bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cancer mortality following X‐ray treatment for ankylosing spondylitis
Authors: Weiss Helen A. , Darby Sarah C. , Doll Richard 
Published: February 2007

AbstractMortality has been studied in 15,577 ankylosing spondylitis (AS) patients diagnosed between 1935 and 1957 in the UK, of whom 14,556 received X‐ray treatment. By January 1, 1992 over half of the cohort had died. Among the irradiated patients, cancer mortality was significantly greater than expected from the national rates for England and Wales, with a ratio of observed deaths to expected (relative risk, RR) of 1.30, and significant increases individually for leukaemia, non‐Hodgkin's lymphoma, multiple myeloma and cancers of the oesophagus, colon, pancreas, lung, bones, connective and soft tissue, prostate, bladder and kidney. Among the unirradiated patients, cancer mortality was lower than expected from national rates (RR = 0.79). Among irradiated patients, the RRs for leukaemia, lung cancer, and all other neoplasms all decreased significantly with increasing time since first treatment following an initial increase. By 35 years after first treatment, the radiation‐related excess for lung cancer had completely disappeared, while for other neoplasms the RR remained significantly raised, although at a lower level than in earlier periods. Most irradiated patients received several courses of treatment within a 5‐year period. Based on a 1 in 15 random sample, the mean total body dose received in this period was 2.64 Gy, with the heaviest dose to the vertebrae. A linear dose‐response model for all neoplasms except leukaemia gave an excess RR of 0.18 Gy−1 in the period 5–24.9 years after first treatment, which decreased significantly to 0.11 Gy−1 in the period more than 25 years after first treatment. There was no evidence that a linear‐quadratic model fitted the data better than a linear model. There were significant dose‐response relationships individually for cancers of the lung, oesophagus, colon, pancreas, prostate, bladder and kidney. © 1994 Wiley‐Liss, Inc.
Enhanced expression of tissue inhibitor of metalloproteinase‐2 (TIMP‐2) in the stroma of breast carcinomas correlates with tumor recurrence
Authors: Visscher Daniel W. , Höyhtyä Matti , Ottosen Susan K. , Liang Chi‐Ming , Sarkar Fazlul H. , Crissman John D. , Fridman Rafael 
Published: February 2007

AbstractThe 72‐kDa (MMP‐2, gelatinase A) and the 92‐kDa (MMP‐9, gelatinase B) matrix metalloproteinases have been associated with tumor cell invasion and metastasis. Immunohistological staining of MMP‐2 and MMP‐9, basal lamina collagen IV and TIMP‐2 were performed on frozen sections of 83 invasive breast carcinomas. MMP‐2 and MMP‐9 were associated with neoplastic cell plasma membrane in 72% of cases and exhibited inter‐tumoral variability of staining intensity. MMP‐2 and MMP‐9 staining was not correlated with presence of metastases at time of diagnosis or with disease outcome. TIMP‐2 was detected in the peri‐tumoral stroma and was present in 87% of cases. Residual benign breast tissue was negative for TIMP‐2 staining. Neoplasms with diffuse TIMP‐2 staining (24%) recurred significantly more frequently (75% recurred) than cases with focal (42% recurred) or absent (27% recurred) TIMP‐2. Presence of collagen IV was negatively correlated with gelatinase staining. We conclude that up‐regulation of MMP‐2 and MMP‐9 expression in breast tumor cells is reciprocally correlated to collagen IV staining. Clinical outcome, however, is more closely related to the presence of TIMP‐2 than the corresponding MMPs. Enhanced TIMP‐2 expression, therefore, may denote a stromal response to tumor invasion, indicative of aggressive behavior in a subset of breast carcinomas. © 1994 Wiley‐Liss, Inc.
Pre‐morbid body size and the prognosis of women with breast cancer
Authors: Jain Meera , Miller Anthony B. 
Published: February 2007

AbstractObesity has been associated with poor prognosis of breast cancer, but studies investigating indicators of adiposity, independent of height, such as skinfold thickness and weight/height ratio, have been limited. From a cohort of 89,835 women in the National Breast Screening Study, data on histologically confirmed, incident cases of invasive carcinoma of breast, diagnosed between January 1981 to June 1992, were analyzed. Body measurements were taken at enrollment and other risk‐factor information from a self‐administered questionnaire completed prior to diagnosis of the breast cancer. Mortality data were obtained by linkage to Statistics Canada, provincial cancer registries, and annual follow‐up of cases through physicians. Of the 5 measures of body size studied among cases, poor prognosis was associated with higher triceps skinfold thickness only. With every 5 mm increase in skinfold, the risk of dying increased approximately 12% (relative risk, 1.12; 95% confidence intervals, 1.01 to 1.24) in the 1033 cases examined and adjusted for age at diagnosis, number of positive axillary nodes involved, and body weight. Compared with women in the lowest quartile of skinfold thickness, women in the fourth quartile had a relative risk (RR) of 1.64 (95% CI, 0.99 to 2.73). None of the other measures—weight, height, body mass index or weight/height ratio—reached any statistical significance. Since the reliability and validity of skinfold measures used in our study were never established, and no data were available for changes in body size after diagnosis, the results of this study on skinfold thickness should be used only as indicative of a need for further studies. © 1994 Wiley‐Liss, Inc.
Proliferating cell nuclear antigen (PCNA) in high‐grade malignant fibrous histiocytoma: Prognostic value in 48 patients
Authors: Dreinhöfer Karsten E. , Åkerman Måns , Willén Helena , Anderson Christina , Gustafson Pelle , Rydholm Anders 
Published: February 2007

AbstractGrading based on histopathologic features is used to predict survival in soft‐tissue sarcoma. However, variations in clinical behavior between tumors of the same grade motivate a search for additional factors that correlate with prognosis. Proliferating cell nuclear antigen (PCNA) is expressed in proliferating cells during the G1 S and G2‐phases. To evaluate a prognostic implication of PCNA, the tumors of 48 patients with malignant fibrous histiocytomas (13 grade III, 35 grade IV) with a minimum follow‐up of 2 years were immunohistochemically studied. We used PC 10, a monoclonal antibody (MAb) directed against PCNA, which allows cell proliferation in formalin‐fixed, paraffinembedded tumor tissue to be evaluated. We appllied a semiquantitative PCNA grading scheme to all stained nuclei of an entire slide. The 3‐year metastasis‐free survival rate was 0.87 for patients in grade A (low PLNA rate), and 0.14 for patients in grade C (high PLNA). Our findings show that immunohistochemical evaluation of cell kinetics in soft‐tissue sarcomas by PCNA might be a useful adjunct to conventional tumor grading. © 1994 Wiley‐Liss, Inc.
Potent stimulatory effect of interleukin‐1α on apolipoprotein D and gross cystic disease fluid protein‐15 expression in human breast‐cancer cells
Authors: Blais Yves , Sugimoto Keiko , Carriere Marie‐Claude , Haagensen Darrow E. , Labrie Fernand , Simard Jacques 
Published: February 2007

AbstractTo better understand the multiple hormonal control of the expression of apolipoprotein D (apo‐D) and gross cystic disease fluid protein‐15 (GCDFP‐15, also designated prolactin‐inducible protein), which are 2 major proteins found in benign breastdisease fluid, we investigated their regulation by interleukin‐Iα (IL‐Iα) in the presence or absence of steroid hormones in ZR‐75‐I human breast cancer cells. Exposure of these cells to IL‐Iα decreased basal cell proliferation by half and markedly reduced the mitogenic action of 17β‐estradiol (E2), the halfmaximal inhibitory effect being exerted at 1.5 pM. In parallel, IL‐Iα stimulated apo‐D and GCDFP‐15 secretion with a similar potency. The antiproliferative effect of IL‐Iα was additive to the inhibition of cell proliferation caused by dihydrotestosterone (DHT) or the glucocorticoid dexamethasone (DEX). In parallel, IL‐Iα‐induced stimulation of apo‐D and GCDFP‐15 secretion was additive to that exerted by DHT or DEX. The sensitivity of the apo‐D and GCDFP‐15 responses to the stimulatory action of DHT or DEX was not changed by the presence of IL‐Iα. IL‐Iα also increased apo‐D and GCDFP‐15 mRNA levels. The present findings demonstrate the potent stimulatory effect of IL‐Iα on basal as well as androgen‐ and glucocorticoid‐induced apo‐D and GCDFP‐15 expression. The present data strongly suggest that IL‐Iα and steroids may modulate the secretion of these 2 proteins through different transduction pathways. © 1994 Wiley‐Liss, Inc.
MAGE‐1 gene product is a cytoplasmic protein
Authors: Schultz‐Thater Elke , Juretic Antonio , Dellabona Paolo , Lüscher Urs , Siegrist Walter , Harder Felix , Heberer Michael , Zuber Markus , Spagnoli Giulio C. 
Published: February 2007

AbstractMAGE‐I gene encodes a human melanoma antigen, recognized by syngeneic cytotoxic T lymphocytes (CTL). MAGE‐I transcripts are also detectable in breast cancers, in non‐smallcell lung carcinomas and in central nervous system tumors. In order to identify, in cellular preparations, the protein encompassing the antigenic peptide, we generated a panel of monoclonal antibodies (MAbs) against the MAGE‐I gene product by using, as immunogen, a full‐length recombinant preparation (rMAGE‐I), obtained through expression cloning of the relevant gene in E. coli. Four reagents were obtained recognizing both rMAGE‐I and the 46‐kDa native protein in cell lines expressing MAGE‐I mRNA. No positivity could be detected in MAGE‐I‐mRNA‐negative melanoma lines. No surface labelling of MAGE‐I‐positive cell lines could be observed. In contrast, on permeabilization of MZ2 melanoma cells, all 4 MAbs induced efficient staining, as detected by cytofluorography. Fluorescence microscopy shows that MAGE‐I gene product is a cytoplasmic protein clustered in paranuclear organelle‐like structures. Thus, MAGE‐I protein location closely resembles that of P9IA and PI98 murine‐tumor antigens. © 1994 Wiley‐Liss, Inc.
Second malignant tumors after elective end of therapy for a first cancer in childhood: A multicenter study in Italy
Authors: Rosso Paolo , Terracini Benedetto , Fears Thomas R. , Jankovic Momcilo , Bellani Franca Fossati , Arrighini Alberto , Carli Modesto , Di Montezemolo Luca Cordero , Garrè Maria L. , Guazzelli Carlo , Izzi Giancarlo , Loiacono Giuseppe , Mancini Antonia , Tamaro Paolo , Testi Anna M. , Masera Giuseppe , Haupt Riccardo 
Published: February 2007

AbstractTo evaluate the incidence of second malignant tumors in a cohort of subjects previously treated for childhood cancer, we analyzed data from the Off‐Therapy Registry (OTR) of the Italian Association of Pediatric Hematology/Oncology, which collects information on children treated for Hodgkin's disease, non‐Hodgkin's lymphoma, Wilms' tumor, acute lymphoblastic leukemia (ALL) and acute non‐lymphatic leukemia and who had been removed from treatment in the absence of clinical signs of disease,i.e.the off‐therapy stage. Second malignant tumors (SMT), diagnosed before December 31, 1988, were identified through a special enquiry to the 36 institutions cooperating in the registry. Observed cases were compared to expected numbers estimated from age‐ and sex‐specific incidence rates derived from the Cancer Registry of the Province of Varese. In a total of 3,310 study subjects, 27 SMTs have been registered. The Cumulative Risk (CR) of SMT was 2.9% 15 years after the end of treatment and the Standard Incidence Ratio (SIR) was 10.8. The ALL sub‐cohort had the highest risk of SMT (SIR 13.6) and 9 cases of CNS tumor occurred in this group (SIR 58.9). All 9 had received prophylactic cranial radiotherapy (CRT) and 5 had been treated on one protocol, characterized by low‐dose intrathecal methotrexate (IT MTX) given monthly for 2 years after CRT. The Off‐Therapy Registry has unique criteria for inclusion; direct comparisons with similar studies are therefore somewhat problematic. However, our data suggest that the risk of SMT in childhood ALL cancer survivors may be greater than previously reported, and that CNS tumors are the most common SMT in this group. The administration schedule of IT MTX may be an important risk factor. © 1994 Wiley‐Liss, Inc.
Micronuclei, a biomarker for chemoprevention trials: Results of a randomized study in oral pre‐malignancy
Authors: Benner Steven E. , Lippman Scott M. , Wargovich Michael J. , Lee J. Jack , Velasco Marco , Martin Jack W. , Toth Bela B. , Hong Waun K. 
Published: February 2007

AbstractBiomarkers are being sought that could serve as surrogate end points for chemoprevention trials. Micronuclei, cytoplasmic fragments of DNA, have been proposed as a biomarker and studied in oral pre‐malignancy. This study evaluated micronuclei frequency in a randomized chemoprevention trial of oral pre‐malignancy. A recent clinical trial evaluated the responses of pre‐malignant oral lesions to 3 months of therapy with isotretinoin followed by 9 months of either low‐dose isotretinoin or beta‐carotene. For 57 study participants, micronuclei were counted in mucosal scrapings of the lesion and in normalappearing mucosa at baseline and following 3 months and 12 months of therapy. Micronuclei counts were higher in scrapings from the lesion than in the normal‐appearing mucosa. Following 3 months of isotretinoin, the micronuclei counts in scrapings of the lesion were significantly reduced. With treatment, the mean micronuclei count declined at 3 months. In a randomized comparison, both isotretinoin and beta‐carotene maintained the suppression of micronuclei. The change in micronuclei count was not associated with the clinical or histological response to treatment. Chemoprevention treatment with isotretinoin led to a reduction in frequency of micronuclei, a marker of recent DNA injury, which was then maintained by both isotretinoin and beta‐carotene. © 1994 Wiley‐Liss, Inc.
Adult T‐Cell leukemia/lymphoma: A working point‐score classification for epidemiological studies
Authors: Levine Paul H. , Cleghorn Farley , Manns Angela , Jaffe Elaine S. , Navarro‐Roman Lydia , Blattner William A. , Hanchard Barrie , De Oliveira M. S. , Matutes Estella , Catovsky Daniel , Shimoyama M. , Tajima Kazuo , Sonoda Shunro , Yamaguchi Kazunari , Takatsuki Kiyoshi 
Published: February 2007

AbstractAdult T‐cell leukemia/lymphoma (ATL) is a malignancy that occurs most frequently in south‐western Japan and the Caribbean basin. The primary etiologic agent for this disease, human T‐lymphotropic virus type I (HTLV‐I), is endemic in these areas. Only a small percentage of individuals infected with HTLV‐I develop ATL. The factors that determine the development of malignant disease as an outcome of HTLV‐I infection in an individual are unknown. ATL is histopathologically heterogeneous and firm diagnosis is made on the contribution of clinical, laboratory and histopathologic features. The wide variety of laboratory assays available to geographically diverse populations has led to a need to standardize the criteria for determining the diagnosis of this disease for epidemiologic studies. This report summarizes current information regarding ATL and proposes a classification facilitating comparison of case series in geographically and ethnically different populations. © 1994 Wiley‐Liss, Inc.
Cross‐sectional study of Opisthorchis viverrini infection and cholangiocarcinoma in communities within a high‐risk area in northeast thailand
Authors: Haswell‐Elkins Melissa R. , Mairiang Eimorn , Mairiang Pisaln , Chaiyakum Jittaroen , Chamadol Nittaya , Loapaiboon Vallop , Sithithaworn Paiboon , Elkins David B. 
Published: February 2007

AbstractWe describe an innovative strategy to quantify risk of cancer associated with varying levels of exposure to chronic parasitic infection through the identification of asymptomatic cases of cholangiocarcinoma within a population‐based survey of Opisthorchis viverrini infection. Stool samples from 12,311 adults over age 24 years from 85 villages in northeast Thailand were examined for intensity of liver fluke infection. People from varying egg count categories were selected for ultrasound examination to identify hepatobiliary disease. Fifteen preclinical cases of cholangiocarcinoma were diagnosed from a total of 1,807 people based on ultrasonographic evidence with confirmation by endoscopy where possible. The prevalence odds of the diagnosis of cholangiocarcinoma increased gradually within the light and moderate intensity groups. In contrast, sharply elevated prevalence odds [age‐, sex‐ and licality‐adjusted prevalence odds ratio (POR) 14.1, p < 0.05] were observed within the most heavily liver fluke‐infected group compared with the uninfected group. Males were more frequently affected than females (crude POR 4.5), but after controlling for intensity of infection, age and locality, the magnitude and significance of this measurement was reduced. Our data clearly demonstrate a significant relationship between intensity of liver fluke infection and cholangiocarcinoma and a strikingly high prevalence of the disease among heavily infected males. © 1994 Wiley‐Liss, Inc.
HLA‐DQB1*0301 association with increased cutaneous melanoma risk
Authors: Lee Jeffrey E. , Reveille John D. , Ross Merrick I. , Platsoucas Chris D. 
Published: February 2007

AbstractSusceptibility to a variety of malignancies has been linked to human leukocyte antigen (HLA) genes, including the HLA class II allele DQBI*0301. To determine whether melanoma risk is associated with HLA class II alleles, molecular oligotyping of HLA class II‐DRBI, ‐DQAI and ‐DQAI genes was performed for 45 patients with melanoma. The DQBI *0301 allele was present in 56% of melanoma patients vs. 27% of 200 local Caucasian controls. This difference was highly significant (Bonferroni'scorrected chi‐square p = 0.003, OR = 3.4). No other class II allele tested was present at significantly increased or decreased frequency in melanoma patients. Furthermore, presence of DQBI*0301 in melanoma patients was associated with advanced disease. Melanoma patients carrying the DQBI*0301 allele presented on average with thicker primary tumors (mean 3.7 mm vs. 1.8 mm, 2‐tailed p = 0.02) and were more likely to present with regional or distant metastatic disease (stages III‐IV, 44% vs. 5%, chi‐square p = 0.003), compared to melanoma patients without DQBI*0301. Risk of melanoma incidence or progression may be influenced by DQBI*0301 or a closely linked gene. © 1994 Wiley‐Liss, Inc.
Changes in p53 and cyclin D1 protein levels and cell proliferation in different stages of human esophageal and gastric‐cardia carcinogenesis
Authors: Wang Li Dong , Shi Stephanie Tao , Zhou Qi , Goldstein Susan , Hong Jun‐Yan , Shao Peter , Qiu Song‐Liang , Yang Chung S. 
Published: February 2007

AbstractThe objective of this study was to quantify the changes in p53 and cyclin DI protein levels in different stages of human esophageal and gastric cardia carcinogenesis in a high‐risk population in Henan, China. Immunoreactivity of p53, cyclin DI and proliferating‐cell nuclear antigen (PCNA) was observed in the cell nuclei of esophageal and gastric cardia biopsies. The number of p53‐immunostaining‐positive cells was low in normal epithelia, slightly increased in basal‐cell hyperplasia (BCH), markedly increased in dysplasia (DYS) (10‐fold), and further increased in squamous‐cell carcinoma (SCC) (40‐fold). This pattern of change was similar to that of cell proliferation as indicated by PCNA immunostaining. On the other hand, the number of cyclin DI‐immunostaining‐positive cells did not increase from BCH to DYS, although a slight increase from DYS to SCC was noted. In the gastric cardia, again, the pattern of change of p53‐positive cells in different stages of lesions paralleled the pattern of cell proliferation. The number of p53‐positive cells was very low, much lower than that of PCNA‐positive cells, in normal, chronic superficial gastritis (CSG) and chronic atrophic gastritis (CAG); therefore, the increase of p53‐positive cells from CAG to DYS was more dramatic (100‐fold). From DYS to adenocarcinoma (AC), the p53‐positive and the PCNA‐positive cells increased 4‐fold. On the other hand, the number of cyclin DI‐positive cells did not increase in pre‐cancerous lesions, but increased slightly in AC. This study demonstrates that p53 protein accumulation increased with the progression of pre‐cancerous lesions, especially in the genesis of dysplasia, both in the esophagus and in the gastric cardia. Our approach of quantitative immunohistochemistry sheds light on the mechanisms of genesis of esophageal and gastric‐cardia cancers, which frequently occur together in many highincidence areas. © 1994 Wiley‐Liss, Inc.
Circadian changes in mitoxantrone toxicity in mice: Relationship with plasma pharmacokinetics
Authors: Lévi Francis , Tampellini Marco , Metzger Gérard , Bizi Ernest , Lemaigre Guy , Hallek Michael 
Published: February 2007

AbstractCircadian time‐dependent differences in clinical toxicity of several anti‐cancer agents were predicted from murine studies. Mitoxantrone is an anthracenedion (an anthracycline‐related class of compounds) of increased clinical use, which may benefit from selective circadian timing. In 3 consecutive studies, a total of 428 male B6D2F1 mice aged from 8 to 10 weeks were synchronized by an alternation of 12 hr of light and 12 hr of darkness (LD 12:12). They received a single i.v. injection of mitoxantrone at one of 6 or 4 circadian stages differing by 4 or 6 hr. A dose‐response relationship characterized body‐weight loss and survival rate. Dose‐toxicity relationship further closely depended upon circadian dosing time. Thus, a dose of 16 mg/kg killed 100% of the mice injected at 3 hr after light onset (HALO), and none of them at 11 or at 15 HALO (p from x2 < 0.001). Body‐weight loss varied from 41% at 3 HALO to 32% at 15 HALO (p from ANOVA < 0.0001). Least hematologic toxicity and fastest recovery of a normal circulating leukocyte count corresponded to mitoxantrone injection near the middle of the dark‐activity span, at 16 HALO. Similar findings characterized colonic and splenic lesions. Moreover, mitoxantrone was both distributed and eliminated faster after injection at 16 HALO. If such data apply to cancer patients, as was the case for other drugs investigated with this methodology, an afternoon infusion should enable high‐dose mitoxantrone to be well tolerated. © 1994 Wiley‐Liss, Inc.
Interclonal heterogeneity in a human epithelioid‐sarcoma cell line (Gru‐1)
Authors: Engers Rainer , Gerharz Claus D. , Moll Roland , Pohl Anke , Sarbia Mario , Gabbert Helmut E. 
Published: February 2007

AbstractThree clonal sub‐populations, GRU‐IA, GRU‐IB, and GRU‐IC, isolated from the human epithelioid sarcoma cell line GRU‐I, were characterized morphologically, cytogenetically and with regard to proliferation kinetics. Immunocytochemically, major differences became evident in the expression of cytokeratin 18 and neurofilament proteins, which are indicative for epithelial and neural differentiation respectively. Vimentin, a mesenchymal differentiation marker, however, could be detected in all tumor cells of each sub‐population. Laminin, a major compound of basement membranes, formed abundant intercellular network‐like patterns in GRU‐IB and GRU‐IC, whereas GRU‐IA was characterized by a diffuse intracellular reaction, suggesting a disorder in laminin secretion. Cytogenetically, all sub‐populations proved to be DNA‐aneuploid, the DNA index ranging from 1.4 to 1.5. Proliferation analysis revealed doubling times ranging from 13 (GRU‐IC) to 19 hr (GRU‐IA). These strictly defined clonal sub‐populations provide a valuable tool for further investigations of the biological behavior of human epithelioid sarcoma with special regard to tumor heterogeneity. © 1994 Wiley‐Liss, Inc.