bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nation‐wide breast cancer screening in the Netherlands: Support for breast‐cancer mortality reduction
Authors: De Koning Harry J. , Fracheboud Jacques , Boer Rob , Verbeek André L. M. , Collette Hubertine J. A. , Hendriks Jan H. C. L. , Van Ineveld B. Martin , De Bruyn Arry E. , Van Der Maas Paul J. 
Published: February 2007

AbstractThe nationwide 2‐yearly breastcancer screening programme in The Netherlands, for women aged 50‐69, started around 1988, and was predicted to result eventually in a 16% reduction in breastcancer mortality in the total female population. We present the results of screening up to January 1, 1993, and compare these with the predicted results from the costeffectiveness analysis, on which basis this mortality reduction had been calculated. At least 550,000 women aged 50‐69 were invited to screening in 1990‐1992, and 75% of these participated. Cancer was suspected from 5,162 examinations and further investigation was therefore required. Excision biopsy was done in 72% of referrals, and 2,515 breast cancers were detected. The results for 404,000 newly invited women compare favourably with expected values (in parentheses): 78% attendance rate (70%), 1.4% screen positive (1.6%), 6.8 cancers detected per 1,000 women screened (6.4) and 38% of these cancers were DCIS or invasive carcinomas smaller than 11 mm in diameter (36%). More data, e.g., on treatment and interval cancers, will follow in the years to come. These first results can be interpreted as strong early signs of a reduction in breastcancer mortality of at least the predicted size. Screening has sufficiently advanced the diagnosis, as well as or better than expected. Breast cancers diagnosed in this age group without screening are diagnosed at a worse stage than expected. Unfavourable sideeffects, especially falsepositive referrals, might be kept lower than those reported in other countries. © 1995 Wiley‐Liss, Inc.
The lower level of natural anti‐thomsen‐friedenreich antigen (TFA) agglutinins in sera of patients with gastric cancer related to ABO(H) blood‐group phenotype
Authors: Kurtenkov Oleg , Klaamas Kersti , Miljukhina Ljudmila 
Published: February 2007

AbstractThe TFA is a tumorassociated, bloodgrouprelated glycosidic precursor structure [Gal(β1‐3)GalNAc]. Its expression in carcinomas is accompanied by a decrease of natural TFA antibodies in serum. The relationship between the ABO(H)‐bloodgroup phenotype and natural anti‐TFA immune response in patients with gastric cancer was studied. The level of TFA agglutinins in the sera of patients with gastric cancer and of healthy controls was examined by the hemagglutination of neuraminidasetreated bloodgroup‐O donor erythrocytes. Individuals were classified as weak or strong TFA responders. They were also classified by ABO(H)‐bloodgroup status, age, cancer stage, tumor morphology and level of isohemagglutinins. The proportion of weak TFA responders (WR) in cancer patients was 33, 50, 50 and 20% (for O, A, B and AB blood groups respectively), as compared with 11.7, 14.5, 13.9 and 26.1% for bloodgrouprelated controls. The difference between cancer patients and controls was significant for all blood groups except group AB. Further analysis showed agedependence in bloodgroup‐O and ‐B controls, with a high level of WR in the older group. Bloodgroup‐A cancer patients had the greatest and uniform suppression of the level of TFA agglutinins, irrespective of age, cancer stage or tumor morphology, and lower levels of anti‐B isohemagglutinins. © 1995 Wiley‐Liss, Inc.
Chromosomal abnormalities in glioblastoma multiforme tumors and glioma cell lines detected by comparative genomic hybridization
Authors: Kim Dong H. , Mohapatka Gayatry , Bollen Andrew , Waldman Frederic M. , Feuerstein Burt G. 
Published: February 2007

AbstractComparative genomic hybridization (CGH) is a recent molecular cytogenetic method that detects and localizes gains or losses in DNA copy number across the entire tumor genome. We used CGH to examine 9 glioma cell lines and 20 primary and 10 recurrent glioblastoma tumors. More than 25% of the primary tumors had gains on chromosome 7; they also had frequent losses on 9p, 10, 13 and Y. The losses on chromosome 13 included several interstitial deletions, with a common area of loss at 13q21. The recurrent tumors not only had gains on chromosome 7 and losses on 9p, 10, 13 and Y but also frequent losses on 6 and 14. One recurrent tumor had a deletion of 10q22‐26. Cell lines showed gains of 5p, 7 and Xp; frequent amplifications at 8q22‐24.2, 7q2l‐32 and 3q26.2‐29 and frequent losses on 4, 10, 13, 14 and Y. Because primary and recurrent tumors and cell lines showed abnormalities of DNA copy number on chromosomes 7, 10, 13 and Y, these regions may play a fundamental role in tumor initiation and/or progression. The propensity for losses on chromosomes 6 and 14 to occur in recurrent tumors suggests that these aberrations play a role in tumor recurrence, the development of resistance to therapy or both. Analysis of common areas of loss and gain in these tumors and cell lines provides a basis for future attempts to more finely map these genetic changes.
Oesophageal cancer in never‐smokers and never‐drinkers
Authors: Cheng K. K. , Duffy S. W. , Day N. E. , Lam T. H. 
Published: February 2007

AbstractAlcohol, tobacco and diet are the most important determinants of oesophageal cancer. Previous studies which examined smoking in non‐drinkers and drinking in non‐smokers did not report the main effects of dietary factors or the smoking and drinking effects adjusted for dietary factors. Data from a hospital‐based case‐control study in Hong Kong Chinese were used to examine the effects of dietary variables as well as tobacco and alcohol in never‐drinkers and never‐smokers. Among the 400 cases, there were 68 never‐smokers and 53 never‐drinkers; 540 were never‐smokers and 407 were neverdrinkers among 1598 controls. In never‐smokers, alcohol drinking was strongly associated with risk. Use of green leafy vegetables and citrus fruits was protective. Among neverdrinkers, smokers had increased risk, but the protective effect of vegetables and fruits did not reach statistical significance. In never‐smokers and in never‐drinkers alike, frequent consumption of pickled vegetables and being born in Teochew or Hokkien were associated with increased risks. This study provides further support for the independent effects of alcohol, tobacco and diet in oesophageal cancer. © 1995 Wiley‐Liss, Inc.
Promotion of experimental liver metastasis by tumor necrosis factor
Authors: Orosz Peter , Krüger Achim , Hubbe Marcus , Rüschoff Josef , Hoegen Paul Von , N. Männel Daniela 
Published: February 2007

AbstractModels for experimental metastasis were established to investigate the influence of rmTNF on tumor‐colony formation in the liver. Highly metastatic lymphoma tumor cells were either injected i.v. or inoculated s.c. to form spontaneous metastases. In both systems, administration of rmTNF to the animals led to significant enhancement of the number of liver metastases in comparison with control groups. The number of metastatic tumor‐cell colonies at an early stage of metastasis was increased, as well as the number of surface metastases in a late stage. Consequently, TNF‐treated animals revealed a higher mortality. The optimal time for TNF to exert this metastasis‐enhancing effect was found to be 7 days after tumor inoculation, In vitro adhesion of the lymphoma tumor cells to a mouse endothelioma cell line was strongly inhibited by monoclonal antibodies interfering with the interaction of VCAM‐1 with VLA‐4. These results support and extend earlier results with a fibrosarcoma lung colonization model. In addition, they show that stimulation of the immune system in tumor‐bearing hosts activates tumor‐promoting pathways, in addition to having possible beneficial effects.
Analysis of the p53 gene in relation to tobacco and alcohol in cancers of the upper aero‐digestive tract
Authors: Franceschi S. , Gloghini A. , Maestro R. , Barzan L. , Bidoli E. , Talamini R. , Vukosavuevic T. , Carbone A. , Boiocchi M. 
Published: February 2007

AbstractTo elucidate the relationship, if any, of p53 gene expression according to smoking and drinking habits, 135 subjects with cancer of the upper aero‐digestive tract were sampled from a case‐control investigation conducted in Pordenone province, Northeast Italy, between 1986 and 1991. Adequate pathological material for immunohistochemical analysis was available for 83 subjects. Level of p53 expression was classified according to intensity on immunoreaction and percentage of p53‐positive cells. Mutations were analyzed by means of single‐strand conformation polymorphism and sequencing in 8 p53‐positive life‐long non‐smokers exposed to various levels of alcohol intake. The association between p53 expression and smoking status and alcohol intake was evaluated by means of odds ratios, and 95% confidence intervals. Significantly, more men (39/65) than women (6/18) had elevated p53 expression. No significant trend of increasing percentage of p53‐positive cancers with increasing smoking and drinking level was detected, especially after allowance for gender. With respect to specific mutation pattern, in 8 life‐long non smokers who drank alcohol, 6 mutations involved G:C base pairs. G‐to‐A transitions were identified in 4 cases. The present study does not support an association between elevated p53 expression and tobacco smoking or alcohol intake. It provides an example of a molecular biology study in the framework of a large epidemiological investigation.
Organisation and gel contraction by human colonic carcinoma (HCA‐7) sublines grown in 3‐dimensional collagen gel
Authors: Kirkland Susan C. , Henderson Karen , Liu Dan , Pignatelli Massimo 
Published: February 2007

AbstractThe role of cell‐matrix interactions in controlling phenotypic heterogeneity in human colonic carcinoma sublines has been investigated. Four cell lines (colony 1, colony 3, colony 6 and colony 30) previously isolated from a single human colonic carcinoma cell line, HCA‐7, were grown in 3‐dimensional collagen gels. In collagen, the growth of the 4 sublines ranged from well‐organised glandular structures (colony 30) to elongated branching structures (colony 3). The capability of cells to organise into glandular structures in collagen correlated with the degree of differentiation observed in their xenografts. Certain sublines, most notably colony 3, were able to contract the collagen gel. Gel contraction could be partially inhibited by a function‐blocking antibody directed to the α2 integrin chain but not by an antibody directed to the α3 integrin chain demonstrating a role for α2 integrin in the contraction process. In addition, colony 3 cultures treated with the function‐blocking α2 antibody formed more compact structures with limited outgrowth, suggesting a role for α2 integrin in cell migration. Gel contraction and cell migration in collagen gel was largely restricted to 1 subline, colony 3. The subsequent demonstration that α2 integrin is involved in both of these processes suggests that integrin expression and function has a role in generating the phenotypic heterogeneity exhibited by these cell lines.
Identification of genital human papillomaviruses in cervical biopsy specimens: Segregation of specific virus types in specific clinicopathologic lesions
Authors: Matsukura Toshihiko , Sugase Motoyasu 
Published: February 2007

AbstractWe have established a critical identification method for the full spectrum of genital human papillomaviruses (HPVs) in clinical specimens. It was based on the recognition of Pstl, Banl and Mspl cleavage patterns of HPV DNA detected by blot hybridization with HPV 58 DNA probe at Tm—40°C. By this method, we identified 24 different types of genital HPV including 5 novel types (HPV 59, 61, 62, 64 and 67) in the specimens collected at one hospital and found almost all the HPVs with the authentic cleavage patterns of their respective prototypes. In 235 cervical biopsy specimens, HPV 6 or 11 was found in exophytic condyloma acuminatum (15/15) but not in any cervical intraepithelial neoplasia (CIN) specimens. In contrast, HPV 18, 30, 43, 54, 56, 59, 62, 66 and 67 were identified in CIN I (28/71) or II (4/56) but not in CIN III, while HPV 16, 31, 33, 35, 39, 51, 52 and 58 were identified in CIN III (83/93) as well as in CIN I (34/71) and II (47/56). The result indicates that heterogeneous genital HPVs prevail all over the world. In addition, HPV 6 and 11 are etiologic agents only of exophytic condyloma, whereas the other HPVs are etiologic agents of CIN with the segregation of specific HPVs in CIN III. We propose a new clinicopathologic grouping of genital HPVs founded on nucleotide homology of the HPV genome. © 1995 Wiley‐Liss, Inc.
Multiple forms of cathepsin b in human lung cancer
Authors: Křepela Evžen , Procházka Jan , Mynaříková Helena , Kárová Bohdana , Polák Jaroslav , Čermák Jan , Roubková Helena 
Published: February 2007

AbstractIn this study we have examined, by means of isoelectric focusing (IEF) in native polyacrylamide gel and contact‐print fluorescence zymography, whether human lung carcinomas and the lung parenchyma contain different pools of multiple charge forms of the cysteine proteinase cathepsin B. The isoelectric point (pl) patterns of cathepsin B from lung carcinoma and matched lung were similar, particularly with regard to 2 major intermediate acidic enzyme pl forms designated as I and II (plapp of 5.10 and 4.93 in tumors, and 5.11 and 4.94 in lungs, respectively). The slightly acidic cathepsin B pl forms (plapp 5.47–5.19) in squamous‐cell lung carcinoma (SQCLC) were significantly more numerous than such enzyme pl forms in lungs. The numbers of the highly acidic cathepsin B pl forms (plapp 4.82–4.33) were significantly higher in SQCLC and lung adenocarcinoma (ACL) than in matched lung. The activity distribution percentage in the set of highly acidic cathepsin B pl forms was significantly higher in SQCLC and ACL than in matched lung. We also observed that cathepsin B from SQCLC and matched lung was fully recoverable by IEF from inhibition by leupeptin. Using the cysteine‐proteinase‐specific inactivator E‐64, we revealed by IEF that some cathepsin B isoforms (charge forms) from SQCLC were more resistant to inactivation by this compound than the corresponding enzyme isoforms from lungs. After IEF, the enzyme isoforms apparently lost their resistance to E‐64. Our results indicate that the pool of multiple charge forms of cathepsin B in SQCLC and ACL is different from that in the lung, and also that there may be an increased level of loose complexes between cathepsin B and some proteins or polypeptides in SQCLC compared to the lung. © 1995 Wiley‐Liss Inc.
Regulation of cytoskeletal organization in tumor cells by protein phosphatases‐1 and ‐2A
Authors: Maier George D. , Wright Mark A. , Lozano Yvonne , Djordjevic Andelka , Matthews John P. , Young M. Rita I. 
Published: February 2007

AbstractNon‐metastatic Lewis lung carcinoma cells (LLC‐C8) become more motile when protein phosphatases (PP‐1 and ‐2A) are inhibited by okadaic acid, attaining the same level of motility as metastatic LLC (LLC‐LN7) variants. This stimulation of LLC‐C8 motility was tempered when protein kinase A activity was inhibited. We examined whether the okadaic acid–stimulated LLC‐C8 motility was associated with alterations in the cytoskeletal organization so that these non‐metastatic cells acquire the rounded morphology and diffuse cytoskeletal organization previously described for metastatic LLC‐LN7 cells. Non‐metastatic LLC‐C8 are typically adherent during culture, achieving a spread morphology. Treatment of non‐metastatic LLC‐C8 cells with okadaic acid resulted in a contraction of most of their extended processes, formation of spikes and membrane blebs within 10 min, and complete cell rounding within 20 min for most of the cells. While the overall level of F‐actin was minimally affected by the okadaic acid, its uniform distribution shifted to localization toward the periphery of the rounded cells, often concentrating at a single focus. Immunofluorescent staining for vimentin showed a similar shift to the cell periphery and similar capping. After okadaic acid treatment, the filamentous network of microtubules in non‐metastatic LLC‐C8 cells disappeared and was replaced with a diffusely staining distribution of β‐tubulin. These results show that PP‐1 and‐2A maintain cytoskeletal organization and that inhibition of this control reduces cytoskeletal organization and increases tumor cell motility. © 1995 Wiley‐Liss, Inc.
The role of TGF‐β production in growth inhibition of breast‐tumor cells by progestins
Authors: Kalkhoven Eric , Kwakkenbos‐Isbrücker Linda , Mummery Christine L. , De Laat Siegfried W. , Van Den Eijnden‐Van Raaij Adriana J. M. , Van Der Saag Paul T. , Burg Bart Van Der 
Published: February 2007

AbstractWe have studied the influence of synthetic progestins on the estrogen‐induced proliferation and type‐β transforming‐growth‐factor (TGF‐β) production of 3 breast‐tumor cell lines. In long‐term growth experiments, progestins inhibited proliferation of T47D cells, while a specific T47D variant and MCF7 cells were not affected, despite the presence of functional progesterone receptors. The effect of progestins was biphasic, since an initial stimulation of proliferation was followed by a prolonged inhibition. This response suggests the involvement of a progestin‐induced negative growth regulator. We show here that TGF‐βs do not fulfill this role since (i) the progestin‐induced T47D cells are not sensitive to TGF‐βI, ‐β2 or ‐β3, (ii) secretion of TGF‐βs is decreased by progestins in all 3 cell lines, and (iii) TGF‐β neutralizing antibodies do not reverse progestin‐induced growth inhibition. Furthermore, evidence was obtained that medium conditioned by T47D cells does not contain any other growth inhibitor to which this cell line responds in a negative autocrine manner. In contrast, MCF7 cells are growth‐inhibited by all 3 TGF‐β isoforms, but are not growth‐inhibited by progestins, suggesting that there is no correlation between growth inhibition by progestins and responsiveness to and production of TGF‐β in vitro. Although TGF‐β is a strong growth inhibitor of normal mammary tissue, recent evidence suggests that, in malignant tissue, enhanced TGF‐β secretion correlates with increased malignancy. Therefore, a progestin‐induced decrease in TGF‐β production, as observed here, may lead to enhanced proliferation of normal but not malignant mammary epithelium. © 1995 Wiley‐Liss, Inc.
Aberrations of p16Ink4 and retinoblastoma tumour‐suppressor genes occur in distinct sub‐sets of human cancer cell lines
Authors: Aagaard Louise , Lukas Jiri , Bartkova Jirina , Kjerulff Anne‐Arnt , Strauss Michael , Bartek Jiri 
Published: February 2007

AbstractThe p16Ink4/MTSI/CDKN2 is a cell‐cycle regulatory inhibitor of cyclin‐dependent kinase 4 (cdk4), and a candidate tumour suppressor whose gene on chromosome band 9p21 is frequently deleted or mutated in diverse types of cancer. Cdk4 in association with its D‐type cyclin partners, together with p16Ink4, and the product of the retinoblastoma tumour‐suppressor gene (pRB), appear to constitute a G1‐phase‐controlling pathway which can become de‐regulated through oncogenic aberrations of any of the components. In an attempt to elucidate the underlying molecular mechanisms, we have now surveyed expression of p16Ink4, at the protein and the mRNA levels, in 21 human cell types expressing normal pRB, as compared with another series of 21 cell lines whose pRB is mutant and/or inactivated through sequestration by DNA tumour virus onco‐proteins. In contrast to aberrant lack of p16 expression in the majority of RB‐positive cell types, expression of apparently normal (as shown by electrophoretic mobility and/or the ability to form protein‐protein complexes with cdk4 in vivo) p16 was uniformly preserved in the cancer cell lines whose RB function was compromised. These data indicate that p16 operates upstream of pRB along the same pathway in G1. The results are discussed in view of the nature of a selective growth advantage potentially gained by cells through de‐regulation of this key cell‐cycle control mechanism. © 1995 Wiley‐Liss, Inc.
Descriptive epidemiology of oral neoplasms in sudan 1970‐1985 and the role of toombak
Authors: Idris A. M. , Ahmed H. M. , Mukhtar B. I. , Gadir A. F. , El‐Beshir E. I. 
Published: February 2007

AbstractData from 1,916 cases of oral neoplasms occurring in the Sudan in a 16‐year period, from January 1970 to December 1985, were retrieved and analysed. The study revealed a relatively high frequency of oral neoplasms in comparison with neighbouring countries. In this study, squamous‐cell carcinoma was the most common oral malignancy (66.5%), followed by tumours of the salivary gland (14.7%), neoplasms of non‐odontogenic and non‐epithelial origin (9.6%) and odontogenic neoplasms (8.6%). Men had a higher frequency than women. The older age group of both genders showed a relatively high frequency of squamous‐cell carcinoma. Among northern Sudanese there was a high rate of squamous‐cell carcinoma, while southern Sudanese showed a high rate of odontogenic and salivary‐gland neoplasms. The use of toombak has been stated to play a major role in the aetiology of oral squamous‐cell carcinoma in the Sudan, and is suspected to be associated with neoplasms of the salivary glands. © 1995 Wiley‐Liss, Inc.
Detection of two epstein‐barr‐virus (EBV)‐carrying leukemic cell clones in a patient with chronic lymphocytic leukemia (CLL)
Authors: Lewin Nongnit , Avila‐Cariño Javier , Minarovits Janos , Lennette Evelyne , Brautbar Chaim , Mellstedt Håakan , Klein George , Klein Eva 
Published: February 2007

AbstractThe leukemic‐cell population of one CLL patient, PG, was found to contain a sub‐set of EBV‐genome‐carrying cells. It was detected directly by the expression of EBNA (EBV‐encoded nuclear antigen) and by its capacity to grow in vitro. The proportion of EBNA‐positive cells (0.1%) was maintained constantly during the period of this study, the final 3 years of the patient's life. EBV‐carrying clonal sibling B‐cell lines were established on 5 occasions. They had identically rearranged JH bands and chromosomal markers corresponding to the ex vivo CLL cells. Analysis of the viral episomes in the lines proved that they were the descendants of one cell. On the last occasion of blood sampling, 8 B‐cell lines were established; 4 of these contained the same clonal markers as the previous lines, while 4 other lines belonged to another clone with identical JH rearrangement. Their abnormal karyotypes were different from the first clone. The chromosomal markers were only partly identical, suggesting secondary diversifications. The EBV sub‐strain carried by this group of lines was different from the sub‐strain of the first clone, as judged by the EBNA size distributions (EBNOtype) and EBV‐DNA analysis. Analysis of the terminal repeat in the viral episomes also showed that the first and the second set of clones represented 2 independent EBV‐infection events in vivo. © 1995 Wiley‐Liss, Inc.