bluuebunny/crossref_metadata_2025_split huggingface dataset:
Appearance of serum antibodies to rat yolk‐sac carcinomas during the latent period prior to primary tumor development
Authors: Lindvall Magnus L. , Alumets Jan , Sjögren Hans Olov 
Published: February 2007

AbstractRat yolk‐sac tumors were induced by intraperitoneal (i.p.) displacement of the visceral yolk sac in fetectomized W/Fu rats. Serum was obtained from each female rat prior to the pregnancy preceding the tumor‐inducing procedure and then once a month during the induction period. The sera were analyzed for the presence of antibodies binding to cultured cells of one of the yolk‐sac tumors. Sera were also assayed for complement‐dependent cytotoxic antibodies on tumor cells. In rats that developed tumors, antibodies reacting specifically with the target tumor cells could be detected in all of 10 rats. Antibodies appeared before tumor detection in all animals but one, and in 6 rats as early as 11 to 25 weeks prior to tumor detection. Nine rats developed antibodies demonstrable in the binding assay and in 6 of those the antibodies appeared 8 to 25 weeks before the tumor became palpable. Analysis of the isotypes of the Ig that bound to tumor cells showed that IgG1 and lgG2b were most frequently present. In one rat lgG2a antibodies appeared one month before tumor detection followed by IgG1 and lgG2b antibodies detectable 4 weeks later. IgG2c and IgM antibodies were not detected in any of the rats. At dilution 1/10, sera of all 10 rats showed specific cytotoxicity to the tumor cells in the presence of added rabbit complement. In 9 of these animals antibodies were demonstrated 1 to 4 months prior to tumor detection.
Interactions of interferons and transforming growth factors during clonal growth of mouse or human cells in soft agar and in mice
Authors: Popik Waldemar , Inglot Anna D. 
Published: February 2007

AbstractThe mouse fibroblast‐like transformed cell line C‐243 adapted to growth in suspension was used as a source of virus‐induced interferons (MulFN‐α, β), and spontaneously produced active growth factors. These factors were purified from C‐243 cells grown as tumors in BALB/c mice, and had properties identical to those of TGF‐α or TGF‐β isolated by others from different tissues. Exogenous TGF‐α, β stimulated colony formation by C‐243 cells in soft agar, whereas MulFN‐α, β inhibited it. Clonal growth of human lung adenocarcinoma AS49 cells in soft agar was inhibited as well by human interferons (types α, β, or γ) as by TGF‐β. Inhibition was dose‐related. Pure EGF, which is an analogue of TGF‐α, diminished the anti‐proliferative activity of interferons α, β, and γ in A549 cells. On the other hand, the anti‐mitogenic action of IFN‐β and TGF‐β was clearly synergistic. In mice bearing C‐243 cell tumors, TGF‐α, β stimulated growth, whereas MulFN‐α, β inhibited it. Stimulation of tumor growth was also observed after administration of anti‐IFN serum that could neutralize endogenous IFN‐α, β. The simultaneous administration of MulFN‐α, β and TGF‐α, β diminished anti‐tumor effects of IFN in mice. Our results suggest that both TGFs and IFNs are autocrine, positive or negative growth factors modulating the rate of proliferation and the neoplastic behavior of the cells. The final effects depend on the target‐cell sensitivity and on the relative concentration of the various hormone‐like factors. Cancer cells overstimulated by TGF‐α, β or by EGF may not respond to IFNs.
A mammalian cell line designed to test the mutagenic activity of anti‐herpes nucleosides
Authors: Pizer Lewis I. , Mitchell Dawn H. , Bentele Beatrice , Betz Joan L. 
Published: February 2007

AbstractThe herpes simplex virus (HSV) thymidine kinase (tk) gene was transfected into Chinese hamster ovary (CHO) 51–11 gly−cells to test its effect on the cytotoxic and mutagenic activity of anti‐herpetic nucleoside analogues. Insertion of the viral tk was verified by Southern blot analysis, by sensitivity to acyclovir, and by elevated in vitro thymidine kinase (TK) activity. TK activity was increased by superinfection with a tk− virus and inhibited by antibody to viral TK. Acyclovir (ACV) was somewhat more cytotoxic in the 51‐D3 cell line that expresses the viral TK than in the 51–11 parent line. Growth in ACV did not increase over background mutations at the hprt locus. FIAC (2′‐fluoro‐5‐iodio‐aracytosine) was slightly cytotoxic to the parent 51–11 line and the tk‐containing clone 51‐D3. FMAU (2′‐fluoro‐5‐methyl‐arauracil) had pronounced cytotoxicity in both cell lines: the 50% survival points were 1.0 μM for 51–11 cells and 0.2 μM for 51‐D3. The clone 51‐D3 was more sensitive than 51–11 to low concentrations of FIAU (2′‐fluoro‐5‐iodo‐arauracil), and when treated with FIAU 51‐D3 had a mutation frequency to glycine independence 5 times greater than that of 51–11 cells. With both cell lines the mutation frequency at the hprt locus did not increase after growth in the presence of FIAC or FIAU. A 7‐fold increase in mutation frequency at the hprt locus was detected after 51‐D3 cells were grown with iododeoxyuridine. Trifluorothymidine was more toxic to 51‐D3 than to 51–11 cells and increased the mutation frequency 2‐ fold. Cytosine‐β‐D‐arabinofuranoside showed no differential cytotoxicity on the two cell lines and did not increase the mutation frequency at the hprt locus.
Regulation of tumor development: The biphasic effects of silica and of lipopolysaccharide on natural resistance
Authors: Sandstrom Paul A. , Chow Donna A. 
Published: February 2007

AbstractThe impact on tumor development of the BRM silica and LPS was assessed through anal/sis of changes in NR parameters in vivo and in vitro. Although injection of the fumed silica Cab‐o‐sil 3 days before a threshold s.c. inoculum of LSI78Y‐F9 cells increased the tumor frequency in syngeneic DBA/2 mice, tumors recovered from silica‐treated animals exhibited an augmented resistance to NAb and to in vivo NR. Cab‐o‐sil increased in vivo NR and induced a biphasic modulation of anti‐tumor NAb and NK activities. The appearance of more autonomous tumors in Cab‐o‐sil‐treated mice corresponding with a stimulation of NR parameters, suggests that the adjuvant activity of silica also contributes to its co‐carcinogenic effect by accelerating tumor development. While injection of LPS 2–3 days before a threshold tumor inoculum lowered the tumor incidence, the survival of tumor cells injected within I day of LPS was increased. A corresponding early decrease in NAb activity occurred, in contrast with increases in NK cell and NAb levels previously observed after 5 days. This biphasic effect of LPS on NR effectors assayed in vitro was also seen on in vivo NR. Although their frequency was higher, tumors initiated during the period of LPS‐induced NR abrogation exhibited greater reductions in NAb binding and sensitivity to NR than tumors from control mice. These data extend the support for NAb acting against tumor cells in vivo and reveal the dual nature of NR in tumor development, (1) defending against small tumor foci and (2) driving the progression of the surviving neoplasm.
Screening for lung cancer‐results from a case‐control study
Authors: Ebeling K. , Nischan P. 
Published: February 2007

AbstractBy means of a case‐control study, a screening programmer originally introduced to control tuberculosis and utilizing biennial chest X‐rays (70 × 70 pa.) was evaluated for its effect on lung cancer mortality. The case group consisted of 130 population‐based deaths from lung cancer (males below 70). One general population‐based and one hospital‐based control group were used, both consisting of 260 males matched for age and alive at the same time as the relevant case. The proportion of exposed persons, i.e. those having had at least one screening test within the 2 years preceding diagnosis, was similar in the case group and in. the 2 control groups: 76, 78 and 75%, respectively. The relative risk of lung cancer death was 0.9 and 1.1 (95% confidence intervals 0.5 to 1.5 and 0.7 to 1.8). There was no trend in relative risks with regard to the number of tests performed and the interval since the last test.
Defective cell‐mediated response to EBV‐transformed B cells in a healthy individual with regular EBV antibody titers
Authors: Bejarano Maria Teresa , Thorsteinsdottir Sigurbjörg , Andersson Jan P. , Andersson Ulf G. , Masucci Maria Grazia , Szigeti Robert , Klein Eva , Klein George 
Published: February 2007

AbstractWe have analyzed the EBV‐related immune parameters of a healthy EBV‐seropositive individual (ST) who has regular antibody titers but defective inhibitory capacity toward the growth of autologous EBV‐infected B cells. This in vitro function reflects the EBV‐specific memory because it does not occur in experiments performed with cells of seronegative individuals. An analysis of events following in vitro EBV infection showed that lymphocytes of ST behaved in some tests in the same way as those collected from seronegative individuals. These parameters were: (I) lack of‐γ‐IFN production 24 hr after EBV infection; (2) low production of soluble factors that inhibit EBV‐induced B‐cell proliferation; (3) lack of generation of LCL selective cytotoxicity after repeated stimulation with autologous LCL; and (4) high proportion of EBNA‐positive cells in 7‐day‐old EBV‐infected cultures. On the other hand, cellular memory to the virus detected by the production of IL–2 24 hr after infection, and by the production of LIF upon exposure to EBV‐encoded antigens, conformed with the results obtained with seropositive individuals. T‐cell‐mediated inhibition of EBV‐induced B‐cell growth in vitro has been regarded as a corollary of in vivo control of EBV‐infected B cells. However, it is absent or has a low efficiency in certain disease categories which are not accompanied by risk of B‐EBV growth. Our results with a healthy individual also indicate that several mechanisms contribute to a harmless lifelong virus carrier state.
Specific chromosome aberration in human renal cell carcinoma
Authors: Kovacs Gyula , Szücs Sandor , De Riese Werner , Baumgärtel Hermann 
Published: February 2007

AbstractUsing G‐banding technique, the chromosomes were studied in short‐term cultures of 25 primary renal‐cell carcinomas (RCC). Phytohaemagglutinin‐stimulated peripheral blood lymphocytes or normal kidney cells of the same patients growing in primary cultures were analysed to define the constitutional karyotype. The modal chromosome number of 23 RCC's was found to be pseudo‐diploid or near‐diploid with only few structural rearrangements, 22 of the RCC's showed an aberration of chromosome 3, deletion of 3p, or translocation of different chromosome segments to the deleted chromosome 3, leading to the loss of variable segments of chromosome 3. The breakpoints in rearrangements of chromosome 3 clustered in the region 3p11.2–p13. Shortest‐region overlap analysis localized a consistent change to a small area of 3p13‐pter. In 8 of the 25 RCCs, the rearrangement of chromosome 3 was the only karyotype change determined, and 4 other tumours had only one chromosomal rearrangement in addition to the aberration of chromosome 3. These results suggest that the aberration of chromosome 3 is the first cytogenetic event in the clonal evolution of RCCs. Translocation 3;5 was preferentially involved in the rearrangements between chromosome 3p and other chromosomes. The breakpoint on chromosome 3 was constant at p13, but the breaks on chromosome 5 varied between bands q11.2 and q22. Monosomy 14 was observed in 10 cases and loss of Y chromosome was detected in 6 of 14 tumours obtained from male patients. Since the normal somatic cells were free of chromosomal aberrations, one may conclude that the loss of 3p13‐pter segment is an acquired, consistent chromosomal aberration which marks human RCCs.
Colorectal polyps and diet: A case‐control study in Marseilles
Authors: Macquart‐Moulin Geneviève , Riboli Elio , Cornée Jacqueline , Kaaks Rudolf , Berthezène Patrice 
Published: February 2007

AbstractThis study investigates the differences in usual past diet between 252 subjects with newly diagnosed adenomatous or villous polyps of the colon and rectum and a group of 238 hospital controls. Cases and controls were interviewed in hospital by 3 nutritionists using a dietary history questionnaire focused on the diet during the preceding year. Nutrient intake was estimated by means of ad hoc food tables adapted from French and British tables. Out of 16 food groups considered in the analyses, the cases reported lower consumption of oil and potatoes and higher consumption of sugar added to food and drink. Among nutrients, we found that cases had a lower consumption of carbohydrates (not taking into account added sugar), potassium, magnesium and vitamin B6. We found a slightly lower intake of fibre and a slightly higher intake of saturated fat among cases, though neither was statistically significant. Intake values for fibre and for carbohydrates were highly Interco related and, due to measurement errors, the effect of one may be masked by the other and vice versa. The hypothesis that some components of carbohydrates (starches, fibre and natural sugars but not added sugar) play a protective role in relation to the biology of tumours of the intestinal tract is considered in further multivariate analyses and in the “Discussion”.
Amplification of the epidermal growth factor receptor gene in the BT20 breast carcinoma cell line
Authors: Lebeau Jérome , Goubin Gérard 
Published: February 2007

AbstractSouthern blot‐hybridization analysis of 10 breast carcinoma cell lines demonstrated an amplification of the epidermal growth factor (EGF) receptor gene in the BT20 cell line. The gene was amplified 10‐to 14‐fold when compared to the level seen in human placental DNA. Northern blot analysis indicated an increased level of transcription in this cell line which probably accounts for the high level of the EGF receptor reported in the BT20 cell line.
The level of expression of class‐I MHC antigens in adenovirus‐transformed human cell lines
Authors: Grand Roger J. A. , Rowe Martin , Byrd Philip J. , Gallimore Phillip H. 
Published: February 2007

AbstractThe level of expression of the class‐l major histocompatibility (MHC) antigen was determined in a series of human embryo cell lines transformed with either adenovirus 12 (Ad 12) early region I (El) or adenovirus 5 (Ad 5) E1 DNA or with combinations of Ad 12 early region IA (El A) or Ad 2 EIA with activated N‐ras DNA. MHC class‐l antigen expression was greatly reduced in all Ad 12 transformants, compared to primary cells. Expression was also reduced in the Ad 5 cell lines transformed with EIA and EIB DNA, but levels were near normal in those lines with only EIA DNA present. Amounts of MHC class‐l antigen on the cell surface, as determined by RIA and FACS analysis, generally reflected total cellular levels as determined by Western blotting. Expression of β2 microglobulin was also much reduced in those cell lines with low levels of MHC class‐l antigen. The treatment of primary cells and all the transformants with human γ‐interferon resulted in increased expression of HLA on the cell surface. Infection of primary human cells with Ad 12 or with a series of Ad 12 mutants did not have any effect on the MHC class‐l antigens present.
Receptors for epidermal growth factor and estradiol in canine mammary tumors
Authors: Nerurkar V. R. , Seshadri Rajeshwari , Mulherkar Rita , Ishwad C. S. , Lalitha V. S. , Naik S. N. 
Published: February 2007

AbstractBoth growth factors and steroid hormones are known to be associated with breast cancer. We have studied the epidermal growth factor receptor (EGFR) in canine mammary tumors and have shown the presence of a single class of 125I‐EGF binding receptor sites in 9 out of 13 (70%) tumors, using Scat‐chard plot. The dissociation contant (KD) was 10−9M. An inverse correlation between EGFR and estrogen receptor (ER) was observed in 54% of the tumors. Our data suggest that EGFR might be used as a biochemical marker in canine mammary tumors.
Serological survey and virus isolation of simian T‐cell leukemia/T‐lymphotropic virus type I (STLV‐I) in non‐human primates in their native countries
Authors: Ishikawa Koh‐Ichi , Fukasawa Masashi , Tsujimoto Hajime , Else James G. , Isahakia Mohamed , Ubhi Narinder K. , Ishida Takafumi , Takenaka Osamu , Kawamoto Yoshi , Shotake Takayoshi , Ohsawa Hideyuki , Ivanoff Bernard , Cooper Robert W. , Frost Eric , Grant Francis C. , Spriatna Yatna , Sutarman  , Abe Kenji , Yamamoto Kohtaro , Hayami Masanori 
Published: February 2007

AbstractInfection with a simian retrovirus (STLV‐I) closely related to human T‐lymphotropic virus type I (HTLV‐I) was investigated in non‐human primates living in their native countries in Africa and Asia. Serum antibodies cross‐reacting with HTLV‐I antigens were detected in 85 of 567 non‐human primates of 30 species. Seropositive animals were found among African green monkeys, olive baboons, Sykes' monkeys, mandrills and patas monkeys in several countries in Africa, and cynomolgus monkeys, Celebes macaques and siamangs in Indonesia. The frequency of seropositivity was much higher in adult than in young African green monkeys, cynomolgus monkeys and Celebes macaques. STLV‐Is were isolated by establishing II lines of virus‐producing lymphoid cells in the presence of interleukin‐2 from 5 species of seropositive non‐human primates, i.e. the African green monkey, Sykes' monkey, Celebes macaque, cynomolgus monkey and siamang. All these cell lines had T‐cell markers and Tac antigen, and the cell lines from the African green monkey and Sykes' monkeys were Leu2a+ while those from other species were Leu3a+. These cell lines expressed viral antigens reacting with human sera from adult T‐cell leukemia (ATL) patients and monoclonal antibodies (MAbs) against p19 and p24 of HTLV‐I core proteins, and produced virus particles having RNA‐dependent DNA polymerase activity. Cellular DNAs from these cell lines contained provirus sequences homologous to HTLV‐I, shown by Southern blot hybridization. The restriction patterns of these provirus genomes were different from those of HTLV‐I and were also dissimilar in the different species.
Loss of basement membrane deposits and development of invasive potential by virally‐transformed rat mammary cells are independent of collagenase production
Authors: Warburton Michael J. , Ferns Sharon A. , Kimbell Rosemary , Rudland Philip S. , Monaghan Paul , Gusterson Barry A. 
Published: February 2007

AbstractThe myoepithelial‐type cell line, Rama 712, derived from a normal rat mammary gland, deposits an extracellular matrix containing type‐IV collagen and other basement membrane proteins round its cellular periphery. After transformation with a temperature‐sensitive mutant of Rous sarcoma virus (tsRSV) the cells fail to deposit an extracellular matrix at the permissive temperature (35°C), but retain the capacity to do so at the non‐permissive temperature (41°C). The synthesis of type‐IV collagen is not affected by the temperature shift. Rama 712 cells fail to form tumours in syngeneic rats. However, Rama 712‐tsRSV cells form tumours that are locally invasive but fail to metastasize. In histological sections, the tumour cells stain with an antibody to type‐IV collagen, but do not deposit any extracellular type‐IV collagen. Cells isolated from the tumours (Rama 712T) remain temperature‐sensitive for the extracellular deposition of type‐IV collagen when grown in vitro. Rama 712, Rama 712‐tsRSV and Rama 712T fail to produce any detectable type‐1 or type‐IV collage‐nase at either 35°C or 41 °C. These results show that in this system extracellular deposits of basement membrane proteins are lost from invasive tumours produced by myoepithelial‐type cells by mechanisms other than those due to the production of collagenolytic enzymes.
Prognostic implications of expression of the cellular genes myc, fos, Ha‐ras and Ki‐ras in colon carcinoma
Authors: Monnat M. , Tardy S. , Saraga P. , Diggelmann H. , Costa J. 
Published: February 2007

AbstractMessenger RNA levels of the c‐fos, c‐myc, c‐Ha‐ras and c‐Ki‐ras genes were studied in 39 tissue samples obtained from 17 patients undergoing surgery for colon carcinoma and other colon diseases. DMA extracted from the same samples was studied by Southern analysis. The tissues were tumors and grossly normal mucosa from each case and in some instances benign polyps and metastases. Our results indicate: (1) that 50% of cases studied show an increase in expression of at least one of the oncogenes studied; (2) that over‐expression is not random, some cases over‐expressing several of the genes studied; (3) that the expression pattern of the oncogenes studied varies between primary tumor and metastases; (4) that amplification is a rare event, being limited to one instance in which c‐myc was amplified in a metastasis; (5) that cases which exhibit high levels of mRNA in one or more genes studied correlate with biologically aggressive tumors; and (6) that “non‐expressors” are at higher risk for local recurrence based on correlations with mucin histochemistry.
Subcellular concentrations of estrone, estradiol, androstenedione and 17β‐hydroxysteroid dehydrogenase (17‐β‐OH‐SDH) activity in malignant and non‐malignant human breast tissues
Authors: Mehta R. R. , Valcourt L. , Graves J. , Green R. , Gupta T. K. Das 
Published: February 2007

AbstractTotal and subcellular (cytosol and nuclear) concentrations of estrone (E1), estradiol (E2), and androstenedione were determined in non‐malignant (n = 61) and malignant (n = 65) human breast tissues obtained from post‐menopausal women. The 17β‐hydroxysteroid dehydrogenase (17 β‐OH‐SDH) activity was determined in 800g supernantant fraction. Total estrogens, E, and E2 levels and 17β‐OH‐SDH activity were significantly (p < 0.005, 0.0005, 0.001, respectively) higher in malignant than In non‐malignant breast tissues. We failed to observe significant changes in subcellular steroid concentrations or enzyme activity associated with patients' obesity or tumor estrogen receptor status. When the steroid levels were analyzed in relation to clinical staging of the disease, nuclear contents of estradiol were significantly higher (p < 0.005) In Stage‐IV patients than in those with less advanced disease (Stages I to III). 17β‐OH‐SDH activity was significantly (p < 0.001) lower in patients with advanced disease than in those with relatively less advanced (Stages I to III) disease and was positively correlated with tissue concentration of androstenedione. Our present data indicate that differential intracellular metabolism of steroid hormones may have some influence on availability of estradiol at nuclear sites. In postmenopausal women, local intercon version of estrogens may provide sufficient estrogenic stimulus to enhance the growth and progression of breast tumors.