bluuebunny/crossref_metadata_2025_split huggingface dataset:
Resistance to a non‐immunogenic tumor, induced by Corynebacterium parvum or Listeria monocytogenes, is abrogated by anti‐interferonγ
Authors: Keller Robert , Keist Ruth , Leist Thomas P. , Van Der Meide Peter H. 
Published: February 2007

AbstractThe complex processes that determine the outcome of the interaction of tumor and host were explored in the operationally simple and reproducible rat D‐12 ascites tumor model. Animals exhibit weak spontaneous resistance against this tumor that is not augmented by repeated inoculation, by various routes, of irradiated syngeneic D‐12 tumor cells, but considerably enhanced after local administration of heatkilled Corynebacterium parvum (CP) or Listeria monocytogenes (LM) organisms. Inoculation of conventional or monoclonal anti‐rat IFNγ antibodies into the same compartment did not affect spontaneous tumor resistance, but largely abrogated the tumor‐protective effect triggered by CP or LM. Our findings support the concept that IFNγ, produced by T cells in the course of the specific immune response raised against immunogenic micro‐organisms, is able to enhance and to maintain local tumor resistance and thus to strengthen the capacity of the host to cope with a non‐immunogenic tumor.
Mapping of linear epitopes of human papillomavirus type 16: The E1, E2, E4, E5, E6 and E7 open reading frames
Authors: Dillner Joakim 
Published: February 2007

AbstractCertain types of human papillomavirus (HPV), especially HPV type 16, are associated with proliferative lesions of the cervix uteri that can progress to malignancy. In order to map the linear epitopes of the HPV‐encoded proteins, we have synthesized the predicted amino acid sequences of the open reading frames (ORFs) in the early region of HPV 16, as a set of 94 synthetic 20‐residue peptides overlapping each other with 5 amino acids. The peptides were tested for reactivity with IgA, IgG and IgM antibodies in the sera of 30 patients with HPV 16‐carrying cervical neoplasia. The E1 ORF had only low immunoreactivity, but several relatively minor epitopes were identified in the carboxyterminal part. The E2 ORF was found to contain several epitopes that were highly immunoreactive with a majority (up to 87%) of the cervical cancer patients' sera. The E4 ORF had one major, regularly IgA‐ and IgG‐reactive epitope, whereas the E5 and E6 ORFs had only a few minor epitopes. The E7 ORF had several epitopes that were highly immunoreactive, but only with a minority of patients' sera. The 10 most immunoreactive peptides were also analyzed for immunoreactivity with 60 control sera, of which 22 were derived from patients with parotid gland tumors and 38 were derived from healthy volunteers. Most of the peptides were also immunoreactive with the control sera. However, the IgA antibodies, and to some extent the IgG antibodies, were found at much lower levels among the controls.
Over‐expression of the epidermal growth factor receptor in human breast cancer cells fails to induce an Estrogen‐independent phenotype
Authors: Valverius Eva M. , Velu Thierry , Shankar Vidya , Ciardiello Fortunato , Kim Nancy , Salomon David S. 
Published: February 2007

AbstractAn association exists in primary human breast tumors between high epidermal growth factor receptor (EGFR) expression and a reduced number or even absence of estrogen receptors (ER). To determine whether an increase in EGFR expression might alter the estrogen responsiveness of an ERpositive human breast cancer cell line, ZR 75‐1 cells were cotransfected with a plasmid containing the full‐length cDNA for the human EGFR under the transcriptional control of the Harvey murine sarcoma virus (HaMSV) long terminal repeat (LTR) and with a pSV2neo plasmid. Two of the isolated G4 18‐resistant clones were found to constitutively express EGFR levels 15‐ to 60‐fold higher than those found on nontransfected ZR 75‐ I cells. The EGFR in these clones were functionally normal since EGF could increase their autophosphorylation and since EGF could enhance the transphosphorylation of p185erbe‐2. No change was seen in either the number or affinity of ER in these clones. In addition, the ability of estrogen to stimulate the anchorage‐dependent and anchorageindependent growth of these clones was not significantly modified. These results suggest that an increase in EGFR expression alone is not sufficient to induce a hormoneindependent phenotype in vitro in human breast cancer cells.
Aluminum phthalocyanines with asymmetrical lower sulfonation and with symmetrical higher sulfonation: A comparison of localizing and photosensitizing mechanism in human tumor LOX xenografts
Authors: Peng Q. , Moan J. , Nesland J. M. , Rimington C. 
Published: February 2007

AbstractA comparison of time‐dependent localization patterns between lower, asymmetrical (AIPCS2a) and higher, symmetrical (AIPCS4) sulfonates of aluminum phthalocyanines in human malignant melanoma LOX transplanted to athymic nude mice from 1 to 120 hr after i. v. administration was made by means of laser scanning fluorescence microscopy. The lipophilic AIPCS2a was distributed mainly in tumor cells, while the hydrophilic AIPCS4, localized only in the vascular stroma of the tumor tissue. Concomitantly, comparative observations on the killing mechanism of photodynamic effects after treatment with a much lower i. v. dose of AIPCS2a and AIPCS4 plus laser light on the human tumor LOX were also made by morphological studies. Light and electron microscopy showed that there was a direct, extensive, photo‐damaging action on all organelles and nuclear structure in the tumor cells after PDT with AIPCS2a; whereas the photo‐induced injury to the tumor tissue after treatment with AIPCS4 and light was largely the consequence of initial functional vasogenic response and ultimate damage to vascular structure. These findings correlate well with the different localization patterns of the 2 dyes observed in human tumor tissues.
Epidermal cell‐shape regulation and subpopulation kinetics during butyrate‐induced terminal maturation of normal and SV40‐transformed human keratinocytes: Epithelial models of differentiation therapy
Authors: Staiano‐Coico Lisa , Steinberg Mark , Higgins Paul J. 
Published: February 2007

AbstractRecent data indicate that malignant human epidermal cells may be appropriate targets for sodium butyrate (NaB)‐mediated differentiation therapy. The response of pre‐ and post‐crisis populations of SV40‐transformed human keratinocytes (SVKs) to this differentiation‐inducing agent was assessed, therefore, within the framework of NaB‐directed normal human keratinocyte (NHK) maturation. NaB augmented cornified envelope (CE) production in NHK and pre‐crisis SVK cultures; the time‐course and efficiency of induced maturation were similar in the 2 cell systems. In NHKs, the percentage of amplifying (“B” substate) cells decreased with time in NaB correlating with increases in both “C” stage keratinocytes and CEs. The latter formed over one or 2 layers of nucleated basal‐like cells. Inductions were accompanied by immediate cell cycle blocks (in both the G1 and G2/M phases), reorganization within the actin cytoskeleton, and transient early increases in cellular actin content. Increased NHK and pre‐crisis SVK cytoskeletal‐associated actin reached a maximum approximately 48 hr after NaB addition and preceded development of CEs. The CE precursors, thus, probably reside in the “B” substate. Post‐crisis SVKs, in contrast, were refractive to NaB‐induced terminal maturation or cell‐cyccle perturbation, failed to initiate actin filament rearrangements, and retained a basal cell‐like phenotype. Stable transformation of human SVKs in post‐crisis phase, therefore, appears to be associated with loss of maturation “competence” within the “B” keratinocyte subpopulation.
The presence of plasmin receptors on three mammary carcinoma MCF‐7 sublines
Authors: Correc Philippe , Fondanèche Marie‐Claude , Bracke Marc , Burtin Pierre 
Published: February 2007

AbstractWe studied plasmin receptors on 3 MCF‐7 sublines: MCF7, MCF7R which was derived by transfection with v‐Ha‐ras oncogene, and MCF7MF which has been studied for the secretion of procathepsin D in the presence of estrogen. All 3 sublines bound plasmin (Pli) with a much higher affinity than plasminogen (Pg). The number of binding sites was increased about 4‐fold by weak proteolytic pretreatment of tumor cells. Transfection by v‐Ha‐ras oncogene did not apparently change the affinity of Pli binding sites (KD 27‐26 nM) and increased their number very slightly (3,800 against 3,200 fmoles/mg protein). However, this number was 5 times higher for MCF7MF (15,000 fmoles/mg protein) and the affinity was 4 times lower (106 nM). MCF7 and MCF7R sublines have previously been reported to be non‐invasive in the in vitro invasion assay system (embryo chick heart muscle) but tumorigenic and metastatic in nude mice. In contrast, the MCF7MF subline has been shown to be invasive in both in vivo and in vitro invasion systems. Thus, the number of Pli binding sites at the MCF7 tumor‐cell surface may be associated directly or indirectly with tumor‐cell invasiveness.
Occurrence of non‐gastric cancer in the digestive tract after remote partial gastrectomy: Analysis of an Amsterdam cohort
Authors: Tersmette Anne C. , Offerhaus Johan G. A. , Giardiello Francis M. , Tersmette W. F. Kasper , Vandenbroucke Jan P. , Tytgat N. J. Guido 
Published: February 2007

AbstractIf peptic ulcer surgery favors the formation of carcinogenic N‐nitroso compounds in the gastric remnant, an increased risk of cancer at sites in the gastrointestinal tract distant from the stomach might be predicted. To estimate the risk of carcinomas in the digestive tract, other than the stomach, occurring after partial gastrectomy, we analyzed an Amsterdam cohort of 2,633 post‐gastrectomy patients operated on for benign disease between 1931 and 1960. Mortality in the study population was compared with the general Dutch population through person‐year analysis. An excess mortality of biliary tract cancer (O/E:2.64; CL:1.32‐4.72; p < 0.01) and pancreatic cancer (O/E:1.65; CL:1.06‐2.44; p < 0.05) was found in males more than 5 years after surgery; females showed only an increased risk of pancreatic cancer in the first 5 years postoperatively (O/E: 15.33; CL: 1.85‐55.43; p < 0.01), probably due to misdiagnosis. All other non‐gastric sites of the digestive tract carried no increased risk for cancer. In males, mortality due to colorectal cancer more than 5 years post‐operatively was significantly decreased (O/E:0.58; CL 0.34‐0.92; p < 0.01). The excess mortality of biliary‐tract and pancreatic cancer in males, which increases with the duration of post‐operative interval, is consistent with a dose‐response phenomenon. This study therefore supports the hypothesis that carcinogens are not only locally activated in the gastric remnant, but are hepatically excreted and initiate cancer in the biliary tree and pancreatic duct. Further exploration of this mechanism of carcinogenesis is warranted, since it may also explain the pathogenesis of pancreatic and biliary cancers in patients without gastrectomy.
Evaluation of CA 125 as a serum marker of hepatocellular carcinoma
Authors: Elias John , Kew Michael C. 
Published: February 2007

AbstractSerum CA 125 concentrations were raised in 90.4% of 115 southern African black patients with hepatocellular carcinoma. Seventy‐four percent of 62 patients with amebic hepatic abscess, 60% of 40 patients with chronic hepatic parenchymal disease (chronic hepatitis or cirrhosis), and 60.9% of 41 patients with acute viral hepatitis also had raised values. The median serum CA 125 concentration for patients with hepatocellular carcinoma differed significantly from the benign hepatic disease groups analysed (p < 0.0002). Serum alphafetoprotein levels were raised in 90.4% of the 115 hepatocellular carcinoma patients. CA 125 is thus a highly sensitive marker for hepatocellular carcinoma, but lacks specificity.
Patterns of expression of the p53 tumour suppressor in human breast tissues and tumours in situ and in vitro
Authors: Bártek Jiří , Bártková Jiřina , Vojtěšek Bořivoj , Stašková Zdenka , Rejthar Aleš , Kovařík Jan , Lane David P. 
Published: February 2007

AbstractAn extensive series of histological sections reflecting the various states of normal breast tissue, and a range of benign and malignant lesions, were examined for the expression of the p53 protein using a panel of anti‐p53 antibodies. In 2 separate series the results of using frozen or methacarn‐fixed, paraffin‐embedded sections were compared. Strong positive staining for p53 was detected in over 50% of the malignant lesions when frozen sections were used. This number fell to just over 20% when methacarn‐fixed sections were examined. In neither series was any p53 staining seen in normal breast or in the benign lesions. Studies by Western blotting on breast cell lines confirmed that this histological signal is due to a pronounced over‐expression of the p53 protein. Earlier studies show that this over‐expression is associated with mutation of the p53 gene. Mutation of the p53 gene with over‐expression of the mutant protein is therefore one of the most frequent specific genetic changes in malignant breast cancer.
Abelson murine leukemia virus transforms preneoplastic Eμ‐myc transgene‐carrying cells of the B‐lymphocyte lineage into plasmablastic tumors
Authors: Sugiyama Hiroyuki , Silva Santiago , Wang Yisong , Weber Gunther , Babonits Magdalena , Rosén Anders , Wiener Francis , Klein George 
Published: February 2007

AbstractEμ‐myc transgenic mice were back‐crossed to BALB/c mice up to back‐cross generation 3. The offspring that included transgene‐carrying and ‐negative mice in approximately equal proportions were randondy divided into 2 groups. Thirty‐four mice (group I) were treated with pristane, fol‐lowed by A‐MuLV, and 40 (groulp II) were injected with AMuLV alone. Altogether, 16 lymphoid tumors developed in group I and 17 in group II. Nine oJ the tumors in group I and 4 in group II appeared as ascitic tumors. The ascites contained lymphoblasts and 10 to 45% plasrriacytoid cells. These tumors were designated as plasmablastic lymphomas (PLs). All tumors except one were transgene‐positive and did not carry translocations. An exceptional tunnor in group I carried a variant 6; 15 translocation but not the transgene. It obviously corresponds to the regular Abelson + pristane‐induced plasmacytoma. Among II tested PLs, 10 had a single retroviral insertion site, while one tumor showed 3. Among 18 untreated transgenic descendants (group III), chosen randomly during serial back‐crosses, 15 (83%) developed lymphomas, with no sign of plasmacytoid differentiation. The incidence was comparable in all 3 groups, assuming 50% of the mice in groups I and II to be transgenic. The time distribution of tumor development was also similar. Spleen cells from transgene‐carrying mice with no clinical sign of lymphoma were infected in vitro with A‐MuLV and transplanted i. p. into BALB/c recipients. PLs developed in 26 of 31 pristane‐treated recipients, but in only one of 18 untreated recipients. One of 6 PLs tested was monoclonal, whereas the remainiing 5 were oligoclonal. They all expressed v‐abl. These results show that some of the preneoplastic B‐cells that expressed constitutively active rnyc transgene turned into plasmablasts after infection with AMuLV. Full development of their neoplastic potential was facilitated by the presence of pristane‐granuloma.
Enhancement of an anti‐tumor effect of interferon by dipyridamole in established human malignant melanoma cell lines
Authors: Kojima Takayuki , Suzuki Nobuo , Sugano Isamu , Hayata Isamu 
Published: February 2007

AbstractEnhancement of the anti‐proliferative effect of human interferon (HuIFN) preparations (α, β and γ) by dipyridamole was detected in a human malignant melanoma cell line, MMICB, which we originally established. Cell growth was inhibited by HulFN alone, but a marked increase in inhibition was noted in vitro and in vivo when dipyrydamole was added. Cellular DNA synthesis, as dletermined by 3H‐deoxythymidine incorporation into the acid‐insoluble cellular fraction, was more inhibited by combined treatment than by any of the agents used alone. Two other melanoma cell lines that we established, MM‐2CB and MM‐3CB, also exhibited sensitivity to combined treatment both in vitro and in vivo. Furthermore, the HMV‐I and SEKI melanoma cell lines were susceptible to the combination. Even non‐cytotoxic concentrations of dipyridamole could enhance the effect of HulFN on MM‐ICB, MM‐2CB, and SEKI cells.
Immunochemical comparison of transformation‐associated protein and secreted phosphoprotein
Authors: Chan James C. , Scanlon Mike , Denhardt David T. , Singh Krishna , Mukherjee Barid B. , Farach‐Carson Mary C. , Butler William T. 
Published: February 2007

AbstractTransformation‐associated protein (TAP) has been detected in MSV‐M‐transformed rat cell lines as glycosylated, weakly phosphorylated protein of molecular weight (Mr) 66,000 and 68,000. In the ts‐MSV‐M‐transformed rat kidney cell line (6m2), the synthesis of TAP and the v‐mos gene product is temperature‐sensitive and accompanies the expression of transformation phenotypes. Therefore, TAP potentially plays a role in cellular transformation. On the other hand, SPP represents a family of glycosylated phosphoprotein with apparent Mr ranging from 42,000 to 69,000. SPP has been detected in osteoblasts and in avian and murine retrovirustransformed rat and mouse epithelial cells. Therefore, the potential relatedness of TAP and SPP was studied. Using the 6m2 cells, we found that SPP was strongly phosphorylated and was synthesized at both the permissive (33°C) and nonpermissive (39°C) temperatures. By contrast, TAP was weakly phosphorylated, and was synthesized, as we found previously, only at the permissive temperature of 33°C. Furthermore, in 35S‐methionine incorporation studies, TAP became heavily labelled whereas SPP was not (consistent with its amino acid composition having few methionine residues). Using 125I‐TAP in both immunoprecipitation and radioimmunoassays, it was found that an antiserum raised against SPP did not cross‐react with 125I‐TAP. Additionally, SPP has now been found in many human and rodent cells, while TAP thus far has only been detected in MSV‐transformed rat cells. These data suggest that structurally, TAP and SPP are not closely related phosphoproteins.
Evidence for the role of 34‐kDa galactoside‐binding lectin in transformation and metastasis
Authors: Raz Avraham , Zhu Daguang , Hogan Victor , Shah Nipa , Raz Tirza , Karkash Rivka , Pazerini Galit , Carmi Pnina 
Published: February 2007

AbstractThe endogenous M, 34,000 galaictoside‐binding lectin (L‐34) is found at elevated levels in a wilde variety of neoplastic cells and correlative evidence suggests that it is involved in tumor metastasis in vivo and in transformation in vitro. We demonstrate here that introduction of recombinant L‐34 into tumorigenic, weakly metastatic UV‐2237‐cl‐ I 5 fibrosarcoma cells results in an increased incidence of experimental lung metastases in syngeneic and nude mice. Transfection of normal BALB/c‐A3 I cloned fibroblasts with functional L‐34 results in acquisition of anchorage‐independent growth and in morphological transformation in vitro but not in tumorigenicity in vivo. These results provide direct evidence that the cellular expression of L‐34 is associated with some aspects of transformation and with metastasis, but not with tumorigenicity per se.
Clonal analysis of tumor‐infiltrating lymphocytes from human primary and metastatic liver tumors
Authors: Shimizu Yukihiro , Iwatsuki Shunzaburo , Herberman Ronald B. , Whiteside Theresa L. 
Published: February 2007

AbstractPhenotypic and functional characteristics of tumor‐infiltrating lymphocytes (TIL) obtained from human primary and metastatic liver tumors were studied. Lymphocytes isolated from 18 tumors and autologous (A) peripheral blood (6 cases) were phenotyped by 2‐color flow cytometry and cloned in a limiting dilution system, which allows virtually all normal T lymphocytes to proliferate; 70‐80% of fresh TIL were T cells (i. e., CD3+), and the ratio of CD4+/CD8+ cells was 1.2 in both primary and metastatic liver tumors. TIL contained significantly more CD56+ (NKHI+) cells, half of which were CD3+ CD56+, CD3+ CD25+ cells and CD3+ HLA‐DR+ cells, than A‐PBL. The frequencies of proliferating T‐cell precursors (PTL‐p) and cytolytic T‐lymphocyte precursors (CTL‐p) reactive with K562, allogeneic tumor cells and autologous tumor cells, were determined. Mean PTL‐p frequencies for TIL from hepatocellular carcinomas, cholangiocarcinomas and metastatic liver tumors were 0.52 (0.22‐0.83), 0.10 (0.05‐0.16) and 0.16 (0.01‐0.30), respectively. The frequency of CTL‐p with natural‐killer‐like activity was lower in TIL than in A‐PBL. The frequency of CTL‐p for autologous tumor cells in fresh TIL isolated from primary liver tumors was 0.02‐0.13 and 12/81 clones were reactive against autologous tumor. In contrast, only 1/66 TIL clones obtained from colon carcinomas metastatic to liver showed autotumor reactivity. No clones reactive with autologous tumor were obtained from peripheral blood of patients with liver cancer. These data indicate that substantial differences in anti‐tumor functions of TIL between primary and metastatic liver tumors exist, which can be detected at a clonal level.
Suppressive effects of intracellular glutathione on hydroxyl radical production induced by tumor necrosis factor
Authors: Yamauchi Naofumi , Watanabe Naoki , Kuriyama Hiroshi , Neda Hiroshi , Maeda Masahiro , Himeno Takeshi , Tsuji Yasushi , Nutsu Yoshiro 
Published: February 2007

AbstractProtective effects of intracellular glutathione (GSH) against the cytotoxicity of human recombinant tumor necrosis factor (TNF) were investigated. Three tumor cell lines (L‐M, B‐16, HeLa) were used as target cells. Exposure of these cells to buthionine sulfoximine (BSO) or diethyl maleate (DEM) resulted in the depletion of intracellular GSH content to 5.2‐43.0% of control values and enhancement of their susceptibility to TNF cytotoxicity. The hydroxyl radical production in L‐M cells stimulated by TNF was increased by treatment with BSO or DEM. These results are consistent with the suggestion that intracellular GSH exerts its protective function against the cytocidal effect of TNF by inhibiting the hydroxyl radical production stimulated by TNF.
Tumor necrosis factor‐α and interleukin‐1α production in cachectic, tumor‐bearing mice
Authors: Lönnroth Christina , Moldawer Lyle L. , Gelin Johan , Kindblom Lars , Sherry Barbara , Lundholm Kent 
Published: February 2007

AbstractWeight‐stable mice bearing a syngeneic, methylcholanthrene‐induced, rapidly growing tumor lost approximately 22% of their lean tissue, became significantly hypoalbuminemic and had a marked increase in serum amyloid P concentrations during progressive tumor growth. Tumors from cachectic mice were producing both TNF‐α and IL‐1α in vivo as documented by the presence of TNF‐α and IL‐1α mRNA and immune‐reactive protein for IL‐1α. Only spleens from tumor‐bearing mice had statistically significantly elevated quantities of IL‐1 mRNA. In general, alterations in tissue concentrations of IL‐1 mRNA in tumor‐bearing animals agreed qualitatively with those found in endotoxin‐stimulated, nontumor‐bearing control mice. However, endotoxin‐stimulated mice had significantly elevated tissue concentrations of TNF mRNA in spleen and livers, while TNF mRNA levels were not significantly increased in any host tissues. Cytokine mRNA levels in tumor tissue were not higher than those found constitutively in various tissues from non‐tumor‐bearing control animals. Plasma from tumor‐bearing mice and endotoxinstimulated controls contained high levels of IL‐6 but low (endotoxin‐stim.) or no measurable levels (tumor‐bearing) of either IL‐1 or TNF. When tumor cells from cachectic mice were placed into long‐term cell culture, immune reactive TNF‐α and IL‐1α were produced, but IL‐6 bioactivity was not produced in measurable amounts.