bluuebunny/crossref_metadata_2025_split huggingface dataset:
Family history of cancer: Pooled analysis in the International Head and Neck Cancer Epidemiology Consortium
Authors: Negri Eva , Boffetta Paolo , Berthiller Julien , Castellsague Xavier , Curado Maria Paula , Maso Luigino Dal , Daudt Alexander W. , Fabianova Eleonora , Fernandez Leticia , Wünsch‐Filho Victor , Franceschi Silvia , Hayes Richard B. , Herrero Rolando , Koifman Sergio , Lazarus Philip , Lence Juan J. , Levi Fabio , Mates Dana , Matos Elena , Menezes Ana , Muscat Joshua , Eluf‐Neto Jose , Olshan Andrew F. , Rudnai Peter , Shangina Oxana , Sturgis Erich M. , Szeszenia‐Dabrowska Neonilia , Talamini Renato , Wei Qingyi , Winn Deborah M. , Zaridze David , Lissowska Jolanta , Zhang Zuo‐Feng , Ferro Gilles , Brennan Paul , La Vecchia Carlo , Hashibe Mia 
Published: September 2008

AbstractAlcohol and tobacco consumption are well‐recognized risk factors for head and neck cancer (HNC). Evidence suggests that genetic predisposition may also play a role. Only a few epidemiologic studies, however, have considered the relation between HNC risk and family history of HNC and other cancers. We pooled individual‐level data across 12 case–control studies including 8,967 HNC cases and 13,627 controls. We obtained pooled odds ratios (OR) using fixed and random effect models and adjusting for potential confounding factors. All statistical tests were two‐sided. A family history of HNC in first‐degree relatives increased the risk of HNC (OR = 1.7, 95% confidence interval, CI, 1.2–2.3). The risk was higher when the affected relative was a sibling (OR = 2.2, 95% CI 1.6–3.1) rather than a parent (OR = 1.5, 95% CI 1.1–1.8) and for more distal HNC anatomic sites (hypopharynx and larynx). The risk was also higher, or limited to, in subjects exposed to tobacco. The OR rose to 7.2 (95% CI 5.5–9.5) among subjects with family history, who were alcohol and tobacco users. A weak but significant association (OR = 1.1, 95% CI 1.0–1.2) emerged for family history of other tobacco‐related neoplasms, particularly with laryngeal cancer (OR = 1.3, 95% CI 1.1–1.5). No association was observed for family history of nontobacco‐related neoplasms and the risk of HNC (OR = 1.0, 95% CI 0.9–1.1). Familial factors play a role in the etiology of HNC. In both subjects with and without family history of HNC, avoidance of tobacco and alcohol exposure may be the best way to avoid HNC. © 2008 Wiley‐Liss, Inc.
Follicular lymphoma B cells induce the conversion of conventional CD4+ T cells to T‐regulatory cells
Authors: Ai Weiyun Z. , Hou Jing‐Zhou , Zeiser Robert , Czerwinski Debra , Negrin Robert S. , Levy Ronald 
Published: September 2008

AbstractThere has been accumulating evidence that CD4+CD25+ FoxP3 expressing regulatory T cells (Treg) are highly concentrated in tumors, thereby fostering an immune‐privileged microenvironment. Some studies have shown that T‐cell receptor (TCR) stimulation can convert conventional T cells into Treg. Follicular lymphoma (FL) B cells can enhance this Treg conversion. We investigated whether FL tumor B cells, as opposed to normal B cells, are unique in their ability to convert effector T cells into Treg. We found that tumor B cells alone, without artificial TCR stimulation, could induce conventional T cells to express FoxP3 and to acquire regulatory function. In contrast to their malignant counterpart, normal B cells did not induce Treg conversion. Treg conversion was independent of the T cell background, as T cells isolated from FL or normal peripheral blood were equally susceptible to being converted by tumor B cells. Our study provides evidence for a tumor‐specific mechanism by which FL tumor cells promote immune escape through the induction of Treg. © 2008 Wiley‐Liss, Inc.
Early aberrant insulin‐like growth factor signaling in the progression to endometrial carcinoma is augmented by tamoxifen
Authors: Strissel Pamela L. , Ellmann Stephan , Loprich Elke , Thiel Falk , Fasching Peter A. , Stiegler Elisabeth , Hartmann Arndt , Beckmann Matthias W. , Strick Reiner 
Published: September 2008

AbstractTamoxifen is an important selective estrogen receptor (ER) modulator for treatment of steroid hormone positive breast cancer. In addition to the beneficial effect, tamoxifen is one risk factor for endometrial carcinoma (EnCa) development. We hypothesized that, (1) dysregulation of gene expression and protein phosphorylation of the insulin‐like growth factor (IGF) and steroid hormone receptor‐signaling occur early in benign endometrial tissues and (2) signaling differences would be detected between patients with or without tamoxifen treatment. Seventy‐eight tissues, including 2 benign cohorts from patients treated with (n = 24) or without tamoxifen (n = 28) (hyperproliferative endometrium, hyperplasia, polyps), EnCa (n = 12) with endometrium controls (n = 14) were analyzed for expression of 15 genes from the IGF and steroid hormone receptor‐signaling, including the target genes Syncytin‐1, PAX2 and c‐myc. Total and phosphorylated protein expression were examined for ERα, PTEN, AKT, mTOR and Syncytin‐1. Compared to controls similar significant deregulation of IGF and steroid hormone receptor‐signaling, Syncytin‐1 and PAX2 occurred in both benign cohorts, irrelevant of tamoxifen treatment. Comparing both benign cohorts with and without tamoxifen significant expression differences were noted. Increased total protein and phosphorylation of pERα‐Ser118, pPTEN‐Thr380, pAKT‐Thr308, pAKT‐Ser473, pmTOR‐Ser2448 and Syncytin‐1 were noted in early benign tissue stages associating with tamoxifen, especially polyps. Functional kinetic studies following tamoxifen treatment of the PTEN mutated RL95‐2 EnCa cell line, demonstrated a doubling of phosphorylation of pERα‐Ser118 and a 4.2‐fold induction of pAKT‐Thr308 along with Syncytin‐1 induction. This study supports that dysregulated IGF and steroid hormone receptor signaling is prominent in endometrial benign stages and these alterations could represent clinical indicators for the risk of EnCa and also help in development of new therapies. © 2008 Wiley‐Liss, Inc.
Imatinib mesylate suppresses bone metastases of breast cancer by inhibiting osteoclasts through the blockade of c‐Fms signals
Authors: Hiraga Toru , Nakamura Hiroaki 
Published: September 2008

AbstractImatinib mesylate (imatinib) is a potent and selective inhibitor of the tyrosine kinases, Bcr‐Abl, c‐Kit and platelet‐derived growth factor receptors (PDGFRs). Recently, it has been reported that imatinib also targets the macrophage colony‐stimulating factor (M‐CSF) receptor c‐Fms. M‐CSF signals are essential for the differentiation of osteoclasts. Bone metastases of breast cancer are frequently associated with osteoclastic bone destruction. Furthermore, several lines of evidence suggest that osteoclasts play central roles in the development and progression of bone metastases. Thus, in the present study, we examined the effects of imatinib on bone metastases of breast cancer. Coimmunoprecipitation assays showed that imatinib inhibited the M‐CSF‐induced phosphorylation of c‐Fms in osteoclast precursor cells as well as the PDGF‐induced PDGFR phosphorylation in MDA‐MB‐231 human breast cancer cells. Imatinib also markedly reduced osteoclast formation in vitro. In contrast, those concentrations of imatinib did not affect osteoblast differentiation. We then examined the effects of imatinib on bone metastases of MDA‐MB‐231 cells in a nude mouse model. Radiographic and histomorphometric analyses demonstrated that imatinib significantly decreased bone metastases associated with the reduced number of osteoclasts. In support of the notion that the inhibition of c‐Fms acts to suppress the development of bone metastases, we found that a specific inhibitor of c‐Fms Ki20227 also decreased bone metastases. In conclusion, these results collectively suggest that imatinib reduced bone metastases, at least in part, by inhibiting osteoclastic bone destruction through the blockade of c‐Fms signals. Our results also suggest that imatinib may have a protective effect against cancer treatment‐induced bone loss. © 2008 Wiley‐Liss, Inc.
Cancer‐retina antigens as potential paraneoplastic antigens in melanoma‐associated retinopathy
Authors: Bazhin Alexandr V. , Dalke Claudia , Willner Nadine , Abschütz Oliver , Wildberger Hannes G. H. , Philippov Pavel P. , Dummer Reinhard , Graw Jochen , de Angelis Martin Hrabé , Schadendorf Dirk , Umansky Viktor , Eichmüller Stefan B. 
Published: September 2008

AbstractMelanoma‐associated retinopathy is a rare paraneoplastic neurological syndrome characterized by retinopathy in melanoma patients. The main photoreceptor proteins have been found to be expressed as cancer‐retina antigens in melanoma. Here we present evidence that these can function as paraneoplastic antigens in melanoma‐associated retinopathy. Sera and one tumor cell line of such patients were studied and ret‐transgenic mice spontaneously developing melanoma were used as a murine model for melanoma‐associated retinopathy. Splenocytes and sera were used for adoptive transfer from tumor‐bearing or control mice to wild‐type mice. Retinopathy was investigated in mice by funduscopy, electroretinography and eye histology. Expression of photoreceptor proteins and autoantibodies against arrestin and transducin were detected in melanoma‐associated retinopathy patients. In tumor‐bearing ret‐transgenic mice, retinopathy was frequently (13/15) detected by electroretinogram and eye histology. These pathological changes were manifested in degenerations of photoreceptors, bipolar cells and pigment epithelium as well as retinal detachment. Mostly these defects were combined. Cancer‐retina antigens were expressed in tumors of these mice, and autoantibodies against arrestin were revealed in some of their sera. Adoptive transfer of splenocytes and sera from tumor‐bearing into wild‐type mice led to the induction of retinopathy in 4/16 animals. We suggest that melanoma‐associated retinopathy can be mediated by humoral and/or cellular immune responses against a number of cancer‐retina antigens which may function as paraneoplastic antigens in melanoma‐associated retinopathy. © 2008 Wiley‐Liss, Inc.
Platelet‐derived microparticles promote invasiveness of prostate cancer cells via upregulation of MMP‐2 production
Authors: Dashevsky Olga , Varon David , Brill Alexander 
Published: September 2008

AbstractProstate cancer commonly affects men in the Western world. A major factor of the life‐threatening course of this disease is the high rate of metastasis, predominantly to bones. Circulating tumor cells encounter platelets and may activate them, resulting in a production of microparticles (MPs). MPs are small platelet fragments expressing membrane receptors as well as cytoplasmic constituents. Here, we report that prostate cancer cells, Clone‐1 (Cl‐1), preincubated with platelet‐derived MPs (PMPs), demonstrate increased invasion through a gelatin‐coated (a denatured form of collagen) membrane of the Boyden chamber system. This effect was accompanied by an increased secretion of metalloproteinase‐2 (MMP‐2) as demonstrated by a gelatin zymography. Application of MMP‐2/9 inhibitor reversed the PMP‐induced tumor cell invasion. PMPs were shown to adhere to Cl‐1 cells, but direct contact between them may not be mandatory for MMP secretion because PMP lysate induced MMP‐2 production by Cl‐1 cells to the same extent as did intact PMPs. PMP‐induced MMP‐2 secretion was inhibited by neutralization of either PKC or total intracellular tyrosine phosphorylation, but was not affected by blocking major intraplatelet cytokines. Actinomycin D (a transcription inhibitor) did not modify this effect, whereas cycloheximide (an inhibitor of protein translation) abolished the MMP‐2 release. MMP‐2 secretion was accompanied by a rapid and transient increase in MMP‐2 mRNA level after a 2‐hr coincubation of prostate cancer cells with PMPs. Thus, PMPs promote tumor invasiveness, at least in part by stimulation of MMP‐2 production. © 2008 Wiley‐Liss, Inc.
Transforming growth factor ß1 induces apoptosis by suppressing FLICE‐like inhibitory protein in DU145 prostate epithelial cells
Authors: Yoo Kiwon S. , Nastiuk Kent L. , Krolewski John J. 
Published: September 2008

AbstractTransforming growth factor ß (TGFß) is a paracrine mediator of prostate epithelial cell apoptosis. In rodents, castration induces production of TGFβ by stromal cells, which leads to apoptosis of epithelial cells. To identify potential mediators of this cell death pathway, we developed a model using DU145 cells, a tumorigenic human prostate epithelial cell line. We discovered that at low density, in low mitogen media, DU145 cells apoptose when treated with TGFβ1. Prior to the onset of death, TGFβ1 treatment downregulated the expression of the caspase inhibitor FLICE‐like inhibitory protein (FLIP), at both the mRNA and protein level, suggesting a causal role between FLIP downregulation and cell death. To confirm the importance of FLIP in TGFβ1‐induced apoptosis, we employed small interfering RNA (siRNA) to silence FLIP expression. Doing so led to apoptosis, which is consistent with the hypothesis that FLIP prevents death in these cells. Furthermore, inhibition of caspase‐8 by siRNA knockdown partially rescued the apoptotic effects of TGFβ1, suggesting a role for death receptor signaling components in TGFß‐mediated death of prostate epithelial cells. © 2008 Wiley‐Liss, Inc.
The topography of some anionic sites at the surfaces of fixed ehrlich ascites tumour cells
Authors: Weiss L. , Jung O. S. , Zeigel R. 
Published: September 2008

AbstractThe distribution of positively charged, colloidal iron hydroxide particles to the surfaces of glutaraldehyde‐fixed Ehrlich ascites tumour cells, was studied in 700Å thick sections. After incubation with neuraminidase and/or ribonuclease, and fixation, cells were also reacted with particles.It was shown that the numbers of bound particles were significantly reduced by enzyme treatment, which had previously been shown to reduce the densities of anionic sites at the cell surfaces. Statistical analyses showed that in the controls and ribonuclease‐treated cells, the particles were adsorbed in surface locations following a Poisson distribution. Following neuraminidase treatment, the particles were arranged in clusters, but the clusters themselves were arranged in a Poisson distribution.The data are tentatively interpreted as indicating the presence of different sized neuraminidase‐ and ribonuclease‐susceptible zones at the cell surface, having a higher than average density of anionic sites.
Feline fibrosarcoma virus: Quantitative focus assay, focus morphology and evidence for a “helper virus”
Authors: McDonald Ruth , Wolfe Lauren G. , Deinhardt Friedrich 
Published: September 2008

AbstractFeline fibrosarcoma virus (FeSV) was assayed by focus formation in feline and marmoset fibroblast cultures overlaid with agar and re‐fed with fluid media. The FeSV titers were consistent from experiment to experiment and were about four times higher in feline fibroblasts than in marmoset fibroblasts in parallel assays. Clones of FeSV‐infected cells grown in soft agar, and foci of transformed cells produced by FeSV in monolayer cell cultures were both of two morphological types: round cells (r) and a loose meshwork of fusiform and round cells (fr). Thermal stability experiments indicated that the morphological differences of the foci were virus‐dependent.The titration pattern of FeSV grown in marmoset or feline cells indicated that these preparations were either competent or contained an excess of helper virus. Preliminary challenge experiments with Snyder‐Theilen FeSV grown in marmoset cells indicated that a 10‐ to 100‐fold excess of non‐transforming, interfering virus (helper virus) was present in this FeSV preparation.
Tumor‐associated immunoglobulins. enhancement of syngeneic tumors by igg2‐containing tumor eluates
Authors: Ran Maya , Witz Isaac P. 
Published: September 2008

AbstractThe present study was intended to establish whether IgG2‐containing eluates, dissociated from carcinogen‐induced tumors by a low pH buffer, have tumor‐enhancing properties.Threshold amounts of cells from mouse tumor lines originally induced by benzo (a)‐pyrene or by methylcholanthrene were mixed and incubated, prior to inoculation, with IgG2‐containing eluates, originating either from the corresponding tumors (autologous eluates) or from other syngeneic tumors (isologous eluates). Tumor cells incubated and injected together with autologous eluates gave in some experiments a higher yield of tumors in syngeneic mice than did cells not subjected to this treatment. Some isologous eluates originating from several primary tumors or from syngeneic tumors belonging to a different line from the one tested, were also capable of enhancing tumor growth.
Absence, or low expression, of leukocyte adhesion molecules CDI1 and CD18 on burkjtt lymphoma cells
Authors: Patarroyo Manuel , Prieto Jacqueline , Ernberg Ingemar , Gahmberg Carl G. 
Published: September 2008

AbstractLeukocyte adhesion to cells is mediated by the cell‐surface glycoprotein complex CDIIa‐c/CD18 and, in some cases, the glycoprotein gp84. The process is associated with leukocyte activation and modulates lymphocyte proliferation and maturation. Epstein‐Barr virus (EBV)‐transformed normal B lymphocytes give rise to lymphoblastoid cell fines (LCLs) which grow as large clusters mediated by adhesion molecules. In contrast, newly explanted EBV‐infected Burkitt lymphoma (BL) cells usually grow as single cells or as loose clusters. We now report that EBV positive‐ and EBV‐negative BL lines lack the adhesive protein complex, or have only low levels of it, whereas LCLs, representing various stages of B‐lymphocyte development, contain considerably higher amounts, as measured by immunofluorescence flow cytometry and immuno precipitation. The level of gp84 expression is of the same magnitude in both types of cells.
Clinical validation of the new ELSA‐CA 125 II assay: Report of a european multicentre evaluation
Authors: Clement Maryvonne , Bischof Paul , Gruffat Claire , Ricolleau Gabriel , Auvray Eliane , Quilien Véronique , Pacheco Carmen , Torres Miguel , Ferdeghini Marco 
Published: September 2008

AbstractThe ELSA‐CA 125 II is a second‐generation radioimmunoassay for the quantification of CA 125 in serum. In a multicentre study involving 49 follow‐ups of patients with ovarian cancers, and 880 other patients, 2.8% of healthy persons, 25% of 149 patients with benign gynaecological diseases and 39% of 82 patients with benign non‐gynaecological diseases had CA 125 levels above 35 U/ml. Using the 35 U/ml cut‐off, sensitivities among epithelial ovarian cancers were found to be 85% in serous tumors, 41% in mucinous tumors and 83% in other types. During follow‐up of patients with serous ovarian cancers, we observed an equivalent behaviour of both assays—first‐ and second‐generation—with the clinical evolution. We also compared results obtained with other assays commercially available; these were significantly different when a polyclonal antibody was used in the sandwich assay. © 1995 Wiley‐ Liss, Inc.
Incidence of cancer among New South Wales adolescents: Which classification scheme describes adolescent cancers better?
Authors: Fritschi Lin , Coates Marylon , McCredie Margaret 
Published: September 2008

AbstractThis report has the dual purpose of describing patterns of cancer incidence among adolescents in New South Wales (NSW), Australia, and comparing adult and childhood cancer classification schemes. All cases of cancer incident between 1972 and 1991 in NSW residents aged 10–19 years were obtained from the population‐based NSW Central Cancer Registry and coded according to Birch and Marsden (1987) in addition to routine coding by the Ninth Revision of the International Classification of Diseases. The average incidence rate for all cancers combined was 158 and 140 per million in males and females respectively. The Birch and Marsden category of “carcinomas and other epithelial neoplasms” comprised 22% of all cancers in male adolescents and 37% in females. Melanoma alone accounted for 16% of all cancers in males and 26% in females. Rates of leukaemias and central nervous system tumours were simitar in the age groups 10–14 years and 15–19 years. By contrast, lymphomas, bone tumours (males only), soft tissue (males only), “germ‐cell, trophoblastic and other gonadal tumours” and “carcinomas and other epithelial neoplasms” were more common in the older age group. The Birch and Marsden classification with its emphasis on morphology provided a clearer picture of some types of cancer which occurred frequently among teenagers. Cancers common in adults did occur in older adolescents but were less well described by the childhood scheme. Cancers of colon and lung were often of unusual histological type compared to adult tumours. It would appear appropriate to use the childhood classification scheme to describe cancer incidence in adolescent age groups, perhaps with minor modification. © 1995 Wiley‐Liss, Inc.
A mother–infant therapy group model for postpartum depression
Authors: Clark Roseanne , Tluczek Audrey , Brown Roger 
Published: September 2008

AbstractThis pilot study examined the feasibility and efficacy of a manualized, 12‐week mother–infant therapy group (M‐ITG) model for women with moderate to severe depressive symptoms during the postpartum period. Study participants were referred to the psychiatric clinic of a university medical center for assessment and treatment for postpartum depression. Results of pre‐ and post comparisons utilizing self‐report and observational measures showed that women in the M‐ITG groups (n = 18) reported significantly fewer depressive symptoms and experienced their infants as more reinforcing following 12 weeks of treatment than did the depressed women in the waitlist control group (WLCG) (n = 14). Mothers in the M‐ITG group also were rated as exhibiting significantly more positive affective involvement and communication in interactions with their infants following treatment than did mothers in the WLCG. The M‐ITG model is described, and the implications of utilizing a mother–infant treatment approach for postpartum depression that focuses on the relationships as well as the mother's depressive symptoms is discussed. The importance of further examining the efficacy of the M‐ITG model for women with postpartum depression and their families in a large‐scale, randomized clinical trial is underscored.
Effects of maternal depression and panic disorder on mother–infant interactive behavior in the Face‐to‐Face Still‐Face paradigm
Authors: Weinberg M. Katherine , Beeghly Marjorie , Olson Karen L. , Tronick Edward 
Published: September 2008

AbstractThe present study evaluated the interactive behavior of three groups of mothers and their 3‐month‐old infants in the Face‐to‐Face Still‐Face paradigm. The mothers had either a clinical diagnosis of major depressive disorder (MDD, n = 33) with no comorbidity, a clinical diagnosis of panic disorder (PD, n = 13) with no comorbidity, or no clinical diagnosis (n = 48). The sample was selected to be at otherwise low social and medical risk, and all mothers with PD or MDD were in treatment. The findings indicated that (a) infants of mothers with PD or MDD displayed the traditional still‐face and reunion effects described in previous research with nonclinical samples; (b) the 3‐month‐old infants in this study showed similar, but not identical, gender effects to those described for older infants; and (c) there were no patterns of maternal or infant interactive behavior that were unique to the PD, MDD, or control groups. These results are discussed in light of mothers' risk status, receipt of treatment, severity of illness, and comorbidity of PD and MDD.