by examining human tumours in situ and following xenograft to nude mice. We have found evidence for the transformation of host stromal fibroblasts both in vivo and following the introduction of the tumours to in vitro culture. The in vitro culture of one such xenograft‐derived from a human prostatic adenocarcinoma‐resulted in the outgrowth of a transformed aneuploid mouse cell line. This transformed line was tumourigenic both in BALB/c nu/nu (nude) mice and in heterozygous nu/+ mice, with the morphology of a spindlecell sarcoma. The cell line did not express human isozymes or human histocompatibility antigens, nor were human chromosomes present. Moreover, human DNA sequences were notdetected by human Alu repeat sequence element probing in the transformed cell line grown either in vitro or in vivo. The line contained retroviral long terminal repeat sequences but there was no evidence of proviral activation. These findings indicate that tumour cells may cause transformation of neighbouring stromal cells; that this transformation may proceed in the absence of DNA transfer or activation of endogenous proviruses; and that the means of this observed transformation may involve humoral factors elaborated by the tumour cells.
Effects of tumor necrosis factor, alone or in combination with topoisomerase‐ii‐targeted drugs, on human lung cancer cell lines
Authors: Giaccone Giuseppe , Kadoyama Chikabumi , Maneckjee Rhoda , Venzon David , Alexander Richard B. , Gazdar Adi F. 
Published: February 2007

AbstractTumor necrosis factor α (TNF) exhibits cytotoxic activity on some solid tumors and has been reported to be synergistic with topoisomerase‐II‐targeted antineoplastic agents. A wide range of TNF concentrations (from 10 to 10,000 U/ml) was tested in 9 human lung cancer cell lines (5 small‐cell and 4 non‐small‐cell carcinomas) using a semi‐automated MTT assay. TNF was not cytotoxic in 8 cell lines, while an adenocarcinoma cell line was marginally sensitive to the cytokine. Using 125I‐TNF we were able to show the presence of specific binding sites for TNF in 4/9 human lung cancer cell lines. Scatchard analysis of the marginally sensitive cell line showed high‐affinity, saturable binding. With 5 cell lines we also tested whether TNF affected the cytotoxicity of doxorubicin and etoposide, 2 topoisomerase II‐targeted drugs which are widely used in the therapy of lung cancer. No significant increase in cytotoxicity was seen when TNF was added to the 2 anti‐neoplastic agents. In contrast to certain other human and mouse lines, human lung cancer cell lines appear to be resistant to TNF, despite the presence of the receptor in some of them; moreover, no synergistic effect of TNF and 2 topoisomerase‐II‐targeted drugs was evident in these human cell lines.
Differential sensitivity of multi‐drug‐resistant and ‐sensitive cells to resistance‐modifying agents and the relation with reversal of anthracycline resistance
Authors: Schuurhuis Gerrit J. , Pinedo Herbert M. , Broxterman Henricus J. , Van Kalken Coenraad K. , Kuiper Catharina M. , Lankelma Jan 
Published: February 2007

AbstractCalcium channel blockers, calmodulin inhibitors, and some other classes of non‐related compounds reverse multi‐drug resistance. In the present study, we found that several resistance modifiers are more toxic for MDR cells than for the corresponding sensitive parent cells, whereas others show the opposite effect. Several calcium channel blockers including bepridil, diltiazem, nifedipine and verapamil, as well as the calmodulin inhibitor trifluoperazine, were more toxic for several MDR cell lines than for the parent cell lines. In contrast, cross‐resistance for cyclosporin A and the verapamil analogue Ro II‐2933/001 was observed in the MDR/sensitive cell couple CHRC5/AUXB1 probably due to a concentration‐dependent stimulation of cell growth in the range of 0–4 μM cyclosporin A and of 1‐4 μ Ro II‐2933/001. In partially revertant CHRC5 cells, growth inhibition by Ro II‐2933/001 at concentrations below I μ, as seen in CHRC5, cells, changed into growth stimulation, and the collateral sensitivity to verapamil and bepridil disappeared almost completely. In the MDR cells CHRC5 2780AD and DC3F/DMXX, cross‐resistance to another calcium channel blocking agent, Ro II‐1781/001 (tiapamil), was observed as well. This compound showed exceptional behavior: it induced marked potentiation of Dx cytotoxicity as well as stimulation of Dx accumulation in AUXB1 cells, even at low tiapamil concentrations, but not in the CHRC5, cells, even at high concentrations. It is concluded that resistance modifiers can selectively influence growth of MDR cells via more than one process, and resulting in either strong growth inhibition in MDR cells relative to the effect on sensitive cells or in growth stimulation.
Risk factors for hepatocellular carcinoma in catalonia, spain
Authors: Mayans M Vall , Calvet X. , Bruix J. , Bruguera M. , Costa J. , Estève J. , Bosch F. X. , Bru C. , Rodés J. 
Published: February 2007

AbstractThe influence of hepatitis B virus infection, alcohol consumption, tobacco smoking and use of oral contraceptives on the risk of hepatocellular carcinoma (HCC) was evaluated in a hospital‐based case‐control study in Catalonia, in the Mediterranean coastal area of north‐eastern Spain. A total of 96 HCC cases (86.5% of them with associated liver cirrhosis) and 190 age‐ and sex‐matched controls were studied. The odds ratio of HCC and 95% confidence interval among hepatitis B surface antigen (HBsAg) carriers was 4.9 (1.3‐21.9). The OR was not significantly elevated in smokers, and a marginally significant increased risk was found among users of oral contraceptives based on 6 female cases. There was a significant dose‐response relationship between alcohol consumption and risk of HCC (X2 for trend: 24.3, p < 0.001). Although hepatitis B infection was strongly associated with HCC, alcohol abuse leading to cirrhosis appears to be one of the main causes of HCC in this region.
Co‐expression of the genes encoding transforming growth factor‐α and its receptor in papillary carcinomas of the thyroid
Authors: Aasland R. , Akslen L. A. , Varhaug J. E. , Lillehaug J. R. 
Published: February 2007

AbstractTransforming growth factor‐α (TGF‐α) is frequently co expressed with its receptor, epidermal growth factor receptor (EGF‐R), in several types of carcinoma and sarcoma. It is believed that this results in an autocrine stimulation of tumor growth in these tumors. We have found that TGF‐α and EGF‐R/c‐erbB RNAs were co‐expressed at significantly higher levels in papillary thyroid carcinomas and their lymph‐node metastases than in non‐neoplastic thyroid tissues. We also observed a low level of expression of RNA specific for insulin‐like growth factor I in these tumors, which was highest in a lymphnode metastasis. Autocrine stimulation by TGF‐α may thus be a common feature of papillary carcinomas of the thyroid. Since EGF is known to induce proliferation and dedifferentiation of normal thyroid cells in culture, TGF‐α and its receptor may play an important role in thyroid carcinogenesis.
The role of alcohol in oral and pharyngeal cancer in non‐smokers, and of tobacco in non‐drinkers
Authors: Talamini R. , Franceschi S. , Barra S. , La Vecchia C. 
Published: February 2007

AbstractData from a hospital‐based case‐control study of oral and pharyngeal cancer conducted in Northern Italy were used to analyse the risk associated with alcohol in non‐smokers and with tobacco in non‐drinkers. Out of a total of 336 cases (291 males and 45 females) and 1,652 controls (1,272 males and 380 females) 27 cases and 572 controls described themselves as lifelong non‐smokers. Odds ratios (ORs) were 1.5 for 14‐55 vs. 0‐13 alcoholic drinks per week and 2.2 for 56 or over; the trend in risk was statistically significant. Among 19 cases and 213 controls who described themselves as non‐drinkers, the ORs were 3.8 and 12.9 for smokers of < 15 and ≥ 15 cigarettes per day, with a highly significant trend. This study therefore confirms that tobacco has an independent role in the aetiology of oral and pharyngeal cancer, and suggests that alcohol may have an independent role as well, even where, as in Northern Italy, wine is its predominant source. Indeed, ORs were similar to those for tobacco and alcohol individually, each adjusted for the other factor, in the overall data‐set.
Lymphokine‐activated killer (lak) cells discriminate between epstein‐barr virus (ebv)‐positive burkitt's lymphoma cells
Authors: Misko Ihor S. , Schmidt Christopher , Martin Nicole , Moss Denis J. , Sculley Thomas B. , Burrows Scott , Burman Kelcey J. 
Published: February 2007

AbstractWe have generated in vitro lymphokine‐activated killer (LAK) cells from healthy donors by stimulating their mononuclear leukocytes with recombinant interleukin‐2 (rIL‐2) (100 U/ml). After 6 days in culture, the lytic properties of the LAK cells were analyzed in the 51Cr‐release assay by utilizing a target panel of 6 paired lines consisting of an Epstein‐Barr virus (EBV)‐positive Burkitt's lymphoma (BL) cell line and an EBV‐transformed lymphoblastoid cell line (LCL) from the same donor, the Raji BL line and the natural killer (NK) cell‐sensitive K562 line. The patterns of lysis showed that the LAK cells discriminated between two categories of BL cell lines. Group l/ll BL tumor cells which expressed the common acute lymphoblastic leukemia antigen (CALLA), the BL‐associated glycolipid antigen (BLA) and phenotypically resembled biopsy cells were strongly lysed whereas group III BL cells which had assumed an LCL‐like phenotype during culture and lacked the CALLA and BLA surface markers were only poorly lysed. The LCL targets were generally resistant to lysis but the K562 cell line was particularly sensitive. The outcome of cell depletion and monoclonal antibody (MAb) studies indicated that the LAK cell populations were phenotypically and functionally heterogeneous and consisted of at least 2 subpopulations of effector cells; a tumor‐specific component and an NK‐cell‐mediated component.
Abnormal expression and structural modification of the insulin‐like growth‐factor‐ii gene in human colorectal tumors
Authors: Lambert Sylvie , Vivario Jeanine , Boniver Jacques , Gol‐Winkler Rosita 
Published: February 2007

AbstractThe insulin‐like growth factor II (IGF‐II) is a small protein implicated in fetal growth and development. It may play a role in the neoplastic process. The IGF‐II gene is located on the short arm of chromosome 11 near insulin and c‐Ha‐ras I genes. Three distinct promoters control the transcription of this gene, leading to different IGF‐II mRNA species. We have analyzed 21 human colorectal tumors and found overexpression of IGF‐II in 6 of them (30%). When compared with expression in normal adjacent tissues, IGF‐II mRNA increase in these tumors was either moderate (2‐ to 15‐fold) or very marked (200‐ to 800‐fold). In situ hybridization experiments confirmed that high IGF‐II mRNA amounts were localized in cancer cells of the tumors overexpressing the IGF‐II gene. In addition, DNA analysis revealed a structural modification of one IGF‐II locus in one tumor characterized by very high IGF‐II mRNA.