bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mortality in a cohort of women given X‐ray therapy for metropathia haemorrhagica
Authors: Darby S. C. , Reeves G. , Key T. , Doll R. , Stovall M. 
Published: February 2007

AbstractMortality to January 1, 1991, has been studied in 2,067 women in Scotland given X‐ray therapy for metropathia haemorrhagica during the period 1940–1960. Average follow‐up was 28 years. Overall, 1,313 deaths were observed compared with 1,297.01 expected from Scottish rates [standardized mortality ratio (SMR): 1.01]. Mortality was increased for cancers of heavily irradiated pelvic sites (SMR 5+ years after irradiation: 1.46) following mean doses to organs in the vicinity of the pelvis in the range 2.6–5.3 Gy. For these cancers the SMR was higher 30+ years after irradiation than at 5–29 years, indicating that the effects of exposure last for over 30 years, and in this period bladder cancer mortality was exceptionally high (SMR = 4.91). Mortality was also raised for leukaemia (SMR 2+ years after irradiation: 2.05), following a mean bone‐marrow dose of 1.3 Gy, and for multiple myeloma (SMR 5+ years after irradiation: 2.59). For leukaemia the SMR was lower 30+ years after irradiation than at earlier periods, but remained greater than unity. For other cancers mortality was similar to Scottish rates, except for breast cancer for which mortality was low (SMR 5+ years after irradiation: 0.53), even in women aged over 50 at irradiation (SMR 5+ years after irradiation: 0.14). The deficit was principally due to a large deficit of breast cancer in women with ovarian doses of at least 5 Gy.
p53 gene mutations in oropharyngeal carcinomas: A comparison of solitary and multiple primary tumours and lymph‐node metastases
Authors: Zariwala Maimoona , Schmid Stephan , Pfaltz Madeleine , Ohgaki Hiroko , Kleihues Paul , Schäfer Reinhold 
Published: February 2007

AbstractDespite the steadily increasing number of patients suffering from squamous‐cell carcinomas of the oropharyngeal region, little is known about the molecular steps involved in the induction of these neoplasms. We investigated oropharyngeal cancers from 38 patients for mutations in the p53 tumour‐suppressor gene. The majority of patients (74%) had a history of tobacco and alcohol abuse. Five had lymph‐node metastases, 3 had multiple primary carcinomas and 2 presented with multiple primary tumours and lymph‐node metastases. Exons 5 through 8 of the p53 gene were screened by single‐strand conformation polymorphism analysis followed by direct DNA sequencing. A total of 16 tumours (42%) contained point mutations which were scattered throughout exons 5 to 8. Most mutations (56%) were transitions, predominantly G→A. Among the transversions, G→T mutations prevailed; these have also been found in smoking‐related lung cancer. One carcinoma of the soft palate showed a mutation which was retained in a lymph‐node metastasis. In another patient, 2 primary carcinomas had different mutations, indicating that they had developed independently. Similar results were obtained in a case with a p53 mutation in the third of 3 primary tongue carcinomas which developed over a period of 23 years. One lymph‐node metastasis had a 12‐bp deletion which was not detected in any of the primary malignancies. The frequent occurrence of p53 mutations in oropharyngeal carcinomas supports the view that they play a role in the initiation or progression of the malignant phenotype.
Risk factors for oesophageal cancer in northeast China
Authors: Hu Jinfu , Nyrén Olof , Wolk Alicja , Bergström Reinhold , Yuen Jonathan , Adami Hans‐Olov , Guo Lihong , Li Hui , Huang Guirong , Xu Xinmin , Zhao Fengquin , Chen Yilang , Wang Chaoxu , Qin Huisheng , Hu Cunlin , Li Youngtang 
Published: February 2007

AbstractA hospital‐based case‐control study of oesophageal cancer was carried out in the Heilongjiang Province, a low‐risk area for oesophageal cancer in China. From May 1985 to May 1989, 196 histologically confirmed cases and 392 controls with other (non‐neoplastic) diseases were personally interviewed in the wards of 5 major hospitals. Information was obtained about usual consumption in the early 1980s of 32 major contributors to the diet in the province, socio‐demographic status, smoking and alcohol consumption. Odds ratios (OR) were obtained from logistic regression models, and confounding was controlled by means of multivariate models. Smoking and alcohol consumption were major risk factors for oesophageal cancer in this population. Smokers of handmade cigarettes exhibited a particularly high risk. A near multiplicative synergism was found between smoking and alcohol consumption. There was a significant inverse dose‐risk trend for combined consumption of vegetables and fruits; a 300‐g increase per day lowered risk by 35%. Vitamin C intake was negatively associated with risk; a 100‐mg increase per day lowered risk by 39%. Our data suggest a modifying effect of vitamin C and β‐carotene on risk associated with smoking, but the power of analyses was low. Salt, salt‐preserved foods and pickled vegetables were not associated with increased risk. High temperature of meals and drinks was a strong risk indicator in this population. The strength of tea and overall tea consumption were independent determinants of the risk. © Wiley‐Liss, Inc.
Association of IgA‐anti‐Fab autoantibodies with disease stage in head‐and‐neck cancer
Authors: Süsal C. , Maier H. , Lorenz K. , Opelz G. 
Published: February 2007

AbstractPatients with head‐and‐neck cancer commonly have immune defects. It was reported that these patients have raised serum IgA levels. We investigated whether IgA‐anti‐Fab autoantibodies, which occur in association with immune dysfunction, are present in patients with head‐and‐neck cancer. Sera of 101 patients with squamous‐cell carcinoma (SCCHN) and 8 patients with adenoid cystic carcinoma (ACCHN) of the head and neck were tested in ELISA for IgA‐anti‐Fab autoantibody activity. IgA‐anti‐Fab serum activity was significantly higher in both SCCHN and ACCHN patients than in healthy controls. In patients with SCCHN, an association between disease stage and IgA‐anti‐Fab activity was established. Stage‐IV patients had significantly higher IgA‐anti‐Fab than stage‐I patients or healthy controls. Stage‐II and stage‐III patients had intermediate levels. Extremely high IgA‐anti‐Fab activity was observed in 7 patients who died within 6 months following testing, suggesting a relationship of autoimmunity with terminal disintegration of physiological body functions. IgA‐anti‐Fab autoantibodies may explain the occurrence of immune defects in patients with head‐and‐neck cancer. © Wiley‐Liss, Inc.
Relationship between loss of estrogen and progesterone receptor expression and of 6q and 11q chromosome arms in breast cancer
Authors: Magdelenat H. , Gerrault‐Seureau M. , Dutrillaux B. 
Published: February 2007

AbstractThe expression of estrogen (ER) and progesterone (PR) receptors was quantified in a series of 95 cytogenetieally characterized breast cancers. The relationship between deficiencies of 6q and Mq arms (where genes for ER and PR are mapped, respectively) and ER and PR expression was analyzed. The range of variations in expression was very large by comparison to that of the number of chromosome arms. Furthermore, low expression without chromosome loss and high expression with chromosome loss were occasionally observed. Thus, major variations in ER and PR expression were independent of the number of copies of the corresponding gene. However, both the decrease in ER expression and 6q arm losses were correlated with cytogenetic evolution of the tumors, this correlation being less significant for PR and the 11 q arm. In addition, 6q‐ but not 11q‐ tumors have, on the average, a low ER/PR ratio, whereas 11q‐ but not 6q‐ tumors have a low PR/ER ratio. When all 6q‐ or 11q‐ tumors were compared to those with no 6q or 11q losses, the average ER or PR value of the former was about half of the later. These data suggest that, in addition to a regulatory change of non‐genetic origin, gene dosage effect plays a secondary, but significant, additional role. © Wiley‐Liss, Inc.
Production and tumour‐binding characterization of a chimeric anti‐CEA Fab expressed in Eschericwa coli
Authors: Chester Kerry A. , Robson Lynda , Keep Patricia A. , Pedlly R. Barbara , Boden Joan A. , Boxer Geoffrey M. , Hawkins Robert E. , Begent Richard H. J. 
Published: February 2007

AbstractA recombinant chimeric Fab (rcFab), with Fv derived from the monoclonal A5B7 antibody to carcinoembryonic antigen (CEA), and with human CHI and Ck was cloned into pUC 19 and expressed in Escherichia coli. rcFab (10 to 12 mg per litre) was produced in bacterial culture fluid, and functional purified rcFab was isolated by affinity chromatography (using antibody to human Ck) and size‐exclusion gel filtration. The re Fab did not show reduced affinity for CEA, and reacted with human colorec‐tal tumours showing a typical anti‐CEA pattern by immunocyto‐chemistry; it was also stable after iodination. Biodistribution studies in nude mice bearing human tumour xenografts showed no toxicity and good turnout‐ localization. Therapeutic ratios at early time points were better than those obtained with whole murine antibody. The results demonstrate that bacterial I y produced anti‐CEA Fab is of use for tumour targeting. © Wiley‐Liss, Inc.
Synergistic effect of retinoids and interferon α on tumor‐induced angiogenesis: Anti‐angiogenic effect on HPV‐harboring tumor‐cell lines
Authors: Majewski S. , Szmurlo A. , Marczak M. , Jablonska S. , Bollag W. 
Published: February 2007

AbstractVarious retinoids and interferons exert anti‐tumor effects both in experimental studies and in clinical trials. Recent reports indicate that they have a synergistic antineoplastic activity. Our study aimed to determine whether these synergistic anti‐tumor effects are related to inhibition of tumor‐cell‐induced angiogenesis. A further aim was to compare the anti‐angiogenic activity of various retinoids including 9‐cis retinoic acid, a ligand for nuclear retinoic acid receptor RXR, given alone and in combination with interferon α‐2a (IFNα‐2a). An in vivo experimental model of cutaneous angiogenesis in the mouse was used. Angiogenesis was induced by intradermal injection of HPVI6‐or HPVI8 DNA‐harboring tumor‐cell lines. All‐trom retinoic acid (all‐trans RA), 13‐cis retinoic acid (13‐cis RA) and 9‐cis retinoic acid (9‐cis RA) as well as 1FNα‐2a applied to mice intra‐peritoneally for S consecutive days before induction of angiogen‐esis resulted in significant inhibition of angiogenesis. Combination of retinoids with IFNα‐2a led to a synergistic inhibition of angiogenesis, as compared to the effects of the drugs given alone. Similar results were obtained when tumor cells were preincubated in vitro with the compounds, before injection into untreated mice. Our findings on synergistic anti‐angiogenic effects of retinoids and IFNα‐2a could explain, at least partially, the anti‐tumor efficacy of combined therapy with these agents, and provide support for the role of angiogenesis in tumor growth. © Wiley‐Liss, Inc.
Androgen responsiveness of the new human endometrial cancer cell line MFE‐296
Authors: Hackenberg Reinhard , Beck Simone , Filmer Angelika , Nia Abdolhamid Hushmand , Kunzmann Regina , Koch Manuela , Slater Emily P. , Schulz Klaus‐Dieter 
Published: February 2007

AbstractMFE‐296 endometrial cancer cells express androgen receptors in vitro. These cells, which are tumorigenic in nude mice, arc derived from a moderately differentiated human endometrial adenoeardnoma. They express vimentin and the cytokeratins 7, 8, 18, and 19. Karyotyping revealed near‐tetraploidy for most of the cells. No marker chromosomes were observed. DNA analyses confirmed the genetic identity of the cell line and the patient from whom the cell line was derived. Proliferation of MFE‐296 cells was inhibited by the progestin RS020 and the androgen dihydrotestosterone (DHT). The inhibition of proliferation by DHT was antagonized by the antiandrogen Casodex, demonstrating the involvement of the androgen receptor. Androgen binding was determined at 22,000 binding sites per cell using a whole‐cell assay (KD = 0.05 nM) and 30 fmol/mg protein with the dextran charcoal method; 7 fmol/mg protein of progesterone receptors were found, whereas estrogen receptors were below S fmol/mg protein. The androgen receptor was functionally intact, as demonstrated by transfection experiments with a reporter‐gene construct, containing an androgen‐responsive element. In MFE‐296 cells the content of the androgen receptor was up‐regulated by its own ligand. © Wiley‐Liss, Inc.
Relaxin influences growth, differentiation and cell‐cell adhesion of human breast‐cancer cells in culture
Authors: Sacchi Tatiana Bani , Bani Daniele , Brandi Maria Luisa , Falchetti Alberto , Bigazzi Mario 
Published: February 2007

AbstractThe effects of different concentrations of relaxin (RLX) on growth and differentiation of a human breast‐cancer cell line (MCF‐7) have been studied after various times of exposure. The cells were cultured for 4 and 7 days in the absence (control) and the presence of highly purified porcine RLX at concentrations of 10−9 M and 10−6 M. (3H)‐Thymidine uptake assay was used to evaluate cell proliferation. Electron microscopy and immunocy‐tochemistry for the cell‐cell adhesion molecule E‐cadherin were carried out to evaluate cell differentiation. Analysis of DNA changes associated with apoptosis was performed to clarify whether RLX induces active cell death in the MCF‐7 cells. The findings obtained show that RLX, when applied at micromolar concentrations, or even at nanomolar concentrations for long exposure times, suppresses proliferation, stimulates differentiation, and enhances expression of the surface molecule E‐cadherin. Growth inhibition is not accompanied by apoptosis. The results of this study show that RLX can be recognized as a novel agent active in influencing growth and differentiation of MCF‐7 breast‐cancer cells. When applied at appropriate concentrations and exposure times, the peptide has a growth‐inhibitory action, thus reversing the growth‐stimulatory effect exerted at low concentrations for short exposure times, and promotes differentiation and cell‐cell adhesion. These last‐mentioned properties might result in a decrease in invasiveness of breast adenocarcinoma cells. © Wiley‐Liss, Inc.
Molecular analysis of chromosomh 1 abnormalities in human gliomas reveals frequent loss of 1p in oligodendroglial tumors
Authors: Bello M. Josefa , Vaquero Jesus , De Campos Jose M. , Kusak M. Elena , Sarasa Jose L. , Saez‐Castresana Javier , Pestana Angel , Rey Juan A. 
Published: February 2007

AbstractAlterations of the short arm of chromosome I are recurrently found in cytogenetic analysis of malignant gliomas, and deletions of Ip36‐p32 region characterize at least the higher‐grade tumors, glioblsstoma multiforme. Molecular analysis of tumor‐derived and normal genomic DNA from 57 cases of gliomas, using a panel of chromosome I‐specific DNA probes showed LOH in 16 tumors. Allelic losses on I p were primarily restricted to glioblastoma multiforme (2/II) and to tumors with a major oligodendroglial component: grade II oligodendrogliomas (6/6), grade III anaplastic oligodendrogliomas (5/6) and grade II‐III mixed oligo‐astrocytomas (2/3). Losses for Iq markers were detected in only I tumor (glioblastoma multiforme). Our data suggest that anomalies of Ip primarily characterize oligodendrogliomas, whereas they are rare events in astrocytic tumors and indicate that a tumor‐suppressor gene on I p36‐p32 is involved in the development of brain tumors with oligodendroglial differentiation. © 1994 Wiley‐Liss, Inc.
Quercetin enhances transforming growth factor β1, secretion by human ovarian cancer cells
Authors: Scambia Giovanni , Panici Pierluigi Benedetti , Ranelletti F. O. , Ferrandina G. , de Vincenzo R. , Piantelli M. , Masciullo V. , Bonanno G. , Isola G. , Mancuso S. 
Published: February 2007

AbstractOur study demonstrates that quercetin (Q)‐induced growth‐inhibitory activity in ovarian cancer cells may be mediated by modulation of transforming growth factor β1 (TGFβ1) production. We used the OVCA 433 cell line which is very sensitive to the anti‐proliferative effect of Q and expresses high‐affinity, low‐capacity TGFβ1 receptors. Conditioned medium (CM) from Q‐treated cells is able to displace 125I‐TGFβ1 from binding to its receptor; moreover Q (10 μM) increases TGFβ1 activity in CM in a time‐dependent fashion starting after 4 hr and reaching a maximum by 24 hr of Q treatment. Q‐induced growth inhibition is reversed by a neutralizing anti‐TGFβ1 MAb both in OVCA 433 and in a clonogenic assay of cells from a primary ovarian tumor. Q‐induced increase of TGFβ1 activity in CM is specific since other anti‐proliferative compounds, such as Dexamethasone, which is as active on the cell cycle as Q, had no effect on TGFβ1 secretion. Northorn‐blot analysis of TGFβ1 mRNA levels at various times of Q (10 μM) exposure revealed that there was no increase, suggesting that regulation of TGFβ1 occurs at post‐transcription at levels. © 1994 Wiley‐Liss, Inc.
Effects of testosterone, dihydrotestosterone and estrogen on 3,2′‐dimethyl‐4‐aminobiphenyl‐induced rat prostate carcinogenesis
Authors: Shirai Tomoyuki , Imaida Katsumi , Masui Tsuneo , Iwasaki Shogo , Mori Toshio , Kato Toshio , Ito Nobuyuki 
Published: February 2007

AbstractPost‐initiation effects of testosterone propionate (TP), α‐dihydrotestosterone (DHT) and ethinyl estradiol (EE) on 3,2′‐dJmethyl‐4‐aminobiphenyl (DMAB)‐prostate carcinogenesis in F344 rats have been investigated by administration of each hormone individually or either androgen in combination with EE. DNAB plus TP resulted in induction of invasive adenocarcinomas in the lateral and anterior prostate and seminal vesicles, as shown in a previous study, whereas DHT did not exhibit any positive modulation potential. Administration of EE together with TP produced increased carcinoma incidence in the lateral and anterior prostate, from 17 and 28% to 70% and 80%, respectively. Dorsal prostate tumors, all of the non‐invasive in situ type, were also evident in 30% of animals receiving both TP and EE. Rats treated with DHT plus EE, however, did not develop tumors. Our experiment thus provides evidence that estrogen may play an important role in prostate carcinogenesis. © 1994 Wiley‐Liss, Inc.
Immunocytological detection of micrometastatic cells: Comparative evaluation of findings in the peritoneal cavity and the bone marrow of gastric, colorectal and pancreatic cancer patients
Authors: Juhl Hartmul , Stritzel Matthias , Wroblewski Andreas , Henne‐Bruns Doris , Kremer Bernd , Schmiegel Wolff , Neumaier Michael , Wagener Christoph , Schreiber Hans‐Wilhelm , Kalthoff Holger 
Published: February 2007

AbstractThe prognosis of digestive cancers is poor mainly due to intraperitoneal relapse by cells which may have already been seeded at the time of surgery. Using immunocytology we investigated the peritoneal cavity and, as a comparison, the bone marrow of 147 patients with gastric, colorectal and pancreatic cancer for micrometastatic cells. Cytological samples from peritoneal cavity lavages and bone marrow aspirates were analyzed using monoclonal antibodies (MAbs) against tumor‐associated antigens (TAA) (CEA, CA‐19‐9, 17‐1‐A, C‐54‐0, Ra96) and compared to a MAb staining cytokeratins (KL‐I). Patients with benign diseases served as controls.Intraperitoneal micrometastatic cells were detected in 27% of colorectal, 43% of gastric and 58% of pancreatic cancer patients. In the bone marrow, the corresponding data were 29% for colorectal, 25% for gastric and 58% for pancreatic cancer patients. Combined evaluation of both compartments increased the detection rate significantly (colorectal cancer: 40%, gastric cancer: 52%, pancreatic cancer: 72%). No unwarranted reactions were found in the control group. Combining 3 antibodies (CA‐19‐9, Ra96, C‐54‐0) enabled good detection for peritoneal cavity samples. In the bone marrow, the use of 2 antibodies (KL‐I and CA‐19‐9) detected 94% of all positive samples, whereas KL‐I and CA‐19‐9 stained approx. 70% of all positive samples in each case. The occurence of stained cells in the peritoneal cavity correlated with classical prognostic factors (TNM classification). © 1994 Wiley‐Liss, Inc.
Partial characterization of a cDNA for human stearoyl‐CoA desaturase and changes in its mRNA expression in some normal and malignant tissues
Authors: Li Juan , Ding Shi‐Fa , Habib Nagy A. , Fermor Beverley F. , Wood Chris B. , Gilmour R. Stewart 
Published: February 2007

AbstractA segment of 712 bases coding for part of the human stearoyl‐CoA desaturase gene was made by polymerase chain reaction (PCR) using primers based on published rat cDNA sequences. The human PCR product was confirmed by DNA sequencing. It was next cloned into a vector from which anti‐sense, highly radioactive RNA transcripts were made in vitro using T7 polymerase. The transcripts were used to probe desaturase mRNA in a number of human tumour and control tissues, using a very sensitive solution hybridization/RNase protection assay. Increased desaturase mRNA levels were found in colonic and oesophageal carcinomas and in hepatocellular adenoma; however, no consistent trend was seen in hepatocellular carcinoma. It is suggested that certain classes of tumour may exhibit increased levels of desaturase mRNA. © 1994 Wiley‐Liss, Inc.
Association of H‐ras mutations with adenocarcinomas of the parotid gland
Authors: van Halteren Henk K. , Top Bert , Moor Wolter J. , Balm Alfons J. M. , Rodenhuis Sjoerd 
Published: February 2007

AbstractWe have examined 17 adenocarcinomas and 2 mixed tumors of the salivary glands for mutational activation of the oncogenes H‐ras, K‐ras and N‐ras. The presence of mutations was determined by in vitro amplification of gene fragments spanning codons 12, 13 and 61 and the use of mutation‐specific oligonucleotide hybridization. ras mutations were present in 3 of 13 adenocarcinomas (23%) of the parotid gland. The mutations were confirmed and characterized by means of cycle sequencing of polymerase chain reaction (PCR) fragments. In all 3 cases, the mutation was an A:T to G.C transition at the second position of codon 61 of the H‐ras gene. This rather unusual ras mutation could provide a clue to identify one or more carcinogens involved in the pathogenesis of parotid cancer. © 1994 Wiley‐Liss, Inc.
Modulation of associated ovarian carcinoma antigens by 5 cytokines used as single agents or in combination
Authors: Imbert‐Marcille B. M. , Thëdrez P. , Saï‐Maurel C. , Francois C. , Auget J. L. , Benard J. , Jacques Y. , Imai S. , Chatal J. F. 
Published: February 2007

AbstractOptimization of intraperitoneal radioimmunotherapy of ovarian cancer depends on increasing the antigenic expression of tumor cells. For this purpose, we studied the effect of 5 cytokines (IFN‐α, IFN‐β, IFN‐γ, TNF‐α and TGF‐β), used as single agents or in combination, on 4 ovarian cancer cell lines which present different antigenic profiles with the monoclonal antibodies (MAbs) tested (OC125, OVTL‐3, MOv 18 and MOv 19). Analyses were performed by flow cytometry and the Scatchard technique in order to study antigenic modulation. The effect on proliferation was determined by cell counting. Expression of O3 antigen, recognized by the OVTL3 MAb, was increased up to 2.5 times after IFNs and TNF‐α (used as single agent) on the 2 lines presenting low basal expression (SHIN‐3 and IGROVI). The expression of CAI25 antigen and the antigens recognized by MOv 18 and MOv 19 MAbs was not increased by any of the cytokines tested. The combination IFN‐γ + TNF‐α was synergistic on cytotoxicity and enhanced O3 expression, providing 10 times as many sites per cell on the SHIN‐3 line. For 3 other associations (IFN‐α + IFN‐γ, IFN‐β + IFN‐γ and IFN‐α + TNF‐α), there was an additive effect on O3 expression and on cell cytotoxicity. © 1994 Wiley‐Liss, Inc.