bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of the E2 prostaglandin enprostil, and the somatostatin analogue sms 201 995, on the growth of a human gastric cell line, MKN45G
Authors: Watson Susan A. , Durrant Lindy G. , Morris David L. 
Published: February 2007

AbstractThe effect of enprostil and the somatostatin analogue SMS 201 995 on the growth of a clonal variant of the human gastric adenocarcinoma cell line, MKN45, was studied. The derived cell line grew twice as fast as MKN45 when grown as a xenograft line in nude mice. However, it did not respond trophically to gastrin either in vitro or in vivo (unlike MKN45) although it possessed the same number of gastrin receptors as the parental line. Gastrin production by the cell line during in vitro culture was twice that of MKN45; thus, the cell line was denoted MKN45G. When MKN45G was grown as xenografts in nude mice (n =10/group), enprostil (20 μg/kg/day) significantly inhibited tumour growth when administered continuously by an osmotic mini‐pump from day 1 to day 7 of a 20‐day experiment, and induced tumour regression when administered from day 7 to day 14. Enprostil reduced post‐prandial serum gastrin levels when administered from day 7 to day 14 and prevented gastrin release by MKN45 in vitro. SMS 201 995 at doses of 25 and 240 μg/kg/day induced tumour regression when administered from day 1 to day 7 and the former dose reduced post‐prandial serum gastrin levels at day 5. Gastrin release by MKN45G was not affected by SMS 201 995 in vitro, thus its effect may not be mediated directly via gastrin, requiring interaction between other hormones or growth factors in the in vivo situation.
Recurrent mutation of immunoglobulin and c‐myc genes and differential expression of cell surface antigens occur in variant cell lines derived from a burkitt lymphoma
Authors: Guy K. , Middleton P. G. , Bansal N. S. , Ross J. A. , Steel C. M. 
Published: February 2007

AbstractThe phenotypic and molecular genetic characteristics of 4 variant sublines of the Burkitt lymphoma cell line Namalwa have been examined. The sublines are DNA‐fingerprint‐identical and derived from a monoclonal tumour, as shown by a rearrangement of the T‐cell‐receptor β‐chain gene common to the 4 sublines. There is non‐co‐ordinate expression of MHC class‐1, MHC class‐II, surface immunoglobulin and a number of antigens recognized by CD MAbs on the different sublines. These different phenotypes of the cells are reminiscent of B cells arrested in varying states of cellular maturity. On Southern blots there are different patterns of restriction fragments hybridizing with Ig heavy‐ and light‐chain gene probes among the sublines, indicating that multiple rearrangements or mutations of 1g genes have occurred in the cells. Different patterns of hybridizing fragments among the sublines were also found by using c‐myc probes, implying the existence of different mutations of the c‐myc locus. The c‐myc mutation found in one of the sublines mapped to the 5′ flanking sequence and in another 3′ to the c‐myc locus. Using the J17BS8 probe, which detects a restriction fragment length polymorphism in the 3′ flanking region of the c‐myc gene, a 4‐fold variation in the gene copy number among the sublines was found and one of the sublines was shown to be hemizygous for c‐myc. Examination of DNA from early cultures of Namalwa cells showed that the alterations in Ig and c‐myc structure had occurred on prolonged culture of the cells.
EGF and TGF‐α, the ligands of hyperproduced EGFR in human esophageal carcinoma cells, act as autocrine growth factors
Authors: Yoshida Kazuhiro , Kyo Eikai , Tsuda Toshitaka , Tsujino Tetsuhiro , Ito Masanori , Niimoto Minoru , Tahara Elichi 
Published: February 2007

AbstractIn order to ascertain autocrine growth factors in esophageal carcinomas, we analysed expression of mRNAs and proteins for epidermal growth factor (EGF), transforming growth factor‐α (TGF‐α) and epidermal growth factor receptor (EGFR) in 6 esophageal carcinoma cell lines. Gene alterations were also examined. All of the esophageal carcinoma cell lines expressed mRNA for EGFR and TGF‐α genes. Interestingly, EGF mRNA of about 5.0 kb was also detected in TE‐1, TE‐2, and TE‐8 cells. Production of protein was also confirmed by binding assay and ELISA on 3 of the 6 cell lines. The cells had a relatively high number of EGFRs and produced TGF‐α and EGF protein at the same time. Furthermore, anti‐EGF (KEM‐10) and anti‐TGF‐α (WA‐3) monoclonal antibodies (MAbs) inhibited spontaneous uptake of tritiated thymidine (3H‐TdR) by TE‐1 cells which expressed EGF, TGF‐α and EGFR mRNA and protein. These results strongly suggest that EGF and/or TGF‐α produced by carcinoma cells function as autocrine growth factors for human esophageal carcinomas.
Oncofetal antigen in Xiphophorus detected by monoclonal antibodies directed against melanoma‐associated antigens
Authors: Claus Gert , Winkler Christoph , Lohmeyer JÜRgen , Anders Fritz , Schartl Manfred 
Published: February 2007

AbstractMonoclonal antibodies (MAbs) directed against Xiphophorus melanoma cells were developed and tested by indirect immunofluorescence and immunoperoxidase staining for reactivity with a panel of 15 allogeneic tissues and 12 allogeneic cell lines. The reactivity of such MAbs was restricted to melanoma cells from tumor biopsies and melanoma‐derived cell lines. In addition, all embryonic cells of all histiotypes from developmental stages later than mid‐organogenesis and from corresponding short term in vitro cultures reacted with these MAbs. In contrast, normal tissues and organs from adult fish displayed no reactivity, thus implying that the melanomaassociated antigens detected by the MAbs described are oncofetal antigens.
Isolation and characterization of 5T4, a tumour‐associated antigen
Authors: Hole Nicholas , Stern Peter L. 
Published: February 2007

AbstractThe monoclonal antibody (MAb) 5T4 defines a human trophoblast antigen marker with a restricted pattern of expression in normal adult tissues but this antigen is expressed on a variety of carcinomas. The purification of 5T4 antigenic molecules is described from term syncytiotrophoblast by a combination of lectin‐ and immunoaffinity chromatography and gel filtration giving up to 10,000‐fold purification with 70% yield. The antigen is carried by non‐associated glycoprotein molecules with an apparent molecular weight of 72 kDa on SDS‐PAGE and a neutral pl. Removal of N‐linked sugars by N‐glycanase reveals a core protein of 42 kDa. Treatment with enzymes that cleave O‐linked sugars does not substantially alter the molecular size. The native 5T4 molecules are very resistant to proteolysis until the N‐linked sugars are removed or the glycoprotein is denatured and reduced. Glycopeptides generated by these approaches will be suitable for amino acid sequencing.
Vaccination against polyoma virus (PYV) tumors using vaccinia‐PYV recombinants: A major tumor‐specific transplantation antigen (TSTA) epitope resides within the C‐terminal segment of middle‐T protein
Authors: Kieny M. P. , Gautier C. , Tomasetto C. , Kuhn I. , Hareuveni M. , Clertant P. , Lathe R. 
Published: February 2007

AbstractWe previously reported that inoculation of rats with live vaccinia virus (VV) recombinants VVpyMT, VVpyLT expressing either the middle‐T (MT) or large‐T (LT) proteins of polyomavirus (PyV) can elicit immunity to challenge with syngeneic PyV‐tumor cells. We now report the results of cross‐vaccination studies. VVpyMT was ineffective against cells expressing LT protein but prevented development of MT‐expressing cells. Conversely, the VVpyLT was ineffective against MT‐expressing cells. In the two experiments performed, tumor growth enhancement rather than retardation was observed in VVpyLT‐vaccinated animals receiving PyV‐LT (FRLTI) challenge tumor cells. To determine the location of the major TSTA within MT, a further VV recombinant (VVpyMT/Cfr) was constructed that expresses only the unique C‐terminal segment of MT. VVpyMT‐Cfr and VVpyMT were equally effective in eliciting tumor immunity, indicating the presence of a major TSTA epitope within the unique C‐terminal region of MT.
Adeno‐associated parvoviruses inhibit growth of cells derived from malignant human tumors
Authors: Bantel‐Schaal Ursula 
Published: February 2007

AbstractInfection of freshly established malignant human tumor cells with the adeno‐associated viruses AAV‐2 or AAV‐5 inhibits cell proliferation. Normal human fibroblasts are also affected, but appear to partially escape the inhibition. In cell cultures of permanent lines of human and rodent origin, cell number reduction could not be observed. The AAV‐mediated influence on cell growth is not due to helper‐independent replication of the virus, since neither of the cell cultures supported AAV propagation in the absence of a viral helper.
Prognostic significance of alpha‐1‐antitrypsin in early stage of colorectal carcinomas
Authors: Karashima Seiichiro , Kataoka Hiroaki , Itoh Hiroshi , Maruyama Riruke , Koono Masashi 
Published: February 2007

AbstractWe have previously shown that human colorectal carcinoma cell lines, RCM‐1 and CoCM‐1, synthesize alpha‐1‐antitrypsin (α1‐AT) in culture. We have studied immunohistochemically the incidence of α1‐AT on histologic sections from paraffin‐embedded tissues of surgically resected colorectal carcinomas and their metastatic foci, polypectomized adenomas, and normal mucosae. α1‐AT was detected in 89 (61%) of 145 carcinomas (including 14 carcinomas in adenoma), and 12 (39%) of 31 adenomas. But only 2 (4%) of 55 normal colorectal mucosae were positive for α1‐AT. In metastatic tumor cells of colorectal carcinomas in lymph nodes and other organs, α1‐AT positivity was 60% and 82%, respectively. The incidence of α1‐AT was markedly higher in advanced adenocarcinomas than in early ones and more frequent in adenocarcinomas of right side (including transverse colon) than those of left side and rectum, regardless of their histological malignancy grades. In mucinous carcinomas the frequency was greater (8 of 9 cases) than in conventional adenocarcinomas.Clinical follow‐up of the patients with colorectal carcinomas suggested that α1‐AT positivity in Dukes' stage A/B tends to correlate with unfavorable prognosis irrespective of the grade of histologic differentiation of carcinoma, but there is no significant relation in Dukes' stage C/D. Our findings suggest that α1‐AT in colorectal carcinoma is related to the invasive and metastatic capacity. It may thus serve as a biologic marker for prognosis of colorectal carcinomas at relatively early stages (Dukes' stage A/B).
Overexpression of the MDRL gene in blast cells from patients with acute myelocytic leukemia is associated with decreased anthracycline accumulation that can be restored by cyclosporin‐A
Authors: Nooter Kees , Sonneveld Pieter , Oostrum Robert , Herweijer Hans , Hagenbeek Ton , Valerio Dinko 
Published: February 2007

AbstractTypical multi‐drug resistance (MDR) in human and animal cell lines is caused by overactivity of a unidirectional drug efflux pump. This pump is composed of a 170‐kDa transmembrane glycoprotein (P‐glycoprotein) that is encoded by the so‐called mdrl gene. The functionally relevant characteristic of MDR cells is a defect in drug accumulation that can be restored by agents which inhibit the P‐glycoprotein pump. The purpose of our study was to find out whether Pglycoprotein inhibitors could increase the daunorubicin (DNR) accumulation in acute myelocytic leukemia (AML) cells, overexpressing the mdrl gene. Using dot blot analysis with an mdrl‐specific cDNA probe, we identified leukemic cell samples, obtained from chemotherapy‐resistant AML patients, that had relatively high levels of mdrl expression. These leukemic cells showed a reduced ability to accumulate DNR in vitro, as quantitated by flow cytometry. Addition of cyclosporin‐A (Cy‐A), a drug known to inhibit the P‐glycoprotein pump, to the incubation medium resulted in an increase (up to 60%) in steady‐state drug uptake by the leukemic cells. The degree of Cy‐A‐induced increase in drug accumulation in the leukemic cells correlated approximately with the level of overexpression of the mdrl gene. Our data indicate that Cy‐A is a good candidate for combination chemotherapy with cytotoxic drugs in clinical trials, aimed at the treatment of drug resistance in AML.
Comparison of dna cleavage induced by etoposide and doxorubicin in two human small‐cell lung cancer lines with different sensitivities to topoisomerase ii inhibitors
Authors: Binaschi Monica , Capranico Giovanni , De Isabella Paola , Mariani Mariangela , Supino Rosanna , Tinelli Stella , Zunino Franco 
Published: February 2007

AbstractIn an attempt to clarify the role of drug‐induced proteinassociated DNA breaks (i.e., DNA topoisomerase II‐mediated DNA cleavage) in the cytotoxic activity of doxorubicin and etoposide, their cellular effects were compared in 2 human small‐cell lung cancer (SCLC) lines, characterized by differential sensitivity to DNA topoisomerase II inhibitors. These drugs were selected for comparative studies since they are among the most effective agents in the treatment of SCLC. H146 and N592 cell lines were obtained from pleural effusion and bone‐marrow aspirate of pretreated patients, respectively. Both cell lines grew as floating aggregates with similar doubling times (30 and 33 hr for N592 and H146 cells, respectively). Although, immediately after 1 hr exposure to equitoxic drug levels, the extent of DNA cleavage produced by doxorubicin was markedly lower than that produced by etoposide, DNA lesions produced by doxorubicin persisted and even increased following drug removal. In contrast, an almost complete disappearance of etoposide‐Induced DNA breaks was noted 1 hr after drug removal. Resealing of strand breaks was faster in N592 than in H146 cells. These findings suggest that reversal of these lesions plays a major role in cell survival rather than the occurrence of DNA breaks immediately following drug exposure. This observation is consistent with the view that inhibition of DNA re‐ligation rather than stimulation of DNA cleavage is the critical step for drug action. The different response of these cell lines to cytotoxic action of the topoisomerase inhibitors is associated with a differential drug effect on DNA integrity (detected as DNA double‐strand breaks and DNA‐protein cross‐links). However DNA lesions were comparable when cells were exposed to equitoxic drug levels. The observation that etoposide‐induced DNA breaks were similar in isolated nuclei from both cell lines suggests that drug‐target interaction is modulated in a different manner in the intact cell. As indicated by doxorubicin uptake and retention, cellular drug pharmacokinetics do not account for the different drug response of the studied SCLC lines, presumably reflecting a different extent of DNA break formation and/or a different cytotoxic consequence of DNA damage.
Estrogen‐ and androgen‐responsive growth of human ovarian adenocarcinoma heterotransplanted into nude mice
Authors: Sawada Masumi , Terada Nobuyuki , Wada Akira , Mori Yoichi , Yamasaki Masato , Saga Tsuneo , Endo Keigo 
Published: February 2007

AbstractA new line of human serous cystadenocarcinoma of the ovary, designated OVA‐5, has been established in athymic nude mice. A strong correlation was noted between tumor volume and plasma CA 125 levels in mice bearing OVA‐5 tumor. Growth of the OVA‐5 tumor in castrated male nude mice was accelerated by s.c. administration of estradiol‐17β and 5α‐dihydrotestosterone but not by progesterone. Estradiol‐17β and 5α‐dihydrotestosterone also accelerated the growth of the OVA‐5 tumor heterotransplanted into sialoadenectomized castrated male nude mice. No remarkable change was observed in the histological appearances of the tumors between control groups and hormone‐treated groups. Receptor assays revealed that the OVA‐5 tumor had both estrogen and androgen receptors. Growth of the OVA‐5 tumor is thus responsive to estrogen and androgen.
Importance of interferon α in the resistance of allogeneic C57B1/6 mice to the multiplication of friend erythroleukemia cells in the liver
Authors: Gresser Ion , Maury Chantal , Bandu Marie‐Thérèse , Belardelli Filippo 
Published: February 2007

AbstractFriend erythroleukemia cells (FLC) (H‐2d) injected intravenously multiply extensively in the livers of syngeneic DBA/2 mice and not at all in the livers of allogeneic C57B1/6 mice. Our results indicate that interferon α (IFN‐α) is an important factor in the resistance of allogeneic mice to the multiplication of FLC in the liver. (a) After i.v. inoculation of FLC there was an inverse correlation between the presence of IFN‐α in the serum and the capacity of FLC to multiply in the liver. Thus, all 44 FLC‐injected adult C57B1/6 mice had circulating IFN‐α and FLC did not multiply in the liver of any of the mice. Interferon was not detected in the serum of 83% of 41 FLCinjected DBA/2 mice (and was found only at a low titer in 17% of the mice) and FLC multiplied in the liver of all mice. (b) FLC did multiply in the livers of newborn C57B1/6 mice and in the livers of irradiated adult C57B1/6 mice, and IFN‐α was not detected in their sera. In contrast, after i.v. inoculation of FLC, IFN‐α was detected in the sera of 3‐week‐old and athymic nu/nu adult C57B1/6 mice while FLC failed to multiply in the liver. (c) FLC also induced IFN‐α in congenic B10.D2 (H‐2d) mice and FLC did not multiply in the liver. We suggest that, depending on the site of tumor implantation, different host mechanisms have various degrees of importance in controlling the growth and/or rejection of allogeneic tumor cells, and that IFN‐α is particularly important when FLC are injected i.v.
Anthropometric variables and risk of breast cancer
Authors: Parazzini Fabio , Lavecchia Carlo , Negri Eva , Bruzzi Paolo , Palli Domenico , Boyle Peter 
Published: February 2007

AbstractThe role of anthropometric variables in the risk of breast cancer has been investigated using pooled data from 2 hospital‐based case‐control studies conducted in Italy for a total data‐set of 3,247 cases and 3,263 controls. No association was observed in pre‐menopausal women between breast cancer risk and height, weight, indices of body mass (W/H2; W/H1.5) and surface area. In post‐menopausal women, the risk of breast cancer was inversely related to height, being 0.8 in taller women (>165 cm) compared with women 155 cm tall or less; the trend in risk, although not constantly decreasing, was statistically significant (ptrend = 0.03). A direct, statistically significant association emerged with weight and indices of body mass and post‐menopausal breast cancer risk. Considering 2 indices of body weight (W/H2 and W/H1.5) and relative to thinner women, the respective estimated risks of post‐menopausal breast cancer increased to 1.4 and 1.3 for grossly obese women, and the corresponding p values for trend were respectively 0.002 and 0.02. The role of overweight was more evident in women with early age at menopause, thus suggesting a duration‐risk effect.
Metallothionein gene expression and resistance to cisplatin in human ovarian cancer
Authors: Schilder R. J. , Hall L. , Monks A. , Handel L. M. , Fornace A. J. , Ozols R. F. , Fojo A. T. , Hamilton T. C. 
Published: February 2007

AbstractIntracellular thiols have been proposed as mediators of resistance to alkylating agents and cisplatin. As metallothionein is the predominant protein thiol, we examined its relationship to cisplatin resistance in human ovarian cancer cell lines. A human ovarian carcinoma cell line, A2780, derived from an untreated patient, was treated with cisplatin in several ways and the induced resistance to cisplatin ranged from 13‐ to 68‐fold. The degree of resistance was dependent upon the method of selection. The drug‐resistant cell lines also developed low levels of cross‐resistance to cadmium. Additional cell lines established from untreated patients or ovarian cancer patients refractory to cisplatin‐ and/or carboplatin‐containing combination chemotherapy were studied. The most cisplatin‐resistant cell lines, OVCAR‐8 and ‐10, were from patients previously treated with intensive chemotherapy. OVCAR‐8 was relatively cross‐resistant to cadmium while OVCAR‐10 appeared relatively sensitive. Cell lines were examined for expression of metallothionein mRNA to evaluate the relationship between cisplatin resistance, cadmium cross‐resistance and metallothionein expression. Only two of the cell lines with in vitro‐induced resistance to cisplatin, 2780E80 and 2780CP70B3, had detectable metallothionein mRNA. The other cell lines selected in vitro for cisplatin resistance, as well as the parental A2780 ovarian cancer cell line, showed no expression at our level of detection. There was variable expression of metallothionein among the OVCAR cell lines. Cell lines from untreated patients, OVCAR‐5 and ‐7, did express metallothionein, while the most cisplatin‐resistant cell lines, OVCAR‐8 and ‐10, did nat. We also examined cisplatin induction of metallothionein mRNA in the cell lines. Only 2780CP70B3 among the cell lines with in vitro‐induced cisplatin resistance showed increased expression after short‐term exposure to cisplatin. OVCAR‐4 also had a slight increase in expression after exposure to cisplatin. Mouse C127 cells transfected with a bovine papilloma virus‐metallothionein gene construct were compared for cisplatin sensitivity to the same cell type transfected with bovine papilloma virus alone. In this model system, metallothionein expression did not influence cisplatin cytotoxicity. On the basis of these studies, we conclude that there is no causal relationship between metallothionein expression and cisplatin resistance.
The locus of the polymorphic epithelial mucin (PEM) tumour antigen on chromosome 1q21 shows a high frequency of alteration in primary human breast tumours
Authors: Gendler Sandra J. , Cohen Edward P. , Craston Ann , Duhig Trevor , Johnstone Gillian , Barnes Diana 
Published: February 2007

AbstractTumour and blood leukocyte DNAs from sporadic breast cancer patients were examined for chromosome 1 loss of heterozygosity using a probe for a polymorphic epithelial mucin, PEM, which is expressed in >92% of breast carcinomas as well as in normal lactating breast tissue. Expression is detected by the monoclonal antibodies (MAbs) HMFG‐1,‐2 and SM‐3 which react with epitopes in the 20 amino‐acid repeat unit of the core protein. The PEM probe has been mapped to the chromosome band 1q21, a region that is often incriminated in chromosomal rearrangements in breast tumours. Loss of heterozygosity or alteration at the PEM locus was detected in 34% of the 70 informative patients examined. Twenty of the 24 individuals showed loss of an allele, whereas 4 showed gain of an additional allele or amplification of an existing allele. Twenty‐eight percent of informative cases exhibited alterations at the MS32 locus, 1q42–43, and 20% had alterations at the short arm locus MSI at 1p33–35. These findings identify the long arm of chromosome 1 and in particular the region around the PEM gene for localization of a gene whose loss or alteration may, in some tumours, contribute to the progression of disease in breast cancer patients.