bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of the platelet‐aggregating activity of cancer cells with different metastatic potential
Authors: Grignani Guido , Pacchiarini Lucia , Almasio Piero , Pagliarino Mauro , Gamba Gabriella , Rizzo Salvatore Carlo , Ascari Edoardo 
Published: February 2007

AbstractWe studied the mechanisms of platelet activation by sublines exhibiting different metastatic potential of two murine experimental tumors: sublines M4 and M9 of the benzopyrene‐induced mFS6 sarcoma and sub‐ lines B77‐AA6 and B77–3T3 of RSV‐transformed BALB/c 3T3 fibroblasts. The neoplastic cells of both models induced platelet aggregation, secretion and prosta‐glandin biosynthesis. In the first model but not in the second, all these processes correlated with the in vivo malignancy of cells. Pretreatment of B77‐AA6 and B77–3T3 cells with apyrase significantly decreased platelet aggregation, while pretreatment of M4 cells was ineffective. However, pretreatment with trypsin or neuraminidase was effective in reducing platelet aggregation induced by M4 cells, but not that induced by any of the others; furthermore, phospholipase A2 reduced the platelet response by all sublines. Finally, platelet‐activating activity was also found in the pellets obtained following centrifugation of culture media. These results suggest that platelets are stimulated by cancer cells through different mechanisms; platelet activation by a sialo‐lipo‐protein complex of the cellular membrane was found to be characteristic of the model in which the platelet‐aggregating activity of neoplastic cells correlated with their in vivo metastatic behavior.
Aspartate‐assisted immune stimulation: Its importance in antitumor and antiviral protection
Authors: Chany Charles , Cerutti Italina 
Published: February 2007

AbstractImmune stimulators such as Cornyebacterium paryum (CP) are useful for antitumoral and antiviral therapy. However, the immune trigger cannot be reactivated without adversely affecting the disease. We have tried to amplify the results yielded by a single injection of CP by using either interleukin‐2 (1L.2) or aspartate salts (ASP). In the present report, we show that 1L2 has no detectable clinical effect. In contrast, the addition of an ASP salt increases the antiviral and antitumoral protection afforded by the CP‐induced trigger. Moreover, treatment using only ASP slightly protects against tumor development and significantly increases antiviral resistance during experimental encephalomyocarditis (EMC) infection. This ASP‐assisted CP immune stimulation improves antitumoral resistance even when ascitic tumors have already developed. In the latter case, tumor regression can even be detected. Since ASP increases T‐cell cytotoxicity in vitro and aggravates spontaneous T‐cell lymphomas in AKR mice, the involvement of T‐cell‐mediated immunity may explain antitumoral and antiviral effects. We propose the use of this therapeutic model for human cancer therapy, and possibly for treating AIDS.
Effect of Fluosol‐DA/O2 on tumor‐cell and bone‐marrow cytotoxicity of nitrosoureas in mice bearing FSA‐II fibrosarcoma
Authors: Teicher Beverly A. , Holden Sylvia A. , Rose Christopher M. 
Published: February 2007

AbstractThe perfluorochemical emulsion, Fluosol‐DA, combined with carbogen breathing, potentiates the effects of radiation and a number of chemotherapeutic agents in several rodent tumors. The interaction of Fluosol‐DA with drugs may be quite complex. In addition to increasing the oxygen supply in the tumor, Fluosol‐DA may alter the pharmacokinetics of the drug and function as a drug delivery system. A series of 4 nitrosoureas of varying lipophilicity were administered as single doses intravenously (i.v.) to C3H/Be/FeJ mice bearing subcutaneous FSa‐11C fibro sarcomas. Doses of 40 mg/kg of CCNU, 15 mg/kg of BCNU, 20 mg/kg of MeCCNU and 15 mg/kg of chlorozoticin followed by 2 hr of breathing 95% oxygen produced tumor growth delays of 7.5, 4.0, 3.8 and 2.7 days, respectively. When the drug injection was followed immediately by 0.3 ml of Fluosol‐DA and 2 hr of breathing 95% oxygen, the tumor growth delay produced by CCNU, BCNU, MeCCNU and chlorozoticin increased 2‐fold, 10‐fold, 4.5‐fold and 3.5‐fold, respectively. Administration of the drugs in Fluosol‐DA followed by 2 hr of 95% oxygen breathing resulted in a 3.5‐fold increase in tumor growth delay with CCNU, a 17‐fold increase with BCNU, a 12.5‐fold increase with MeCCNU and a 6‐fold increase with chlorozoticin compared to drug and 95% oxygen breathing. These results are quantified in terms of cell survival by the tumor excision assay. Effects on the bone marrow from each treatment were measured using the granulocyte‐monocyte colony‐forming units (CFU‐GM) assay. There was no correlation between the lipophilicity of the nitro sources tested and the tumor growth delay produced by each treatment.
The immune system during the pre‐cancer and the early cancer period. IL‐2 production by PBL from post‐menopausal women with and without endometrial carcinoma
Authors: Yron I. , Schickler M. , Fisch B. , Pinkas H. , Ovadia J. , Witz I. P. 
Published: February 2007

AbstractWe report on alterations in IL‐2 production and cell proliferation following PHA stimulation of peripheral blood lymphocytes (PBL) from stage‐1 endometrial carcinoma (EC) patients, and on mechanisms involved in these alterations. Our study includes 3 groups: EC patients, post‐menopausal women at high risk of developing EC, and age‐matched healthy women. IL‐2 production was markedly lower in most EC patients than in healthy controls. Varying levels of IL‐2 were produced by PBL from women in the high‐risk group. The proliferative response of PBL to PHA appeared to correlate with levels of IL‐2 production. Our results suggest that macrophages are involved, in part, in the modulation of T‐cell functions of EC patients.
S‐phase fraction of human brain tumors in situ measured by uptake of bromodeoxyuridine
Authors: Hoshino Takao , Nagashima Tadashi , Cho Kyung G. , Murovic Judith A. , Hodes Jonathan E. , Wilson Charles B. , Edwards Michael S. B. , Pitts Lawrence H. 
Published: February 2007

AbstractOne hundred fifty‐four patients with brain tumors of various types were given an intravenous infusion of the thymidine analogue bromodeoxyuridine (BUdR), 200 mg/m2, at the time of surgery but before biopsy of the tumor to label S‐phase cells. Excised tumor specimens were fixed, sectioned, and stained by immunoperoxidase methods to detect BUdR. The labelling index (LI), or percentage of BUdR‐labelled cells, was calculated for each tumor specimen. The LIs of glioblastomas, medulloblastomas, and most highly anaplastic astrocytomas were 5% to 20%. The majority of moderately anaplastic astrocytomas showed LIs of less than 1 %, but 30% of them had LIs similar to those of highly malignant gliomas. Most pituitary adenomas and neurinomas showed LIs of less than 1%. Non‐ malignant meningiomas had LIs of less than 1%, whereas malignant meningiomas had LIs higher than 2.7%. This is an important observation, because malignant meningiomas are not well‐defined histopathologically and their growth rate and rate of recurrence cannot be predicted by current diagnostic procedures. By estimating the proliferative potential of individual tumors more precisely, the BUdR LI supplements histopathological diagnosis, allowing a more accurate estimate of prognosis and facilitating the design of treatment regimens for individual patients.
Effects of mouse interferon on human tumour xenografts in the nude mouse host
Authors: Balkwill F. R. , Proietti E. 
Published: February 2007

AbstractMurine interferon (IFN) inhibited the growth of 3/3 human tumour xenografts growing in nude mice. This inhibition was independent of the sensitivity of the xenograft to human IFN. In contrast to human IFN, the murine IFN did not directly affect the human tumour cells in vitro as measured by levels of the IFN‐ induced enzyme 2–5A synthetase or elevation of HLA expression. In preliminary investigations into the role of the host in the murine IFN‐mediated tumour inhibition, we found equal activities of this IFN in nude and in beige (NK‐deficient) nude mice. Moreover, murine IFN did not elevate levels of NK‐cell activity in either of these mouse strains. We conclude that murine IFN mediates this tumour inhibition via an effect on the tumour‐bearing host that may or may not involve immune mechanisms.
Recombinant human interferon gamma suppresses HTLV‐III replication in vitro
Authors: Nakashima Hideki , Yoshida Tsutomu , Harada Shinji , Yamamoto Naoki 
Published: February 2007

AbstractEffect of human interferon gamma (rINF‐γ) on HTLV‐III replication was evaluated quantitatively via a novel infection system using HTLV‐I‐carrying MT‐4 cells. Treatment of HTLV‐III‐infected MT‐4 cells with different concentrations (1–1,000 U/ml) of rINF‐γ, which did not affect the growth or viability of uninfected cells, significantly blocked the appearance of immunofluorescent antigens of HTLV‐III and the virus‐induced cytopathic effect in a dose‐dependent manner. A plaque assay was applied to measure the exact amount of viral particles released from HTLV‐III‐infected MT‐4 cultures either untreated or treated with rINFγ after infection. The number of plaques per dish decreased with increasing drug concentrations. About 50% and 80% of HTLV‐III replication were inhibited by the addition of 100 and 1,000 U/ml of rINF‐γ, respectively. The effects of INF were observed by day 5 of incubation with the chemical. However, longer treatment of cells with rINFγ permitted a gradual increase in viral replication. Re‐addition of fresh INF into cultures did not change this pattern significantly.
Early spontaneous metastasis in the human epidermoid carcinoma HEp3/Chick embryo model: Contribution of incidental colonization
Authors: Gordon Joseph R. , Quigley James P. 
Published: February 2007

AbstractIn the experimental model system where human tumor cells (HEp3) are implanted on the chorioallantoic membrane (CAM) of the chick embryo, metastasis of HEp3 cells to the embryonic lung occurs within a few days. Such rapidity in tumor dissemination makes this an attractive and potentially useful model for studying the metastatic process. The model, however, involves microvascular trauma at the site of implantation and thus tumor cells may accidentally enter the circulation during implantation or shortly thereafter. If these cells are the cause of the lung metastasis subsequently measured, the model would be in effect a colonization system and not a true, spontaneous metastasis system. The possible contribution of accidental lung colonization to secondary tumor growth was therefore critically examined in this model. In standard metastasis assays, HEp3 was inoculated onto the CAMs of 10‐day embryos, which were then incubated for various periods of time. The embryos' lungs were passaged to a second group of CAMs, incubated for 7 days to allow expansion of any HEp3 cells present, and then assayed for HEp3 cells by both microscopy and measurement of human plasminogen activator (PA) activity. Metastasis was evidenced by PA values above background (30mU/mg protein). Morphological analysis of HEp3 cells in the embryonic lung correlated closely with PA values. To focus on the early stages of tumor dissemination when colonization might occur, the primary tumor was surgically excised from 38 embryos at various intervals after tumor inoculation, and after the operation embryos were allowed to develop to day 17. This procedure increased estimated assay sensitivity down to the level of 1 to 10 cells per lung in embryos operated on within 2 days of inoculation. Median PA values in the transplanted lungs were 13, 3, 37, 1,290 and 3,765 mil/mg protein in the groups operated on at 4 hr, 1, 2, 3 and 4 days after inoculation, respectively. Thus very few or no HEp3 cells arrest and grow in the lungs during the first 24 to 48 hr, but extensive metastasis occurs by 72–96 hr. Accidental colonization therefore plays no major part in the rapid pulmonary spread of HEp3 in this model.
Expression of HLA‐D sub‐region products on human colorectal carcinoma
Authors: Ghosh A. K. , Moore M. , Street A. J. , Howat J. M. T. , Schofield P. P. 
Published: February 2007

AbstractThe major histocompatibility complex (MHC) status of normal, inflamed, pre‐malignant and malignant epithelia of the human gastrointestinal tract was investigated by immunocytochemical methods using monoclonal antibodies (MAbs) directed against heavy (α)‐and light (β2m)‐chain Class‐I molecules and sub‐locus products (DP, DQ, DR) of the HLA‐D region. Class‐I expression on epithelial cells appeared to vary little with pathological status except in the case of 4/32 (13%) colorectal carcinomas in which the antigens were undetectable or scanty. The pattern of Class‐II expression was more complex. The antigens were readily detectable on normal stomach epithelium, in villous adenomas and in inflammatory bowel mucosa. In each of these situations DR was the predominant specificity, followed by DP and DQ. Expression on normal colonic epithelium was usually negative but, in the vicinity of a neoplasm or an area of marked leukocyte infiltration, Class‐II molecules (DR>DP>DQ) were detectable. A similar pattern of non‐coordinate expression was found on 23/32 (72%) colorectal carcinomas, but on the remaining 28% no Class‐II products were detectable, under conditions wherein stromal leukocytes were strongly stained. The data suggest that In a significant proportion (nearly 30%) of primary colorectal carcinomas, the capacity for Class‐II induction, a constitutive or acquired feature of normal colorectal epithelium, is either diminished or lost. Also, tumor Class‐II status is not correlated to Dukes' stage or differentiation.
Imbalance of sex chromosomes, with gain of early‐replicating X, in human solid tumors
Authors: Dutrillaux B. , Muleris M. , Seureau M. Gerbault 
Published: February 2007

AbstractAn imbalance of sex chromosomes was observed in several cases of solid tumors: colorectal, anal canal and breast carcinomas. Replication studies, using BUdR incorporation, show that in males there is a tendency towards a gain of early‐replicating X and a deficiency of Y chromosomes. In females, there is a tendency towards a gain of early‐replicating X and a loss of late‐replicating X chromosomes. Although almost no replication studies have been published in the literature, making it impossible to distinguish between late‐and early‐replicating Xs, it is likely that a similar situation exists for several solid tumors other than those we have studied. A possible consequence of this imbalance is briefly discussed.
STLV‐I antibodies in feral populations of East African vervet monkeys (Cercopithecus aethiops)
Authors: Dracopoli Nicholas C. , Turner Trudy R. , Else James G. , Jolly Clifford J. , Anthony Robert , Gallo Robert C. , Saxinger W. Carl 
Published: February 2007

AbstractSerum samples from feral populations of African green monkeys (Cercopithecus aethiops) were screened for antibodies to the simian T‐lymphotropic virus, type I (STLV‐I). Blood samples had been collected from 336 monkeys in 4 regions of central and southern Kenya in 1978 and 1979, from 114 monkeys in central Ethiopia in 1973, and from 85 monkeys from the Kampala region of Uganda in 1966. A total of 178/535 monkeys (33%) were seropositive (STLV‐I+). Only 4/114 monkeys (4%) from Ethiopia were seropositive compared to 25/85 Ugandan monkeys (29%) and 149/336 Kenyan monkeys (44%). Epidemiological analysis of the Kenyan monkeys showed that 37% of the males and 54% of the females were STLV‐I+, and that there was a progressive increase in the proportion of STLV‐1+ monkeys of both sexes with age, rising from an average of 16% in infants (< 9 months) to an average of 69% in adults (> 42 months). The proportion of STLV‐I+ monkeys was higher among females in each age category. Seropositivity for antibodies to STLV‐I had no apparent effect on the health of monkeys, and no association with the occurrence of Hepatocystis parasitemia was seen in this species. The analysis of data from infants of STLV‐I+ mothers showed that seroconversion had occurred in I of 3 cases, suggesting that vertical transmission of the STLV‐I virus is not an inevitable consequence for infants of seropositive mothers.
Identification of a cell‐surface glycoprotein mediating cell adhesion in EBV‐immortalized normal B cells
Authors: Patarroyo Manuel , Beatty Patrick G. , Nilsson Kenneth , Gahmberg Carl G. 
Published: February 2007

AbstractPhorbol ester treatment markedly enhanced aggregation of Epstein‐Barr virus (EBV)‐immortalized normal B cells. Monoclonal antibody (MAb) 60.3, recognizing a leukocyte common antigen, completely inhibited intracellular adhesion, whereas MAbs reacting with leukocyte common antigen T200, C3b receptor, T‐cell‐associated antigen TA‐I, C3d (EBV) receptor, brain‐granulocyte/T‐lymphocyte antigen, transferrin receptor, surface immunoglobulin, Class‐I or Class‐II transplantation antigens or a B‐cell‐specific antigen (BI) showed no inhibitory effect. Both the spontaneous and phorbol‐ester‐enhanced cell aggregations were similarly inhibited by Fab fragments made from antibody 60.3. Phorbol esters also enhance binding between EBV‐immortalized normal B cells and autologous or allogeneic blood mononuclear cells depleted of B lymphocytes. This process, which is independent of immunity to EBV, was similarly blocked by the antibody fragments. Antibody 60.3 precipitated 3 non‐covalently associated surface gylcopolypeptides with apparent MW of 90, 130 and 160/kDa from EBV‐infected B cells. Although dissociation of a similar protein complex from granulocytes by sodium dodecyl sulfate treatment clearly indicated the presence of the epitope on the smallest component, the same treatment did not dissociate the protein complex from EBV‐immortalized normal B cells, ft is thus concluded that the 90‐kDa glycopolypeptide, either alone or associated with the larger glycopolypeptides, mediates cell adhesion of the B cells.
Specificity of a monoclonal antibody to drosophila melanogaster neoplastic hematopoietic cell surfaces as detected by immunofluorescence
Authors: Steinberg M. Gwen , Poodry Clifton A. 
Published: February 2007

AbstractWe have generated, and characterized the immunological specificity of, a monoclonal antibody (MAb) termed 2B3G8 that recognizes cell‐surface determinant(s) of D. melanogaster neoplastic hematopoietic tissue. This antibody was generated against antigens of a tumor line derived from neoplastic lymph glands, the hematopoietic organs, of a growth control mutant, Tumorous‐lethal (Turn1). 2B3G8 does not recognize any of a panel of normal Drosophila cells or transformed cell lines from mouse or human sources as assayed by indirect immunofluorescence. Enzymatic digests did not remove this antigen from neoplastic blood cells or uncover the antigen in normal blood cells. Thus, we have generated a MAb that serves as a marker for the neoplastic hematopoietic condition in Drosophila which is a model for vertebrate neoplasia. This antibody is potentially useful for the study of oncodevelopmental antigens in developing hematopoietic systems and for detecting the onset of the neoplastic condition.
Tumor‐associated glycoprotein (TAG‐72) detected in adenocarcinomas and benign lesions of the stomach
Authors: Ohuchi Noriaki , Thor Ann , Nose Masato , Fujita Jun , Kyogoku Masahisa , Schlom Jeffrey 
Published: February 2007

AbstractMurine monoclonal antibody (MAb) B72.3, prepared against a membrane‐enriched extract of metastatic carcinoma and reactive with a high‐molecular‐weight determinant, designated tumor‐associated glycoprotein (TAG)‐72, was shown to be reactive immunohistochemically with 97% of a variety of primary adeno‐carcinomas of the stomach (n = 40). All “early” gastric carcinomas were reactive with MAb B72.3, although the average percentage cellular reactivity was lower than in “advanced” carcinomas. TAG‐72 antigen was detected in benign lesions (i.e. adenomatous polyps and hyperplastic polyps) with intestinal metaplasia. Dysplastic lesions characterized by cellular atypia, abnormal differentiation, and disorganized mucosal architecture demonstrated higher TAG‐72 expression than non‐dysplastic epithelia. In contrast, normal gastric mucosa was generally non‐reactive with MAb B72.3. Assays using serial sections of normal, benign and malignant gastric tissues with two MAbs (B1.1 and COL‐6) directed against distinct epitopes of carcinoembryonic antigen (CEA) demonstrated differential reactivity, confirming that TAG‐72 and CEA are distinct, non‐coordinately expressed antigens. Our results suggest that TAG‐72 antigen may be expressed in malignant and dysplastic epithelial cells, as well as in intestinalized epithelium of the stomach which has been closely related to subsequent carcinoma development. Hence, MAb B72.3 may be a useful immunohistochemical adjunct for detecting early foci of adenocarcinomas and premalignant lesions of the stomach.
Differential expression of cellular oncogenes in benign and malignant human breast tissue
Authors: Whittaker Joanne L. , Walker Rosemary A. , Varley Jennifer M. 
Published: February 2007

AbstractWe have examined 62 specimens of benign fibrocystic breast tissue, fibroadenomas, carcinomas and surrounding non‐malignant tissue excised from 50 patients to determine the level of expression of 4 cellular oncogenes, c‐myc, c‐H‐ras, c‐K‐ras, and c‐N‐ras. Our results demonstrate that in breast carcinoma the frequency and relative level of expression of these oncogenes are significantly greater than those found for benign breast tissue. However, some fibrocystic specimens having prominent hyperplastic features also exhibited enhanced oncogene expression. In view of the association between the increased frequency of carcinoma of the breast in women with a previous history of benign breast disease, it will be interesting to follow up donors of benign specimens to see if there is any relationship between the expression of oncogenes in such lesions and the development of carcinomas.
Formaldehyde and cancers of the pharynx, sinus and nasal cavity: I. Occupational exposures
Authors: Vaughan Thomas L. , Strader Clifton , Davis Scott , Daling Janet R. 
Published: February 2007

AbstractA population‐based case‐control study was undertaken in 13 counties of western Washington to determine if occupational formaldehyde exposure was related to cancer of the oro‐ and hypopharynx (OHPC, N = 205), nasopharynx (NPC, N = 27) or sinus and nasal cavity (SNC, N = 53). Controls were selected by random digit dialing (N = 552). A telephone interview inquired about lifetime occupational history as well as a number of potential confounding factors, including smoking and drinking. Approximately half (N = 143) of the case interviews were with next‐of‐kin. Occupational formaldehyde exposures were assessed by application of job‐exposure matrix developed for this study which classified unique job codes into 4 categories based on judgement of likelihood and intensity of formaldehyde exposure. Exposure scores were calculated by weighting the number of years in a formaldehyde‐associated job by the assigned exposure level. The effects assuming a 15‐year induction period were also investigated. Logistic regression was used to estimate exposure odds ratios (OR) while taking into account multiple risk factors for each site. No significant associations were found between occupational formaldehyde exposure and any of the cancer sites under study. However, relative risk estimates associated with the highest exposure score categories were elevated for OHPC (OR = 1.3, 95% Confidence Interval = 0.6–3.1) and NPC (OR = 2.1, 95% CI = 0.4–10.0) when an induction period was accounted for. When only live interviews were considered, the odds ratios for OHPC and NPC increased to 1.7 and 3.1 respectively. Several limitations in the study tend to conservatively bias the results and must be taken into account in its interpretation.