bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of dietary stearic acid on the genesis of spontaneous mammary adenocarcinomas in strain A/ST mice
Authors: Bennett Alice S. 
Published: February 2007

AbstractStrain A/ST female mice maintained on a high fat (15%) diet in which stearic acid was the major lipid component developed initial spontaneous mammary adenocarcinomas at an older age than mice fed a low fat (4.5%) stock diet. Mice placed on the SA diet at weaning developed tumors at 15.7 ± 0.87 months compared to 12.7 ± 0.43 months for those retained on the stock diet (p<.05). Placing mice on the SA diet at 11.5 months resulted in a smaller but significant increase in the latency period (5.0 ± 0.86 vs 3.0 ± 0.57 months ± 0.57 mo), (p< .05). Fatty acid analyses of non‐tumorous mammary tissue from mid‐pregnant mice and of tumor tissues showed that feeding large amounts of 18:0 did not result in increases in the proportion of 18:0. Significant reductions in the percentages of polyun‐saturated fatty acids (PUFA) was found in tissues on mice fed the SA diet. The percentage of 18:2 was reduced in both types of tissues; 20:3 and 20:4 was reduced in tumor tissues. Distribution of C18 fatty acids in plasma membranes of tumors of mice fed the two diets were similar; percentages 18:2 was higher in plasma membranes of non‐tumorous tissues of mice fed the SA diet. These results suggest that dietary stearic acid interferes with the availability of certain PUFA required for tumor production.
Differential growth response of normal human diploid fibroblasts and in vitro transformed human fibroblasts in serum‐free defined culture medium
Authors: Namba Masayoshi , Kusaka Takashi , Fukushima Fujiko , Kimoto Tetsuo 
Published: February 2007

AbstractTwo neoplastic human cell lines, WI‐38 CT‐1 and SUSM‐1, which were transformed in vitro with gamma rays and 4‐nitroquinoline 1‐oxide, respectively, grew continuously in a serum‐free defined medium. The defined medium used was a 1:1 mixture by volume of Dulbecco's modified Eagle's medium and Ham's F12 (DF) supplemented with 0.1% bovine serum albumin fraction V, 10 μg/ml of transferrin, 1 μg/ml of insulin, and 5 of μg/ml oleic acid. In the case of SUSM‐1, 100 μg/ml of fetuin were added to cultures when the cells were subcultured. Under these conditions the growth rates of the two transformed human cell lines were almost the same as those in a DF medium containing 10% fetal bovine serum (FBS). In addition, the defined medium permitted the cells to grow indefinitely without a lag period when they were transferred from serum‐containing medium into this defined medium, indicating that no selection or adaptation of the cells had occurred. Interestingly, these cell lines did not require for their growth any polypeptide growth factors such as epidermal, platelet‐derived or fibroblast growth factors. On the other hand, the control WI‐38 cells stopped growing in the defined medium after about 2 divisions. Another control normal cell strain of fibroblasts derived from a human embryo showed a decreased growth rate in the defined medium as compared with that in the DF medium with 10% FBS. These results suggest that the defined medium described here is useful for the selective growth of human cells transformed in vitro after treatment with carcinogens from an untransformed cell population. In addition, the defined medium for transformed human cells should contribute to studies on their growth mechanisms.
Suggestive evidence that the highly metastatic variant ESB of the T‐cell lymphoma eb is derived from spontaneous fusion with a host macrophage
Authors: Larizza L. , Schirrmacher V. , Graf L. , Pflüger E. , Peres‐Martinez M. , Stöhr M. 
Published: February 2007

AbstractTwo lines of evidence are reported which suggest that the highly metastatic variant ESb of the T‐cell lymphoma Eb is derived from spontaneous fusion with a host macrophage. Firstly, ESb cells are shown to express the macrophage differentiation antigen Mac‐1 which was not found on Eb cells or on any other tumor cells tested except the macrophage tumor line Pu5. Secondly, the progression from low to high metastatic capacity could be reproduced in vitrofollowing hybridization of thioguanine‐resistant Eb cells (EbTGR) with syngeneic bone‐marrow‐derived macrophages. Two HAT medium‐selected hybrid tumor lines (Eb‐F1 and Eb‐F2) could be established. They were found to express cell surface markers of both parental lines: T lymphoid differentiation antigens from T‐lymphoma and macrophage antigens (Mac‐1, class II MHC antigens) from the normal cell fusion partner. The antigens were identified on the hybrids and subclones thereof by means of monoclonal antibodies and 3 different detection assays: cytofluorography, complement‐dependent cytotoxocity and immunoprecipitation followed by gel electrophoresis. Animals inoculated s.c. with the parental line EbTGR developed local tumors but not metastases and survived for more than 40 days. In contrast, animals inoculated similarly with Eb‐F1 or Eb‐F2 cells quickly developed metastases in visceral organs and died as early as 10‐14 days following inoculation. In many but not all respects, the in vitro‐derived Tlymphoma‐macrophage hybrids resembled the spontaneous in vivo‐derived variant ESb. These findings, together with the presence of Mac‐1 antigen on ESb cells, suggest (1) that ESb variant cells may be derived from spontaneous fusion with a host cell, most likely a macrophage and (2) that somatic cell fusion may be an important mechanism of genetic rearrangements leading to metastatic variants. The new highly metastatic tumor lines which were developed under well‐defined in vitro conditions, and their subclones, may become very useful tools for studying the contribution of specific genetic traits and of membranerelated structures to various steps of the metastatic process.
Use of the micronucleus test to monitor the effect of vitamin A, beta‐carotene and canthaxanthin on the buccal mucosa of betel nut/tobacco chewers
Authors: Stich Hans F. , Stich Waltraud , Rosin Miriam P. , Vallejera Mythyl O. 
Published: February 2007

AbstractThe frequency of exfoliated cells with micronuclei in buccal swabs was used to estimate the protective effect of vitamin A, beta‐carotene and canthaxanthin (4,4′‐diketo‐beta‐carotene) on the buccal mucosa of betel (areca) nut/tobacco chewers. Micronuclei were scored on exfoliated cells taken by swabbing and stained with the Feulgen reaction and fast green. The betel (areca) nut/tobacco chewers served as their own controls. Prior to the administration of vitamin A and beta‐carotene, the examined betel quid chewers had elevated frequencies of micronucleated buccal mucosa cells, averaging 4.03% ± 1.24 sd (n = 26) and 3.43% ± 1.22 sd (n = 25), respectively. The frequency of micronucleated buccal mucosa cells in non‐chewers and non‐smokers was 0.51% (n = 52). Following a 9‐week ingestion of vitamin A (150,000 IU/week) and beta‐carotene (180 mg/week in 6 capsules), the frequency of micronucleated cells decreased significantly (p<0.001) to 1.70% and 1.16%, respectively. No significant shift in the frequencies of micronucleated cells was observed following the intake of canthaxanthin (180 mg/week in 6 capsules) for 9 weeks or that of a placebo. The lack of protective activity of canthaxanthin, which is a good trapper of oxygen singlets but cannot be converted into vitamin A, suggests that vitamin A and beta‐carotene exert their inhibitory effect on the formation of micronuclei by a mechanism not involving the scavenging of free radicals. The efficacy of beta‐carotene as an inhibitor of micronucleated cell formation, the lack of toxicity, and its availability from a multitude of dietary sources should focus attention on this carotenoid as a promising chemopreventive agent.
The proliferative response of low‐density human cell cultures to tumor promoters and its relevance to carcinogenic mechanisms in vitro
Authors: Kopelovich Levy , Chou Ting‐Chao 
Published: February 2007

AbstractThe effects of the tumor promoter 12‐O‐tetradecanoyl phorbol‐13‐acetate, its analogues, and other tumor promoters, on the proliferation of human skin fibroblasts (SF) have been investigated. We have previously shown (Kopelovich and Bias, 1979), that TPA caused a biphasic (upward concave) dose effect in the cloning efficiency assay of normal and mutant human fibroblastic cell strains. Here we report that the biphasic dose response pattern, consisting of an inhibitory phase and a stimulatory phase, was shared by the active analogues of TPA, e.g., phorbol‐12, 13‐dibutyrate and phorbol‐12, 13‐dibenzoate. This biphasic dose effect relationship, however, was not seen with phorbol‐12, 13‐diacetate or the inactive analogues of TPA such as phorbol and 4‐O‐methyl‐12‐O‐tetradecanoyl phorbol‐13‐acetate, nor was it seen with mezerein, teleocidin, or bile‐acid derivatives of humans. An analysis of the cloning efficiency data by the median‐effect equation (Chou and Talalay, 1981) showed that in low‐density cultures both the inhibitory phase and the stimulatory phase of the dose‐effect relationships of TPA, its analogues, mezerein, and teleocidin exhibited a linear median‐effect plot and thus closely followed the basic mass‐action principle. The median‐effect plot of these data allowed quantitative determination of growth curve characteristic such as regression coefficient, slope (a measure of sigmoidicity), median‐effect concentrations such as I50 for the inhibitory effect, and A50 for the stimulatory effect (i.e., the relative potency of the analogues) and the transition point of the biphasic phenomenon in the case of the phorbol esters. In additon, we have demonstrated a relationship between the dose response effect of TPA on the proliferation of various human cells and tumor progression in vitro.
Induction of IL‐2 production, IL‐2 receptor expression and proliferation of T3− T‐PLL cells by phorbol ester
Authors: Vyth‐Dreese Florry A. , De Vries Jan E. 
Published: February 2007

AbstractLeukemic T cells from the peripheral blood of a patient with T‐prolymphocytic leukemia (T‐PLL) were investigated for their potential to differentiate in vitro upon exposure to 12‐O‐tetradecanoyl‐phorbol‐13‐acetate (TPA). The T‐PLL cells, identified as typical PLL cells by nuclear morphology, were typed as E+ sIg−OKTI+3−4+6−8−11+ cells lacking reactivity with OKI‐I or OKM‐l. In addition, between 3% and 10% of the cells reacted with monoclonal antibodies against T10. In contrast to normal T cells, the T‐PLL cells could not be induced to proliferate by mitogenic lectins or alloantigens in the presence or absence of human interleukin‐l (IL‐I), interleukin‐2 (IL‐2) or allogeneic monocytes and did not produce IL‐2. They also failed to proliferate in response to TPA or TPA in the presence of phytohemagglutinin (PHA), but under these conditions T‐PLL cells secreted high levels of IL‐2 activity. Incubation in the presence of PHA + TPA or TPA for 48 h induced T‐PLL cells to become blasts exhibiting enhanced protein synthesis, and induced a 10‐fold increase in the percentage of cells reactive with monoclonal antibodies against T10. At the same time, about 15% of the cells developed receptors for IL‐2 as monitored by their reactivity with anti‐Tac monoclonal antibody. Washing of these T‐PLL cells to remove TPA resulted in the induction of proliferation upon subsequent culture in the presence of IL‐2 or in medium only. Since proliferating T‐PLL cells still failed to express T3 antigens, it was concluded that these leukemic cells represent a T‐cell differentiation stage or a T‐cell subset which can be activated via a T3‐independent pathway.
In vitro analysis of the epstein‐barr virus: Host balance in long‐term renal allograft recipients
Authors: Yao Q. Y. , Rickinson A. B. , Gaston J. S. H. , Epstein M. A. 
Published: February 2007

AbstractFour indlces of the EB virus carrier state, for which quantitative in vitro assays now exist, have been monitored in 55 renal allograft recipients under long‐term immunosuppression, each patient being tested on a single occasion. By comparison with parallel data from healthy control donors, the results indicate the extent to which virus replication in the throat and virusinfected B cells in the blood are increased as a result of immunosuppression; the concrodance between these two independent indices of the level of EB virus infection in vivo, first noted with healthy donors, was again observed within this large group of patients. Immunosuppression also leads to an impairment of virus‐specific memory T‐cell responsiveness and to an increase in anti‐viral antibody titres, but the results show that the level of virus infection prevailing in any one individual cannot be inferred directly from these immunological indices of the virus: host balance. In allograft patients on stable levels of immunosuppression, virus and host appear to establish a new equilibrium. Limited prospective studies suggest that the position of this new equilibrium depends critically upon the virus: host balance prevalling in the same individuals before immunosuppression began. This may be an important consideration in identifying patients for whom immunosppression may carry a particularly high risk of developing EB virus genome‐positive lymphoma.
Herpes simplex virus type 2 and human papillomavirus type 16 in cervicitis, dysplasia and invasive cervical carcinoma
Authors: Prakash S. S. , Reeves William C. , Sisson Gary R. , Brenes Maria , Godoy Julio , Bacchetti Silvia , de Britton Rosa C. , Rawls William E. 
Published: February 2007

AbstractSera and biopsies of cervical lesions from 55 women with benign or malignant disease were analyzed for evidence of infection with herpes simplex virus type 2 (HSV‐2) or human papillomavirus (HPV). In addition, information regarding known risk factors for cervical cancer was obtained by interview. The sera were tested for HSV‐2 antibodies and the biopsies were tested for HPV or HSV DNA sequences by Southern blot hybridization. HSV‐2 sequences were detected in 2/13 (15%) invasive neoplasms and in 1/12 (7%) benign lesions. Under non‐stringent conditions of hybridization, reactions with HPV DNA were detected in biopsies of 2/17 (12%) inflammatory lesions, 6/12 (50%) intraepithelial neoplasms and 13/20 (65%) invasive neoplasms. All but one of the positive biopsies of invasive cancer, but only 4/11 biopsies of non‐invasive lesions, contained HPV‐16 DNA as determined by stringent hybridization conditions. Women with cervical cancer possessed the risk factors associated with the disease. Cigarette smoking and the presence of HPV‐16 DNA were the most prominent risk factors. No evidence of an interaction between HSV‐2 and HPV‐16 was found among the cases of invasive cervical cancer.
Endocrine sensitivity of the receptor‐positive T61 human breast carcinoma serially grown in nude mice
Authors: Brünner N. , Spang‐Thomsen M. , Poulsen H. Skovgaard , Engelholm S. A. , Nielsen A. , Vindeløv L. 
Published: February 2007

AbstractA study was made of the effect of ovariectomy, 17β‐oestradiol, and tamoxifen on the oestrogen and progesterone receptor‐positive T61 human breast carcinoma grown in nude mice. The effect of the treatment was evaluated by the specific growth delay calculated on the basis of Gompertz growth curves, and by the changes in the cell cycle distribution monitored by flow cytometric DNA analysis. The results demonstrated that both oestradiol and tamoxifen induced a temporary growth delay, whereas ovariectomy of the host had no effect on the growth of the tumour. The oestradiol‐induced tumour growth delay was accompanied by a decrease in the G1 fraction, an accumulation of cells in the S‐phase, and polyploidy, whereas neither treatment with tamoxifen nor ovariectomy influenced cell cycle distribution. The results indicate that oestradiol and tamoxifen have different mechanisms of action. In addition, they were interpreted as indicating different mechanisms regulating ovariandependent tumour growth, on the one hand, and oestrogen and tamoxifen‐induced tumour growth inhibition, on the other. The results support the view that the presence of receptors may be of importance but is not a sufficiently clear marker to allow prediction of the endocrine sensitivity of individual breast tumours.
Infectious transmission of human T‐cell leukemia virus to rabbits
Authors: Miyoshi I. , Yoshimoto S. , Kubonishi I. , Fujishita M. , Ohtsuki Y. , Yamashita M. , Yamato K. , Hirose S. , Taguchi H. , Niiya K. , Kobayashi M. 
Published: February 2007

AbstractA rabbit lymphoid cell line (Ra‐I) was established by co‐cultivation with a human T‐cell line (MT‐2) carrying human T‐cell leukemia virus (HTLV). The Ra‐l cell line is chromosomally male and is persistently infected with HTLV. Ra‐l cells, with or without mitomycin‐C treatment, were inoculated intravenously (i. v.) into 3 female rabbits. All 3 animals responded with the production of antibodies to HTLV antigens. Lymphocytes from one of these seroconverters were cultured in the presence of T‐cell growth factor (TCGF) and HTLV particles were detected in the TCGF‐grown lymphocytes which were chromosomally female. Co‐cultivation of lymphocytes from the 2 other seroconverters with lymphocytes from 2 anti‐HTLV‐negative healthy men gave rise to the establishment of an HTLV‐producing T‐cell line derived from each individual. Blood transfusion from one of the HTLV‐infected rabbits into 2 female rabbits also resulted in the seroconversion of both recipients. An HTLV‐carrying lymphoid cell line (Ra‐2) was established from one of the transfusion‐related seroconverters. The Ra‐2 cell line was initially TCGF‐dependent but later became TCGF‐independent. These results indicate that HTLV can be transmitted to rabbits. These animals may provide a suitable model system for studying the mode of transmission and pathogenicity of HTLV.
Radioimmunodetection of murine mammary adenocarcinoma (TA3/Ha) lung and liver metastases with radioiodinated PNA
Authors: Shysh A. , Eu S. M. , Noujaim A. A. , Suresh M. R. , Longenecker B. M. 
Published: February 2007

AbstractOrgan‐specific lung and liver metastatic variants of the murine TA3/Ha mammary adenocarcinoma cell line were selected by sequential in vivo growth with intervening in vitro cell culture. These variants readily formed specific lung or liver metastatic lesions upon i. v. injection into A/J mice. TA3/Ha cells produce a large cell surface glycoprotein called epiglycanin, which contains a high proportion of Thomsen‐Friedenreich (TF) antigenic structures. The presence of non‐cryptic TF has been associated with malignancy in humans and animals. We used peanut lectin agglutinin (PNA), which has a preferential affinity for TF antigenic structures, to determine whether these selected metastatic variants retained the TF antigen expression. In vitro, the TA3/Ha etastatic variant lines exhibited strong PNA binding similar to that seen with human RBC after neuraminidase treatment to expose the cryptic TF antigen. In contrast, the non‐epiglycaninproducing TA3/St subline did not bind PNA appreciably. Autoradiography of liver sections with TA3/Ha metastatic lesions after 125I‐PNA i. v. indicated an avid uptake throughout the viable tumor mass and FITC‐PNA staining of these tissue sections readily identified the metastatic tumors under fluorescence microscopy. Tissue biodistribution studies revealed that lung or liver containing the TA3/Ha metastatic variant nodules retained about 7 to 8 times as much of an i. v. dose of radioiodinated PNA as did controls, allowing for clear delineation of tumor‐infiltrated lung or liver by gamma xintigraphy. These in vitro and in vivo tests confirm that the selected organ‐specific TA3/Ha variants retained the binding characteristics of the parent TA3/Ha line. These observations illustrate the potential utility of radiolabelled PNA for the detection of TF‐antigen‐expressing tumors and metastases. This murine system with organ‐specific TA3/Ha metastatic variants also provides a model for evaluation of various other macromolecular probes for tumor radioimmunodetection of metastatic lesions.
Anti‐tumor effect of inelammatory neutrophils: Characteristics of in vivo generation and in vitro tumor cell lysis
Authors: Lichtenstein Alan , Kahle Janet 
Published: February 2007

AbstractInflammatory neutrophils elicited by intraperitoneal injection of Corynebacterium parvum, thioglycollate or proteose peptone were capable of lysing different murine and human tumor targets in a shortterm chromium‐release assay. A single‐cell cytotoxicity assay, which evaluated effector‐target cell interactions at the single‐cell level, confirmed a PMN‐mediated tumor‐lytic effect. Optimal lysis was achieved by PMNs obtained 6 hr after injection of C parvurn and 16 hr after injection of thioglycollate. In vitro, loss of tumor cell membrane integrity occurred extremely rapidly following conjugation with inflammatory PMNs (beginning within 15 min of the binding step). By 45 min, the lytic event was completed. Addition of catalase or superoxide dismutase to the cytotoxicity assays prevented tumor lysis in a concentration‐dependent fashion, indicating that hydrogen peroxide and superoxide, products of the PMN respiratory burst, are mediators of the lytic reaction.
An analysis of some risk factors for lung cancer in Hong Kong
Authors: Koo L. C. , Ho J. H‐C. , Lee N. 
Published: February 2007

AbstractLung cancer has been the major cause of cancer death in Hong Kong for more than a decade. Although it is known that some 95% of male cases can be attributed to smoking, the etiological factors in women remain elusive. Among “never‐smoked” female cases, increases in attributable risk from passive smoking were limited to only some of the histological types of lung carcinomas, and an overall analysis of all types did not reveal any significant increase in relative risk from this source. Other environmental factors which encourage bronchial irritation are suspected. Methodological differences may explain the differences in proportional distributions of histological lung tumor types noted between previous reports, and the risk values attributed therein to active and passive smoking.
Gastric cancer risk in chronic atrophic gastritis: Statistical calculations of cross‐sectional data
Authors: Slpponen Pentti , Kekki Matti , Haapakoski Jaason , Ihamäki Timo , Siurala Max 
Published: February 2007

AbstractRelative risk (RR) and cumulative risk of gastric cancer (GCA) were calculated for different grades of atrophic gastritis (AG) of the antrum and body. Cross‐sectional data on the occurrence of AG in a representative population sample (371 subjects), and Finnish Cancer Registry data on GCA were used in the calculations. The RR was increased significantly in severe AG of the antrum and the body (18.1 and 4.6 times, respectively), but not significantly in the less severe grades of AG. As a risk factor, severe antral and body gastritis were independent of each other. The cumulative risk, i. e., the probability of contracting GCA within the following 10 years in age groups 50–54 … 70–74 years was calculated to vary from 2.3% to 9.3% and from 8.7% to 31.9% in severe antral AG and from 0.9% to 4.5% and from 3.6% to 16.6% in severe body AG in males and females, respectively.