bluuebunny/crossref_metadata_2025_split huggingface dataset:
Occurrence of a fetal fibroblast phenotype in familial breast cancer
Authors: Schor S. L. , Haggie J. A. , Durning P. , Howell A. , Smith L. , Sellwood R. A. S. , Crowther D. 
Published: February 2007

AbstractWe have previously shown that fetal and adult human skin fibroblasts display distinctive migratory phenotypes when cultured on 3‐dimensional collagen gels in vitro. In the present study, we have used this information to assess the migratory behavior of fibroblasts obtained from patients with either benign or malignant breast disease, and correlated this with the presence of a family history of breast cancer. We have observed that fibroblasts from 17/34 patients with no previous family history of breast cancer displayed fetal‐type behavior in our assay system; in contrast, fibroblasts from 15/16 patients with a positive family history of breast cancer behaved abnormally. This apparently increased probability of expressing a fetaltype migratory phenotype in the patients with a family history is statistically significant (p > 0.008). Skin fibroblasts obtained from 2 healthy and unaffected first‐degree relatives (one male and one female) of patients with a family history of breast cancer also exhibited a fetal‐type migratory phenotype.
A case‐control study of dietary factors and stomach cancer risk in Poland
Authors: Jedrychowski W. , Wahrendorf J. , Popiela T. , Rachtan J. 
Published: February 2007

AbstractWe report results from a case‐control study on stomach cancer conducted in 1980–81 in Cracow, Poland, where the risk of this disease is among the highest reported world‐wide. One hundred and ten cases from a surgical clinic were matched by age and sex to the same number of controls from the same hospital. A matched series from a population‐based health survey was also considered. After adjusting for residency, smoking and various food items, cases and hospital controls showed significant differences in consumption of fruits (RR rarely vs. daily: 3.24; 95% Cl: 1.56–6.77), joint consumption of vegetables, salads and fruits (RR low vs. high: 4.23; 95% Cl: 1.41–12.63), and consumption of protein‐containing foods (RR low vs. high: 0.23; 95% Cl: 0.08–0.61). Consumption of strong alcoholic beverages on an empty stomach (before breakfast) was associated with an RR of 2.09 (1.04–4.22). The findings are discussed in relation to the apparent urban/rural difference in stomach cancer incidence in Poland and the possible underlying etiological factors involved.
A monoclonal antibody cibr17 recognizes a myoepithelium‐specific antigen in human mammary gland
Authors: Dempsey Peter J. , de Kretser Theonne A. , Brown Robert W. , Whitehead Robert H. , Jose David G. 
Published: February 2007

AbstractA murine monoclonal antibody (MAb) CIBr17, raised against the human breast carcinoma cell line PMC42, reacts specifically with myoepithelial cells in normal human breast. This IgGI antibody recognizes a ∼ 110kDa glycoprotein that is expressed on the cell surface and junctional membranes of PMC42 mono‐layer cultures. The CIBr17 antigen is present in two major glycosylated forms with approximate pls of 5.2 and 5.5 respectively in PMC42 cells. The tissue specificity of CIBr17 was assessed on frozen sections of PLP‐fixed tissues by means of a 4‐layer immunoperoxidase technique. CIBr 17 has reacted with a variety of epithelium‐derived tissues and some smooth muscle cells. Within many epithelial tissues, CIBr17 has demonstrated specific staining of particular epithelial cell types. Within normal breast and most benign breast lesions, antibody CIBr17 stained only myoepithelial cells. No staining of luminal epithelium, basement membranes or stromal elements was observed. In sclerosing adenosis, CIBr17 stained areas of pronounced myoepithelial differentiation, while in duct epitheliosis variable staining of proliferating cells was observed. In breast carcinomas, CIBr17 demonstrated variable antigen expression. In most tumors, CIBr17 either did not stain any tumor cells or stained only a small number of tumor cells spread randomly throughout the tumor. In several ductal carcinomas, however, CIBr17 stained the majority of tumor cells.
Products of cells cultured from gliomas. IV. Extracellular matrix proteins of gliomas
Authors: McKeever Paul E. , Fligiel Suzanne E. G. , Varani James , Hudson Jerry L. , Smith David , Castle R. Lynn , McCoy J. Philip 
Published: February 2007

AbstractFive primary and 3 established human glioma cell lines were cultured with ascorbate and examined for expression of extracellular matrix components. All lines except C6 expressed collagen as assessed by silver impregnation, immunofluorescence and lectin staining and expressed laminin and fibronectin. None expressed a lectin marker for endothelial cells. Both epithelial and mesenchymal collagens were expressed. While extracellular components of glioma lines resembled those of fibroblasts more closely than other cell types, subtle differences between gliomas and fibroblasts were present. These included more laminin and collagen type‐IV antigenic reactivity and more 11–12 nm diameter extracellular fibrils from individual gliomas, and slight differences in spectra of low‐molecular‐weight extracellular proteins assessed by gel elec‐trophoresis. One primary and two established glioma lines analysed for DNA content were aneuploid in contrast to diploid fibroblasts. Simultaneous expression of mesenchymal and epithelial markers suggests a dual differentiation potential of glioma cells. Results do not support an endothelial origin for cells cultured from gliomas.
Suppression of tumorigenicity by the cell‐cycle‐dependent control of cellular differentiation and proliferation
Authors: Wille John J. , Scott Robert E. 
Published: February 2007

AbstractThe experiments described in this report were designed to determine if suppression of tumorigenicity can be mediated by cell‐cycle‐dependent mechanisms that control cellular differentiation and/or proliferation in mesenchymal stem cells of the 3T3 T type. These cells were employed because they possess distinct, well‐characterized cell‐cycle‐dependent mechanisms to control both cellular differentiation and proliferation. To achieve our goal we developed by non‐mutagenic procedures 23 clonal variants of 3T3 T stem cells that expressed one of 4 distinct phenotypes for the regulation of cellular differentiation and proliferation. Six clones expressed combined defects in the control of differentiation and proliferation; 6 expressed intact mechanisms to control proliferation but defects in the control of differentiation; and 3 expressed intact mechanisms to control differentiation but defects in the control of proliferation. Finally, 8 clones expressed no detectable phenotypic defects in the control of either differentiation or proliferation. Once isolated and characterized, each of these clones was assayed for its tumorigenic potential. The results establish that clones which express combined defects in the control of differentiation and proliferation are highly tumorigenic. By contrast, tumorigenicity is markedly suppressed in clones that maintain the ability to control their proliferation or their differentiation. Furthermore, clones that maintained the ability to control both proliferation and differentiation showed no evidence of tumorigenicity. These data are interpreted to suggest that stringently regulated control of cellular differentiation and/or proliferation can act as a cancer suppressor mechanism.
A radiobiological comparison of human tumor soft‐agar clonogenic assays
Authors: West Catharine M. L. , Sutherland Robert M. 
Published: February 2007

AbstractRadiation survival curves have been generated for 3 human tumor cell lines as a means of comparing and evaluating the validity of human tumor soft‐agar clonogenic assays. The assays investigated were the Hamburger‐Salmon, Courtenay‐Mills, Courtenay‐Mills plus additions, soft agar (no additions), and soft agar plus additions. The additions were formulated to supplement the media used in soft agar assays of primary ovarian and cervical carcinoma specimens. Supplementing the media with additions led to a 2‐ to 3‐fold increase in PE of CaSki cells but had no effect on the PEs of ME180 and OWI cells. Radiation survival curves were similar in all assays for CaSki and OWI but differed for ME180 cells. For ME180 cells, the Courtenay‐Mills and soft agar assays plus additions produced the most radioresistant curves (Do = 2.2 Gy); the cells were more responsive when assayed by the Hamburger‐Salmon method (Do = 1.5 Gy), and the soft agar and Courtenay‐Mills assays gave the most radiosensitive curves (Do = 1.2 Gy). These results demonstrate that the PE of human tumor cell lines may be increased with no effect on radiation survival; radiation survival may be altered without changes in PE and neither may be altered by applying modifications and supplements to existing clonogenic assays.
Augmentation of B16 melanoma lung colony formation in C57BL/6 mice having marked granulocytosis
Authors: Ishikawa Makoto , Koga Yutaka , Hosokawa Masuo , Kobayashi Hiroshi 
Published: February 2007

AbstractThe effect that polymorphonuclear leukocytes (PMN) may have on the metastatic colonization of tumor cells is controversial: some laboratories have reported that PMN can inhibit metastasis whereas others have shown an augmentation effect. We have exploited our finding that a particular fibrosarcoma (BMT‐II) transplanted subcutaneously into syngeneic C57BL/6 mice induces a progressive increase in the number of circulating PMN, to re‐examine this question. We used such “granulocytosis‐positive” mice as recipients of B16 melanoma cells to examine the influence of significant granulocytosis on the level of lung tumor colonies. The number of B16 melanoma lung colonies detected after intravenous (i.v.) injection was significantly higher in BMT‐II tumor‐bearing mice with granulocytosis than in control (non‐tumor‐bearing) mice. Retention of 125IUdR‐labelled B16 cells 24 hr after the i.v. injection was 3 to 10 times greater in mice with granulocytosis than in controls. Either simultaneous injection, or preinjection of PMN with B16 cells, increased the lung‐colonizing capacity of B16 melanoma cells. These results suggest that abnormally increased numbers of PMN in the peripheral blood, particularly in the lung circulation, can enhance the ability of tumor cells to colonize or metastasize.
Cancer incidence in Murcia, Spain, in 1982: First results from a population‐based cancer registry
Authors: Navarro Carmen , Perez‐Flores Domingo , Coleman Michel P. 
Published: February 2007

AbstractThis report presents the first findings of the Murcia Cancer Registry, a population‐based cancer registry set up in May 1981 in the Murcia region of southeast Spain (955,487 inhabitants). Descriptive epidemiological methods have been applied to study cancer incidence in 1982. The validity of cancer registration has been assessed for both completeness and accuracy. Altogether 1,987 cases were registered in 1982, the crude (all‐ages) annual incidence rates per 100,000 being 238 in males and 179 in females. Excluding non‐melanoma skin cancer, which seems to be incompletely registered, age‐standardized rates for Murcia are very similar to those of other registries in Spain in males, but lower in females. The risk was higher in males than in females for all sites and for the great majority of specific sites, especially larynx, oesophagus and bladder. The age‐standardized rate for cancer of the larynx was 26 times higher in men than in women. Lung cancer was the most common cancer in males: the risk was 8 times that in females. Lung cancer rates were higher, in both males and females, than in other Spanish registries. Cancer of the larynx was the second most common site in males when either truncated rates (35–64 years) or cumulative incidence rates up to 64 years of age were used. The age‐standardized rate (18 per 100,000) supports previous studies suggesting that the risk for this cancer in Spain and other Mediterranean countries is very high. The lung/larynx rate ratio in men was two. Cancer of the breast is the most common cancer among women, as in other registries in Spain and in most other countries. The age‐standardized rate (29.4 per 100,000) is lower than breast cancer rates elsewhere in Spain. This difference may be partly explained by incompleteness of ascertainment in Murcia. The incidence rate for cancer of the cervix uteri was 4.9 per 100,000, excluding carcinoma in situ. Despite the limitations of the data, cervical cancer incidence in Murcia is likely to be similar to that in other regions of Spain.
Characteristics of a cell line established from a patient with multiple osteosarcoma, appearing 13 years after treatment for bilateral retinoblastoma
Authors: Fodstad Øystein , Brøgger Anton , Bruland Øyvind , Solheim Oyvin P. , Nesland Jahn M. , Pihl Alexander 
Published: February 2007

AbstractAn osteosarcoma cell line, OHS, was established from a patient with multiple skeletal manifestations of osteosarcoma, developing after bilateral retinoblastoma. The tumor cells expressed sarcoma‐associated antigens and showed rapid growth in monolayers and as multicellular spheroids. They formed distinct colonies in soft agar, and subcutaneous tumors in nude mice. Morphological studies indicated that OHS cells had retained important characteristics of the cells of origin. No deletion of the retinoblastoma genes on chromosome 13q 14 could be demonstrated with the banding techniques used. However, cytogenetic studies revealed double minute chromosomes, as evidence of gene amplification, as well as translocations involving chromosomes 1,6,11 and 13. The OHS line can be used to study the genetic basis of tumor initiation and growth, and to elucidate factors predisposing for second primary cancers in retinoblastoma patients.
Studies in healthy human T‐cell‐leukemia lymphoma virus (HTLV‐I) carriers from the Caribbean
Authors: Matutes E. , Dalgleish A. G. , Weiss R. A. , Joseph A. P. , Catovsky D. 
Published: February 2007

AbstractSix healthy relatives of 3 adult T‐cell leukemia lymphoma (ATLL) patients and 6 members of a Caribbean family immigrant to the UK have been investigated for the presence of HTLV‐I and expression of interleukin 2 (IL‐2) receptors. Serum antibodies to HTLV‐I were detected in all but 4 samples. Four to 10% of circulating cells from 3/4 seropositive donors studied displayed IL‐2 receptors (anti‐Tac+) and were shown to be convoluted lymphocytes by light microscopy morphology and immunoelectronmicroscopy. After 5 to 28 days in culture, cells from 4 seropositive donors reacted with monoclonal antibodies (MAbs) against the HTLV‐I core proteins, p19 and p24, and released retrovirus particles. Similar experiments with blood from 3 seronegative donors from the same families and 4 normal controls proved negative. Our findings indicate that seropositive individuals harbour the virus in a population of T‐lymphocytes which may then acquire receptors for IL‐2. These individuals are at risk of developing ATLL.
The epithelial cell surface antigen 17–1A, a target for antibody‐mediated tumor therapy: Its biochemical nature, tissue distribution and recognition by different monoclonal antibodies
Authors: Göitlinger Heinrich G. , Funke Ilona , Johnson Judith P. , Gokel Josef M. , Riethmüller Gert 
Published: February 2007

AbstractThe antigen defined by MAb 17–1A, raised against colorectal cancer cells and currently used in immuno‐therapy trials, is a 37 kDa protein containing N‐linked glycans as demonstrated by inhibition of glycosylation with tunicamycin. The 17–1A antigen (17–1A Ag) is broadly distributed in normal epithelial tissues and is also found in various types of carcinoma. Quantitative differences in expression between normal and malignant tissues were only apparent in gastric carcinomas. After immunizing mice with fresh colon carcinoma tissue, 4 MAbs were obtained that showed the same tissue reaction pattern as MAb 17–1A and recognized the 17–1A Ag as judged from precipitation and immunoblotting experiments. MAbs M72 and M74 reacted with an anti‐idiotypic serum directed against the original MAb 17–1A and were able to block 17–1A binding. In contrast, M77 and M79 are directed against a different epitope. This makes them potentially interesting for passive immunotherapy in regimens involving a combination of MAbs.
Enhancement of experimental metastasis by pretreatment of tumour cells with hydroxyurea
Authors: McMillan T. J. , Rao J. , Hart I. R. 
Published: February 2007

AbstractThe effect of treatment with hydroxyurea (HU), on subsequent experimental metastasis formation by cells of 3 murine melanoma lines has been examined. In vitro treatment of B16‐F1, B16‐F10and K‐1735‐clone 19 cells with 0.1 mM or 0.3mM HU, followed by a period of recovery in drug‐free medium, resulted in a significant increase in the number of lung nodules formed in syngeneic mice following i.v. injection of the cells. The maximum effect obtained was observed when cells were injected 6 hr after removal of HU and it occurred in spite of the cytotoxicity of the doses used. Six hours after release from treatment with 0.3 mM HU cells were synchronized in the G2 phase of the cell cycle but the consequent increase in cell volume was not responsible for increased metastasis through enhancement of tumour‐cell arrest, since lodgement of 51Cr‐labelled, HU‐treated cells was no greater than that of control cells. The results obtained suggest that the chemotherapeutic agent HU may facilitate tumour progression via a direct action on neoplastic cells.
Expression of protooncogenes in murine osteosarcomas
Authors: Schön A. , Michiels L. , Janowski M. , Merregaert J. , Erfle V. 
Published: February 2007

AbstractThe expression of 7 protooncogenes (c‐sis, c‐abl, c‐mos, c‐bas, c‐Ki‐ras, c‐fos, c‐myc) was examined in transplants and established cell lines from spontaneous and radiation‐induced murine osteosarcomas. The transplant tumors were compared with different tissues, particularly skeletal tissue (sternum), and the osteosarcoma cell lines with fibroblast lines from the same mouse strains. C‐sis was expressed above the level of controls in 2 osteosarcomas (TV, Os5). Three osteosarcomas showed over‐expression of c‐abl (TVK, DOS, Os5), c‐bas (DOS, Os5 and V893) and c‐fos (TVK, DOS, Os5), and 4 osteosarcomas showed over‐expression of c‐Ki‐ras (TVK, DOS, Os5, Os16) and c‐myc (TVK, DOS, TV, Os5). C‐mos expression was not observed under the conditions used. One cell line (Os5) showed an altered transcript (1 kb transcript of c‐fos). Apart from the relatively frequent increase in expression of the c‐myc and c‐ras‐family, there was no indication that any particular protooncogene or combination of protooncogenes was associated with murine osteosarcomas.
Gut‐associated lymphoid tissue and 1,2‐dimethylhydrazine intestinal tumors in the rat: An histological and immunoenzymatic study
Authors: Martin M. S. , Hammann A. , Martin F. 
Published: February 2007

AbstractThe association between chemically‐induced intestinal carcinoma and gut lymphoid patches was studied in 20 male Sprague‐Dawley rats 7 months after the first of 16 weekly injections of 1,2 dimethylhydrazine (DMH). The lymphoid patches of DMH‐treated rats and of 14 untreated control animals were systematically studied histologically on sections of “swiss‐rolled” whole intestine. It was found that 78% of the small‐intestine carcinomas and 73% of the colorectal carcinomas were associated with intestinal lymphoid patches. Furthermore, misplaced and often atypical glandular crypts were often found in the parafollicular or interfollicular areas of lymphoid patches, in treated as well as in control animals. These glands could be the origin of the lymphoid‐patch‐associated carcinoma. Immunohistological staining with monoclonal antibodies (MAbs) against T‐lymphocyte antigens or anti‐IgM serum labelling B lymphocytes clearly localized early carcinoma and atypical glands in the T‐dependent, interfollicular and parafollicular area of lymphoid follicles. An MAb directed against la‐antigen stained some well‐differentiated carcinomas and some atypical glands found in control rats. On the other hand, lymphoid patches, when not invaded by a carcinoma, were not modified in their number, size, morphology or cellular composition in DMH‐treated rats as compared to control animals.
Post‐exposure treatment with monoclonal antibodies in a retrovirus system: Failure to protect cats against feline leukemia virus infection with virus neutralizing monoclonal antibodies
Authors: Weijer Kees , Uytdehaag Fons G. C. M. , Jarrett Oswald , Litz Hans , Osterhaus Albert D. M. E. 
Published: February 2007

AbstractWe have attempted to protect kittens against oronasal infection with FeLV (strain A/Glasgow‐I) by treatment with a mixture of two virus‐neutralizing (VN) MAbs (IgGI, K) directed against the same epitope of the viral glycoprotein gp70. Ten SPF 9‐week‐old kittens were infected on day 0 with 106 ffu FeLV and subsequently inoculated i.m. with MAbs every 2 days over a 20‐day period at different times after infection. The results clearly show that no protection was achieved. It is unlikely that the amount of VN antibodies, the mode and route of their application or the infectious dose of FeLV used can account for the failure to protect cats against infection. Other possibilities which may explain the lack of protective effect are that (i) the restricted epitope specificity of the MAb preparation used may have led to selection of neutralization‐resistant virus mutants, or that (ii) other mechanisms than virus neutralization (complement‐mediated lysis, antibody‐dependent cell cytotoxicity), that may be involved in protection, function less efficiently with MAb. However, in the light of our finding that an early anti‐idiotypic response is observed in all cats following administration of the MAb preparation, the rapid clearance of anti‐FeLV MAb from the circulation is a more likely explanation. The data presented support our hypothesis that by administration of MAb—as compared to polyclonal antibody—a more vigorous anti‐idiotypic response is elicited due to the presentation of only a limited set of idiotopes. This potential drawback of rapid clearance of MAbs as a consequence of an anti‐idiotypic response might be overcome by the use of mixtures of MAbs resulting in a more heterogeneous set of idiotypic determinants.
Molecular expression of epitopes recognized by monoclonal antibodies HMFG‐1 and HMFG‐2 in human breast cancers: Diversity, variability and relationship to prognostic factors
Authors: Turnbull J. E. , Baildam A. D. , Barnes Diana M. , Howell A. 
Published: February 2007

AbstractEpitopes recognised by the monoclonal antibodies HMFG‐1 and HMFG‐2 are found on glycoprotein components in human breast cancers. This study used immunobiotting techniques to ascertain their molecular diversity, assess their relationship to known prognostic factors, and investigate their expression in sequential samples of breast tumours from individual patients. Both epitopes were expressed on components of a wide variety of molecular weights (HMFG‐1, 130 to 450kDa; HMFG‐2,90 to 450kDa). The HMFG‐2 epitope was expressed more frequently on components of <200kDa (p < 0.0001). Progesterone receptors (PR), small tumour size and low histological grade correlated significantly with HMFG components ⩾300kDa. Higher staining intensity was associated with increased likelihood of PR positivity. Paired sequential samples were taken, with a median interval of 8 days, from 38 patients, 23 of whom were administered tamoxifen. In the majority of tumours profiles of expression of components carrying the epitopes were identical in both samples (HMFG‐1, 30/38; HMFG‐2, 22/38). Overall the results suggested that there was no consistent relationship between the differences observed and tamoxifen administration. We conclude that expression of the HMFG‐1 and HMFG‐2 epitopes is relatively constant in most tumours, but variable (and possibly subject to modulation) in others, and that their expression, particularly on high molecular weight components, is related to factors associated with good prognosis (PR, small size, low grade), and may be of independent prognostic value.