bluuebunny/crossref_metadata_2025_split huggingface dataset:
Tumorigenic conversion of xeroderma pigmentosum lymphoblastoid cells without karyotypic alteration
Authors: Tachibana Akira , Toyoda Mariko , Mitani Hiroshi , Sasaki Masao S. , Arita Izumi , Takebe Hiraku , Tatsumi Kouichi 
Published: February 2007

AbstractIn order to examine the process of malignant transformation of human somatic cells, we studied the tumorigenic conversion of an Epstein‐Barr‐virus‐immortalized lymphoblas‐toid cell line (LCL) derived from a patient with xeroderma pigmentosum (XP) complementation group A. Repeated irradiation of the XP cells, XP7NI, with UV‐light and subsequent treatment with l2‐0‐tetradecanoylphorbol‐l3‐acetate (TPA) resulted in the acquisition of tumorigenicity in athymic nude mice. The tumorigenicity of XP7NI cells was also induced by TPA treatment alone. The tumors formed in athymic mice were of B‐cell lymphoma with characteristic histology, cell surface immunoglobulins and an antigen as detected by a B‐cell‐specific monoclonal antibody (MAb), CD20. The surface immunoglobulins and the HLA type of these tumor cells were identical with those of the parental cells. These malignantly transformed cells retained the same UV sensitivity, serum requirement, colony‐forming ability in soft agar, and normal human karyotype as the parental cells. Unlike other tumorigenic lymphoblastoid cell lines, this XP lympho‐blastoid cell line provides a unique case in that process(es) leading to tumorigenicity may be induced by UV and TPA without apparent karyotypic changes.
Bladder cancer and occupational exposure to polycyclic aromatic hydrocarbons
Authors: Bonassi Stcfano , Mfrlo Franco , Pearce Neil , Puntoni Riccardo 
Published: February 2007

AbstractThe association between occupational exposure to polycy‐clic aromatic hydrocarbons (PAH) and bladder cancer development was investigated in a population‐based case‐control study carried out in the Bormida valley, Italy. One hundred and twenty‐one male cases and 342 male controls, matched by age were collected from local hospitals. Occupational exposure to PAH and aromatic amines (AA) was evaluated by means of a job exposure matrix, constructed specifically for this study. Subjects considered as sharing a “definite exposure to PAH” showed an increased risk even after adjustment for cigarette smoking and exposure to AA (OR = 2.14, 95% CL 0.82‐5.60). No elevation in risk was found for the category “possible exposure to PAH” (OR = 1.05, 95% CL 0.45‐2.44). The findings of this study are consistent with previous studies indicating PAH as a risk factor for bladder cancer. A possible residual confounding effect due to AA impurities is discussed.
Bispecific antibodies reactive with the multidrug‐resistance‐related glycoprotein and CD3 induce lysis of multidrug‐resistant tumor cells
Authors: van Dijk J. , Tsuruo T. , Segal D. M. , Bolhuis R. L. H. , Colognola R. , van de Griendleuren R. J. , Fleuren G. J. , Warnaar S. O. 
Published: February 2007

AbstractWe describe the lysis of multidrug‐resistant (MDR) tumor cells by various lymphocytic effector cells, retargeted with bispecific antibodies (heteroconjugates). The Ab‐hetero‐conjugate used was prepared by chemically cross‐linking the OKT3 monoclonal antibody (MAb) reactive with CD3 antigen on T lymphocytes, with the MRKI6 MAb, which recognizes the MDR‐associated P‐glycoprotein. Cloned TCRαβCD3+ T lymphocytes, OKT3‐activated peripheral‐blood mononuclear cells and peripheral‐blood mononuclear blood lymphocytes, stimulated with allogeneic irradiated cells in a mixed lymphocyte culture, could be induced to lyse MDR ovarian tumor cells in the presence of Ab‐heteroconjugate CD3/MRKI6, whereas the drug‐sensitive parental tumor cells lacking the P‐glycoprotein were not lysed by these retargeted effector cells. Cloned TCRγδ5/CD3+ T lymphocytes showed a high MHC‐unrestricted lysis of MDR tumor cells. Addition of Ab‐heteroconjugate CD3/MRKI6 could therefore not enhance target‐cell lysis. Melanoma tumor cells transfected with the mdr‐l gene which codes for the P‐glycoprotein were also efficiently lysed by Ab‐heteroconjugate retargeted cloned TCRαβ/CD3+ T cells. Tumor cell lines derived from organs known to express the P‐glycoprotein also were lysable by the retargeted effector cells.
Frequent clonal chromosomal changes in human non‐malignant tumors
Authors: Teyssier J. R. , Ferre D. 
Published: February 2007

AbstractA cytogenetic analysis has been performed on 109 nonmalignant human solid tumors of various histological types after short‐term culture. These tumors were derived from epithelial, mesenchymal, embryonal and neurogenic tissues. The chromosome count was in the diploid range in virtually all specimens. Clonal chromosomal changes were found in 37% of tumors: 20% had numerical deviations, 12% structural rearrangements, and 5% both karyotypic alterations. Chromosome 7 was most frequently involved in 25% of abnormal specimens. Our results suggest that chromosomal changes contribute to non‐malignant tumorigenesis and that their analysis may provide information about the genetic events which shift benign tumor cells to malignant behavior.
Risk of cancer in women receiving hormone replacement therapy
Authors: Adami Hans‐Olov , Persson Ingemar , Hoover Robert , Schairer Catharine , Bergkvist Leif 
Published: February 2007

AbstractCancer risk following treatment with non‐contraceptive estrogens was studied in a population‐based cohort of 23,244 women. Complete follow‐up for an average of 6.7 years revealed 1,087 incident cancers versus 962.5 expected (relative risk/RR/= 1.13; 95% confidence interval 1.10–1.20). We confirmed the recent findings of a more detailed analysis of the same cohort, based on a I‐year shorter follow‐up period, namely: a markedly increased risk of endometrial cancer (RR = 1.8; 1.5–2.1), notably in women receiving potent estrogens, i.e., conjugated estrogens or estradiol (RR = 2.0; 1.6–2.4), and a slightly increased risk of breast cancer (RR = 1.1; 1.0–1.2). A slightly decreased risk of invasive cervical cancer (RR = 0.8; 0.5–1.2) is most likely due to more frequent smear taking than in the background population. There was no increase in the risk of cancer of ovary (RR = 1.0; 0.8‐1.2), pancreas (RR = 0.8; 0.5–1.2), large bowel (RR = 1.0; 0.8–1.2) or kidney (RR = 1.0; 0.7–1.4). The risk of developing cancer in liver or biliary tract was lower than expected (RR = 0.4; 0.2–0.7), particularly in women who had used potent estrogens (RR = 0.3; 0.1–0.6), an unexpected finding which warrants further studies. Increased risks of malignant melanoma (RR = 1.5; 1.0–2.1) and lung cancer (RR = 1.3; 0.9–1.7) need cautious interpretation because of their low magnitude, the absence of a biological gradient when subgroups were analyzed and the slightly higher prevalence of smokers in the cohort than in the background population.
Staurosporine stimulates expression of the urokinase‐type (u‐PA) plasminogen activator in LLC‐PK1 cells
Authors: Dierks‐Ventling Christa , Knesel Jaromir , Nagamine Yoshikuni , Hemmings Brian A. , Pehling Gundula , Fischer Franz , Fabbro Doriano 
Published: February 2007

AbstractIn LLC‐PK1 porcine epithelial cells, the urokinase‐type plasminogen activator (u‐PA) mRNA and protein can be induced either by stimulation of the protein kinase C (PKC) pathway using a tumor promoter (PMA) or by stimulation of the protein kinase A (PKA) pathway with calcitonin (SCT). By contrast, addition of 10−7 M staurosporine, an inhibitor of PKC, to LLC‐PK1 cells also stimulated urokinase production. In contrast to the in vitro situation (where staurosporine inhibited PKC activity), in the cell‐culture system the microbial agent caused an early translocation of PKC and inhibited PKA. Addition of staurosporine together with PMA or with SCT further increased urokinase mRNA and protein synthesis. Maximal stimulation was obtained when all 3 agents were added together. We thus assume that in LLC‐PK, cells the PKA and PKC signal‐transferring pathways can function independently.
Morphological and immunological characteristics of a rat choriocarcinoma
Authors: Verstuyf A. , Sobis H. , Vandeputte M. 
Published: February 2007

AbstractA post‐gestational rat choriocarcinoma has been studied for its immunological and morphological characteristics. The tumor can be transplanted in syngeneic (WKA/H rats) as well as in allogeneic rats (BN, R/A). Even after immunization of the allogeneic hosts with tissues of the WKA/H rats, the development of the tumor was not inhibited. This neoplasm is composed of giant cells, surrounding spaces filled with blood, and of proliferating cytotrophoblasts. Ultrastructurally, these cells are very similar to those found in normal rat placenta. In some rats lung metastases were also observed. The tumor is hormonally active as demonstrated by proliferation of and secretions from the mammary glands in tumor‐bearing animals and by the presence of Δ5‐3β‐hydroxysteroid dehydrogenase in the giant cells of the neoplasms. These 2 findings indicate that the rat choriocarcinoma cells secrete lactogen and might produce progesterone, like cells of rat placenta. All the described features of this tumor point to its similarity to human choriocarcinoma.
Suppression of focus formation by bovine papilloma virus‐transformed cells by contact with non‐transformed cells: Involvement of sugar(S) and phosphorylation
Authors: Yoshikura H. 
Published: February 2007

AbstractFocus formation by bovine papilloma virus‐transformed C127 cells was inhibited by direct contact with non‐transformed C127 cells. The suppressive capacity of C127 cells was abolished by introduction of the neomycin resistance gene (neor) but not by that of the hygromycin resistance gene (hygrr).Though both genes code for phosphotransferase which inactivates the aminoglycoside antibiotics, their substrates are different, i.e.,there is no cross‐resistance between them. As the neomycin phosphotransferase phosphorylates the specific hydroxyl group of the sugar in the aminoglycosides, such as 3′OH of the glucose residue of kanamycin A, some specific sugar(s) on the molecules exposed on the cell surface must be responsible for the suppressive signal and their phosphorylation must have resulted in the loss of that signai. The sugar must have the structure shared by kanamycin, neomycin or G418 but not by hygromycin B. Involvement of sugar was also suggested by the observation that conca‐navalin A partially abrogated the suppressive capacity of C127 cells.
Synergism of cisplatin and mitomycin C in sensitive and resistant cell subpopulations of a tumor model
Authors: Durand Ralph E. 
Published: February 2007

AbstractCisplatin is a widely‐used anti‐neoplastic agent with activity against a broad spectrum of human solid tumors. It is, however, seldom curative as a single agent. In an in vitro tumor model system, V79 spheroids, the non‐cycling, hypoxic cell subpopulations are most resistant to cisplatin, suggesting that combination chemotherapy with cisplatin and a drug which preferentially killed hypoxic cells might prove useful. Mitomycin C has the latter activity, and was thus evaluated. Not only was the expected complementary toxicity observed in combination treatments, but synergism between the drugs was found at clinically relevant drug doses. Further, both the net pattern of cell killing and the degree of interaction between the agents were a function of the dose ratios of the drugs in the combination treatments. The ability of mitomycin C to potentiate the response of cells resistant to cisplatin as a single agent may thus prove of value in clinical protocols.
Factors influencing the time and site of leukemic transformation of factor‐dependent cells after injection into irradiated recipient mice
Authors: Dührsen Ulrich , Metcalf Donald 
Published: February 2007

AbstractAfter cells of the non‐tumorigenic‐factor‐dependent line FDC‐PI are injected into irradiated DBA/2 mice a progressive increase occurs in the number of engrafted FDC‐PI cells and eventually leukemic transformation occurs. Step‐wise increase in the number of cells injected led to an increasingly rapid accumulation of untransformed FDC‐PI cells in the hemopoietic organs and some shortening of the pre‐leukemic phase. FDC‐PI cells explanted from pre‐leukemic mice differed from primary FDC‐PI cells in that they were able to undergo leukemic transformation in non‐irradiated recipients after short latent periods. Pre‐leukemic populations contained FDC‐PI variants with an improved ability to proliferate in non‐irradiated tissues. Co‐injection of normal marrow cells delayed the leukemic transformation of injected FDC‐P cells. The accelerating effect of prior irradiation of the recipient on leukemia development was also abrogated when the injection of FDC‐PI cells was delayed by several weeks. No specific site of transformation could be determined in mice with very early leukemias. Proliferation of untransformed FDC‐PI cells and the emergence of variants with improved adaptation to in vivo conditions appear to be important and possibly necessary steps in the pathogenesis of the disease. Whether the host contributes actively to the final transformation process remains speculative.
Volatile nitrosamine levels and genotoxicity of food samples from high‐risk areas for nasopharyngeal carcinoma before and after nitrosation
Authors: Poirier S. , Bouvier G. , Malaveille C. , Ohshima H. , Shao Y. M. , Hubert A. , Zeng Y. , De Tehé G. , Bartsch H. 
Published: February 2007

AbstractTraditional life‐style, especially food habits, infection by Ep‐stein‐Barr virus (EBV) and genetic factors, have been associated with an increased risk of nasopharyngeal carcinoma (NPC). N‐Nitroso compounds and other carcinogens either present in food or formed endogenously, as well as food constituents that activate EBV, have been suspected as etiological factors in NPC pathogenesis. For their characterization preserved food items, frequently consumed in NPC endemic areas in Tunisia, South China and Greenland, were sampled and screened for the presence of mutagens and volatile nitro‐samines before and after nitrosation. Aqueous extracts as well as 2 organic extracts of the samples were assayed for genotoxicity in 2 Salmonella typhimurium strains and the SOS chromotest. The same extracts had previously been analyzed for volatile nitrosamines and for EBV‐activating substances in Raji cells. In our study, 13 out of 16 food samples showed a weak, directly‐acting genotoxicity in the SOS chromotest in at least one of the extracts, but only one sample from Greenland was found to be weakly mutagenic in Salmonella TA 98. Chemical nitrosation for 9 out of 15 samples of aqueous food extracts increased the genotoxic effect in the SOS chromotest. Levels of volatile nitrosamines were also elevated for 12 out of 15 samples; highest levels of N‐nitroso‐dimethylamine were found in hard salted and dried fish from China (1,200 μg/kg) and highest N‐nitrosopyrrolidine levels in a Tunisian spice (3,840 μg/kg). In non‐nitrosated aqueous food extracts, the level of volatile nitrosamines and genotoxic activities were not correlated with the EBV‐inducing activity of the same samples. After chemical nitrosation, EBV‐inducing activity was decreased or showed no change and was not correlated with increases in either the genotoxicity or the nitro‐samine levels. Our results suggest that EBV‐activating compounds belong to a different class of substances. However, there was an association between the changes in genotoxicity and nitrosamine levels due to nitrosation.
Measurement of 5′‐methylthioadenosine in patients with neoplasms
Authors: Kaneko Kiyoko , Fujimori Shin , Kanbayashi Takaaki , Miyazawa Yukihisa , Kumakawa Toshiro , Fujii Hisaichi , Miwa Shiro , Kamatani Naoyuki , Akaoka Leo 
Published: February 2007

AbstractThe amount of polyamines in urine from patients with various neoplasms is larger than in normal subjects. We have determined the concentration of 5′‐methylthioadenosine (MTA), a by‐product of the polyamine biosynthesis, in patients with malignancies as well as normal subjects. Our studies indicate that the amount of MTA in urine from patients with leukemias and malignant lymphomas was higher than in normal subjects (p <0.005). Urine samples from patients with other malignancies contained normal amounts of MTA. The levels of blood MTA in patients with leukemias before treatment or in relapse was higher than in control subjects (p <0.005), while in patients with other malignancies and leukemia in remission, the levels were not different from control subjects. Peripheral blood MTA levels clearly decreased after effective chemotherapy. The measurement of MTA levels in urine and blood may not be as useful as polyamine assays for the detection of malignancies, but blood levels of MTA may be useful as an indicator of the efficacy of chemotherapy in leukemic patients.
Chromosome aberrations in metastatic ovarian cancer: Relationship with abnormalities in primary tumors
Authors: Bello M. Josefa , Rey Juan A. 
Published: February 2007

AbstractTwenty malignant effusions secondary to ovarian cancer have been cytogenetically analyzed directly and after short in vitro culture. With the exception of one sample characterized by trisomy 3, all cases displayed clonal structural rearrangements. Chromosomes 1 and 3 were most frequently involved in the genesis of markers. Abnormalities of chromosomes 5, 6, 9, 11 and 12 were also recurrently found, and double minutes (DM) were observed in 2 samples. Our results agree with previous findings on the preferential involvement of chromosomes 1, 3 and 6 in ovarian carcinomas, and suggest that rearrangements of certain chromosomes are non‐random but are secondary to the malignant progression of these tumors.
Murine spontaneous T‐cell leukemia constitutively expressing IL‐2 receptor—a model for human T‐cell malignancies expressing IL‐2 receptor
Authors: Lugasi Hefziba , Hajos Silvia , Murphy John R. , Strom Terry B. , Nichols Jean , Peñarroja Carlos , Naor David 
Published: February 2007

AbstractWe describe a new, spontaneously occurring BALB/c‐derived murine T‐cell leukemia. The leukemic cells, designated LB, grow rapidly and progressively in the syngeneic host with no signs of effective immunological resistance. LB cells expressed the Thy‐1+, Lyt‐2+, L3T4‐, CD3‐ class‐1+, CD25+ (IL‐2 receptor, IL‐2R), class‐II‐, gp70‐ phenotype. As LB cells express IL‐2, as indicated by staining with 2 distinct anti‐CD25 IL‐2R monoclonal antibodies (MAbs), the therapeutic efficacy of IL‐2‐diphtheria toxin‐related protein was tested on this leukemic model. IL‐2‐diphtheria toxin, but not diphtheria toxin, efficiently inhibited the proliferation of LB cells. The proliferation of a murine myeloma cell line, which does not express IL‐2R, was not inhibited by IL‐2‐diphtheria toxin. The possible implantation of this animal model in fundamental and practical studies is discussed.
A possible mechanism for increased breast cell proliferation by progestins through increased reductive 17β‐hydroxysteroid dehydrogenase activity
Authors: Coldham N. G. , James V. H. T. 
Published: February 2007

AbstractWe have investigated whether progestins may be able to regulate breast cell proliferation by altering the fraction of oestradiol relative to oestrone, using the human breast cancer cell line MCF‐7. The ability of the two oestrogens, oestradiol and oestrone, to stimulate breast tumour cell proliferation was investigated. Oestradiol in concentration was of 10‐fold greater proliferative potency than oestrone. The progestin MPA increased both reductive and oxidative 17β‐hydroxysteroid oxidoreductase activity when the tissue culture media pH indicator phenol red was included in the media. When phenol red was excluded from the tissue culture media, MPA increased predominantly the reductive 17β‐hydroxysteroid oxidoreductase activity, and to a far greater extent than in the presence of phenol red. Other progestins such as levonorgestrel, norethisterone and norethisterone acetate also increased predominantly reductive 17β‐hydroxysteroid oxidoreductase activity in the absence of phenol red. The action of MPA on reductive 17β‐hydroxysteroid oxidoreductase activity was increased by treatment with oestradiol to a small but significant extent. We propose that the progestational increase of reductive 17β‐hydroxysteroid oxidoreductase activity is a possible mechanism by which progestins may increase breast cell proliferation in vivo.
Screening for lung cancer in the middle‐aged
Authors: Berndt R. , Nischan P. , Ebeling K. 
Published: February 2007

AbstractA screening programme for lung diseases has been in operation in the German Democratic Republic for more than 3 decades. The programme is based on biennial chest X‐rays (70 × 70 mm posterior‐anterior) of the population 40 years of age or over. With respect to lung cancer the results show that, for the population under 60 years of age, the adjusted relative risk of dying from lung cancer among subjects who took part in the last screening round compared with subjects who did not but were screened at least once during the preceding 10‐year period was 0.93 (95% confidence interval 0.65–1.33).
Procoagulant activity of mononuclear phagocytes from different anatomical sites in patients with gynecological malignancies
Authors: Semeraro N. , Montemurro P. , Conese M. , Giordano D. , Stella M. , Restaino A. , Cagnazzo G. , Colucci M. 
Published: February 2007

AbstractMononuclear phagocytes exhibit complex interactions with cancer cells and might contribute to fibrin formation associated with malignancy through the production of procoagulant activity (PCA). We have studied the PCA of peritoneal macrophages in 8 patients with advanced (stages III or IV) ovarian cancer and of macrophages from regional lymph nodes in 14 patients with limited (stages I or II) uterine cancer; peritoneal and lymph‐node macrophages from patients with benign gynecological tumors were used as reference cell populations. In all patients, PCA of blood monocytes was also studied. Peritoneal and lymph‐node macrophages obtained from patients with ovarian and uterine cancer, respectively, expressed far higher levels of basal PCA than the corresponding cell populations from patients with benign tumors (p <0.001). PCA of blood mononuclear cells from patients with ovarian, but not with uterine cancer, was significantly higher (p <0.001) than that of control cells. High levels of D‐dimer, a specific product derived from plasmin‐induced degradation of stabilized fibrin, were found in all ascitic fluids and in all plasma samples but one from patients with ovarian cancer. In contrast, all controls and all uterine cancer patients but one had normal plasma D‐dimer. Our findings suggest that local activation of host macrophages for PCA production might contribute to fibrin formation within the tumoral mass. In advanced cancer, blood monocytes may also be activated to produce PCA and thus contribute to activation of intravascular coagulation and, possibly, to thrombo‐embolic complications frequently associated with disseminated malignancy.