bluuebunny/crossref_metadata_2025_split huggingface dataset:
Enhancement of azoxymethane‐induced colon carcinogenesis in spontaneously hypertensive rats
Authors: Tatsuta Masaharu , Iishi Hiroyasu , Baba Miyako , Taniguchi Haruo 
Published: February 2007

AbstractThe incidence, number, location, and histological types of colon tumors induced by azoxymethane (AOM) and the tissue norepinephrine concentration of the colon wall were investigated in spontaneously hypertensive (SH) rats and in control normotensive Wistar Kyoto (WKY) rats. All rats received 10 weekly s.c. injections of AOM. At week 30, the incidence of colon tumors was significantly higher in SH than in WKY rats. Colon tumors were chiefly located in the proximal colon in WKY but were found with significant frequency in the distal colon in SH rats. The colon tumors induced were mainly adenocarcinomas, but no significant difference in histological type of adenocarcinoma was found between the 2 strains of rat. At weeks 8 and 30, the norepinephrine concentration and labelling index of the distal colon, but not of the proximal colon, were significantly higher in SH than in WKY rats. These findings indicate that increased sympathetic nervous system activity enhances the development of colon tumors.
The use of a genotypic marker to demonstrate clonal dominance during the growth and metastasis of a human breast carcinoma in nude mice
Authors: Price Janet E. , Bell Carl , Frost Philip 
Published: February 2007

AbstractWhen a mixture of 11 clones of a human breast carcinoma (MDA‐MB‐435)—each clone transfected with pSV2neo and identified as having a unique insertion site of the gene—was injected into nude mice, the resulting tumors were found to contain only one clone (Neo 24). This clone, identified by the unique restriction fragments on Southern blot analyses, was also found in metastases recovered from the lungs and lymph nodes of the animals. The individual clones showed no differences in in vitro growth, while in vivo the Neo 24 cells produced the largest tumors. Thus, one explanation for the observed clonal dominance in this study could be the more rapid growth in vivo of the Neo 24 cells. This study illustrates how an introduced selectable gene marker can be used in lineage studies of human tumor cell populations.
Cytokinetic investigation of lung tumors using the anti‐bromodeoxyuridine (BUDR) monoclonal antibody method: Comparison with dna flow cytometric data
Authors: Teodori Laura , Trinca Maria Luisa , Goehde Wolfgang , Hemmer Jorg , Salvati Franco , Storniello Giuseppe , Mauro Francesco 
Published: February 2007

AbstractIn order to investigate the cytokinetics of malignant tumors and non‐malignant lesions of the lung, tissue samples from 57 patients affected by non‐small‐cell carcinoma (NSCLC), small‐cell carcinoma (SCLC), and benign and inflammatory lesions have been analyzed using the BUdR monoclonal antibody (MAb) method. This method is based on the preparation, at the time of surgery, of viable monocellular suspensions (using collagenase and DNase treatment) and the concomitant administration of BudR. The percentage of BudR‐labelled cells was monitored by fluorescent microscopy using an FITC‐labelled second antibody. In NSCLC, each histological group showed a wide range of labelling index (LI) values. On the contrary, SCLC exhibited a more homogeneous kinetic behaviour as evidenced by a narrowly distributed, higher LI. Tumors shown to be diploid by flow cytometry did not show a lower LI than aneuploid tumors. Furthermore, differences were constantly observed between the S‐phase percent calculated using BUdR and that calculated using the DNA flow cytometric (FC) histogram, the latter always showing higher S‐phase values. In an attempt to study the intratumor proliferative heterogeneity, multiple‐site sampling was performed. Proliferative heterogeneity seemed to be higher inter‐tumor than intra‐tumor. Finally, a positive correlation (p < 0.05) was found between LI and the actual doubling time (DT) of the primary tumor mass, evaluated using sequential radiographs. In conclusion, the present BUdR method can be considered a useful source of relevant information on in vivo cell growth, in parallel to other clinical (DT) and biological (DNA content) approaches.
Purification and characterization of a peanut‐agglutinin‐binding pancreatic‐cancer‐related serum mucus glycoprotein
Authors: Ching C. K. , Rhodes Jonathan M. 
Published: February 2007

AbstractA high‐molecular‐weight (approximately 3.5 × 103 kDa) peanut agglutinin (PNA)‐binding glycoprotein was previously identified as a tumour marker in pancreatic cancer sera. In the present study the density of this glycoprotein has been estimated and further analysis performed using sequential lectin blotting combined with serial mild acid hydrolysis followed by repeated Smith degradation. This has allowed partial in‐situ characterization of the carbohydrate side‐chains. The PNA‐binding glycoprotein variably expresses the blood group H and sialylated Lewisa antigens. H and sialyl Lea expression disappeared after mild acid hydrolysis and T (PNA acceptor) disappeared after the first Smith degradation step. T (βgal(1‐3)αgalNAc) expression reappeared after a second Smith degradation, suggesting that the backbone regions of the mucin side‐chains with this core sequence are built up by the further addition of at least 2 monosaccharides. A model has been constructed showing the minimum variations in side chain structure that would explain the results of the serial degradation and lectin blotting. Purification and caesium chloride density gradient centrifugation show that the infact PNA‐binding glycoprotein has a density of >1.48 g/ml, characteristic of a mucin. The development of assays using a panel of monoclonal antibodies (MAbs) or lectins directed against the different carbohydrate epitopes expressed on this mucin may provide better diagnostic accuracy for pancreatic cancer than current marker assays which rely on detection of a single epitope.
Inhibitory effect of quercetin on the synthesis of a possibly cell‐cycle‐related 17‐kDa protein, in human colon cancer cells
Authors: Hosokawa Nobuko , Hosokawa Yohei , Sakai Toshiyuki , Yoshida Mitsunori , Marui Nobuyuki , Nishino Hoyoku , Kawai Keiichi , Aoike Akira 
Published: February 2007

AbstractQuercetin inhibits growth of COLO320 DM cells, derived from a human colon cancer. The inhibitory effect is partially reversible when quercetin is removed from the culture medium. Flow cytometric analysis has revealed that quercetin causes perturbation of the cell cycle, inducing a frozen cell‐cycle pattern and a block at the G1/S boundary. The synthesis of a 17‐kDa protein was specifically inhibited by the addition of quercetin, and recovered when the cells at the G1/S boundary progressed into S‐phase after the removal of quercetin from the culture medium. Furthermore, using synchronized cells obtained by centrifugal elutriation, we have shown that the rate of synthesis of a 17‐kDa protein was low in G1, and high in S‐phase of the cell cycle. Thus, this protein appears to be cell‐cycle‐related.
Differentiation capacity of human non‐small‐cell lung cancer cell lines after exposure to phorbol ester
Authors: Salge Ursula , Kilian Peter , Neumann Kurt , Elsässer Hans‐Peter , Havemann Klaus , Heidtmann Hans‐Heinrich 
Published: February 2007

AbstractThree cell lines of squamous‐cell carcinoma and 3 of large‐cell carcinoma origin were investigated for the expression of differentiation markers and functional parameters (proliferation, morphology, cornified envelope formation, involucrin staining, transglutaminase activity, adhesiveness and migration) under normal cell culture conditions and after treatment with the tumor promoter phorbol‐12‐myristate‐13‐acetate (PMA). Although all original tumors had been described as poorly differentiated by histological grading, we found significant heterogeneity in the expression of differentiation markers in cell culture. A systematic grading of the cell lines became possible only after PMA stimulation. PMA generally increased expression of differentiation markers in cell lines of comparably low grades of differentiation, as indicated by dose‐dependent inhibition of proliferation and cloning efficiency, induction of squamous markers, and decreased adhesiveness and cell motility. In contrast, cell lines of apparently higher differentiation by these criteria showed little response to PMA. The results presented show that the assessment of differentiation capacity by comparison of differentiation markers under normal cell culture and PMA‐stimulated conditions in established NSCLC cell lines allows for a refined cell culture grading, which might advance the classification and characterization of such cell lines which, otherwise, appear to be very heterogeneous. It may also help to correlate cellular functions with various states of differentiation in vitro.
Differentiation and the tumorigenic and metastatic phenotype of murine melanoma cells
Authors: Kameyama Koichiro , Vieira Wilfred D. , Tsukamoto Katsuhiko , Law Lloyd W. , Hearing Vincent J. 
Published: February 2007

AbstractUsing B16 F10 murine melanoma cells and sublines generated from the JB/MS melanoma which exhibit various degrees of melanogenesis, the relationships among differentiation, tumorigenicity, and metastatic potential were examined. The effect of melanocyte‐stimulating hormone (MSH), which specifically stimulates differentiation of melanocytes, was also studied. All melanoma lines tested were capable of growing as experimental pulmonary metastases but, surprisingly, the undifferentiated and amelanotic JB/MS‐w cells failed to grow as primary subcutaneous tumors. JB/MS‐w cells, which had few surface MSH receptors, did not respond to MSH with an increase in melanin production, unlike the other cell lines. Although in vitro treatment with MSH did not change the rates of growth of primary tumors by these cell lines, such treatment decreased the number of pulmonary metastases from B16 F10, JB/MS cells, JB/MS‐b1 cells and JB/MS‐w cells. Conversely, MSH treatment significantly increased the rates of pulmonary metastases from JB/MS‐p cells. The expression of surface melanoma antigens, urokinase‐type plasminogen activity and susceptibility to natural killer cells were examined. MSH did not significantly alter surface melanoma antigen expression, but increased the natural killer cell susceptibility of B16 F10, JB/MS and JB/MS‐b1 cells, cells which possess abundant surface MSH receptors. There was an inverse correlation between differentiation (pigmentation) and proliferation in vitro, and the more pigmented melanoma cells (B16 F10, JB/MS and JB/MS‐b1) expressed relatively lower levels of class‐1 MHC, relatively higher levels of class‐11 MHC and the highest metastatic capacity. These results demonstrate that MSH possesses the capacity to regulate not only melanogenesis, but also other factors critical to the metastatic growth of the cells.
Inhibition of N‐methyl‐N′'‐nitro‐n‐nitrosoguanidine‐induced methotrexate and adriamycin resistance in CHO cells by adeno‐associated virus type 2
Authors: Yalkinoglu A. Özkan , Schlehofer Jö Rg R. , Hausen Harald Zur 
Published: February 2007

AbstractWe studied the effects of helper‐dependent parvovirus AAV [adeno‐associated virus] type 2 on carcinogen‐inducible resistance to methotrexate (MTX) and adriamycin (ADR) in Chinese hamster ovary cells. Both types of drug resistance were monitored by determination of the number of drug‐resistant colonies normalized for the respective value of plating efficiency under non‐selective conditions. Treatment of cells with N‐methyl‐N′‐nitro‐N‐nitrosoguanidine (MNNG) drastically enhanced the frequency of resistance to MTX and ADR. By contrast, infection of cells with AAV‐2 prior to treatment with MNNG markedly inhibited carcinogen‐induced drug resistance. Infection by AAV alone did not exert any effect. Analysis of the dihydrofolate reductase (dhfr) gene copy numbers of individual MTX‐resistant clones derived from MNNG‐treated and non‐treated cultures revealed similar frequencies (60–18%) and amplitudes of dhfr gene amplification (2‐ to 8‐fold) irrespective of prior AAV treatment. Hence, carcinogen‐induced enhancement of MTX‐resistance could reflect an increase in the frequency of dhfr gene amplification among the survivors of MNNG treatment. On the other hand, inhibition of carcinogen‐inducible drug resistance by AAV suggests an interference of the virus with cellular responses to genotoxic stress, thus leading to enhanced cell killing under altered growth conditions. Possible mechanisms responsible for the inhibitory effect of AAV and its relevance in relation to tumor chemotherapy are discussed.
Presence of hpv 16 sequences in laryngeal carcinomas
Authors: Pérez‐ayala M. , Ruiz‐Cabello F. , Esteban F. , Concha A. , Redondo M. , Oliva M. R. , Cabrera T. , Garrido F. 
Published: February 2007

AbstractHuman papillomavirus types HPV 16 and HPV II DNA sequences were analyzed in normal and neoplastic tissues of the larynx, using the technique of polymerase chain reaction (PCR). An amplified region of E6 ORF was hybridized with 3′ end‐labelled oligonucleotide probe. Twenty six out of 48 (54%) squamous‐cell carcinomas, and 3 out of 3 verrucous‐cell carcinomas hybridized with HPV 16 DNA sequences, whereas we did not detect HPV II sequences. HPV 16 DNA sequences were also found in normal, autologous mucosa and lymphnode metastases, although these were absent in other tissues analyzed. HPV‐16‐positive tumors were most frequently poorly differentiated squamous‐cell carcinomas.
Human meningiomas co‐express platelet‐derived growth factor (pdgf) and pdgf‐receptor genes and their protein products
Authors: Maxwell Marius , Galanopoulos Theofanis , Tessa Hedley‐Whyte E. , McL. Black Peter , Antoniades Harry N. 
Published: February 2007

AbstractThe present studies investigated the expression of the platelet‐derived growth factor (PDGF) and PDGF‐receptor genes in human meningiomas. Northern blot analysis demon strated that all meningiomas examined expressed both the c‐sis/PDGF‐2 proto‐oncogene and the PDGF‐receptor gene. In situ hybridization localized the c‐sis mRNA and the PDGF receptor mRNA in the tumor cells of the meningioma tissues. Control pachymeninges derived from adult individuals, with out meningiomas, expressed only PDGF‐receptor mRNA but not the c‐sis mRNA. Immunocytochemistry studies detected both the c‐sis and the PDGF‐receptor protein products in me ningioma tissues but only the PDGF‐receptor protein prod ucts in control pachymeninges. These findings indicate the presence of an autocrine mechanism in human meningiomas based on the co‐expression of the c‐sis/PDGF‐2 proto‐onco gene and PDGF‐receptor gene and their protein products. This co‐expression of a potent mitogen and its receptor may contribute to the growth and maintenance of human menin giomas.
Circulating antibodies against c‐MYC oncogene product in sera of colorectal cancer patients
Authors: Ben‐Mahrez Kamel , Sorokine Irène , Thierry Dominique , Kawasumi Toshiyuki , Ishii Sunsuke , Salmon Remy , Kohiyama Masamichi 
Published: February 2007

AbstractWe developed a Western blot assay using purified human c‐myc protein expressed in E. coli in order to look for circulating anti‐c‐myc antibodies in human sera. The presence of IgG antibodies against c‐myc was observed in 25 out of 44 sera from patients with colorectal cancer diagnosed and treated at the Hǒpital Curie in Paris, compared to the sera of 46 normal donors of which only 8 samples were positive (p = 0.001).
Estrone sulfate stimulates growth of nitrosomethylurea‐induced breast carcinoma in vivo in the rat
Authors: Santner Steven J. , Levin Michael C. , Santen Richard J. 
Published: February 2007

AbstractConcentrations of estradiol in human breast tumors from pre‐ and post‐menopausal women are similar whereas plasma levels are 5‐ to 60‐fold lower in post‐menopausal women. The mechanism for maintaining high tumor tissue estrogen levels in post‐menopausal women is unknown but could be related to the ability of plasma estrone sulfate to serve as a precursor for estradiol synthesis in tumor tissue. Estrone sulfate plasma levels are 30‐fold higher than free estradiol levels in postmenopausal women and estrone sulfatase is present in many tissues, including breast tumors, supporting this hypothesis. In this study, we examined the ability of exogenously administered estrone sulfate to stimulate growth of a carcinogeninduced, hormone‐dependent rat mammary tumor and measured the rate of conversion of estrone sulfate to free estrone and estradiol. Castrate rats bearing nitrosomethylurea‐induced mammary tumors were infused with estradiol as a control or estrone sulfate over a 14‐day period. Estradiol at low doses significantly increased tumor volume whereas higher amounts paradoxically inhibited growth. By comparison, estrone sulfate infusions significantly increased tumor volume over that observed in castrate animals on both days 7 and I4 of infusion. To determine whether estrone sulfate was converted to free estrone and estradiol during this protocol, 3H‐estrone sulfate was substituted for unlabelled steroid and castrate animals were again infused for 14 days. At 7, 10 and 14 days of infusion, 18‐26% of estrone sulfate was converted to free estrone and 9‐16% to free estradiol. There were no significant differences between the 2 doses used and the rates of conversion were stable over the infusion period. Conversion of estrone sulfate to free estradiol was also demonstrated by radioimmunoassay of free estradiol in plasma during estrone sulfate infusions. These data demonstrate that exogenously administered estrone sulfate can stimulate mammary tumor growth in castrate animals and support the possibility that estrone sulfate may serve as an important source of tumor tissue estradiol.
Increased fucosylation of high‐molecular‐weight glycoproteins accompanies retinoic‐acid‐induced differentiation of f‐9 embryonal carcinoma cells
Authors: Amos Brad , Lotan Dafna , Lotan Reuben 
Published: February 2007

AbstractRetinoic acid (RA) treatment of F‐9 embryonal carcinoma cells resulted in cell flattening and increased production of laminin Bl chain, both indicating differentiation to endoderm‐like cells. In addition, RA caused a time‐ and dose‐ dependent decrease in growth rate in monolayer culture and a dose‐dependent decrease in the ability of the cells to form colonies in soft agarose. Differentiation was accompanied by an increase in the fucosylation of specific high‐molecular‐weight cellular and cell‐surface glycoproteins. The fucosylation of glycoproteins of Mr 175,000 (gp175), 250,000 (gp250), and 400,000 (gp400) increased as early as 24 hr after the addition of 5 ± 10−6 M RA to the culture medium. These changes preceded both growth inhibition and the induction of laminin BI expression, which were detected 48 to 72 hr after addition of RA. The increased fucosylation of these glycoproteins showed a distinct dose‐response relationship. Both gp 175 and gp250 showed the greatest increase in fucosylation at 10−5 M, which was also the dose at which RA induced laminin maximally, while the fucosylation of gp400 was greatest at 10−8 M RA and declined at higher concentrations. The overall synthesis of large fucosylated glycopeptides decreased in RA‐treated cells, in spite of the increases in the fucosylation of specific cellular glycoproteins. RA‐induced differentiation of F‐9 cells was also accompanied by a time‐ and dose‐dependent increase in fucosyltransferase activity. Although the functions of these glycoproteins are not currently known, the early increase in their fucosylation can be considered as a marker of differentiation in this system.
Establishment of highly metastatic variants of murine colon adenocarcinoma 26 under serum‐free conditions
Authors: Sugimoto Yoshikazu , Oh‐hara Tomoko , Heike Yuji , Watanabe Masahiko , Nakatsuru Yoko , Ishikawa Takatoshi , Tsuruo Takashi 
Published: February 2007

AbstractTumor cell variants were established in vitro by treating a metastatic variant of murine colon adenocarcinoma 26 (P‐26‐select) in serum‐free RPMI 1640 medium for 6 to 10 weeks. Five tumor cell lines were established from independent cultures and designated PS‐I to PS‐5. The PS cells showed higher growth potential in vitro under serum‐free or low‐serum conditions than the parental P‐26‐select. In comparison to P‐26‐select, the PS cell lines possessed enhanced lung‐colonizing ability after i. v. inoculation and metastasized spontaneously to the lung following s. c. inoculation into the flank or the right fore‐footpads of BALB/c mice. Metastatic nodules were also observed in the liver. Spleens and livers of the tumor‐bearing mice were enlarged mainly as a result of hematopoiesis, suggesting the production of CSF‐like substance(s) by the tumor cells. The PS cells secreted increased amounts of putative autocrine growth factor(s) and CSF‐like substance(s) in vitro. These characteristics might be related to the in vivo metastatic ability of the PS cells.
Cancer mortality in rio de janeiro
Authors: Pinto Cynthia Boschi , Coleman Michel P. 
Published: February 2007

AbstractCancer mortality data for 1979‐81 are presented for the state of Rio de Janeiro, Brazil. The population in 1980 was over II million, and more than 30,000 deaths (11% of the total) were certified as being due to cancer during the 3‐year period. Death certification was fairly complete, and for two‐thirds there was complementary medical evidence of the certified cause of death. Cancers of the stomach, lung and female breast accounted for one‐third of all cancers, and cancers of the oesophagus and liver ranked 4th and 5th, respectively, among both sexes combined. Lung cancer mortallty was higher in both sexes (ASR 27.9 in males, 6.1 in females) than elsewhere in Brazil. Mortality from liver cancer (ASR 5.9 in males, 4.5 in females) was more than 8 times higher than in the city of So Paulo. Cervix cancer mortality was only one‐third of that of Fortaleza, a rural state. The results confirm large regional differences in the pattern of cancer mortality within Brazil.
Possible prognostic value of pulmonary ah‐locus‐linked enzymes in patients with tobacco‐related lung cancer
Authors: Bartsch H. , Hietanen E. , Petruzzelli S. , Giuntini C. , Saracci R. , Mussi A. , Angeletti C. A. 
Published: February 2007

AbstractAs prognosis in breast cancer patients has been related to the AHH activity in their breast tissue, we have conducted a similar analysis on pulmonary drug metabolizing enzymes as prognostic markers for male lung cancer patients, primarily investigated for other reasons. A subset of 50 patients with lung cancer related to tobacco use, who had undergone thoracic surgery, was re‐analyzed. The activity of parenchymal aryl hydrocarbon hydroxylase (AHH) and epoxide hydrolase (EH) that had been determined previously in homogenates of non‐neoplastic surgical lung specimens, was used for comparisons of the patients' survival after surgery. When the crude mortality percentages at 1 and 2 years by AHH or EH activity, subdivided into quarters of the distribution, were calculated, a lower mortality was related to lower enzyme levels. Subjects in the 1st and 4th quarters of the distribution showed significant differences in their 1‐year survival for AHH (p = 0.05) and EH (p < 0.01) activities. This relationship could not be accounted for by age, cumulative lifetime smoking, recent or continuing smoking, stage or histological type of disease. Thus, the levels of pulmonary AHH and EH may have some prognostic significance in tobacco‐related lung cancer.