bluuebunny/crossref_metadata_2025_split huggingface dataset:
Alteration of the extracellular matrix of cultured human keratinocytes by transformation and during differentiation
Authors: Brown Keith W. , Parkinson E. Kenneth 
Published: February 2007

AbstractWe have investigated the production of 3 extracellular matrix proteins (fibronectin, laminin and entactin) and glycosaminoglycans (GAGs) by keratinocytes derived from human squamous‐cell carcinomas (SCCs). All the SCC lines retained the ability to synthesize fibronectin, laminin and entactin, and to incorporate them into an extracellular matrix. In some of the SCC lines fibronectin production was higher than in normal keratinocytes, and in most lines laminin production was equal to or higher than that seen in normal keratinocyte strains. All the tumorigenic SCC lines produced less entactin than normal keratinocytes. Five out of 7 SCC lines showed a shift in GAG production compared with normal keratinocytes, so that in these lines heparan sulphate was the major GAG as opposed to hyaluronic acid in the normal keratinocytes. As these changes could have been a consequence of the reduced differentiation found in the SCC lines, we fractionated normal keratinocytes into 4 size classes corresponding to different stages of differentiation, using Percoll gradient centrifugation. It was found that the ability to produce these extracellular matrix glycoproteins and GAGs was lost as keratinocytes terminally differentiated. However, this did not explain the matrix changes seen in the SCC lines, since the undifferentiated normal keratinocytes produced a normal pattern of extracellular matrix components. Nonetheless, the loss of extracellular matrix production may well explain the reduction in substratum adhesiveness which occurs as keratinocytes terminally differentiate.
Down‐regulation of peripheral blood cell interferon receptors in chronic myelogenous leukemia patients undergoing human interferon (HuIFNα) therapy
Authors: Maxwell Beth Lynn , Talpaz Moshe , Gutterman Jordan U. 
Published: February 2007

AbstractOur interest in studying interferon (IFN) receptor activity in peripheral blood cells (PBCs) from patients with chronic myelogenous leukemia (CML) receiving therapeutic doses of partially purified leukocyte IFN (IFNα) stems from a need for more adequate monitoring of IFN therapy. The binding of 35S‐labelled recombinant DNA‐derived leukocyte clone A IFN (35SrlFNαA) to PBCs from 8 patients with CML was determined before and during IFNα treatment. The patients′ mean pretherapy binding level (0.049 femtomoles of bound 35S‐rlFNαA) was in the range of values obtained from 4 normal donors (mean of 0.054 femtomoles bound). Within 24 hr of the first IFNα dose, the mean femtomoles bound decreased 10‐fold and remained low during the course of IFNα treatment. In I/I patient, we demonstrated that this decreased binding was due to a loss in number of IFN receptors. The apparent number of receptors after 5 doses of IFNα decreased from approximately 600 receptors per cell at pretherapy to approximately 75 receptors per cell, with no difference in the dissociation constants (1.13 × 10−10M, 0.968 × 10−10M, before and during treatment, respectively). In 4/4 patients, we demonstrated indirectly that the decreased binding was not due to receptor saturation as a result of residual circulating IFNα. In 3/3 patients, we demonstrated a gradual recovery of binding capacity after incubating the patients′ PBCs at 37°C. Within 2–7 days in vivo recovery of binding, comparable to pretherapy levels, was observed in 3/3 patients whose IFNα therapy was discontinued. Combining all these data, we conclude that in both responding and nonresponding patients with CML, IFNα exposure induces decreased binding of labelled IFN when a single recombinant DNA‐derived IFN species is used. We feel the supporting data indicate that the decreased binding capacity may be due to receptor down‐regulation. In the limited number of patients studied thus far, there was no correlation between clinical hematologic response and occurrence of down‐regulation, however, down‐regulation of cell surface receptors may be required to sustain a biological effect. Further studies of both the kinetics of down‐regulation and activation of key enzyme systems are required to fully evaluate the relevance of these findings.
Phenotypic dynamics of tumor progression in human malignant melanoma
Authors: Bröcker Eva‐Bettina , Suter Ludwig , Brüggen Josef , Ruiter Dirk J. , Macher Egon , Sorg Clemens 
Published: February 2007

AbstractThe phenotypic changes in human melanoma cells during the course of tumor progression were studied with monoclonal antibodies (MAbs) against the melanoma‐associated antigens (MAA) M.2.2.4, H.2.8.10, K.1.2, A.1.43, and A.10.33, and HLA‐(A.B.C and D). Cryostat sections of 172 primary melanomas of the skin, 157 melanoma metastases and 56 nevi were investigated with an indirect immunoperoxidase method. Phenotypic heterogeneity was observed within lesions at all stages, and also within different tumors of the same patients. Despite this heterogeneity, principles of antigen expression were found. From the reaction pattern of MAbs, the following classifications of antigens were derived: “constitutive” markers of nevomelanocytic cells (M.2.2.4 and H.2.8.10) were found expressed over a wide range of local and systemic tumors. One MAA. K.I.2 (Suter et al., 1985), hat declines with progression of melanoma, was classified as an “early” antigen, whereas MAA that appear in primary melanoma in proportion to invasiveness, and which are expressed in metastases of lymph nodes and visceral organs (A.I.43, and A.10.33), were classified as „late”︁ markers of tumor progression. HLA‐antigens were classified as „intermediate”︁ markers, HLA‐A,B,C, as an „early‐intermediate”︁, and HLA‐DR as a „late‐intermediate”︁ marker. The occurrence of class II HLA, A.I.43‐, and A.10.33‐positive tumor cells in primary melanoma indicates a high metastatic potential of tumors, independent of tumor thickness. The data show that local and systemic progression of melanoma is associated with qualitative changes in tumor cells which can be recognized by MAbs.
Serum micronutrient levels in relation to gastric pathology
Authors: Haenszel William , Correa Pelayo , López Alfredo , Cuello Carlos , Zarama Guillermo , Zavala Diego , Fontham Elizabeth 
Published: February 2007

AbstractAs part of an ongoing cohort study of gastric cancer precursors in Narino, Colombia, blood levels of ascorbic acid, vitamin E, retinol, pre‐albumin, retinol binding protein and carotenoids were measured and correlated with histopathologic findings of gastric biopsies. Carotene levels in both sexes and vitamin E levels in males were significantly lower in subjects with gastric dysplasia than in subjects with normal mucosa and subjects with less advanced gastric lesions (chronic atrophic gastritis and intestinal metaplasia). No other significant correlations were found.
Case control study of cervical cancer in Herrera Province, Republic of Panama
Authors: Reeves William C. , Brinton Louise A. , Brenes Maria M. , Quiroz Evelia , Rawls William M. , De Britton Rosa C. 
Published: February 2007

AbstractA previous survey found the average annual age‐adjusted incidence of cervical cancer in Herrera Province, Panama, to be 79/100, 000, exceeding any other reported world rate. In an effort to clarify the reasons for this excessive occurrence, a case‐control study was conducted among patients diagnosed between 1974‐1980. Sixty‐six percent of cervical cancer patients from Herrera Province were alive and were contacted by the study team; of these 91% were successfully interviewed and provided serum specimens. The total study encompassed 156/169 surviving patients and 309 age‐neighborhood matched controls. Sexual promiscuity was uncommon, but it exerted a major effect, with those reporting 4 or more life‐time sex partners being at a 4‐fold excess risk compared to those reporting only one partner. First intercourse at a young age was common (21% began sexual activity prior to age 16) but it failed to alter risk once number of partners was taken into account. Oral contraceptive use was associated with a 2‐fold excess risk and this was not substantially affected by controlling for sexual parameters. Thirty‐three percent of the study subjects had anti‐herpes‐simplex type‐2 antibody as measured by both neutralization and radioimmunoassays. Although results of the neutralization test were not predictive of risk, women with a radioimmunoassay indicative of HSV‐2 infection were at a 40% excess risk for cervical cancer after adjustment for sexual characteristics.
Multipotentiality of yolk‐sac carcinoma cell clones
Authors: Van Hove L. , Sobis H. , Lu Y. L. , Vandeputte M. 
Published: February 2007

AbstractYolk‐sac carcinoma (YSCa) clones were isolated by manual cloning under visual control. By morphology, immunohistology and histochemistry the clones were shown to differentiate in vitro into visceral and parietal yolk‐sac cells and in vivo into visceral and parietal yolk‐sac cells, trophoblast and mesenchyme. Trophoblast and mesenchyme were only recorded in rat YSCa derived from displaced yolk sac but not in embryoderived YSCA. Hence YSCa cells displaying a visceral and parietal yolk‐sac pattern as well as the trophoblastic and the mesenchymal structures should have a common cell ancestor.
Characterization of human tumor necrosis factor produced by peripheral blood monocytes and its separation from lymphotoxin
Authors: Kelker Hanna Chroboczek , Oppenheim Joel D. , Stone‐Wolff Donna , Henriksen‐DeStefano Dorothy , Aggarwal Bharat B. , Stevenson Henry C. , Vilček Jan 
Published: February 2007

AbstractCultures of human peripheral blood leukocytes (PBL) induced with phytohemagglutinin (PHA) and the phorbol ester 12‐0‐tetradecanoylphorbol 13‐acetate (TPA) produced two types of cytotoxic proteins, indistinguishable in the in vitro assay employing murine L 929 cells as targets. One of these proteins had the antigenic and physicochemical properties of lymphotoxin (LT). We have identified the other cytotoxin as tumor necrosis factor (TNF), mainly on the basis of antigenic cross‐reactivity demonstrated with antiserum to TNF, and also by its characteristic physicochemical properties and cell source. Unlike LT, PBL‐derived TNF did not bind to Concanavalin A‐Sepharose or to several other agglutinin‐Sepharose columns specific for carbohydrate moieties common in glycoproteins. The molecular weight of native TNF determined by gel filtration was approximately 40,000 while SDS‐PAGE revealed a single sharp peak of 16,500 ± 500. When cultures of monocytes and lymphocytes separated by elutriation were stimulated with PHA and/or TPA, monocytes were the major source of TNF. In contrast, only lymphocytes produced LT. A mixture of antisera to TNF and LT neutralized all cytotoxicity of crude human lymphokine preparations for L 929 cells, suggesting that TNF and LT are either the only, or the major, cytotoxic proteins present in such crude lymphokine preparations demonstrable in this assay.
Selective dna‐amplification induced by carcinogens (initiators): Evidence for a role of proteases and DNA polymerase alpha
Authors: Heilbronn Regine , Schlehofer Jörg R. , Yalklnoglu A. Oüzkan , Hausen Harald Zur 
Published: February 2007

AbstractInhibitors of DNA polymerase alpha (aphidicolin, phosphonoacetic acid, phosphonoformic acid) efficiently inhibit initiator‐induced amplification of SV40 DNA sequences in the SV40‐transformed Chinese hamster cell line C0631. Amplification is also inhibited by various protease inhibitors (antipain, leupeptin, aprotinin, alpha‐I‐antitrypsin, epsilon‐amino‐caproic acid, soy‐bean protease inhibitor), by the non‐initiating but DNA‐damaging agent caffeine, and by sodium butyrate, which inhibits DNA synthesis by histone modification. In contrast, an inhibitor of topoisomerase II, nalidixic acid, enhances amplification when applied simultaneously with initiating treatment. This latter compound does not induce amplification when applied without initiator. Cycloheximide induces DNA amplification in the same way as chemical and physical carcinogens. This amplification can still be observed when protein synthesis is completely blocked. The data suggest a complex mechanism of selective DNA amplification. The possible involvement of proteases leading to a functional modification of DNA polymerase alpha is discussed.
Biological effects of γ‐interferon on human tumor cells: Quantity and affinity of cell membrane receptors for γ‐IFN in relation to growth inhibition and induction of HLA‐DR expression
Authors: Ücer Ugur , Bartsch Helge , Scheurich Peter , Pfizenmaier Klaus 
Published: February 2007

AbstractA large difference in the number of γ‐IFN receptors was found on a variety of human tumor cell lines with a range of 0.4 to 15 × 103 binding sites/cell. The receptor number did not correlate with the potential responsiveness of the cells to γ‐IFN, in regard to either growth inhibition or induction of HLA‐DR expression, two independently regulated γ‐IFN effects. However, with respect to HLA‐DR expression it was found that the γ‐IFN sensitivity of inducible cell lines depended on the number of receptors, so that with increasing number of receptors present on these cells lower doses of γ‐IFN were required for induction of the γ‐IFN effect.
Lysis of type‐i collagen by squamous carcinomas of the head and neck
Authors: Burman J. F. , Carter R. L. 
Published: February 2007

AbstractLysis of type‐1 collagen by squamous carcinomas of the head and neck has beeen studied in freshly excised tissues, xenografts and established cell lines. Investigations with 35 freshly excised tumours showed only low levels of active and total collagenase in both carcinomas and controls. A difference became apparent when the tissues were set up in explant organ culture where a significant (P < 0.05) increase in total collagenase was found in 13/19 tumours compared with paired control tissues over a 4–week culture period. Two xenografts showed little capacity to lyse collagen in vitro and there was only limited evidence of an increase in total collagenase after explantation and growth in organ culture. Twenty tumour cell lines showed low levels of active collagenase. Total collagenase levels were significantly increased (p < 0.05) in 4 of the the cell lines derived from cancers of the tongue; this activity was sustained in subsequent passages. Six control fibroblastoid cell lines also showed low levels of active collagenase. Levels of total collagenase were consistently high, but this activity was transient and declined in subsequent passages. Co‐cultivation experiments with 11 tumour‐cell lines and 5 fibroblastoid cell lines showed some enhanced, synergistic destruction of collagen. Parallel experiments with supernatant media from the carcinoma and fibroblastoid lines showed no enhancement, indicating that intact carcinoma cells and fibroblastoid cells are requited for synergistic collagenolysis to take place.
In vitro and In vivo antitumor activity of lymphokine‐induced cytotoxic cells
Authors: Ting Chou‐Chik , Wunderlich John R. , Hargrove Myrthel E. , Winkler David 
Published: February 2007

AbstractThe present study demonstrates that LICC possess both in vitro and in vivo antitumor activity. The LICC were generated by culturing normal spleen cells with syngeneic peritoneal cells and indomethacin, or with a conditioned medium containing IL 2 with or without a putative new lymphokine, the CCDF. The LICC thus generated selectively killed the lymphoid or solid tumor targets of different H‐2 haplotypes and of different etiological origins. The precursors of LICC were probably NK‐like cells. The effectors were neither classical NK nor classical cytotoxic T lymphocytes. The LICC were very effective in preventing growth of both lymphoid and solid tumors in vivo, and Thy I+ cells were essential for the anti‐tumor effect. The ability to generate LICC was preserved in the tumorbearing hosts until the terminal stage of tumor growth, when the generation of suppressor T‐cells interfered with LICC induction. LICC seem to play an important role in defense against non‐immunogenic tumors.
Gastrointestinal carcinoma‐associated antigen detected by a monoclonal antibody in dysplasia and adenocarcinoma associated with chronic ulcerative colitis
Authors: Olding Lars B. , Åhren Christer , Svalander Christian , Thurin Jan , Karlsson Karl‐Anders , Koprowski Hilary 
Published: February 2007

AbstractColorectal tissue specimens from 13 patients with chronic ulcerative colitis, of whom all had epithellal dysplasia and 2 had adenocarcinoma, were tested for the presence of gastrointestinal carcinoma‐associated antigen (GICA), using an immunoperoxidase technique with a monoclonal antibody (MAb) against this antigen. GICA was present in the formaldehyde‐fixed and paraffin‐embedded sections of dysplastic and cancer tissue but absent from normal or hyperplastic epithelium. However, the pattern and extent of staining with the antibody did not correlate with the degree of dysplasia, i.e., ‘mild’ dysplasia was often positive, and ‘severe’ dysplasia was sometimes negative. Changes classified as ‘indefinite for dysplasia but probably negative’ were variable in their expression of GICA. The adenocarcinomas were selectively labelled within cell clusters. In contrast, ulcerative colitis (UC) patients with severe inflammatory changes but with no detectable dysplasia were negative for GICA. GICA could be eluted from paraffin blocks of dysplastic tissue and biochemically characterized as a glycolipid. The detection of this antigen might be a useful complement to morphological examination in discriminating between precancerous and benign epithelial lesions of the colon.
SQM1 Antiody defines a surface membrane antigen in squamous carcinoma of the head and neck
Authors: Boeheim Klaus , Speak Jonathan A. , Frei Emil , Bernall Samuel D. 
Published: February 2007

AbstractWe produced murine monoclonal antibodies (MAbs) directed against the surface membrane of squamous‐cell carcinoma of the head and neck (SCCHN). One antibody, SQMI, was determined by immunofluorescence and radioimmunoassay to be reactive with 13/13 SCCHN cell lines derived from different sites of the head and neck area. No binding reaction was observed with normal fibroblasts, red blood cells, nucleated bone‐marrow cells or epithelial cells from normal oral mucosa. SQMI reactivity was observed with primary cultures of normal epidermal and bronchial epithelial cells. Significant reactivity was found with 2/4 cell lines derived from small‐cell carcinoma of the lung but little or no reactivity was found with other lung cancer cell lines. Various cell lines derived from other cancers including breast, colon, and ovarian carcinomas, melanoma, neuroblastoma and leukemia were generally unreactive. Seventeen out of 18 fresh frozen specimens of SCCHN were strongly reactive with SQMI antibody. However, autopsy specimens from the heart, liver, kidney, spleen, colon, subcutaneous fat and skin connective tissue were unreactive. SQMI antibody may be useful in biological and clinical studies of the head and neck region.
Prostaglandin and hydroxyeicosatetraenoic acid synthesis by human mesenchymal tumors
Authors: Knazek Richard A. , Yee Carole L. , Costa Jose 
Published: February 2007

AbstractThe metabolism of arachidonic acid was investigated by radioimmunoassay and chromatographic techniques in 5 sarcomas and one embryonal carcinoma of human origin maintained as transplantable tumors in nude mice. The results obtained indicate that: (1) the absolute quantities of arachidonic acid metabolites produced by a given tumor varied between experiments but the overall distribution pattern of these products, in general, remained constant from passage to passage; (2) each tumor showed a different arachidonic acid metabolite profile in quality and quantity; (3) 2 sarcomas of the same histological type could be clearly distinguished by their arachidonic acid metabolites; (4) the predominant product in all tumors was 12‐HETE3 or 15‐HETE, whereas thromboxane A2 was synthesized in low quantities by all tumors; (5) PGF2α was synthesized at the highest rate by an alveolar rhabdomyosarcoma; (6) PGE2 synthesis was highest in a malignant fibrous histiocytoma; and (7) total prostaglandin synthesis was low in the chondrosarcoma and synovial‐cell sarcomas.All results reported in this study are for the complete tumor which includes both neoplastic and stromal cells. The role that these products play in the biological behavior of mesenchymal tumor cells and normal tissues of the host remains to be determined.
Host cell range of adult t‐cell leukemia virus I. Viral infectivity and binding to various cells as detected by flow cytometry
Authors: Sinangil Faruk , Harada Shinji , Purtilo David T. , Volsky David J. 
Published: February 2007

AbstractAdult T‐cell leukemia virus is the member of a human type‐C retrovirus family (HTLV) found to be associated with adult T‐cell leukemia (ATL) in Japan. In our study, HTLV was isolated from the MT‐2 cell line, purified on sucrose gradient and labelled with fluorescein‐isothiocyanate (FITC‐HTLV). The protein pattern of the virus was determined by SDS‐gel electrophoresis and assured by Western blotting using ATL patient serum. Fresh human lymphocytes, separated Band T cells, mouse and rabbit lymphocytes, mouse fibroblasts, and 13 different tumor cell lines were tested in parallel for binding of FITC‐HTLV and infectability by the virus. Virus binding to cell receptors was assayed by flow cytometry. Successful infection was monitored by following the expression of HTLV determined antigen (HTLA). Most of the cells bound FITC‐HTLV at levels ranging from 5% to 130% of the MT‐2 cell binding. Only fresh human T, mouse and rabbit lymphocytes were infectable by cell‐free virus preparations. The results demonstrate that HTLV receptors are present on different types of cells of both human and animal origin, and that infection by the virus is restricted to fewer host cells but not limited to a specific class of human lymphocytes.
Changes in plasma hormone profiles after tumor transplantation into syngeneic and allogeneic rats
Authors: Besedovsky Hugo O. , Rey Adriana Del , Schardt Martin , Sorkln Ernst , Normann Sigurd , Baumann Joyce , Glrard Jürg 
Published: February 2007

AbstractTransplantation of 2 chemically (DMBA, MCA)‐induced tumors into syngeneic female or male DA strain rats elicited hormonal changes during tumor growth. Plasma levels of 7 different hormones were studied. Tumor cells in syngeneic recipients produced a biphasic decrease in insulin, an early increase in prolactin, and a late‐phase decrease in thyroxine. Corticosterone decreased in female tumor bearers but increased in males. This difference may reflect differences in the tumors transplanted. Male rats had a decrease in testosterone during the late phase of tumor growth, while females had a biphasic decrease in progesterone and a late‐phase increase in growth hormone. The tumors used were moderately immunogenic in syngeneic recipients. However, tumor transplantation to allogeneic recipients produced an early decrease in growth hormone and no change in insulin, corticosterone or thyroxine. Further, transplantation of normal liver cells to syngeneic or allogeneic recipients produced no hormonal abnormalities.This study demonstrates that hormonal changes which are not observed with normal cells or allogeneic tumor transplantation can occur within 2 days of syngeneic tumor transplantation. Progressive tumor growth is characterized by a worsening endocrine imbalance which involves multiple hormone systems.