bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inhibitory action of ASPARAGUS racemosus on DMBA‐induced mammary carcinogenesis in rats
Authors: Rao A. R. 
Published: February 2007

AbstractThe present paper reports the inhibitory effect of Asparagus racemosuson DMBA‐induced mammary tumorigenesis in rats of Holtzman strain. When virgin female rats, normal or primed with 17‐β‐estradiol treatment, are put on diets containing 0.25%, 0.5%, 1% or 2% Asparagus root extract powder prior to their exposure to DMBA, mammary tumor incidence shows a sharp decline.
Production of T‐cell lines with inhibitory or stimulatory activity against syngeneic tumors in vivo. A preliminary report
Authors: Mulé J. J. , Forstrom J. W. , George E. , Hellström I. , Hellström K. E. 
Published: February 2007

AbstractWe obtained Thy‐1‐positive cells directly from growing methylcholanthrene‐induced (MCA‐1510) sarcomas using fluorescence‐activated cell sorting, then cultured these lymphocytes in medium containing Interleukin‐2 and tested their activity in vivo against various MCA‐sarcoma lines with the Winn assay. We found that cultured T cells from small MCA‐1510 tumors (17 days after transplantation) significantly inhibited the growth of that particular sarcoma, but not of three other MCA‐tumor lines tested, while cultured T cells from large MCA‐1510 sarcomas (41 days after transplantation) significantly enhanced the growth of that tumor, but not of an unrelated tumor, MCA‐1460. The former cells were primarily Lyt‐1+, 2+ while the latter were primarily Lyt‐1−, 2+.
Regulation of gene expression by tumor promoters. III. Complementation of the developmental program in myeloid leukemic cells by regulating mRNA production and mRNA translation
Authors: Hoffman‐Liebermann Barbara , Liebermann Dan , Sachs Leo 
Published: February 2007

AbstractRegulation of gene expression has been analysed in different clones of mouse myeloid leukemic cells treated with the tumor promoter 12‐O‐tetradecanoyl‐phorbol‐13‐acetate (TPA), the macrophage‐ and granulocyte‐in‐ducing protein MGI, and combined treatment with TPA and MGI. Two‐dimensional gel electrophoresis was used to measure changes in the rate of synthesis of specific proteins and in the amount of corresponding translatable mRNAs assayed in the reticulocyte cell‐free translation system. TPA induced different subsets of differentiation‐associated protein changes in the different clones and the degree of response to TPA was not necessarily related to the degree of response to MGI. It is shown that TPA can induce protein changes either by inducing the synthesis of new mRNA, by increasing or decreasing the amount of pre‐existing mRNA, or by modulating the translation of a constant amount of mRNA. Combined treatment with TPA and MGI resulted in an enhancement of protein changes induced by MGI or TPA alone and induced differentiation‐associated protein changes not induced by either compound separately in differentiation‐defective clones. This complementation of gene expression appeared to be due to each compound inducing functions not induced by the other, so that the combined treatment resulted in new gene expression. Complementation also occurred at the level both of mRNA production and of mRNA translation. It is suggested that the ability of TPA to regulate gene expression at the level of mRNA production and mRNA translation and to complement changes in gene expression induced by other compounds such as MGI are important functions for its role as a tumor promoter.
Enhancing effects of dimethylnitrosamine on aflatoxin B1 hepatocarcinogenesis in rats
Authors: Angsubhakorn Subhkij , Bhamarapravati Natth , Romruen Kanda , Sahaphong Somphong 
Published: February 2007

AbstractIn a study of possible enhancing effects of dimethylnitrosamine (DMN) on aflatoxin B1 (AFB1) hepatocarcinogenesis, male Buffalo strain rats were fed diets containing 1 ppm AFB1, 25 ppm DMN, and a combination of 1 ppm AFB1 and 25 ppm DMN (AFB1 + DMN). The diets were replaced by chow pellets after 6 months, and animals were killed 3,6,9 and 12 months after the onset of the experiment. In the untreated control group animals were free of hepatocellular carcinoma but the treated groups fed AFB1, DMN and AFB1 plus DMN developed hepatic lesions ranging from multiple cysts, altered cell foci and neoplastic nodules to hepatocellular carcinomas. Hepatocellular carcinomas developed in 79%, 45% and 5% of rats fed AFB1 plus DMN, AFB1 and DMN respectively at the end of the experiment. Multiple cysts were also found in all periods in animals fed AFB1 plus DMN, whereas rats fed AFB1 and DMN separately developed a few multiple cysts by the end of the experiment. These findings suggest that DMN potentiates the hepatocarcinogenesis induced by AFB1 in rats.
Natural killer cell activity in reticulum‐cell sarcomas of SJL/J mice. II. Analysis of RCS‐associated NK activity
Authors: Fitzgerald Karen L. , Ponzio Nicholas M. 
Published: February 2007

AbstractLymphoid cells taken from the grossly enlarged lymph nodes (LN) and spleens of SJL/J mice bearing transplantable reticulum‐cell sarcomas (RCS), showed increased levels of natural killer (NK) cell activity, when compared to LN and spleen cells taken from normal SJL mice. The NK susceptible target cells used for these studies included RL‐1 and YAC‐1. Target cells that were not susceptible to NK lysis by CBA/J effector cells (high NK strain) were also resistant to lysis by RCS tumor cells. Although significant lysis of target cells was detectable at 4 h, optimal NK cytotoxicity was observed in a 16‐h 51Cr‐release assay. In terms of lytic unts (LU)/107 effector cells, greater NK activity was observed in RCS effectors than was apparent in normal CBA/J lymphoid cells. Depletion of macrophages from RCS cell preparations had no effect on the observed NK activity. Purified Mu‐IFN‐α stimulated a small increase in the NK activity expressed by SJL lymphoid cells; however RCS‐derived supernatants (containing Mu‐IFN‐γ) did not augment NK activity of SJL effector cells, nor were they cytotoxic for NK target cells. Therefore, tumor‐derived soluble factors appear not to be involved in the observed RCS‐associated NK activity. The data presented in this report further define the parameters of the NK activity manifested by RCS tumor cell preparations. The accompanying article characterizes the nature of the NK effector cells present within RCS tumors of SJL mice. Taken together, these data indicate that the RCS tumors represent either neoplastic expansion of conventional NK cells with somewhat modified properties, or else an entirely new class of cytotoxic effector cells.
Estrogen receptor quantitation and staging as complementary prognostic indicators in breast cancer: A study of 583 patients
Authors: Godolphin W. , Elwood J. M. , Spinelli J. J. 
Published: February 2007

AbstractEstrogen receptor (ER) quantity was measured at the time of primary diagnosis on 583 patients with breast cancer seen at the major treatment centre in British Columbia between 1975 and 1979. Survival rates (overall, recurrence‐free and post‐recurrence) were assessed relative to ER concentration, staging, menopausal status, age, differentiation, and therapy. A linear trend in increased survival was demonstrable through variations in ER concentration from ⩽1 to ⩾260 fmoles/mg cytosol protein. This trend was highly significant and remained after adjustment for stage, menopausal status, and age, and was seen for all groups of patients except those with metastatic disease. The association of high ER concentration with increased recurrence‐free survival was not due to differing responses to adjuvant therapy, but the trend in post‐recurrence survival was only significant in patients who had received hormonal therapy. Survival was as strongly associated with receptor concentration as with staging, and these two factors were almost completely independent. A proportional hazards model was fitted to produce predictions of survival, and showed that TNM stage III patients with high ER concentrations have a better survival than stage I or II patients with lower ER concentrations. This suggests that quantitative assessment of ER status is essential to definition of risk in breast cancer patients and that stratification in clinical trials and consideration for adjuvant therapy ought to be guided, in part, by a standardized ER‐quantitative determination performed on the primary tumor.
Induction of cytotoxic activity in human lymphocytes against autologous and allogeneic melanoma cells in vitro by culture with interleukin 2
Authors: Hersey P. , Bindon C. , Edwards A. , Murray E. , Phillips G. , McCarthy W. H. 
Published: February 2007

AbstractThe influence of interleukin 2 (IL2) on the cytotoxic activity of lymphocytes from patients with melanoma against autologous and a variety of allogeneic melanoma cells was studied. IL2 was produced from blood lymphocytes cultured for 24 h with phytohaemagglutinin (PHA) and purified by membrane chromatography to exclude PHA. Lymphocytes from 13 patients with melanoma at various clinical stages were cultured for 6 days with IL2 (2 U/ml) and then tested for cytotoxic activity against autologous melanoma cells, three allogeneic melanoma and three non‐melanoma cells. Autologous cytotoxicity was generated by culture with IL2 alone and was not increased by culture with both IL2 and autologous tumour cells. Marked increases in cytotoxic activity were also generated against the allogeneic target cells and were maximal against the NK‐insensitive Chang target cells. Similar degrees of cytotoxicity were induced by IL2 stimulation of lymphocytes from melanoma patients, patients with non‐melanoma carcinoma and normal subjects against the allogeneic target cells. Cold target inhibition studies were carried out against IL2 induced autologous cytotoxicity in five patients. In four of five studies the autologous target cells inhibited more than the allogeneic target cells. There was no significant difference between the inhibition produced by allogeneic melanoma cells and that produced by non‐melanoma cells. Similarly, in studies against allogeneic target cells, there was no significant difference in the inhibition produced by allogeneic melanoma compared to non‐melanoma target cells. This applied irrespective of whether effector cells were from melanoma or non‐melanoma subjects. These results suggest that lymphocytes from patients with melanoma are primed against autologous antigens in vivo and that provision of a second signal, IL2, in vitro can induce cytotoxicity against the autologous tumour. The cytotoxicity generated against the allogeneic target cells did not appear to have specificity to melanoma. Several results, such as the pattern of cytotoxicity against the target cells and changes in cell surface markers on the lymphocytes during culture, suggested that cytotoxicity was mediated by activated T cells rather than by natural killer cells. These findings appear to have important implications both in the understanding of tumour host relationships and for the use of IL2 in therapy.
Studies on long‐term T‐cell‐mediated immunity to epstein‐barr virus in immunosuppressed renal allograft recipients
Authors: Crawford D. H. , Edwards J. M. B. , Sweny P. , Hoffbrand A. V. , Janossy G. 
Published: February 2007

AbstractPeripheral blood lymphocytes from normal seropositive donors and renal transplant recipients on various immunosuppressive regimens have been tested for their ability to mount a cytotoxic response when cultured with autologous EB virus‐infected B cells and thereby to cause regression of proliferating B‐cell foci. Cultures from 10 normal seropositive donors all showed the normal pattern of regression. Lymphocytes from patients receiving Cyclosporin A therapy with or without prednisolone completely failed to cause regression, thus allowing B‐cell lines to proliferate unchecked. Cells from two of 17 patients treated with azathioprine and prednisone also failed to cause regression. The cells from the remaining 15 individuals showed regression responses varying from minimal to normal. These results suggest a mechanism by which EB virus‐related tumours may arise in immunosuppressed renal allograft recipients.
Intestinal M3 antigen, A marker for the intestinal‐type differentiation of gastric carcinomas
Authors: Bara J. , Hamelin L. , Martin E. , Burtin P. 
Published: February 2007

AbstractThe mucus‐associated intestinal M3 antigen, normally restricted to intestinal goblet cells, was found in 35 out of 100 gastric adenocarcinomas belonging to intestinal (19/64) as well as diffuse (16/36) types according to Laurén's classification, often accompanying the other mucus‐associated gastric Ml and M2 antigens. This M3 antigen was predominant over the gastric M antigens in 25 of these 35 tumors; 18 of these belonged to the histological intestinal type. According to the WHO classification, the M3 antigen was found to predominate in all mucinous adenocarcinomas (7/7), was never present in the undifferentiated carcinomas (0/8), but was also found in some tubulo‐papillar (16/57) and signet‐ring cell (12/27) adenocarcinomas. This antigen could be used as a new criterion and incorporated into a point system containing morphological and tumor cell behavioral considerations; then it would appear to be a good marker for intestinal‐type differentiation. Indeed, 22 of these 25 gastric adenocarcinomas which produced predominantly M3 antigen showed such an intestinal‐like differentiation. The M antigenic pattern of gastric carcinoma suggested a duodenal rather than colonic‐type differentiation.
The role of chromosome 15 in murine leukemogenesis. I. Contrasting behavior of the tumor vs. normal parent‐derived chromosomes no. 15 in somatic hybrids of varying tumorigenicity
Authors: Spira Jack , Wiener Francis , Babonits Magda , Gamble Jenny , Miller Jacques , Klein George 
Published: February 2007

AbstractG‐banding analysis was carried out on a series of hybrids derived from the fusion of a chromosome 15‐trisomic murine T‐cell leukemia of AKR origin and normal diploid fibroblasts or lymphocytes of the CBT6T6 strain. Due to the 14; 15 translocation involved in the generation of the T6 marker, the chromosomes No. 15 and 14 derived from the normal and the tumor parent can be distinguished cytogenetically. Highly tumorigenic, in vitro maintained hybrids, and high‐tumorigenic segregants of originally low‐tumorigenic in vitro hybrids, selected by in vivo passage, showed a similar cytogenetic pattern. It was characterized by the amplification of the tumor‐derived chromosomes No. 15 from the expected 3 to 5.5 ± 0.2 copies and a concomitant decrease of the normal derived T(14;15)6 from 2 copies to 0.9 ± 0.2. All other autosomes except No. 14 showed only minor random variations, around the expected number of 4 copies. The tumor‐derived chromosome 14 was amplified from the expected 2 to 3 copies. The lowtumorigenic hybrids showed the opposite pattern with a decrease in the number of the tumor‐derived 15 chromosome from 3 to 2.6 ± 0.1 and the maintenance of the two normal parent derived T(14;15)6 chromosomes. These findings suggest the existence of a qualitative difference between the 15 chromosomes derived from the tumor vs. the normal parent, due to mutation or proviral DNA insertion in the tumor‐derived homologue. Amplification of the changed locus and a decrease in the dosage of its normal counterpart appear to favor tumorigenicity.
Luteinizing hormone‐releasing factor increases release of human chorionic gonadotrophin in isolated cell columns of normal and malignant trophoblasts
Authors: Bützow R. 
Published: February 2007

AbstractThe effect of synthetic luteinizing hormone‐releasing factor (LRF) on release of human chorionic gonadotrophin (hCG) was studied by isolated cell columns of normal syncytiotrophoblasts and choriocarcinoma (BeWo) cells. After LRF stimulation the release of hCG by the normal trophoblasts increased up to 4‐fold and release by the malignant trophoblasts increased up to 6‐fold, indicating a specific effect of LRF on normal and malignant trophoblast cells.
Age at menarche, probability of ovulation and breast cancer risk
Authors: Macmahon Brian , Trichopoulos Dimitrios , Brown James , Andersen A. P. , Aoki Kunio , Cole Philip , Dewaard Frits , Kauraniemi Tapani , Morgan Robert W. , Purde Maret , Ravnihar Božena , Stormby Nils , Westlund Knut , Woo Ngai‐Chen 
Published: February 2007

AbstractAn analysis is undertaken of the frequency of ovulation in 17 groups of women aged 15 to 19 who had been the subjects of other studies. A urine specimen of at least 8 h accumulation had been provided on the 20th or 21st day of a menstrual cycle by 681 women. Analysis is restricted to 431 specimens which had been collected between 11 and 3 days prior to the onset of the subsequent menstrual period. A pregnanediol concentration of less than 1 mg per litre in such a specimen was taken as evidence that the cycle was anovular. The probability of a cycle being anovular was inversely and significantly related to the number of years since menarche, and, with years since menarche held constant, was positively but not significiantly associated with age at menarche. This observation indicates that women with early menarche do not have a longer duration of exposure to anovular cycles than do those whose menarche is delayed, and that variation in the duration of exposure to post‐menarcheal anovular cycles does not explain the association of breast cancer risk with early age at menarche. The 17 groups of women were classified into four categories according to ethnic origin and breast cancer incidence in the populations from which they derived. Anovular cycles were not more common in the high‐risk groups; indeed, the two centers in the lowest risk category had the highest proportion of anovular cycles.
Serum concentrations of total and non‐protein‐bound oestradiol in patients with breast cancer and in normal controls
Authors: Moore J. W. , Clark G. M. G. , Bulbrook R. D. , Hayward J. L. , Murai J. T. , Hammond G. L. , Siiteri P. K. 
Published: February 2007

AbstractIn premenopausal women with breast cancer, total serum oestradiol (E2) concentrations are normal but nonprotein‐bound E2, concentrations are significantly raised. This is not due to low sex‐hormone‐binding‐globulin (SHBG) binding capacities which are within the normal range and is unlikely to be due to the small but significant decrease in albumin concentrations. In post‐menopausal patients, both total and non‐protein‐bound E2 are significantly raised: this may be explained partially by lower SHBG binding capacities. In patients and controls there is a highly significant correlation between non‐protein‐bound E2 and SHBG but, for a given SHBG binding capacity, the patients have more non‐bound E2 than controls. It is concluded that the breast in women with breast cancer may be exposed to elevated levels of biologically active E2 although the reasons for this remain obscure.
Modulation of T leukaemic cell phenotype with phorbol ester
Authors: Delia D. , Greaves M. F. , Newman R. A. , Sutherland D. R. , Minowada J. , Kung P. , Goldstein G. 
Published: February 2007

AbstractA panel of monoclonal antibodies and other markers (e.g., terminal deoxynucleotidyl transferase, sheep erythrocyte rosettes, peanut agglutinin) have been used in conjunction with flow cytometry and biochemical analysis to monitor the induction of maturation in human thymic (T) leukaemic cell lines by phorbol ester (TPA). Seven cell lines underwent multiple phenotypic alterations in response to TPA but were unresponsive to synthetic thymic hormones (TP5, FTS) or to other compounds (e.g. DMSO, retinoic acid) which induce maturation in other types of leukaemia. The changes parallel those observed in normal T‐cell differentiation and partly reflect alterations in glycosyl transferase activity, altered synthesis of proteins and regulation of cell surface receptors (for transferrin) associated with rapid growth and metabolism. These studies further illustrate the reversibility of maturation arrest in human leukaemia and provide support for the view that leukaemia may involve regulatory defects in the coupling of proliferation and maturation. Induction or promotion of terminal differentiation in leukaemic equivalents of T‐cell precursors may provide a convenient system for the study of biochemical and molecular events involved in T‐cell development and diversification.
Characterization of human cells persistently infected with cytomegalovirus and exposed to a chemical carcinogen
Authors: Li Jui‐Lien H. , Albrecht Thomas 
Published: February 2007

AbstractA non‐productive, persistent human cytomegalovirus (CMV) infection was developed in human embryo lung (LU) cells by initially using supraoptimal temperatures to restrict the replication of a recent CMV isolate (76‐24). Although CMV replication was observed in some cells within a few weeks of shifting the cultures to 37°C and subculturing, CMV cytopathic effects and infectious CMV were not detected with further subculturing during the next 5 weeks. CMV‐specific nuclear antigens were, however, observed in most cells (designated LU‐76‐24) for 38 additional culture passages made during the following 12 months. Although the LU‐76‐24 cells were morphologically distinct from LU cell cultures carried in parallel as controls, the LU‐76‐24 were contact‐inhibited in spite of a somewhat disoriented growth pattern. Treatment of LU‐76‐24 cells with 0.05 μ/ml of the chemical carcinogen 4‐nitroquinoline I‐oxide (NQO) induced a lytic CMV infection from which a clone of cells (designated LUC‐NQO) was isolated. No effect was seen when LU cells were treated with the same dose of NQO. LUC‐NQO cells were morphologically altered from LU‐76‐24 cells and had lost contact inhibition. Even though CMV‐specific nuclear antigens were observed in LUC‐NQO cells, infectious CMV was not detected in lysates of these cells, nor was CMV rescued by co‐cultivation of these cells with susceptible cells or by induction with 5‐iodo‐2′‐deoxyuridine. LUC‐NQO, but not LU or LU‐76‐24 cells, plated with good efficiency in semi‐solid medium. The results indicate that long‐term, non‐productive, persistent CMV infections can be established in vitro and suggest that such cells may be more susceptible than non‐infected cells to the action of chemical carcinogens.
Synergistic effect of cis‐dichlorodiammineplatinum and 5‐aza‐2′‐deoxycytidine on mouse leukemic cells in vivo and in vitro
Authors: Veselý J. 
Published: February 2007

Abstractcis‐Dichlorodiammineplatinum and 5‐aza‐2′‐deoxycytidine display a considerable synergistic effect in L1210 and La mouse leukemia in vivo; the combination of both drugs is also clearly synergistic in vitroas evidenced by the effects on cell growth and cell survival in soft‐agar medium. In exponential but not in stationary growth of L1210 cells, the drugs interfere with DNA and RNA synthesis.
Clinical evaluation of NCA in patients with chronic myelocytic leukemia
Authors: Wahren B. , Rudén U. , Gahrton G. , Hammarstöm S. 
Published: February 2007

AbstractNCA, a normal colon and granulocyte antigen, which has been found in large amounts in myelocytes and metamyelocytes and in smaller amounts in neutrophil granulocytes, was studied in 50 CML patients in various stages of the disease. Radioimmunoassay was used to demonstrate NCA in serum. Untreated CML patients had a mean level of 732 μg NCNI, poorly controlled patients 421 μg/l and well‐controlled patients 160 μ/I. These valuer differ significantly from the mean of healthy persons, which was 71 μg NCN/I. The serum NCA levels were related to the number of maturing myeloid cells in blood, and to the clinical course in the chronic phase of CML In blast crisis low values with a mean of 109 μg NCNI was found. Patients with ANLL had a low mean level, 50 &I. Low levels of NCA could not be attributed to antibodies to NCA. NCA is a normal myeloid differentiation antigen. Despite this, its Occurrence in serum in leukemic patients differs from normai. This probably has to do with the abnormal amount as well as the release of NCA by leukemic maturing myeloid cells.