bluuebunny/crossref_metadata_2025_split huggingface dataset:
Indications of future decreasing trends in skin‐melanoma mortality among whites in the United States
Authors: Scotto Joseph , Pitcher Hugh , Lee John A. H. 
Published: February 2007

AbstractTrends in skin melanoma death rates during a 35‐year period, 1950‐84, were analyzed according to age, sex, and birth cohort for whites in the United States. In contrast to upward trends observed for older men and women (i.e., over 40), downward trends were noted for younger age groups. The risk of dying from skin melanoma appears to have peaked for male cohorts born during the 1950s and for female cohorts born during the 1930s. Assuming no future environmental or lifestyle changes, the upward trend in age‐adjusted mortality rates, which averaged 2 to 3% per annum since 1950, is projected to discontinue and bend downward by the second decade of the 21st century. Skin melanoma incidence data, which was limited to a series of 12 years (1973‐84) and inadequate for cohort analyses, were included to demonstrate that trends in age‐specific rates were comparable with those observed for mortality during the overlapping time period. Incidence trends according to anatomical site are also described. These results indicate that baseline data necessary for assessing the potential effects on this disease from future depletions of the ozone layer, and predicted increases of solar ultra‐violet radiation exposure, would be improved with the inclusion of cohort data and age‐specific trend analyses.
The systemic complement activation caused by interleukin‐2/lymphokine‐activated killer‐cell therapy of cancer causes minimal systemic neutrophil activation
Authors: Moore Francis D. , Schoof Deric D. , Rodrick Mary , Eberlein Timothy J. 
Published: February 2007

AbstractTwenty‐three cancer patients undergoing therapy with interleukin‐2 and lymphokine‐activated killer cells were studied for evidence of complement activation and systemic neutrophil activation occurring during the course of therapy. Patient plasma samples demonstrated evidence of marked complement activation, with 3‐fold elevations of C3a desArg concentrations by the 8th day of therapy. Concentrations of C4a desArg were also elevated by the end of therapy. In vitro chemotaxis of patients' neutrophils both to C5a and to the synthetic peptide chemotaxin, FMLP, was initially normal and then fell progressively to 60% of normal by the end of treatment. Mean neutrophil cell‐surface expression of complement receptor Type 1 and complement receptor Type 3 increased in inverse temporal relationship to the deficit in chemotaxis, but showed no consistent pattern for individuals and was only doubled at maximum. Thus, despite a degree of complement activation which should have produced pronounced neutrophil activation, the response of the circulating neutrophils was diminished. In view of this discrepancy, the toxicity of this therapy may not be mediated by activation of circulating neutrophils.
Dietary factors and stomach cancer in Spain: A multi‐centre case‐control study
Authors: González Carlos A. , Sanz J. Miguel , Marcos Guillermo , Pita Salvador , Brullet Enric , Saigi Eugeni , Badia Asunción , Riboli Elio 
Published: February 2007

AbstractA multi‐centre case‐control study of diet and gastric cancer was carried out in 4 regions of Spain (Aragon, Castile, Catalonia and Galicia). We selected 354 cases of pathologically confirmed gastric adenocarcinoma from 15 hospitals, representative of nearly all those in the study areas. A control for each case, matched by age, sex and area of residence, was selected from the same hospital as the case. Habitual diet was investigated by the dietary history method, and past diet by means of frequency questionnaire. The results regarding consumption of food items are presented here. With respect to habitual diet, an increase in risk was associated with consumption of preserved fish, cold cuts and oleaginous fruits. A high intake of cooked green vegetables, fresh noncitrus fruit and dried fruit showed an inverse association with the risk of gastric cancer. Simultaneous intake of 2 groups of food which increase or decrease the risk of cancer strengthens the respective individual effect. The intake of protective food items seems to neutralize the effects of food items which increase risk. With reference to past diet, possible a protective effect was observed for daily consumption of fresh fruit and green vegetables.
Survival of breast cancer patients in relation to factors which affect the risk of developing breast cancer
Authors: Ewertz Marianne , Gillanders Sonya , Meyer Lesley , Zedeler Karin 
Published: February 2007

AbstractIn order to evaluate the prognostic significance of risk factors for developing breast cancer, a population‐based study was conducted of 2,445 breast cancer patients diagnosed in Denmark, 1983‐1984. Data on clinical and pathological characteristics of breast cancer were derived from the Danish Breast Cancer Cooperative Group and data on risk factors from self‐administered questionnaire. Among 1,744 patients (71%) with complete information, survival was determined primarily by size of the tumour, skin invasion, number of positive lymph nodes and grade. No significant association was found between survival and reproductive or hormonal risk factors, dietary variables, alcohol consumption and smoking. Low current body weight and weight loss indicated a poor prognosis, independent of the clinical characteristics of the tumour.
Abnormalities of the EGF receptor system in human thyroid neoplasia
Authors: Lemoine Nicholas R. , Hughes Christine M. , Gullick William J. , Brown Christopher L. , Wynford‐Thomas David 
Published: February 2007

AbstractThe epidermal‐growth‐factor receptor (EGF‐r) and its ligands are involved in the control of proliferation of both normal and neoplastic thyroid epithelium. Autocrine stimulation of growth involving this receptor system has been identified in several types of human neoplasia and we were interested to determine whether it might occur in human thyroid tumours. We have therefore examined an archival series of thyroid tumours and non‐neoplastic pathologies for expression of the EGF‐r and 2 of its ligands, transforming growth factor alpha (TGF‐α) and epidermal growth factor (EGF), using immunohistochemistry. We found evidence of expression of both the EGF‐r and the TGF‐α in the majority of thyroid tumours, with a trend to higher expression in more malignant neoplasms. We also found variable levels of expression of EGF‐r and TGF‐α in all cases of thyroiditis examined. We conclude that there is a potential autocrine loop involving the EGF‐r system in both neoplastic and non‐neoplastic conditions of the human thyroid.
Combined in vitro modulation of adriamycin resistance
Authors: Meijer C. , Mulder N. H. , Timmer‐Bosscha H. , Petfrs W. H. M. , de Vries E. G. E. 
Published: February 2007

AbstractIn a P‐glycoprotein‐negative cell line, GLC4‐Adr90, a 75‐fold acquired Adriamycin (Adr) resistance coincided with a reduced cellular Adr level, an increased detoxifying capacity (glutathione (GSH) and glutathione S‐transferase (GST) elevated), and a reduced topoisomerase‐II (topo‐II) activity compared with the parent cell line GLC4. The effect on Adr resistance of buthionine sulfoximine (BSO, GSH synthesis inhibitor), was studied alone or in combination with verapamil (drug‐efflux inhibitor), docosahexaenoic acid (membrane lipid domain affector), ethacrynic acid (GST inhibitor), aphidicolin (DNA‐ polymerase‐α inhibitor) or novobiocin (NOV, topo‐II inhibitor). Cytotoxicity was tested using a microculture tetrazolium assay. In GLC4‐Adr90, BSO and NOV increased Adr‐induced cytotoxicity 12.9‐fold and 1.8‐fold respectively. The combination of BSO plus NOV showed an additive effect, decreasing the Adr resistance factor from 75 to 2.7. Combination of modulators of Adr resistance directed at different resistance mechanisms appears promising in vitro.
Induction of multiple‐drug resistance during anti‐neoplastic chemotherapy in vitro
Authors: Licht Thomas , Fiebig Heinz‐Herbert , Bross Klaus J. , Herrmann Friedhelm , Berger Dietmar P. , Shoemaker Robert , Mertelsmann Roland 
Published: February 2007

AbstractInduction of P‐glycoprotein‐related multi‐drug‐resistance (MDR) has been shown innormal and malignant tissues to result from environmental stresses such as heat shock, exposure to carcinogens or X‐ray irradiation. To identify conditions under which MDR is enhanced during anti‐neoplastic chemotherapy, a cell line showing low‐level intrinsic MDR was investigated. In the pleural mesothelioma cell line, PXF1118, < 1% of cells ex‐ pressed P‐glycoprotein (P‐gp), as shown by immunocytochemical staining with monoclonal antibody (MAb) MRK16. Exposure of PXF1118 to vincristine, vindesine, vinblastine or doxorubicin for 2‐3 weeks led to an increase in the MDR cell fraction of up to 15‐28% during 2 to 3 weeks. For doxorubicin and vindesine, dose‐dependence was observed: drug concentrations not capable of eliciting cytotoxicity failed to induce significant P‐gp expression. Nutrient starvation in aging medium, exposure to activated cyclophosphamide (even at high concentrations) or cisplatin caused only negligible MDR induction. After exposure to vindesine for 6 weeks, tumor colonies exhibited highly enhanced resistance to Vinca alkaloids, doxorubicin, etoposide and dacarbacine, whereas their sensitivity to mitomycin, activated cyclophos hamide or cisplatin remained unchanged. As determined by [3H]‐thymidine uptake and proliferation antigen expression, induction of MDR phenotype was observed at minimal proliferative activity with no change in cell count during exposure to anti‐cancer drugs, thus suggesting that the drug treatments changed the phenotype of the cells rather than selecting for a resistant sub‐population. In addition, changes in cell differentiation were observed during MDR induction. Induction of P‐gp during exposure to anti‐cancer drugs thus provides a model for MDR development during initially successful chemotherapy.
Ethnic differences in the anatomical location of colorectal adenomatous polyps
Authors: Offerhaus G. Johan A. , Giardiello Francis M. , Tersmette Kasper W. F. , Mulder Jan‐Willem R. , Tersmette Anne C. , Moore G. William , Hamilton Stanley R. 
Published: February 2007

AbstractThe ratio of right‐ to left‐sided colonic cancer is increasing, but data on the distribution of its usual precursor lesion, the colorectal adenoma, are contradictory. Therefore, we investigated the prevalence of right‐ and left‐sided colorectal adeno‐matous polyps from January I, 1970, to September 30, 1989, using the study design of „epidemiologic necropsy”︁ and the autopsy files of The Johns Hopkins Hospital.Compared with the decade of the 1970's, the 1980's showed a slight decrease in the overall prevalence of right‐sided adenomas (6.4 per 1,000, 95% confidence limits 4.7‐8.8 vs. 5.1 per 1.000, 95% CL 3.6‐6.5), but a marked decrease occurred in left‐sided adenomas (11.8 per 1,000,95% CL 9.3‐14.3 vs. 6.7 per 1,000, 95% CL 4.8‐8.6). As a result, the ratio of right‐sided to left‐sided adenomas increased from 0.55 in the 1970's to 0.77 in the 1980's. This increased ratio occurred in both sexes, although prevalences were lower in females, and in whites. Unexpectedly, blacks had a ratio of right‐sided to left‐sided adenomas greater than unity in both the 1970's and 1980's (1.19 vs. 1.79) due to a relatively high prevalence of right‐sided adenomas (5.8 per 1,000, 95% CL 3.6‐8.0 in 1970's; 5.8 per 1,000, 95% CL 3.3‐8.3 in 1980's), but low prevalences of left‐sided adenomas (4.9 per 1,000, 95% CL 3.0‐6.8 in 1970's; 3.2 per 1,000, 95% CL 1.2‐5.2 in 1980's). The overall adenoma prevalence in blacks was lower than in whites.We conclude that the right‐sided predominance of colorectal adenomas in blacks suggests ethnic differences in the pathogenesis of colorectal adenomas. This observation may have important implications for secondary prevention of colorectal cancer.
Tissue concentrations of prostate‐specific antigen in prostatic carcinoma and benign prostatic hyperplasia
Authors: Pretlow Thomas G. , Pretlow Theresa P. , Yang Bin , Kaetzel Charlotte S. , Delmoro Carrie M. , Kamis Sheryl M. , Bodner Donald R. , Kursh Elroy , Resnick Martin I. , Bradley Edwin L. 
Published: February 2007

AbstractProstate‐specific antigen (PSA), as measured in peripheral blood, is currently the most widely used marker for the assessment of tumor burden in the longitudinal study of patients with carcinoma of the prostate (PCA). Studies from other laboratories have led to the conclusion that a given volume of PCA causes a much higher level of PSA in the peripheral circulation of patients than a similar volume of prostate without carcinoma. We have evaluated PSA in the resected tissues immunohistochemically and in extracts of PCA and of prostates resected because of benign prostatic hyperplasia (BPH) with an enzyme‐linked immunosorbent assay. Immunohistochemical results were less quantitative than but consistent with the results of the ELISA of tissue extracts. Immunohistochemically, there was considerable heterogeneity in the expression of PSA by both PCA and BPH both within and among prostatic tissues from different patients. While the levels of expression of PSA in these tissues overlap broadly, PSA is expressed at a lower level in PCA than in BPH when PSA is expressed as a function of wet weight of tissue (p = 0.0095), wet weight of tissue/% epithelium (p < 0.0001), protein extracted from the tissue (p = 0.0039). or protein extracted/% epithelium (p < 0.0001).
Association of C‐erbB‐2 protein over‐expression with high rate of cell proliferation, increased risk of visceral metastasis and poor long‐term survival in breast cancer
Authors: Kallioniemi Olli‐P. , Holli Kaija , Visakorpi Tapio , Koivula Timo , Helin Heikki H. , Isola Jorma J. 
Published: February 2007

AbstractC‐erbB‐2 protein over‐expression was studied immunohis‐tochemically in 319 paraffin‐embedded breast carcinomas representing 89% of all breast‐cancer cases operated in the Tampere University Hospital between 1977 and 1981. The immunohistochemical evaluation of c‐erbB‐2 was optimized using protease pre‐treatment and verified using antibodies for both the external and the internal domains of the protein. c‐erbB‐2 over‐expression was found in 72 (23%) of the 319 cases and was associated with high histological and nuclear grade (p< 0.0001), DNA aneuploidy (p= 0.003), high tumor S‐phase fraction (p< 0.000l), and lack of estrogen (p< 0.0001) and progesterone (p= 0.03) receptors. Overall, breast‐cancer patients with c‐erbB‐2 over‐expression had about 2.2‐fold relative risk (RR) of death (p< 0.001) as compared with those without over‐expression. According to a multivariate analysis, c‐erbB‐2 over‐expression was an independent prognostic factor in the whole material as well as in the node‐negative sub‐set. In node‐negative breast‐cancer tumor size, S‐phase and c‐erbB‐2 status defined a large patient group with only 4% 5‐year and 15% 10‐year mortality rate without adjuvant therapy. In comparison with c‐erbB‐2‐negative tumors, those with over‐expression of this gene metastasized 3 times more often (p= 0.0002) to the lungs, liver and brain and 3 times less often to the bone. Our findings suggest that the prognostic value of c‐erbB‐2 over‐expression may be related not only to increased cell proliferation rate but also to a distinctive pattern of metastasis.
Allelic loss on the short arm of chromosome 11 in non‐small‐cell lung cancer
Authors: Ludwig Christian U. , Raefle Gaby , Dalquen Peter , Stulz Peter , Stahel Rolf , Obrecht Jean‐Paul 
Published: February 2007

AbstractForty‐eight samples of primary non‐small‐cell lung cancer (nsclc) and normal tissue from the same patients were analyzed for allelic deletions on chromosome 11p. five polymorphic loci were assessed to determine the incidence of 11 p sequence deletions and to define hot‐spots of deletions. information was obtained from all patients in at least one locus. our data show that the deletions observed were not randomly scattered over the short arm of chromosome i i. rather, 2 hot‐spots of deletions were observed: one in the area of the genes for catalase and β‐fsh corresponding to band ii p13, the other close to the igf‐ii locus corresponding to band ii p15. a high incidence of loss of heterozygosity (loh) was found with the probe for catalase (21/29), a locus flanking the centromeric region of the wilms' tumor locus. most of the samples exhibiting loh of one or more of the alleles analyzed remained heterozygous for at least one other chromosome iip allele. furthermore, duplication of the intensity of the remaining allele was rarely observed. our results indicate that loh on the short arm of chromosome ii is a common event in nsclc and that the chromosomal region containing the wilms' tumor locus is most commonly involved.
Distribution of collagenase and tissue inhibitor of metalloproteinases (TIMP) in colorectal tumours
Authors: Hewitt Robert E. , Leach Iain H. , Powe Desmond G. , Clark Ian M. , Cawston Tim E. , Turner David R. 
Published: February 2007

AbstractIncreased collagenase activity in colorectal carcinomas has recently been shown to be associated with increased malignant potential. To determine the tissue distribution of collagenase and its specific inhibitor, tissue inhibitor of metalloproteinases (TIMP), we carried out an immunohistochemical study on colorectal carcinomas (n = 20), adenomas (n = 7) and normal mucosa (n = 6). We found increased staining for collagenase in the connective tissue stroma of carcinomas, as compared with adenomas and normal mucosa. Little evidence of epithelial cell staining for collagenase was seen in any tissue. In carcinomas, both stromal fibroblasts and collagen fibres stained strongly and stromal staining was strongest close to neoplastic glands. Vascular staining was more prominent in neoplastic than normal tissues, perhaps reflecting the increased proteolytic activity during tumour angiogenesis. The pattern of TIMP immunostaining was similar to that of collagenase, although basement membrane staining for TIMP was generally more intense. Another difference was that, unlike TIMP, staining for collagenase was often increased at the invasive edge of carcinomas, perhaps reflecting increased collagenase activity at this location.
Inhibitory effect of maternal antibody on mother‐to‐child transmission of human T‐lymphotropic virus type I
Authors: Takahashi Kazuo , Takezaki Toshiro , Oki Toshitaka , Kawakami Kiyoshi , Yashiki Shinji , Fujiyoshi Toshinobu , Usuku Kouichiro ,   THE MOTHER‐TO‐CHILD TRANSMISSION STUDY GROUP, Mueller Nancy , Osame Mitsuhiro , Miyata Kouichiro , Nagata Yukihiro , Sonoda Shunro 
Published: February 2007

AbstractIn order to evaluate the protective role of the maternal antibody against mother‐to‐child transmission of HTLV‐I, we followed a total of 780 children born to HTLV‐I carrier mothers by investigating the level of anti‐HTLV‐l antibody transferred in utero, decline of the maternal antibody and seroconversion in post‐natal life. The anti‐HTLV‐1 antibody was positively detected within the first 3‐6 months of life and declined at 6‐12 months after birth in all children. After the maternal antibody declined, seroconversion occurred in some of the children following either breast feeding or bottle feeding. The seroconversion rates of short‐term (≦6 months) and long‐term (≧7 months) breast feeders were 4.4% (4/90 cases) and 14.4% (20/139 cases), and the rate of bottle feeders was 5.7% (9/158 cases). Long‐term breast feeding yielded more seroconverters than short‐term breast feeding; 14.4% (20/139 cases) vs. 4.4% (4/90 cases), RR = 3.68, p = 0.018. The seroconversion rate of short‐term breast feeders was nearly equal to that of bottle feeders; 4.4% (4/90 cases) vs. 5.7% (9/158 cases), RR = 0.770, p = 0.471. When neonatal lymphocytes were cultured with breast milk cells of HTLV‐I carrier mothers, the in vitro infection of HTLV‐I was inhibited by the addition of HTLV‐I‐seropositive cord‐blood plasma. Our results suggest that the maternal antibody may inhibit HTLV‐I infection by short‐term breast feeding but not by long‐term breast feeding after decline of the maternal antibody.
Synergistic cytotoxicity of different alkylating agents for epithelial ovarian cancer
Authors: Lidor Y. J. , Shpall E. J. , Peters W. P. , Bast R. C. 
Published: February 2007

AbstractAlkylating agents have been used individually and in combination to treat epithelial ovarian carcinoma. In this study, the cytotoxicity of 7 alkylating agents has been measured using a serial dilution clonogenic assay. When individual agents were evaluated, markedly different activity was observed against several ovarian cancer cell lines. Among 4 cell lines tested, OVCA 432 was the most sensitive to cisplatin, thiotepa and melphalan. When alkylating agents were used in combination against OVCA 432, synergistic activity was observed with cisplatin and each of several other alkylating agents including thiotepa, melphalan, 4‐hydroperoxycyclophosphamide (4HC) and carboplatin. The combination of cisplatin and thiotepa also exerted synergistic activity against the OVCA 420, 429 and 433 cell lines, but had only additive or subadditive activity against the NIH:OVCAR‐3 cell line. Sequential treatment of tumor cell lines with the different alkylating agents was as effective as simultaneous treatment. Synergistic anti‐tumor activity in cell culture is consistent with clinical observations that alkylating agents in combination appear more effective than single agents for treatment of advanced epithelial ovarian cancer. In addition, our study suggests that cisplatin in combination with thiotepa, 4HC or melphalan might prove useful for high‐dose therapy with autologous bone‐marrow support.
Pentoxifylline enhances lung colonization and alters cell adhesion and glycosaminoglycan synthesis by metastatic B16 melanoma cells
Authors: Edward Michael , Mackie Rona M. 
Published: February 2007

AbstractThe effect of pentoxifylline on B16 melanoma cell lung colonization, synthesis and properties of glycosaminoglycans (GAGS), and adhesion to and degradation of subendothelial extracellular matrix was examined. Pentoxifylline inhibited cell growth, cell numbers being reduced by 50% following incubation for 4 days in the presence of 250 μg/ml pentoxifylline, while the treated cells appeared more flattened, possessed numerous but short dendritic processes, and exhibited greatly enhanced tyrosinase activity and melanin synthesis. Pentoxifylline treatment increased the cells' ability to colonize the lungs of syngeneic C57BL mice following tail‐vein injection of 105 cells. The number of lung tumours increased from 16.7 ± 6.1 to 52.2 ± 17.8. In addition, pentoxifylline‐treated cell GAG synthesis was reduced by 36%, and the charge density of chondroitin sulphate reduced, while tumour‐cell aggregation and adhesion to subendothelial extracellular matrix was increased, as was the tumour‐cell‐mediated release of 35SO4, from radiolabelled subendothelial matrix. The observed changes in GAG synthesis may contribute toward the increased cell adhesiveness which, in addition to increased degradation of certain components of the subendothelial extracellular matrix, may account, at least in part, for the enhancement of lung colonization.