bluuebunny/crossref_metadata_2025_split huggingface dataset:
Anthropometric and reproductive variables and exocrine carcinoma of the pancreas: A population‐based case‐control study in The Netherlands
Authors: De Mesquita H. B. Bueno , Maisonneuve P. , Moerman C. J. , Walker A. M. 
Published: February 2007

AbstractDuring 1984–88 a population‐based case‐control study was carried out in The Netherlands, in collaboration with the International Agency for Research on Cancer, to examine the possible relationship between aspects of medical history and exocrine pancreatic carcinoma in 176 cases and 487 controls. About 58% of patients were interviewed directly. In women, a significant, positive dose‐response effect of height was seen (p‐value trend < 0.005). Compared with ages 14 or more, women with an early age at menarche, i.e., 11 years or less, had a 3‐fold increase in risk (15 cases vs. 23 controls, OR 3.07, 95% Cl 1.35 to 7.00). Other aspects of the reproductive history were not related to risk. In brief, the results of the present study support the hypothesis that, in women, early menarche and greater adult stature may be early predictors of the development of cancer of the pancreas later in life. © 1992 Wiley‐Liss, Inc.
Immunoreactivity, pharmacokinetics and bone marrow dosimetry of intrathecal radioimmunoconjugates
Authors: Moseley R. P. , Papanastassiou V. , Zalutsky M. R. , Ashpole R. D. , Evans S. , Bigner D. D. , Kemshead J. T. 
Published: February 2007

AbstractTen patients with neoplastic meningitis were treated with a variety of 1311‐monoclonal antibody (MAb) conjugates, chosen to bind to their particular malignancy. Pharmacokinetic studies revealed that MAbs leave the ventricular compartment, enter the sub‐arachnoid space and then pass into the blood. Once the MAbs enter the blood compartment, their clearance is determined by factors such as circulating anti‐mouse Ig and circulating antigens. These lead to complex formations and the clearance of the conjugate by the ireticuloendothelial system. In one individual, the anti‐mouse Ig response observed systemically was not mirrored within the CSF, which has implications for planning future therapy of this type. In other patients, formation of immune complexes was due to binding to circulating antigen within the blood. The major toxicity associated with the intrathecal administration of 1311‐MAbs was bone‐marrow suppression. The doses to the bone marrow, resulting from the form of therapy, were calculated but showed no direct correlation with WHO grade 3/4 toxicity. Doses to the ventricular lining werct also calculated, but due to the complex geometry of the compartment, calculation of potential tumour doses was not practicable. © 1992 Wiley‐Liss, Inc.
Expression of genes related to the human erbB, erbA, pdgf and pdgf‐r in tumors of different etiology in Xiphophorus
Authors: Zechel C. , Peters H. , Schleenbecker U. , Anders F. 
Published: February 2007

AbstractThe melanoma determining; Tu locus of the teleost Xiphophorus contains an accessory gene, x‐erbB*a, which is closely related to the EGF receptor gene family, and is probably oncogenic. x‐erbB*a exists in allelic forms that are specific for distinct Tu‐loci, and shows high homology to a non‐allelic non‐oncogenic counterpart x‐erbB*i which is transcribed into mRNA of 4.6 kb in non‐tumorous and tumorous tissues of fish harboring and lacking Tu. Expression of a 4.0‐kb mRNA in tumors (melanoma and fibrosarcoma) of different etiology is strictly correlated with the inheritance of X. maculatus x‐erbB*a alleles; transcripts of 8.0 kb were detected in melanoma and carcinoma of fish harboring a certain x‐erbB*a of X. variatus. The expression of the putative x‐erbB*a transcripts parallels the stage of malignancy of the tumor. The expression of the xiphophorine EGF receptor gene (x‐erbB) was detected in almost all tumors, is strongly enhanced in carcinoma, and is positively correlated with the degree of malignancy of melanoma and fibrosarcoma. Some tumors show expression of erbA‐related genes. The PDGF receptor mRNA is expressed in all tumors analyzed and shows enhanced expression in malignant tumors of neurogenic, epithelial and mesenchymal origin. Expression of x‐pdgf was observed in several cases of melanoma, but more frequently in carcinoma and fibrosarcoma. We conclude that x‐erbB*a might be involved in initiation of tumors of different cellular origin and etiology in fish harboring Tu, as well as in the determination of the malignancy of the tumor. Furthermore, we assume that x‐erbB*i, x‐erbB, x‐pdgf and x‐pdgf‐r play a role in secondary events in tumorigenesis by, e.g., conferring a selective growth advantage to the tumor cells. © 1992 Wiley‐Liss, Inc.
Differentiation‐related expression of adhesion molecules and receptors on human neuroblastoma tissues, cell lines and variants
Authors: Gross Nicole , Favre Simone , Beck Daniel , Meyer Manuela 
Published: February 2007

AbstractThe expression of cellular adhesion molecules (CAM) involved in cell adhesion and immune recognition was measured on neuroblastoma tissue samples, on a neuroblastoma (NB) cell line, SK‐N‐SH, and on 3 phenotypically different variants, SH‐SY5Y, SH‐EP, SH‐IN, representing neuronal, Schwannian/ glial or intermediate NB‐cell types. Immunohistochemical analysis of CAM expression by NB and related tumors at different stages of differentiation revealed a co‐expression of several CAM (ICAN‐1/CD54, LFA‐3, VLA‐2 and HLA‐ABC) associated with low stages and more highly differentiated NB tumors and peripheral neuroepitheliomas (PN). In contrast, N‐CAM was uniformly expressed on all NB tumors. Flow cytometric analysis of CAM surface expression by SK‐N‐SH and variant cells revealed highly variable phenotypes. Expression of ICAM‐1, LFA‐3, VLA‐2 and HLA‐ABC molecules was associated with the epithelial cell type represented by the SH‐EP variant. In contrast, low expression of these molecules and high expression of N‐CAM was associated with the neuronal SH‐SY5Y cells. Exposure of the NB cells to differentiation inducers (retinoic acid, 5′‐brornodeoxyuridine and phorbol esters) and cytokines (τ‐interferon, α‐tumor necrosis factor) resulted in a variable up‐regulation of the expression of all CAMs, except N‐CAM, regardless of the type of differentiation induced. In an attempt to establish a link between the pattern of expression of CAM on NB cells and their susceptibility to natural killer (NK) or lymphokine‐activated killer (LAK) cell lysis, the analysis revealed that NB cells expressing CAM and a differentiated phenotype were less susceptible to NK lysis, but no difference in the sensitivity of the NB cell types to LAK effectors was observed. Treatment of NB target cells with cytokines or PMA decreased their susceptibility to NK and LAK lysis, while induction of differentiation with RA or BUdR resulted in no changes in the sensitivity to NK and LAK lysis. In conclusion, expression of HLA‐ABC and several co‐regulated CAMs was shown to be associated with a differentiated phenotype in NB, with an overall decreased sensitivity to NK/LAK effector cells. © 1992 Wiley‐Liss, Inc.
Orthotopic and ectopic organ environments differentially influence the sensitivity of murine colon carcinoma cells to doxorubicin and 5‐fluorouracil
Authors: Wilmanns Christoph , Fan Dominic , O'Brian Catherine A. , Bucana Corazon D. , Fidler Isaiah J. 
Published: February 2007

AbstractWe determined the effects of organ environment on the response of murine CT‐26 colon carcinoma cells to 2 structurally and pharmacologically distinct chemotherapeutic agents. CT‐26 cells were injected i.v. (to produce lung lesions), s.c., into the cecal wall, and into the spleen (to produce spleen and liver lesions). Doxorubicin (DXR) at 10 mg/kg, 5‐fluorouracil (5‐FU) at 20 mg/kg, or saline (control) was injected intravenously on different schedules after tumor‐cell implantation. The in vivoresponses of the tumors growing in the cecum, spleen, liver, lung and subcutis were compared. Colon carcinomas growing in the subcutis were most sensitive to DXR. Tumors growing in the spleen and cecum were most sensitive to 5‐FU and less so to DXR. Tumors in the liver were highly resistant to both drugs, whereas experimental lung metastases were sensitive to 5‐FU but resistant to DXR. The differential responses of the tumors to the drugs were not due to drug distribution. The level of protein‐kinase‐C activity was elevated in the spleen, liver and cecum tumors as compared with s.c. tumors and correlated with the in vivo DXR resistance of the tumor cells. This correlation suggested that organ environment may modulate the chemosensitivity of tumor cells, at least in part, by perturbing signal transduction pathways. Collectively, the data indicate that the organ environment has profound effects on the response of tumor cells to chemotherapy. A molecular understanding of this phenomenon should facilitate the design of more effective systemic chemotherapy for cancer metastases. © 1992 Wiley‐Liss, Inc.
Secretion of autocrine growth‐promoting activity by renal‐carcinoma cells treated with 5‐fluorouracil
Authors: Nishimura Naoki , Kanda Shigeru , Yogi Yasuo , Kawamura Masaya , Nakamura Mikio , Hyakutake Hiroyuki , Kanetake Hiroshi , Saito Yutaka 
Published: February 2007

AbstractA study was made of the auto‐proliferative activity of human renal‐carcinoma cells in the supernatant from a carcinoma‐cell culture in serum‐free medium to which an anticancer agent had been added (5‐FU). The human renal‐cancer cells used in this study were of 3 strains: ACHN, VMRC‐RCW and NT. When each line was cultured in medium containing no 5‐FU, the supernatant showed almost no activity for stimulating DNA synthesis. However, when the line was cultured in the presence of 5‐FU, the supernatant showed autocrine growth‐promoting activity which strongly stimulated DNA synthesis of 3 renal‐cancer cell lines in a dose‐dependent manner. Activity could be detected in a 4‐ to 6‐kDa fraction by gel filtration. This fraction increased the DNA‐synthesis‐promoting activity of epidermal growth factor, transforming growth factor‐β, basic fibroblast growth factor and insulin, and was acid‐ and heat‐stable. It was also stable against pepsin and dithiothreitol. DNA synthesis in BALB/c 3T3, adult rat hepatocytes and rabbit renal tubular cells was not affected by this fraction which was thus considered not to affect non‐cancerous cells. Renal‐cell carcinoma responds poorly to anticancer agents, and the autocrine activity of the fraction may possibly be a factor accounting for this resistance. © 1992 Wiley‐Liss, Inc.
Human carcinoembryonic antigen cDNA expressed in rat carcinoma cells can function as target antigen for tumor localization of antibodies in nude rats and as rejection antigen in syngeneic rats
Authors: Pèlegrin André , Terskikh Alexei , Hayoz Daniel , Chalandon Yves , Olsson Nils‐Olivier , Folli Silvio , Buchegger Franz , Kromer Beril , Schwarz Klaus , Martin Monique , Martin Francois , Mach Jean‐Pierre 
Published: February 2007

AbstractWe have tried to develop a new model consisting of rats transplanted with syngeneic colon carcinoma PROb cells transfected with cDNA coding for the carcinoembryonic antigen (CEA), the human tumor marker most commonly used as target for MAbs. The antigenic density of the 4 CEA‐expressing clones selected for a precise characterization ranged from 5 × 104 to 1 × 106 CEA molecules per cell. In all clones the CEA was shown to be attached to the membrane by a phosphatidylinositol (PI) anchor. Using a panel of radiolabeled MAbs directed against the 5 major epitopes described on the CEA molecule, we showed that all these CEA epitopes were expressed by the 4 transfectants. Southern‐blot analysis showed that the entire CEA cDNA was present in the transfectants. Western‐blot analysis, however, showed that the size of the CEA expressed by the 4 transfectants was slightly smaller than that of CEA produced by 2 reference human colon‐carcinoma cell lines. Two clones, expressing 1 × 105 and 1 × 106 CEA molecules per cell, respectively, were grafted s.c. in nude mice and rats. Injection of radiolabeled anti‐CEA F(ab')2 fragments into these animals showed specific tumor localization with the highest percentages of injected doses for the transfectants expressing the highest CEA level. When grafted into immunocompetent syngeneic BDIX rats, the CEA‐expressing clones induced a strong antibody response against CEA and tumor rejections in a majority of the animals. Although the analysis of the immune response against the CEA‐cDNA‐transfected carcinoma cells is under investigation, the present results demonstrate that human CEA could function as a rejection antigen when transfected into rat carcinoma cells. © 1992 Wiley‐Liss, Inc.
Jumping translocations originate clonal rearrangements in SV40‐transformed human fibroblasts
Authors: Hoffschir F. , Ricoul M. , Lemieux N. , Estrade S. , Cassingena R. , Dutrillaux B. 
Published: February 2007

AbstractA comparative study of chromosomal rearrangements occurring in 4 independent clones obtained from SV40‐transformed cornea and skin human fibroblasts was performed. Rearrangements principally affect some constitutive heterochromatin and, to a lesser degree, telomeric regions. This results in multiple exchanges between a limited number of chromosome structures, i.e., in jumping translocations. Such rearrangements occur even at early passages and some of them give rise to clonal rearrangements that accumulate at late passages. This process is responsible for progressive modification of the karyo‐types, principally characterized by deletion of a number of chromosome segments. Thus, clonal rearrangements are selected among many others not occurring at random. The selective pressure retaining clonal rearrangement seems to be similar for the 4 independent clones, since selection of the derivative chromosomes leads to the same imbalances, whatever the origin of the clone. This sequence of events recalls that of human solid tumors, since jumping rearrangements are generally observed in pre‐malignant conditions or in low‐grade malignancies, whereas clonal rearrangements leading to typical imbalances are detected in more advanced malignant tumors. © 1992 Wiley‐Liss, Inc.
Effect of MHC class‐I transfection on local tumor growth and metastasis in an H‐2‐negative clone derived from a chemically induced fibrosarcoma
Authors: Mialdea M. J. , Martin J. , Gaforio J. J. , Algarra I. , Pérez M. , Gonzalez A. , Ljunggren H. G. , Garrido F. 
Published: February 2007

AbstractGR9 is a chemically induced fibrosarcoma composed of clones with different H‐2 class‐I expression. These clones differ with respect to local growth and spontaneous metastasis. The B9 clone (H‐2 negative) is highly tumorigenic (local growth) but of low metastatic potential (spontaneous metastasis assay). We have analyzed the effect that transfection of H‐2Dd and H‐2Kdgenes on this clone have upon local growth, lung colonization after i.v. injection and ability to form spontaneous metastases. The results showed that the effect on local growth of transfection of the Kd‐gene was stronger than that of the Dd gene. In addition, B9 co‐transfected with H‐2Kd and Dd genes showed the highest immunogenic properties in syngeneic BALB/c mice. Interestingly, the pSV2‐neo transfected clone gave almost the same result as that obtained with Dd transfection. Lung colonization after i.v. injection of the different clones (experimental metastasis), paralleled the results obtained for local growth: the number of lung nodules followed the cadence KdDd < Kd < Dd < pSV2. Survival of mice was always inversely correlated with local growth, e.g., all mice injected with 5 × 105 B9 H‐2KdDdtransfected cells survived. In contrast, no mice injected with the B9 control did. These differences were abrogated in irradiated and nude BALB/c mice. Finally, all transfected clones remained non‐metastatic in a spontaneous metastasis assay, behaving as the control, non‐transfected B9 cells. © 1992 Wiley‐Liss, Inc.
p53 over‐expression is an early event in the development of human squamous‐cell carcinoma of the larynx: Genetic and prognostic implications
Authors: Dolcetti Riccardo , Doglioni Claudio , Maestro Roberta , Gasparotto Daniela , Barzan Luigi , Pastore Antonio , Romanelli Massimiliano , Boiocchi Mauro 
Published: February 2007

AbstractThe tumor‐suppressor protein p53 is over‐expressed in a large fraction of squamous‐cell carcinomas of the larynx (LSCCs). p53 overexpression is dependent upon the synthesis of mutated versions of the protein and has been associated with the malignant progression of certain tumor types. In order to examine the prognostic value of p53 immunodetection in LSCCs, we performed a retrospective analysis on a selected series of tumors, using the PAb 1801 and CMI antibodies. No significant difference in the frequency of p53 over‐expression was observed between tumors from patients with early relapse (67%) and those who had been disease‐free for more than 5 years (84%). The lack of correlation of p53 immunoreactivity with clinical stage and differentiation grade of LSCCs, together with the coordinated expression of pS3 in primary tumors and the corresponding lymph‐node metastases, indicate that p53 over‐expression is probably unrelated to the biological aggres‐siveness of these tumors. In addition, the detection of p53 immunostaining in pre‐invasive areas as well as in preneoplastic lesions suggests that p53 abnormalities probably constitute a very early event in LSCC development. © 1992 Wiley‐Liss, Inc.
pS2 protein and steroid hormone receptors in invasive breast carcinomas
Authors: Koerner Frederick C. , Goldberg Diane E. , Edgerton Susan M. , Schwartz Laurent H. 
Published: February 2007

AbstractWe have used immunohistochemical and hormone‐binding techniques to determine the presence of estrogen receptors, estrogen‐receptor protein, progesterone receptors and pS2 protein in 97 invasive breast cancers. Our group of tumors displayed the same frequency of estrogen receptors and progesterone receptors as other comparable groups, but it contained more tumors containing pS2 protein. We also observed staining of morphologically normal cells in lobules adjacent to the tumors and in several fibroadenomas; both findings vary from some other reports. We attribute these variations to the use of a sensitive immunohistochemical method and choice of the lowest possible threshold to classify a tumor as pS2‐positive. If we used a higher threshold, then about 95% of the tumors containing pS2 protein also contained estrogen receptor protein. Our results add further weight to the assertion that tumors containing pS2 protein also display estrogen receptors. The data also provide theoretical and indirect support to the clinical prediction that tumors containing pS2 protein are more likely to respond to hormonal therapy and may have a more indolent course than tumors lacking the molecule. © 1992 Wiley‐Liss, Inc.
Progression of human cutaneous melanoma is associated with loss of expression of c‐kit proto‐oncogene receptor
Authors: Natali P. G. , Nicotra M. R. , Winkler A. B. , Cavaliere R. , Bigotti A. , Ullrich A. 
Published: February 2007

AbstractMutations at the white spotting (w) locus in mice have deleterious effects on germ cells, melanocytes and hematopoietic stem cells. The w locus encodes the c‐kit tyrosine‐kinase receptor whose ligand is the product of the SI locus. Using monoclonal antibodies (MAb(s) ) to the extracellular domain, we have evaluated the expression of c‐kit in normal and transformed melanocytes. This cell lineage synthetizes a receptor with a mw of 145 kDa. The gene product is expressed in epidermal melanocytes and in a fraction of nevocytic and blue nevi. In primary melanomas, loss of the receptor is observed in more invasive lesions. Only 30% of the metastatic lesions express detectable levels of the receptor. These findings demonstrate that the c‐kit product is down‐regulated in melanocytes following malignant transformation. The functional relevance of this modulation remains to be evaluated. © 1992 Wiley‐Liss, Inc.
Phenotypic overlaps between pleomorphic malignant T‐cell lymphomas and mixed‐cellularity Hodgkin's disease
Authors: Tosi Piero , Leoncini Lorenzo , del Vecchio Maria Teresa , Spina Donatella , Lorenzini Letizia , Barbini Paolo , Massai Maria Rita , Pileri Stefano , Sabattini Elena , Kraft Rainer , Cottier Hans 
Published: February 2007

AbstractHistologically diagnosed, or in part questionable, malignant pleomorphic peripheral T‐cell lymphomas (pPTCLs, n = 16) and mixed‐cellularity Hodgkin's disease (MCHD, n = 12) were objectively compared by the use of combined immunohistochemistry on paraffin sections, test‐point analysis of tissue components, and semi‐automated nuclear morphometry on semi‐thin resin sections. Classical, qualitative histomorphological distinction of these sub‐types of lymphomas proved to be valid and is probably still the best method. Quantitative discriminant features, in order of decreasing significance, were: (i) expression by large atypical cells (LACs) of CD45RO, CD43 and CD45 in pPTCLs, and of CD30 and GD15 in MCHD; (ii) means and standard deviations (SDs) of LAC nuclear‐profile areas (greater in MCHD than in pPTCLs); (iii) expression of CD3 by LACs in pPTCLs; (iv) prominence of small lymphoid cells in MCHD; (v) higher percentage of medium‐sized lymphoid cells in pPTCLs; and (vi) higher SDs of nuclear‐profile circularity factor of small lymphoid cells in MCHD. The medians of the largest nucleolar profile areas in LACs per field did not differ in pPTCLs and MCHD, but dispersion of individual values towards higher levels was significantly greater in the latter. Stepwise discriminant analysis of test point and nucleometric variables that best distinguished pPTCLs from MCHD revealed considerable overlaps, and questionable cases tended to be intermediate between the two. In conclusion, our results confirm and expand the notion of intra‐group heterogeneity, with indistinct borders and the existence of intermediate phenotypes between these two taxonomic categories of malignant lymphomas. © 1992 Wiley‐Liss, Inc.
Expression of HER‐2/neu in renal‐cell carcinoma. Correlation with histologic subtypes and differentiation
Authors: Rotter Michael , Block Thomas , Busch Raymonde , Thanner Stefanie , Höfler Heinz 
Published: February 2007

AbstractTwenty‐four renal‐cell carcinomas (RCC) and corresponding non‐neoplastic kidney tissue were examined for amplification and expression of the HER‐2/neu gene. Gene amplification was examined by slot‐blot analysis, mRNA expression by in situ hybridization and Northern blot analysis, and protein expression by immunohistochemistry. Northern‐blot analysis revealed lower expression of HER‐2/neu mRNA in clear‐cell (p < 0.001) and compact (p < 0.001) tumor subtypes, while chromophilic, chromophobic and tubulo‐papillary subtypes did not show significant differences in HER‐2/neu gene expression, as compared with non‐neoplastic kidney tissues. HER‐2/neu gene expression was not significantly associated with tumor stage. Low differentiation (G3) was associated with lower HER‐2/neu gene expression, but the number of G3 cases was too small for statistical analysis. HER‐2/neu gene amplification was not found in any of the tumors. The results of in situ hybridization and immunohistochemistry generally agreed with those of Northernblot analysis. We conclude that HER‐2/neu gene expression correlates with Thoenes' classification of RCC and may be inversely related to tumor differentiation; it is probably not involved in progression of RCC, in contrast to carcinomas of other locations (e.g. breast, ovary). © 1992 Wiley‐Liss, Inc.