bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ouabain‐resistant non‐small‐cell lung‐cancer CELL LINE SHOWS COLLATERAL SENSITIVITY TO cis‐diamminedichloroplatinum(II) (CDDP)
Authors: Ohmori Tohru , Nishio Kazuto , Ohta Sei , Kubota Naohiro , Adachi Mitsuru , Komiya Kazuhide , Saijo Nagahiro 
Published: February 2007

AbstractWe have reported that the cellular uptake of cis‐diamminedi‐chloroplatinum(11) (CDDP) was inhibited by an Na+,K+‐adenosine triphosphatase (ATPase) inhibitor, ouabain, in a human non‐small‐cell lung‐cancer cell line, PC‐14, but not in its CDDP‐resistant cell line, PC‐14/CDDP. [3H]Ouabain binding of PC‐14/CDDP was about 50% lower than that of PC‐14. Accordingly, we speculated that a decrease in Na+,K+‐ATPase activity in PC‐14/CDDP might contribute to the decrease in cellular CDDP accumulation. To clarify the relationship between the activity or expression of Na+,K+‐ATPase and cellular CDDP accumulation, we established an ouabain‐resistant non‐small‐cell lung‐cancer cell line (PC‐14/OB300), which showed 1.9‐fold resistance to the cytotoxicity of ouabain. Interestingly, this cell line was 4.2‐fold more sensitive to CDDP than PC‐14. The accumulation of CDDP in PC‐14/OB300 was increased to 2.7‐fold that in PC‐14. This elevation of CDDP accumulation was not considered to be caused by increased passive diffusion, because the accumulation of CDDP in PC‐14/OB300 was also inhibited by ouabain compared to PC‐14. As one of the indices of Na+.K+‐ATPase activity, we determined cellular 86Rb+ influx rates. The 86Rb+ influx rate was 1.5‐fold higher in PC‐14/OB300 and fell to 0.7‐fold in PC‐14/CDDP compared with PC‐14. The mRNA expression of Na+,K+‐ATPase was increased in PC‐14/OB300 and decreased in PC‐ 14/CDDP. There was no difference in cellular [3H]ouabain binding between PC‐14/OB300 and PC‐14. It is passible that Na+,K+‐ATPase of PC‐14/OB300 has a different affinity for ouabain from that of PC‐14. Our results suggest that the enzyme activity or the level of expression of Na+,K+‐ATPase may contribute to the cellular uptake of CDDP and determine the sensitivity to CDDP. © Wiley‐Liss, Inc.
The effect of vitamin and mineral supplementation on esophageal cytology: Results from the linxian dysplasia trial
Authors: Mark Steven D. , Liu Shu Fan , Li Jun Yao , Gail Mitchell H. , Shen Qiong , Dawsey Sanford M. , Liu Fusheng , Taylor Philip R. , Li Bing , Blot William J. 
Published: February 2007

AbstractThe population of Linxian in China has one of the world's highest rates for esophageal/gastric cardia cancer, as well as documented nutritional deficiencies. To determine whether dietary supplementation with a multi‐vitamin multi‐mineral preparation could reduce the risk of esophageal cancer and favorably influence precursor lesions, 3,318 individuals age 40‐69 with cytologically determined grade I or grade 2 esophageal dysplasia were randomly assigned to receive either an active multi‐vitamin multi‐mineral supplement or a placebo. Pills were distributed at monthly visits and incident cancers or deaths were recorded. At 30 and 72 months subsequent to randomization all living participants without a known incident cancer were asked to undergo repeat cytological examination of their esophagus. Based on these procedures participants were classified as having no dysplasia, dysplasia grade I, dysplasia grade 2 or near cancer dysplasia. Diagnoses of cancer were based on the cytology findings plus available histologic, radio‐logic and clinical materials. At the end of the study there was little overall difference in cumulative risk of esophageal cancer between those receiving vitamin/mineral supplementation and those receiving placebo. There was, however, a significant increase in reversion to non‐dysplastic cytology among the group receiving the active treatment. The odds of not having any dysplasia at the two post‐randomization screens was 1.23 times higher in the active treatment group than in the placebo group. Within each treatment group higher categories of dysplasia were associated with higher rates of cancer. © 1994 Wiley‐Liss, Inc.
Expression of MUC1, MUC2, MUC3 and MUC4 mucin mrnas in human pancreatic and intestinal tumor cell lines
Authors: Hollingsworth Michael A. , Strawhecker Judith M. , Caffrey Thomas C. , Mack David R. 
Published: February 2007

AbstractWe examined the steady‐state expression levels of mRNA for the MUC1, MUC2, MUC3 and MUC4 gene products in 12 pancreatic tumor cell lines, 6 colon tumor cell lines, and one ileocecal tumor cell line. The results showed that 10 of 12 pancreatic tumor cell lines expressed MUCI mRNA and that 7 of these 12 lines also expressed relatively high levels of MUC4 mRNA. In contrast, MUC2 mRNA was expressed at only low levels and MUC3 was not detected in the pancreatic tumor cell lines. All 7 intestinal tumor cell lines examined expressed MUC2, and 5 of 7 expressed MUC3; however only one expressed significant levels of MUCI and 2 expressed low levels of M0C4 mRNA. This report of high levels of MUC4 mRNA expression by pancreatic tumor cells raises the possibility that mucin carbohydrate epitopes defined by antibodies such as DuPan 2 may be expressed on a second mucin core protein produced by pancreatic tumor cells. © 1994 Wiley‐Liss, Inc.
Reversal of multidrug resistance by tyrosine‐kinase inhibitors in a non‐P‐glycoprotein‐mediated multidrug‐resistant cell line
Authors: Takeda Yuichiro , Nishio Kazuto , Niitani Hisanobu , Sajio Nagahiro 
Published: February 2007

AbstractWe have already established a human leukemia sub‐line resistant to the growth‐inhibitory effect of TPA (12‐O‐tetradecanoylphorbol 13‐acetate) (K562/TPA) derived from K562. KS62/TPA was found to be a non‐P‐glycoprotein‐mediated multidrug‐ resistant cell line, in which intracellular drug accumulation was not reduced. In K562/TPA, adriamycin (ADM) was distributed mainly in the cytoplasm and was scarcely observed in the nucleus. We determined the relative levels of multidrug‐resistance‐associated protein (MRP), which was recently identified as the novel transporter. The relative levels of MRP in K562/TPA were the same as in K562. Although the catalytic activity of K562/TPA topoisomerase II was about hall that of the parental cells, resistance to other drugs could not be explained by topoisomerase‐II activity. To elucidate the mechanism of drug resistance in K562/TPA, we tried to find chemicals that would reverse the drug resistance. Tyrosine‐kinase inhibitors enhanced the cytotoxicity of anti‐neoplastic drugs against K562/TPA. Therefore we examined the modification of nuclear ADM accumulation in K562/TPA by one of these tyrosine‐kinase inhibitors, genistein. Although the amount of ADM was decreased in the nuclei of K562/TPA cells, it was significantly increased after incubation in the presence of genistein. The formation of DNA single‐strand breaks by ADM. etoposide and ACNU was significantly lower in K562/TPA than in K562, but was significantly increased in the presence of genistein. These results suggest that genistein could overcome drug resistance by enhancing the accumulation of drug into the nuclear fraction of K562/TPA. © 1994 Wiley‐Liss, Inc.
Suppressive effect of recombinant human Cu, Zn‐superoxide dismutase on lung metastasis of murtne tumor cells
Authors: Yoshizaki Naohito , Mogi Yoshihiro , Muramatsu Hirohito , Koike Kazuhiko , Kogawa Katsuhisa , Niitsu Yoshiro 
Published: February 2007

AbstractThe inhibitory effect of recombinant human Cu++Zn++superoxide dismutase (rhSOD) on metastasis of tumor cells in the mouse was investigated. In an experimental pulmonary metastasis model employing Moth A cells as inoculum, significant inhibition of metastasis was obtained by intravenous pre‐ and post‐administration of rhSOD. An inhibitory effect of rhSOD was also observed in a spontaneous pulmonary metastasis model with ILL cells as the inoculum. rhSOD was not observed to have any significant effects on the platelet‐aggregating activity of tumor cells, the adhesiveness of tumor cells to vascular components (endothelial cells, laminin and type‐IV collagen), or the growth of tumor cells either in vitro or in vivo. However, rhSOD suppressed invasion of Meth A and 3LL cells into Matrigel (an artificially reconstituted basement membrane of collagen, laminin and heparan sulfate) in the presence of hypoxanthine and xanthine oxidase, in vitro producers of superoxide. Thus, the present study shows that rhSOD is able to inhibit both experimental and spontaneous pulmonary metastasis, possibly through the suppression of tumor cell invasion into the extracellular matrix. © 1994 Wiley‐Liss, Inc.
HLA restriction and T‐cell‐receptor Vβ gene expression of cytotoxic T lymphocytes reactive with human squamous‐cell carcinoma of the head and neck
Authors: Yasumura Satoshi , Weidmann Eckhart , Hirabayashi Hideki , Johnson Jonas T. , Herberman Ronald B. , Whiteside Theresa L. 
Published: February 2007

AbstractA human cytotoxic‐T‐lymphocyte (CTL) line capable of killing autologous tumor (AuTu) cell targets was established from peripheral‐blood lymphocytes of a patient with squamous‐cell carcinoma of the tongue. The cultured CTL were CD3+CD8+CDIIb‐HLA‐DR+T cell receptor (TCR) α/β+. When tested in 4‐hr 51Cr‐release assays against various lines of squamous‐cell carcinoma of the head and neck (SCCHN) and a variety of non‐squamous human tumor and normal cell targets, the CTL were found to lyse the autologous SCCHN cell line (PCI50) and 7 allogeneic SCCHN lines: PCI‐1, ‐2, ‐4A, ‐4B, ‐13, ‐30 and ‐38. Of these tumor cell lines, PCI‐13, ‐30 and ‐38 shared HLA‐A2 locus with the AuTu, PC1‐50, while PCI‐4A and ‐4B shared HLA‐B44 with AuTu. Lysis of AuTu (A2+B44+), PCI‐13 (A2+B44‐) and PCI‐4B (A2‐ B44+) by the CTL was efficiently inhibited by monoclonal antibodies (MAbs) to CD3, CD8, TCRα/β or the major‐histocompatibility‐complex(MHC)‐class‐l antigens. MAbs to HLA‐A2 antigens inhibited lysis of PCI‐50 or PCI‐13 targets by the CTL. In cold‐target inhibition assays, unlabeled PCI‐4B or PCI‐13 cells inhibited CTL lysis of AuTu targets. The CTL incubated in the presence of the HLA‐A2+ SCCHN PCI‐50 or ‐13, but not an HLA‐A2+ gastric carcinoma, produced TNF‐α, IFN‐γ and GM‐CSF. The CTL were tested for their TCR Vβ gene expression by polymerase chain reaction (PCR). At week 10 in culture, the time of the highest AuTu cytotoxicity mediated by the CTL line, Vβ was expressed by 26% of T cells. Three clones, obtained by limiting dilution from 10‐week CTL and selected for high cytotoxicity against AuTu, were found to be Vβ+. Further analysis of the specificity of these clones indicated lytic activity against PCI‐13 (A2+B44‐), but not PCI‐4B (A2‐B44+) targets. In 16‐week cultures, which retained AuTu cytotoxicity as well as Vβ expression, TCR Vβ2 was also expressed at high frequency (29%), and AuTu‐reactive clones were found to be Vβ2+. Our results indicate that at least 2 different CTL populations (Vβ2+ and β2+) are able to recognize SCCHN‐associated antigen(s) and that the Vβ6+ T cells are HLA‐A2 restricted, while Vβ6+ T cells are HLA‐A2 restricted, while Vβ2+ T cells may be HLA‐ B44 restricted. © 1994 Wiley‐Liss, Inc.
A prospective study of weight, body mass index and other anthropometric measurements in relation to site‐specific cancers
Authors: Chyou Po‐Huang , Nomura Abraham M. Y. , Stemmermann Grant N. 
Published: February 2007

AbstractThe association of weight, body mass index and other anthropometric measurements with cancer was investigated in a cohort of 7,840 men, examined and interviewed from 1965‐1968 in Hawaii. After 23 years of follow‐up, histologically confirmed incident cases of prostate (n = 306), colon (n = 289), lung (n = 236), stomach (n = 229) and rectal (n = 108) cancer were identified. Body weight was positively associated with prostate cancer. This direct association was stronger for cases diagnosed II or more years after examination than for those diagnosed earlier. A similar pattern was also present for the risk of colon cancer,in association with weight and body mass index. For lung cancer, increased subscapular and triceps skinfold thickness were each associated with decreased risk with adjustment for cigarette smoking, but the inverse association did not persist as the time interval from exam to cancer diagnosis lengthened. There was no significant association between anthropometric measurements and stomach or rectal cancer. © 1994 Wiley‐Liss, Inc.
Intestinal metaplasia types and the risk of gastric cancer: A cohort study in Slovenia
Authors: Filipe M. Isabel , Muñoz Nubia , Matko Ivan , Kato Ikuko , Pompe‐Kirn Vera , Jutersek Albert , Teuchmann Sibylle , Benz Maja , Prijon T. 
Published: February 2007

AbstractBetween 1967 and 1976, 1,525 Slovenian patients with a histological diagnosis of intestinal metaplasia (IM) were classified according to subtype of IM based on morphology and mucin staining; 518 cases were diagnosed with type I, 197 with type II and 275 with type III, but in 291 the diagnosis of IM was not confirmed. Patients who had developed cancer or died up to 1986 were identified by record linkage at the Slovenia Cancer Registry and the Central Population Registry in Slovenia. A total of 34 incident cases of gastric cancer occurring at least 6 months after the diagnosis of IM were identified. The standardised incidence ratio (SIR) for stomach cancer was 2.23 in the whole cohort. It was highest for IM type III, followed by type II and IM‐unconfirmed, but not increased for type I. The relative risk (RR) of developing gastric cancer based on Cox's proportional hazards model was 2.14 for type II and 4.58 for type III, compared with type I. The RR was especially increased for a subgroup of type III secreting sulphomucins in their goblet cells in comparison with types I‐II negative to sulphomucins. Our results confirm that subtyping of IM is useful for identifying individuals at high risk for gastric cancer. © 1994 Wiley‐Liss, Inc.
Cea expression of colorectal adenocarcinomas is correlated with their resistance against lak‐cell lysis
Authors: Kammerer R. , von Kleist Sabine 
Published: February 2007

AbstractWe have investigated the in vitro interaction of LAK cells with 20 different human tumor cell lines freshly isolated from colorectal carcinoma (CRC) specimens. Three steps of LAK cell/tumor cell interaction, namely adherence, infiltration and lysis, have been studied. All are important for the cytotoxic effect of LAK cells against solid tumors: LAK‐cell adherence was studied on tumor‐cell monolayer cultures, the infiltration capacity of LAK cells using tumor‐cell spheroids and the resulting cytotoxic effects of LAK cells against CRC cells grown as spheroids or monolayers. Finally, we correlated the degree of lysis of the CRC cells with their carcinoembryonic antigen (CEA) production, the secretion of which varied in a broad range from not detectable to 2,800 ng/day in culture medium. Cytotoxicity experiments showed a good correlation between CEA expression of CRC cells and their resistance against allogeneic LAK cells. Spheroids of CEA‐producing cells prevented LAK‐cell infiltration resulting in high resistance against LAK‐cell lysis. Adhesion of LAK cells on monolayers of CEA‐expressing CRC cells was minimal. Our results indicate that CEA expression may be an escape mechanism protecting colon carcinoma cells from an attack by cytotoxic cells. © 1994 Wiley‐Liss, Inc.
Expression of APO‐1 (CD95), a member of the NGF/TNF receptor superfamily, in normal and neoplastic colon epithelium
Authors: Möller Peter , Koretz Karin , Leithäuser Frank , Brüderlein Silke , Henne Christof , Quentmeier Armin , Krammer Peter H. 
Published: February 2007

AbstractAPO‐I is a 48‐kDa cell‐membrane protein identical to the Fas antigen now designated CD95. It is a member of the NGF/TNF receptor superfamily. Anti‐APO‐I monoclonal antibody induces apoptosis in a variety of cell types expressing this antigen. We immunohistochemically investigated APO‐I expression in normal colon mucosa, 20 adenomas, 258 colon carcinomas and 10 liver metastases and carried out in vitro studies using a panel of colon‐carcinoma cell lines. Immunohistochemically, APO‐I was regularly expressed at the basolateral membrane of normal colon epithelia. In a minor fraction of colon adenomas and in 39.1% of colon carcinomas APO‐I expression was diminished and in 48.1% of carcinomas, predominantly of the non‐mucinous type, APO‐I expression was completely abrogated. The normal level of APO‐I in carcinomas was correlated with the mucinous type. Reduced/lost APO‐I expression was more frequent in rectal carcinomas. Complete loss of APO‐I was more frequent in tumors that had already metastasized. APO‐I expression in liver metastases essentially corresponded to that of the primary tumors. Comparative analysis with data from previous studies revealed that the mode of APO‐I expression is correlated with that of HLA‐A,B,C./β2m, HLA‐DR, HLA‐D‐associated invariant chain and of the secretory component. Surface expression of APO‐I was heterogeneous in colon‐carcinoma cell lines; SW480 expressed considerable amounts of APO‐I on all cells, while HT‐29 constitutively did less so and only in a minority of cells. Surface density of APO‐I and the fraction of positive cells in HT‐29 was enhanced by interferon‐gamma (IFN‐γ) and, additively, by tumor necrosis factor‐alpha (TNF‐α), whereas in SW480 APO‐I expression was not modulated by these cytokines. We conclude that neoplastic transformation of colon epithelium often leads to a loss of the physiologic, high level of surface APO‐I by giving rise either to a stable lack of APO‐I or to an IFN‐γ/TNF‐α‐sensitive phenotype of inducible APO‐I expression. © 1994 Wiley‐Liss, Inc.
Derivation of androgen‐independent human LNCaP prostatic cancer cell sublines: Role of bone stromal cells
Authors: Wu Hsi‐Chin , Hsieh Jer‐Tsong , Gleave Martin E. , Brown Nicholas M. , Pathak Sen , Chung Leland W. K. 
Published: February 2007

AbstractA model of human prostate cancer was established to study cellular interaction between prostate cancer and bone stroma in vivo. In this model, subcutaneous co‐injection of 2 non‐tumorigenic human cell lines‐LNCaP, a prostate cancer cell line, and MS, a bone stromal cell line‐into intact adult male mice resulted in formation of carcinomas that secreted prostate‐specific antigen (PSA), a clinically useful human serum prostate cancer marker. In castrated hosts, upon cellular interaction with bone fibroblasts, we observed the progression of these tumors from an androgen‐dependent (AD) to an androgen‐independent state (AI). We derived 4 LNCaP cell sublines from the chimeric LNCaP/MS tumors: the M subline from intact hosts and the C4, C4‐2 and C5 sublines from castrated hosts. The LNCaP sublines had chromosomal markers similar to those of the parental LNCaP cells and distinctly different from those of the MS bone stromal cell line. Although the parental and derived cell lines expressed similar steady‐state levels of orni‐thine decarboxylase transcript, the sublines expressed 5‐ to 10‐fold higher basal steady‐state levels of PSA transcript than did the parental LNCaP cell line. The LNCaP sublines formed 13‐ to 26‐fold more soft‐agar colonies than the parental LNCaP cell line. The sublines became tumorigenic, yielding an incidence of tumors in intact athymic mice of 7‐75%. The LNCaP sublines C4 and C5 (but not the parental and M cell line) formed tumors in castrated hosts when co‐injected with bone fibroblasts. A second‐generation LNCaP subline, C4‐2, was derived from a chimeric tumor induced by co‐inoculating castrated mouse with C4 cells and MS cells. We found that C4‐2 subline was tumorigenic when inoculated into castrated hosts in the absence of inductive fibroblasts. Moreover, C4‐2 was the only subline capable of forming soft‐agar colonies when cultured in serum‐free medium. In comparison with the parental LNCaP cells, the C4‐2 subline expressed lower steady‐state levels of androgen receptor (AR) protein and mRNA transcript and lost its androgen responsiveness in vitro. Our results suggest that certain genetic traits of prostate cancer cells may be selected or altered through an “adaptive” mechanism that involves cellular interaction with the bone stromal cells. © 1994 Wiley‐Liss, Inc.
Isolation of naturally processed peptides recognized by cytolytic T lymphocytes (CTL) on human melanoma cells in association with HLA‐A2.1
Authors: Wölfel Thomas , Schneider Jörg , Zum Büschenfelde Karl‐Hermann Meyer , Rammensee Hans‐Georg , Rötzschke Olaf , Falk Kirsten 
Published: February 2007

AbstractCytolytic T lymphocyte (CTL) clones have previously been derived from peripheral blood of melanoma patient SK29(AV). They lyse autologous melanoma cells but not autologous Epstein‐Barr virus (EBV)‐transformed B lymphocytes. Immunoselection experiments indicate that these CTL clones recognize 4 different antigens (Aa, Ab, B, C) in association with a single HLA restriction element, HLA‐A2.1. While the expression of antigens B and C appears to be confined to SK29‐melanoma cells, antigens Aa and Ab are shared by a high proportion of allogeneic HLA‐A2‐positive melanoma lines. HLA‐A2.1 and total HLA class 1 molecules have now been purified from SK29‐melanoma cells using affinity chromatography and associated peptides have been eluted. Peptide pools eluted from HLA‐A2.1 and total class 1 were separated by reversed phase high performance liquid chromatography (HPLC). Individual HPLC fractions were tested for their ability to sensitize target cells for recognition by SK29‐CTL clones. The presence of antigens Aa, Ab, B and C was detected in distinct HPLC fractions that were identical for both peptide pools. As target for detection of peptide antigens in HPLC fractions, the use of the HLA‐A2.1‐positive antigen processing mutant cell line CEM x 721.174.T2 (T2), pre‐incubated with anti‐HLA‐A2 monoclonal antibody (MAb) MA2.1, was shown to be essential. Single‐peak target‐sensitizing activity was found for antigens Ab and B, whereas multi‐peak sensitizing activity was reproducibly detected for antigens Aa and C. We reason that at least some of these melanoma peptide antigens might occur in biochemically distinct isoforms. © 1994 Wiley‐Liss, Inc.
Association between HLA‐DQB1 alleles and risk for cervical cancer in African‐American women
Authors: Gregoire Lucie , Lawrence W. Dwayne , Kukuruga Debra , Eisenbrey A. Bradley , Lancaster Wayne D. 
Published: February 2007

AbstractSquamous‐cell carcinoma of the cervix and its precursor lesions are associated with human papillomavirus (HPV) infection. Epidemiological studies indicate that HPV infection in itself is not sufficient for cervical‐cancer induction, suggesting that other factors contribute to carcinogenesis. We have investigated the potential role of host genetic background as one such factor. We screened a series of squamous‐cell carcinomas of the cervix for HLA‐class‐II DQBI* alleles by the polymerase chain reaction and site‐specific oligonucleotide probe hybridization and for HPV type from African‐American women using a local, ethnically matched control panel. Statistically significant associations for increase in relative risk for cervical cancer were seen for DQBI*0303 and DQBI*0604. DQBI*0201 and the hetero‐zygote DQBI*0301/*0501 showed a decrease in relative risk for cervical cancer. HPV typing revealed no association between virus type and DQBI alleles. Our results confirm other studies showing an increase in relative risk for cervical cancer associated with HLA‐DQ3 alleles in Caucasians. © 1994 Wiley‐Liss, Inc.