bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stimulation by EGF of the growth of EGF receptor‐hyperproducing tumor cells in athymic mice
Authors: Ozawa Soji , Ueda Masakazu , Ando Nobutoshi , Abe Osahiko , Hirai Masamichi , Shimizu Nobuyoshi 
Published: February 2007

AbstractEGF receptor‐hyperproducing cells of squamous carcinoma origin were inoculated s.c. into the bilatero‐abdominal regions of athymic mice and a mini‐osmotic pump containing EGF was implanted on the back. After 2 weeks the tumors formed from 5 different cell lines in the presence of EGF weighed 3 to 6 times more than those formed in the absence of EGF. The cells recovered from these tumors maintained their original characteristics such as the amplified EGF receptor gene, high numbers of EGF receptors and a sensitivity to EGF‐mediated inhibition of growth in vitro. These results suggest that EGF plays an important role in promoting growth of squamous‐cell carcinoma in vivo.
Analysis of the chromosomal abnormalities of a woodchuck hepatocellular carcinoma‐derived cell line (WH257GE10)
Authors: Matsushita Fumiaki , Ohno Shinsuke , Unoura Masashi , Kobayashi Kenichi , Tanaka Nobuyoshi , Fukuoka Kenichi , Morioka Takeshi , Kaneko Shuichi , Aoyama Syou , Migita Shunsuke , Hattori Nobu 
Published: February 2007

AbstractThe normal woodchuck karyotype was determined by the G‐banding technique, and the chromosomal abnormalities of a woodchuck hepatocellular carcinoma‐derived cell line (WH257GE10) were analyzed and compared with it. The normal woodchuck karyotype was 38, XY in a male, and 38, XX in a female. Autosomes were classified into 2 groups (A and B). Group A consisted of 13 pairs (1–13) of metacentric or submetacentric chromosomes, and group B consisted of 5 pairs (14–18) of telocentric or sub‐telocentric ones. The X chromosome was sub‐metacentric, and the Y chromosome was telocentric. In WH257GE10, the modal number was 36. Deletion of one of the chromosome 5 pair, of the chromosome 13 pair, and of the Y chromosome was observed. Two marker chromosomes (M1and M2) were found. These markers showed the same G‐banded patterns except for a small chromosome fragment at the distal part of the long arm of M1. The chromosome aberrations were very stable through successive passagesin vitro.These findings suggest that the chromosomal abnormalities found in WH257GE10 might be associated with the pathogenesis of woodchuck hepatocellular carcinoma.
Epidemiological features of HTLV‐I carriers and incidence of ATL in an ATL‐endemic island: A report of the community‐based co‐operative study in Tsushima, Japan
Authors: Tajima Kazuo , Kamura Sueo , Ito Shin‐Ichiro , Ito Mizuko , Nagatomo Masazumi , Kinoshita Ken‐Ichiro , Ikeda Shuichi 
Published: February 2007

AbstractTo extend the epidemiological study on adult T‐cell leukemia‐lymphoma (ATL) in japan, the geographical and demographic characteristics of carriers of human T‐lymphotropic virus type I (HTLV‐I) and patients with ATL were analyzed in Tsushima Island, which is one of the typical endemic areas of ATL in Kyushu, japan. Even on the small island of Tsushima (710 km2; pop. 48,875; 123 villages), the positive rates of anti‐HTLV‐1 antibody among the 58 villages studied varied from 2% to 50%, a fact that is probably associated with the historical events affecting the movement of the indigenous population of Tsushima Island. The positive rate of anti‐HTLV‐1 antibody in males increased little with age; however, the female rate increased distinctly with age in moderate and high HTLV‐1‐endemic villages where more than 15% of the inhabitants had positive anti‐HTLV‐1 antibody. Analysis of anti‐HTLV‐1 antibody positivity between spouses confirmed that HTLV‐1 was more contagious from husband to wife than from wife to husband, which corresponded to the fact that the positive rate of anti‐HTLV‐1 antibody in females older than 30 years was higher than that in males. Recently the rate of carrier children from HTLV‐1 carrier mothers was estimated at around 20%. The recent annual incidence rates of ATL among 1,000 HTLV‐1 carriers older than 40 years living in Tsushima Island was estimated at 2.2 in males, 0.8 in females.
Antibody‐antigen complex formation following injection of OC125 monoclonal antibody in patients with ovarian cancer
Authors: Haisma Hidde J. , Battaile Anne , Stradtman Earl W. , Knapp Robert C. , Zurawski Vincent R. 
Published: February 2007

AbstractMonoclonal antibody (MAb) OC125 binds to approximately 80% of epithelial ovarian cancers. Serum antigen, CA125, can be detected in these patients. 1311‐OC125‐F(ab)2 was injected into 5 ovarian carcinoma patients with preinjection serum levels of 150 to 9,000 CA125 U/ml. Patients received the antibody intravenously in doses ranging from 0.46 to 0.94 mg with a specific activity of approximately 2.5 mCi/mg 1311. The half‐ life in the circulation was approximately 30 hr and was independent of serum CA125 levels. Clearance of 1311 from the circulation fitted an open, one‐compartment mathematical model. Gel filtration chromatography revealed antibody‐antigen complexes in sera 15 min after injection of the radiola‐belled antibody. By 5 days after injection, the free form of OC 125 antibody could not be detected in the serum. The rate of complex formation correlated well with the observed preinjection serum CA125 levels. This direct correlation was verified in vitro using purified CA125 antigen and radiola‐beled OC125 F(ab)2 fragments. The specific effects of complex formation on tumor localization remains unclear. However, the presence of complexes should not be ignored, when planning for diagnostic imaging or immunotherapy with OC 125 or other MAbs reacting with circulating antigen.
Absence of the hybrid bcr‐abl mRNA in Ph1‐positive B lymphoblastoid cell lines established from a patient with chronic myelogenous leukemia
Authors: Yamada Toshiyuki , Oikawa Tsuneyuki , Kuzumaki Noboru , Takagi Nobuo , Sasaki Motomichi 
Published: February 2007

AbstractThe expression of c‐abl, c‐sis, c‐myc and N‐ras oncogenes was examined in 2 lymphoblastoid cell lines, one with Ph1 (PB‐1049) and the other without Ph1 (LN‐1049), both established from a patient with chronic myelogenous leukemia (CML), and in a Ph1‐positive cell line (PB‐1049‐T) derived from a tumor formed after transplantation of PB‐1049 cells in a nude mouse with reference to their tumorigenic potential in nude mice. The normal transcripts of c‐abl were detected in all 3 lymphoblastoid cell lines. Although in situ hybridization of v‐abl proved, and restriction endonuclease analyses of the bcr region strongly indicated the occurrence of bcr‐abl rearrangement in PB‐1049 and PB‐1049‐T, we could not obtain any evidence for the expression of the hybrid bcr‐abl mRNA. These results indicate that the Ph1 translocation does not ensure the production of the hybrid bcr‐abl mRNA, and that the expression of hybrid bcr‐abl gene is not essential for the maintenance of tumorigenicity of these cell lines. Expression of c‐sis was not detected in any of the cell lines examined, whereas the expression of c‐myc was uniformly higher in the 3 cell lines than in normal control cells. The levels of N‐ras expression varied considerably, probably in parallel with the changes in tumorigenicity of the cell lines. N‐ras expression in the PB‐1049 and PB‐1049‐T cell lines was higher than that in the LN‐1049 line when they retained tumorigenic potential, but it fell to the level of LN‐1049 with loss or decline of tumorigenicity.
Carcinogenicity of diethylnitrosamine in vitamin‐A‐deficient mice
Authors: Santhanam Uma , Lautha V. S. , Bhide S. V. 
Published: February 2007

AbstractThe effect of suboptimal levels of dietary vitamin A on diethylnitrosamine (DEN) carcinogenesis was studied in BALB/c and Swiss mice. Two different dietary regimens were employed to induce vitamin A deficiency and DEN was administered by gavage at 2 dose levels: 0.6 mg/kg as a single dose and 200 mg/kg in 4 divided doses. Shark liver oil (SLO) which was the main source of vitamin A in the standard diet, was deleted in one regimen and reduced to 25% in the other. The mice maintained on the former diet were given a high dose of DEN and those on the latter diet received a low dose. In both strains the deficient mice had a greater tumour incidence than those on standard diet with a marginal reduction in the latent period. At the low level of DEN there was shift in organotrophy, i.e. from liver in controls to lung in the vitamin‐A‐deficient mice of BALB/c strain. With the higher dose, lung adenomas predominated in deficient as well as control groups in both the strains. Forestomach carcinomas appeared in deficient mice and not in the controls.
Interaction of different steroid hormones during progression of tumour cells to steroid autonomy
Authors: Darbre Philippa D. , King R. J. B. 
Published: February 2007

AbstractProgression to steroid insensitivity poses a major problem in therapy of breast cancer, but studies of the origin of steroid‐insensitive cells have been few and have concentrated in any one system on the loss of response to only one steroid. Since both normal and tumour mammary cells have complex endocrine requirements, we wondered how different steroids might interact during loss of steroid sensitivity. Cloned cells from the androgen‐responsive Shionogi 115 mouse mammary carcinoma respond in vitro to both androgens and glucocorticoids in terms of both cellular and molecular parameters but, following prolonged absence of any steroid, these cells become unresponsive. We show here that 2 steroids can interact to prevent the progression to steroid insensitivity since the S115 cells can be protected against any loss of response to either androgen or glucocorticoid with either steroid alone. Androgen protects against loss of glucocorticoid sensitivity and glucocorticoid protects against loss of androgen sensitivity. The clinical implications are discussed.
Estrogen control of lactate dehydrogenase isoenzyme‐5 in human breast cancer
Authors: Nagai M. A. , Sonohara S. , Brintani M. M. 
Published: February 2007

AbstractDeterminations of estradiol receptor (ER), progesterone receptor (PR), total lactate dehydrogenase activity (LDH) and electrophoretic separation of LDH isoenzymes were performed in cytosols from 118 samples of primary infiltrating ductal mammary carcinoma. ER + PR + tumors demonstrated a significant increase in the proportion of the LDH muscle‐type isoenzyme (LDH5) as compared to ER‐PR‐ samples (p < 0.002). Tumors lacking one of the receptors presented intermediate LDH5 percentages. As total LDH activity bore no relation to either the presence or absence of receptors, the increased proportion represents an absolute elevation of LDH5, suggesting that LDH5 may be a promising hormone‐dependence marker. As an in vitro model to study whether LDH5 was induced by estradiol via ER, we have used two human breast cancer cell lines, MCF‐7 and T47D. In both cell lines LDH5 was the sole isoenzyme. Total ER and PR have been determined by a whole‐cell method, in MCF‐7 cells (with high ER levels), after incubation with 10−10 m estradiol, maximal induction of LDH had already been achieved. In relation to T47D (low ER levels) estradiol did not evoke an induction of LDH5 at any concentration examined. In MCF‐7 cells, the level of LDH5 induction paralleled processing of ER. The processing effect was rapid, beginning within 5 min of estradiol addition, and was completed within 1 hr. With 10−6 m tamoxifen, LDH5 induction was suppressed and this effect was reversed by estradiol. Such antiestrogenic effects of tamoxifen on LDH5 have not been observed in T47D cells. Agonistic effects of low doses of tamoxifen on LDH5 were not observed. Our studies suggest that estrogen stimulation of LDH5, involves ER.
Hepatocellular carcinoma: Clinical, aetiological and pathological features in British patients
Authors: Dunk Arthur A. , Spiliadis Haris , Sherlock Sheila , Fowler Martin J. F. , Monjardino Jon P. , Schruer Peter J. , Thomas Howard C. 
Published: February 2007

AbstractWe have examined the clinical, prognostic, aetiological and pathological features of 41 consecutive British patients with hepatocellular carcinoma (HCC). Presenting symptoms were often vague, and patients were generally in poor condition at diagnosis, 56% being of WHO grade 2 performance score or higher. Ascites (46%) and jaundice (35%) were often present at diagnosis, and the median duration of survival from diagnosis was only 6 weeks. Only initial performance grade (p<0.0001) and serum bilirubin concentration (p = 0.02) significantly affected prognosis. Serum alphafoetoprotein (AFP) was positive by counter‐immune electrophoresis in only 34%, but increased to 68% when radioimmunoassay was used. Cirrhosis was present in 33 patients (80%) and was most often cryptogenic (12) or alcoholic (7) in origin. Serum HBsAg was detected in 5 patients (12%) and, of the remainder tested, 21 % had serological evidence of past HBV exposure. None of 8 serum HBsAg‐negative tumour specimens had detectable HBV‐DNA integration into the tumour cell genome. Liver‐cell dysplasia was noted in 56% of patients with liver biopsies predating the diagnosis of HCC, and in 78% of biopsies taken at the time of HCC diagnosis. The commonest histological pattern was trabecular (71%). Other forms were rare; the fibrolamellar pattern was only seen in 2 patients.
Mutation analysis of the N‐ras proto‐oncogene in active and remission phase of human acute leukemias
Authors: Senn H.‐P. , Trǎn‐Thang Ch. , Wodnar‐Filipowicz A. , Jiricny J. , Fopp M. , Gratwohl A. , Signer E. , Weber W. , Moroni Ch. 
Published: February 2007

AbstractDNA isolated from blood or bone‐marrow samples from 18 patients with acute non‐lymphocytic leukemia (ANLL) and 14 patients with acute lymphocytic leukemia (ALL) was analyzed for the presence of mutations in the N‐ras gene. Using synthetic oligonucleotide probes we detected mutations in 5 cases of ANLL; 4 GGT → GAT transitions in codon 12 and one CAA → AAA transversion in codon 61. One case exhibited homozygosity for the mutation. No mutations could be detected at these codons in the DNA of the 14 ALL patients. In a follow‐up study with 3 of the above 5 patients, the mutation could no longer be detected in 2 cases following successful induction of clinical remission by chemotherapy. However, the mutated N‐ras persisted in one patient who did not achieve remission. We show that oligonucleotide hybridization is a sensitive assay for the detection of N‐ras point mutations, which in ANLL could be used to follow the fate of the leukemic clone during (and after) therapy.
Establishment and characterization of a new human bladder cancer cell line showing features of squamous and glandular differentiation
Authors: Russell Pamela J. , Jelbart Margaret , Wills Edward , Singh Sardool , Wass Jane , Wotherspoon John , Raghavan Derek 
Published: February 2007

AbstractTumour‐cell heterogeneity has been studied in a continuous cell line, UCRU‐BL 17CL, established from a xenografted human primary bladder carcinoma. The cell line, grown in vitro for more than 30 generations, reflects the pathology of both the xenograft from which it was derived and the original human tumour. It comprises mainly adenocarcinoma cells which secrete mucin in vitro, as well as squamous and transitional carcinoma cells. Features of both adenocarcinomatous and squamous differentiation have been observed within the same cell. The line expresses ABH blood group isoantigens, binds to peanut lectin and reacts with monoclonal antibodies (MAbs) raised against keratin and against normal and malignant epithelial cells. It also reacts with MAbs against ras p21 proteins and the epidermal growth factor receptor (EGFR). It shows high levels of lactic acid dehydrogenase jsozyme 5, consistent with a high‐grade tumour, forms colonies in meth‐ylcellulose and is tumorigenic in nude mice. The karyotype (human) shows many marker chromosomes, consistent with expression of EGF receptors and ras p21 proteins, and an 11:13 translocation. DNA content, as studied by flow cytometry, reveals a shift from tetraploid to near triploid. This line may provide a useful model for studies of the histogenesis of bladder cancer and the relationship between transitional‐cell carcinoma and the other histological subtypes of this disease.
Burkitt's lymphoma cell lines reveal different degrees of tumorigenicity in nude mice
Authors: Gurtsevitch V. E. , O'Conor G. T. , Lenoir G. M. 
Published: February 2007

AbstractA quantitative in vivo assay for evaluating the tumorigenicity of Burkitt's lymphoma (BL) cell lines in nude mice is described. It is based on the dose‐response kinetics of BL cell tines in pre‐irradiated (480 rad) nude mice following the s.c. injection of 4 different cell doses. This model system was used to estimate the xenografting potential of 26 BL cell lines derived from BL patients of different geographic and ethnic origins, as well as lymphoblastoid cell lines (LCLs) established by Epstein‐Barr virus (EBV) immortalization of normal B lymphocytes. The results indicate that most BL cell lines are tumorigenic, but LCLs fail to produce progressively growing tumours in nude mice. However, BL cell lines revealed individual degrees of tumorigenicity and accordingly could be divided into 4 groups with high, moderate, low or no tumorigenicity. Preliminary attempts to correlate the xenografting phenotype of BL lines with other characteristics indicate that: (1) the aberrations of chromosome I are more often encountered in cell lines with high and moderate tumorigenicity; (2) EBV‐positive BL lines do nat reveal a higher tumorigenic phenotype in comparison with EBV negative ones; (3) cell lines carrying translocations t(8;22) and t(2;B) might fall more frequently in the group of lines with high and moderate tumorigenicity; and (4) when LCLs grow in nu/nu mice, rejection always occurs and is associated with massive tumour necrosis. These findings suggest that the tumorigenicity of BL cell lines in immunosuppressed animals is nat related with EBV, but with certain chromosomal abnormalities (BL‐specific and nonspecific) indicating that this in vivo model system can be instrumental for the identification of other factors or stages involved in BL development.
Antibody targeting to the murine lymphoma ESb‐MP: Increased accumulation due to reduced internauzation into lymphoma cells as compared to normal lymphoid cells
Authors: Matzku S. , Kirchgessner H. , Schirrmacher V. 
Published: February 2007

AbstractUsing rat monoclonal antibody (MAb) (2–;15A against the spontaneously metaxtasizing mouse lymphoma variant ESb‐MP, we elaborated conditions for targeting. In vitro, high binding of labelled antibody to ESb‐MP cells and low binding to Iymphoid cells (e.g., spleen cells) was noted. In vivo, we observed pronounced accumulation in spleen, lymph nodes and bone marrow, the uptake kinetics indicating high accessibility of the target antigen in these tissues, and rapid clearance of radioactivity from blood and most normal tissues, indicating degradation of the antibody and excretion of the label. Binding to lymphoma tissue was slow but persistent, resulting in high tumor:tissue ratios only after 2–3 days. Biodistribution could be dramatically changed by pre‐treatment of animals with excess cold antibody, which reduced trapping of labelled antibody in normal lymphatic tissue, leading to prolonged persistence in the blood and preferential uptake into tumor tissue. Monovalent 12–15A fragments showed less pronounced binding to lymphatic tissue, while being rapidly cleared from the circulation by virtue of their inherent tendency to bind to kidney tissue. Tumor:tissue ratios up to 56:1 were obtained by a combination of pre‐treatment with unlabelled 12–15A IgG or Fab fragment, followed by injection of labelled fragment or IgG, respectively. This is interpreted on the basis of differences in the internalization and retention of antigen‐antibody complexes. Pre‐treatment obviously leads to a temporary blockade or removal of the target antigen, which is much more efficient with normal lymphoid cells than with tumor cells. Thus, it may become possible to target antibodies into the tumor despite concurrent antigen expression on normal tissue.
Formation of dna adducts and water‐soluble metabolites of benzo[a]pyrene in human monocytes is genetically controlled
Authors: Nowak Dennis , Schmidt‐Preuss Ute , Jörres Rudolf , Liebke Frank , Rüdiger Hugo W. 
Published: February 2007

AbstractFormation of DNA adducts and of water‐soluble metabolites was studied in monocytes of 86 first‐degree relatives of 15 families. Tests were performed with blood monocytes using (G‐3H)‐benzo[a]pyrene as a model pro‐carcinogen. Variance analysis revealed significantly higher inter‐familial than intra‐familial variations. From these data we conclude that the formation of DNA adducts is genetically controlled. Therefore the enhanced formation of benzo[a]pyrene DNA adducts in lung cancer patients found in earlier studies may reflect a genetic predisposition for lung cancer in some patients.
P53 expression in breast cancer
Authors: Cattoretti Giorgio , Rilke Franco , Andreola Salvatore , D'Amato Lucia , Delia Domenico 
Published: February 2007

AbstractImmunohistochemical evaluation of 200 primary breast cancers with the anti‐p53 mouse monoclonal antibody (MAb) PAb421 showed positivity in nuclei of malignant cells in 31 cases (15.5%). PAb421+ cases were significantly more frequently epidermal growth factor receptor (EGF‐R)‐positive (67.7%; p < 0.001) and estrogen receptor (ER)‐negative (73.3%; p < 0.001); they displayed surface histocompatibility class‐1 (80.6%; p < 0.01) and II (74.2%; p < 0.05) antigens. Low values for progesterone receptor (mean 67.20 ± 25.2 fmol/mg; p < 0.05) and a high number of cells positive for the proliferationassociated antigen Ki‐67 (log mean 6.88 ± 0.33; p < 0.01) were found in PAb421+ tumors as well as a high number of grade‐3 infiltrating duct carcinomas (70%; p = 0.01). Of the 200 cases of mammary carcinoma, 88 were further analyzed using another human specific anti‐p53 MAb PAb1801, and 40 (45.5%) were found positive. This MAb stained all the PAb421+ cases and was significantly associated with negative ER status (39.5%; p < 0.05) and high Ki‐67 scores (log mean 6.93 ± 0.24; p = 0.001). Analysis of PAb1801+/Pab421− cases for HLA antigens, EGF‐R and ER showed a phenotype similar to that of the p53−ve/ER+ carcinomas, except for the high Ki‐67 score. No differences in age of the patient, number of involved nodes, tumor size, ploidy or labelling index scores were evident between p53+ and − carcinomas. We concluded that p53 in mammary carcinomas is associated with ER‐negative, growth factor receptor‐positive, high‐grade tumors, and is a promising new parameter to evaluate the cellular biology and prognosis of breast cancer.
Estimates of the worldwide frequency of sixteen major cancers in 1980
Authors: Parkin D. M. , Läärä E. , Muir C. S. 
Published: February 2007

AbstractThe numbers of new cancer cases in 16 common sites occurring in 1980 have been estimated for 24 areas of the world for which the United Nations produces population estimates. For the world as a whole, the total number of new cases was 6.35 million, almost exactly evenly divided between the developed and developing countries. In males, the most important sites were lung, stomach, colon/rectum, mouth/pharynx, prostate and oesophagus, and in females breast, cervix, colon/rectum, stomach, corpus uteri and lung. When the two sexes are combined, stomach cancer emerges as the most common cancer in 1980 (669,400 new cases per year), but this estimate is only slightly greater than that of lung cancer (660,500 new cases), and comparisons with earlier estimates for 1975 suggest that, with declining incidence rates for stomach cancer and the continuing rise for lung cancer, the latter would become the most common cancer in the world by the end of 1981. The implications for cancer control in the developed and developing countries of the world are discussed.