bluuebunny/crossref_metadata_2025_split huggingface dataset:
Recombinant human tumor necrosis factor‐α: Thrombus formation is a cause of anti‐tumor activity
Authors: Shimomura Kyoichi , Manda Toshitaka , Mukumoto Sueo , Kobayashi Katsumasa , Nakano Kazuo , Mori Jo 
Published: February 2007

AbstractIn a previous study we showed that recombinant human tumor necrosis factor‐α (rTNF‐α) has no cytolytic effect on Meth A fibrosarcoma cells in vitro but that it has a strong anti‐tumor activity in vivo. In the present work, we define the in vivo mode of action of rTNF‐α on solid‐form Meth A fibrosarcoma implanted intradermally (i.d.) in mice. rTNF‐α exhibited strong anti‐tumor activity when given intravenously (i.v.) 7 or 10 days after tumor implantation, but not when given 3 days after implantation. Light and electron microscopy showed that rTNF‐α impaired microcirculation by producing fibrin‐like substances in newly formed microcapillaries in 7‐day‐old tumor tissue. An anti‐coagulant, dicoumarol, abrogated the effect of rTNF‐α. Injection of carbon particles showed that the development of capillaries in 7‐day‐old tumors was more extensive than in 3‐day‐old tumors, and suggested that the anti‐tumor activity of rTNF‐α depends upon a fully developed fine network of induced capillaries in the tumor. Electron microscopy showed that rTNF‐α increases the number of primary and secondary lysosomes in the cytoplasm of 7‐day‐old tumor cells. The results suggest that rTNF‐α selectively stems the blood flow in newly formed microcapillaries, eventually leading to autolysis of the tumor cells.
JB/MS murine melanoma: A new model for studies on the modulation of differentiation and of tumorigenic and metastatic potential
Authors: Hearing Vincent J. , Cannon Grace B. , Vieira Wilfred D. , Jiménez‐Atiénzar Mercedes , Kameyama Koichiro , Law Lloyd W. 
Published: February 2007

AbstractThe recently obtained JB/MS melanoma (induced by DMBA in C57BI/6 mice) has been successfully established in culture, and characterization of various parameters of these cells, as they have been serially passaged in vivo and in vitro, has begun. The culture lines were initially highly dendritic and melanotic, growing slowly in vitro and extremely slowly in vivo. During serial passage in vivo and in vitro the cell lines have gradually evolved into less melanotic, but more proliferative, tumorigenic and metastatic cells. We have been able to demonstrate that the JB/MS melanoma shares the common melanoma TSTA previously reported for B16, K1735 and JB/RH melanomas, but does not cross‐react with the S91 melanoma or with other non‐melanoma cell lines used as specificity controls. The JB/MS cells can be induced to differentiate in vitro by α‐melanocyte stimulating hormone, a physiologically relevant agent, and studies have been initiated to detail the level at which this induction occurs. These sublines should prove to be excellent models for study of the progression of transformed cells from non‐tumorigenic to tumorigenic phenotypes, and for progression through stages of varying metastatic potential, immunogenicity and differentiation.
The reversal of doxorubicin resistance by verapamil is not due to an effect on calcium channels
Authors: Huet S. , Robert J. 
Published: February 2007

AbstractUsing a model of doxorubicin‐resistant rat glioblastoma cells, we have studied the relationship between the reversal of multi‐drug resistance by verapamil and calcium fluxes into the cells. Although it is known to be a voltage‐dependent calcium channel blocker, verapamil exerted no effect on calcium entry into the cells. In the absence of calcium in the medium, drug resistance was not affected and verapamil was still active. It was possible to modify calcium fluxes into the cells by using manganese ions (decreasing calcium uptake) or the calcium ionophore A23187 (increasing calcium uptake). These agents had only a marginal effect on the expression of drug resistance by the cells and did not prevent the action of verapamil on its reversal.
Fucosylated type‐2 chain polylactosamine antigens in human lung cancer
Authors: Zenita Koichi , Kirihata Yoshiko , Kitahara Aiko , Shigeta Katsuyoshi , Higuchi Kayoko , Hirashima Kunimi , Murachi Takshi , Miyake Masayuki , Takeda Toshio , Kannagi Reiji 
Published: February 2007

AbstractFour specific monoclonal antibodies (MAbs) have been used to study distributions of fucosylated type‐2 chain polylactosamine antigens, Lex, poly Lex, Ley and sialylated Lex‐i antigens, in human lung cancer tissues and in the serum of patients with lung cancers. Radioimmunoassay frequently showed abnormally high antigen levels in the sera of 66 lung cancer patients tested. When histological typing was performed, high serum levels of the above 4 antigens were most frequently observed in patients with adenocarcinoma of the lung; i.e., after combining the results from the 4 antigens, 75% of the sera from patients with lung adenocardnoma were positive (50% in the case of large‐cell carcinoma, 30% in the case of squamous‐cell carcinoma and 27% for small‐cell carcinoma). Among the 4 antigens, the sialylated Lex‐i antigen had the highest positive incidence, 58%, in the sera of patients with adenocarcinoma of the lung, compared to 33% for Ley 29% for poly Lex, and 8% for Lex antigen. On the other hand, when the distributions of these antigens in the lung cancer tissues of 42 patients were studied by immunohistological techniques, the Lex antigen had the highest positive incidence, 100%, in lung adenocarcinoma tissues, poly Lex antigen had 86%, sialylated Lex‐i antigen had 71%, and Lex antigen had 29%. In cancer tissues, the incidence of non‐sialylated antigens, such as Ley, poly Lex and Lex antigens, often exceeds the positive incidence of the sialylated antigen, but the sialylated form of the antigen, such as sialylated Lex‐i antigen, appears more often than the non‐sialylated form in patients' sera.
Sister chromatid exchanges and chromosomal aberrations in lymphocytes of nurses handling cytostatic agents
Authors: Benhamou Simone , Pot‐Deprun Jacques , Sancho‐Garnier Hélène , Chouroulinkov Ivan 
Published: February 2007

AbstractA cohort study of 29 nurses who constantly handled cyto‐static drugs, and 29 controls matched according to sex and age, was carried out between 1983 and 1986. Cytogenetic damage was assessed by sister chromatid exchanges (SCE) and chromosomal aberrations. No significant increase in mean number of SCE was found for nurses (7.37) as compared to matched controls (7.00), whereas a significant excess of SCE (p < 0.001) was observed for smokers (8.23) as compared to non‐smokers (6.75). The number of SCE was studied in relation to the amount and nature of cytostatics handled as well as to the duration of exposure. A significant association (p < 0.05) was found between individual mean number of SCE and the total number of drugs handled after adjustment for confounding factors. In contrast, the number of SCE was not significantly related to the nature of drugs handled or to the duration of exposure. With regard to chromosomal damage, no significant difference was observed between nurses and controls in gap, break, dicentric and translocation frequencies.
Tumor‐associated alpha‐2‐macroglobulin in human melanomas
Authors: Matoska J. , Wahlstrom T. , Vaheri A. , Bizik J. , Grofova M. 
Published: February 2007

AbstractWe and others have previously shown that human melanoma cell lines in culture synthesize alpha‐2‐macroglobulin (α2M). We have now studied melanomas from 30 patients for the presence of α2M using the peroxidase anti‐peroxidase technique on histologic sections from paraffin‐embedded tissues and primary antibody raised against tumor‐associated α2M in rabbits. α2M was detected in 10 of the 30 melanomas studied. In all but 2 cases the presence of α2M was restricted to solitary tumor cells or to solitary foci of tumor tissue. In one case of melanoma almost all tumor cells were positive for α2M, while in the others between 20% and 50% of tumor cells were positive. In all but one of the melanomas, the positivity was characteristic of epithelioid or large‐cell type or was confined to this component in melanomas with more than one cell type. In 4 positive cases, differences in the extent of α2M‐containing tumor tissue were observed between primary tumor and metastases or metastases from different localizations, with equivocal trend. Clinical follow‐up of the melanoma patients suggested that α2M‐positivity tends to correlate with an unfavorable prognosis.
Absence of expression of a human endogenous retrovirus is correlated with choriocarcinoma
Authors: Kato Nobuyuki , Larsson Erik , Cohen Maurice 
Published: February 2007

AbstractWe examined the RNA expression of a human endogenous provirus, termed ERV3, in 170 human tissue and cell specimens. The highest expression was found in normal placental chorionic villi as mRNAs of 9, 7.3, and 3.5 kb. The 7.3‐kb RNA species was found only in the placenta. ERV3 mRNA was expressed in most other normal and malignant tissues at a level which was 2‐10% of that seen in placenta. However, several tissues and tumor cell lines had higher transcnptional levels, equal to 10–60% of the placental level. In contrast, an almost complete abrogation of ERV3 mRNA expression was noted in choriocarcinoma cell lines and in an invasive hydatidiform mole tissue biopsy. This abrogation was not linked to deletions or rearrangements of the ERV3 genome. It appeared to be unassociated with methylation because the ERV3 provirus was similarly methylated in the DNA of placental chorionic villi and choriocarcinoma cells, and ERV3 transcription in choriocarcinoma cells was not induced by 5‐azacytidine. These results suggest that the loss of ERV3 mRNA expression is associated with susceptibility to choriocarcinoma.
Tamm‐horsfall protein is a marker of renal and extra‐renal rhabdoid tumours
Authors: Kumar S. , Jakatte S. M. , Marsden H. B. , Kumar P. , Jasani B. 
Published: February 2007

AbstractA monoclonal antibody (MAb) to Tamm‐Horsfall protein (THP) was used to stain 6 renal rhabdoid tumours (RRT) and 2 primary extra‐renal rhabdoid tumours (E‐RRT). One of the E‐RRT was a tumour from the posterior fossa of a 3‐year‐old child and the other was a lump from the right side of the neck in an 18‐month‐old girl. Five of 6 RRT and both cases of E‐RRT were positive for THP. Both cases of E‐RRT also reacted with vimentin and cytokeratin MAbs. On electron microscopy, cells from both E‐RRT were seen to contain concentric whorls of intermediate filaments characteristic of rhabdoid tumours. Viable tissues from one RRT and one E‐RRT (the posterior fossa tumour) were available for tissue culture. Ninety‐five percent of the cells growing out of both tumours were polygonal and approximately 5% of these cells were THP‐positive.
Methylxanthines and breast cancer
Authors: Rohan Thomas E. , McMichael Anthony J. 
Published: February 2007

AbstractThe association between intake of methylaxnthines and risk of breast cancer was examined in this population‐based case‐control study conducted in Adelaide, South Australia. The study included 451 cases, and one control was matched to each case for age (to the nearest year). Overall, and within the post‐menopausal stratum, there was relatively little variation in the risk of breast cancer in association with total caffeine and total methylxanthine intake. In pre‐menopausal women, risk was increased at the higher levels of intake, but the increase in risk was not dose‐dependent. There was no evidence for an effect of methylxanthines at high levels of fat intake. Prior epidemiological and experimental studies have not provided strong support for a positive association between intake of methylxanthines and risk of breast cancer. However, the possibility that they are linked through an association between methylxanthines and those histological subcategories of benign breast disease which are strongly associated with risk of breast cancer is discussed.
Elevated antibody titers against cytomegalovirus among patients with testicular cancer
Authors: Mueller Nancy , Hinkula Jorma , Wahren Britta 
Published: February 2007

AbstractThe epidemiology of testicular cancer (TC) has 2 distinguishing features. First, it has an unusual unimodal age‐incidence curve which peaks about age 30, and decreases with increasing age. Second, risk of the disease has been consistently associated with a high standard of living inasmuch as it is a disease of young white men of generally higher social class in economically developed populations. These features suggest that risk may be related to relatively late age of exposure to common infectious agents resulting in damage to the developing testis. We evaluated this hypothesis in a serologic case‐control study in which subjects were compared for both prevalence and level of antibody to the following agents: measles, mumps, rubella, varicella (VZV), herpes simplex {HSV), cytomegalovirus (CMV), toxoplasmosis, Chlamydia, and Mycoplasma hominis. The TC cases included 50 with seminoma, 50 with embryonal carcinoma, and 17 with other sub‐classification. There were 100 male controls of comparable age. No consistent differences were found for any of the non‐herpes viruses. For VZV, cases generally had elevated titers, significantly so for the seminoma patients, relative risk (RR) = 6.3 (95% confidence interval, 3.0–13.3) adjusted for the titer distributions of HSV and CMV. For HSV, seminoma patients also had elevated titers, RR = 2.6 (1.0–6.4). The strongest association was with CMV. Patients had a higher prevalence rate than controls, RR = 2.0 (1.1–3.6), and a gradient of risk with titer level. Overall, those in the highest titer quartile had an RR of 4.9 compared to those with no antibody, with a significant trend (p = 0.0002). Since age at CMV infection is directly related to social class, these findings suggest that delayed exposure to CMV, resulting in a more severe infection, may be related to risk of TC. However, confounding by immune status of the cases or by other risk factors of TC could not be evaluated and may account for this observation.
Role of concomitant resistance in the development of murine lung metastases
Authors: Bonfil R. Daniel , Ruggiero Raul A. , Bustuoabad Oscar D. , Meiss Roberto P. , Pasqualini Christiane Dosne 
Published: February 2007

AbstractAn attempt was made to explain the distinct lung metastatic patterns of 2 mammary adenocarcinomas with a common BALB/c origin: M3, which does not induce spontaneous metastases, and MM3 with an almost 100% incidence. No difference between the 2 tumors was detected with respect to host mononuclear cell content, degree of immunogenicity or lung‐colony‐forming ability. Conversely, there was a marked difference in the capacity to induce concomitant resistance: M3‐bearing mice induced stronger and earlier resistance against i.v. challenge of both M3 and MM3 tumor cells than MM3‐bearing mice; this resistance was expressed as lower number of lung metastases and lower tumor‐cell proliferation in metastatic nodules. M3 was also able to control the development of spontaneous metastases: metastases developed in all M3‐excised mice, compared with none in M3‐bearing mice, while MM3‐bearing mice also bearing a secondary M3 tumor developed fewer metastases than mice bearing MM3 only. This anti‐metastatic effect does not appear to depend on classical immunological mechanisms since no difference could be detected between the 2 tumors in response to T cells, NK, macrophages or antibodies.
Effects of metastatic cascades on metastatic patterns: Studies on colon‐26 carcinomas in mice
Authors: Weiss Leonard , Ward Pamela M. 
Published: February 2007

AbstractThe present studies are based on autopsy data showing that in upper esophageal and lower rectal carcinomas, hematogenous metastasis occurs mainly first to the lungs, and cancer cells from pulmonary metastases generate arterial metastases. In lower esophageal and upper rectal carcinomas, he‐matogenous metastases occur first in the liver, then in the lungs, and are further disseminated by the arterial route. The arterial metastatic patterns are different in the 2 groups. One possible explanation for these differences in pattern is that liver “residence” is associated with different metastatic behavior; this has been tested in a model system. Experiments with the transplantable colon‐26 carcinoma in mice reveal that, when cancer cells from common s.c. transplant sites are grown in the liver, lungs or liver‐and‐lungs, and then injected into the bloodstream of fresh recipients via the left ventricle, the portal vein or the tail vein, different patterns and degrees of colonization of 11 different target sites are observed. These results are consistent with the hypothesis that growth of cancers in different anatomic sites may modify the subsequent arterial metastatic patterns, due to site‐induced changes occurring in cancer cell populations, which influence metastasis from metastases or so‐called “cascade” processes.
Establishment and characterization of cisplatin‐resistant sublines of human lung cancer cell lines
Authors: Hong Weon‐Seon , Saijo Nagahiro , Sasaki Yasutsuna , Minato Koichi , Nakano Hidehiko , Nakagawa Kazuhiko , Fujiwaka Yasuhiro , Nomura Kazuhiro , Twentyman Peter R. 
Published: February 2007

AbstractHuman lung cancer sublines resistant to cisplatin (CDDP) have been developed by continuously exposing cells to gradually increasing doses of CDDP and use of the limiting dilution technique. The cell lines used were PC‐7, PC‐9 and PC‐14 (pulmonary adenocarcinoma) and H69 and N23I (small‐cell lung cancer). The resistant phenotype of the resistant sublines was stable for more than 2 months in the absence of drug. PC‐7/1.2 (i.e., PC‐7 cells growing stably in medium containing 1.2 μg/ml of CDDP), PC‐9/0.5, PC‐14/1.5, H69/0.4, and N23I/ 0.2 have been developed, which are 22.9, 7.1, 3.1, 25.6, and 8.4 times more resistant to CDDP than the respective parent cell line in terms of IC50 in the soft agar colony assay with continuous drug exposure. Cloning efficiency decreased significantly in N23I/0.2. The doubling times increased significantly in most of the resistant sublines. Cellular DNA contents increased in all resistant sublines, but statistical significance was observed only in H69/0.4 (p<.0.05). Cells of the resistant sublines of PC‐7, PC‐9, PC‐14 and H69 were larger than cells of the parent lines, but the differences were not significant. The growth morphologies of all resistant sublines in the drug‐free medium were similar to those of parent cell lines. All resistant sublines tested were significantly cross‐resistant to carboplatin. The patterns of cross‐resistance, cross‐sensitivity and collateral sensitivity to adriamycin, mitomycin‐C, 5‐fluorouradl, vindesine, etoposide, aclacinomycin and vincristine were different in each resistant subline. Verapamil (1.3 μg/ml) showed little modifying effect on CDDP resistance in 5 CDDP‐resistant sublines tested except N231/0.2 (Modification Index: 0.49). Cy‐closporin A (5.0 μg/ml) modified CDDP resistance in CDDP‐resistant small‐cell lung cancer sublines (H69/0.4 and N23I/0.2) (Modification Index: 0.45 and 0.07, respectively), while in CDDP‐resistant NSCLC sublines (PC‐7/1.0 and PC‐9/0.5). cyclosporin A reduced the sensitivity to CDDP.
Development of an enzyme‐linked immunosorbent assay (ELISA) for detecting IgA antibodies to the epstein‐barr virus
Authors: Uen Wu‐Ching , Luka Janos , Pearson Gary R. 
Published: February 2007

AbstractA 3‐step enzyme‐linked immunosorbent assay (ELISA) was developed for detecting IgA antibodies Co purified Epstein‐Barr virus (EBV) polypeptides. The 3‐step procedure included the use of a mouse anti‐human IgA monoclonal antibody (MAb) to amplify the IgA reaction. The 2 major EBV proteins used in this assay were the 125‐kDa component (gpl25) associated with the viral capsid antigen (VCA) complex and a major glycoprotein (gp 250/200) associated with the membrane antigen (MA) complex. Eighty‐two sera were tested on ELISA plates containing either both of the glycoproteins or each one separately. These included 45 IgA antibody‐positive sera from patients with nasopharyngeal carcinoma {NPC). With these sera, there was a good correlation, both qualitatively and quantitatively, between results with the immuno‐fluorescence (IF) and ELISA procedures. Although most IgA antibody‐positive sera contained antibodies reactive with both gpl2S and gp250/200, a number of sera contained antibodies reactive with one of the glycoproteins but not with both. The data indicated that both of these glycoproteins should be used in assays for detecting IgA antibodies to EBV, to avoid false‐negative results. This assay should be useful for screening large populations for IgA antibodies to EBV and also possibly for monitoring disease course in patients with NPC.
Non‐ocular cancer in patients with hereditary retinoblastoma and their relatives
Authors: Derkinderen D. J. , Koten J. W. , Nagelkerke N. J. D. , Tan K. E. W. P. , Beemer F. A. , Otter W. Den 
Published: February 2007

AbstractIn The Netherlands, retinoblastoma patients have been registered in the Utrecht national retinoblastoma registry since 1862. This register is virtually complete from 1945 onwards. We describe a unique epidemiological survey of the occurrence of non‐ocular cancer in all patients registered during the period 1945‐1970. The occurrence of non‐ocular cancer in relatives of patients with hereditary retmoblastoma is also reported. One hundred and forty‐one patients with hereditary retinoblastoma were studied for non‐ocular second primary cancer. Nineteen patients died of retrnoblastoma. The median follow‐up of the surviving 122 patients was 25 years. Seventeen of these patients developed a second primary cancer, most frequently soft‐tissue sarcoma. The cumulative incidence of non‐ocular cancer was I at the age of 35, i.e., a 14‐fold increase as compared to the general population. Twelve patients with hereditary retinoblastoma died of non‐ocular cancer whereas none of 252 patients with non‐hereditary retinoblastoma died of non‐ocular cancer. Furthermore, among the parents of our hereditary retinoblastoma patients, 24 (born before 1945) had also been affected by retinoblastoma or had affected sibs. In the parents, 4 tumors occurred, of which 2 were rhabdomyosarcomas and 2 were urinary bladder cancers. Both types of non‐ocular cancer were also encountered among the 122 patients with hereditary retinoblastoma. In 103 fathers and 103 mothers of patients with hereditary retinoblastoma who did not have retinoblastoma themselves, there was no previous family history of retinoblastoma. The fathers had a relative risk of 8.3 for pancreatic cancer compared to the general population. There was no significant increase in the number of non‐ocular tumors in 332 sibs of patients with hereditary retinoblastoma.