bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of a novel neuroglandular antigen (NGA) expressed on abnormal human melanocytes
Authors: Sikora L. K. J. , Demetrick D. J. , Dixon W. T. , Jerry L. M. , Pinto A. , Urbanski S. J. , Temple W. 
Published: February 2007

AbstractMurine monoclonal antibodies (MAbs) were produced with reactivity to human malignant melanoma. Six MAbs, 3 of the IgGI (LS113, LS140, LS152) and 3 of the IgG2a (LS59, LS62, LS76) subclasses, were selected for their binding, with an identical pattern of reactivity, to a novel melanoma‐associated antigen. As characterized by the enzyme‐linked immunosorbent assay (ELISA), these MAbs were found to be positive on n‐octyl‐β‐D‐glucopyranoside extracts of all 10 melanoma cell lines tested and on extracts of 22 metastatic melanoma tumors. The antibodies had minimal reaction with a panel of 14 normal adult tissue extracts. A degree of crossreactivity was observed with 50% of 39 non‐melanoma tumor extracts. The results obtained with the ELISA on cell line and tissue extracts were duplicated using the ABC method of peroxidase staining. The pattern of cross‐reactivity, as demonstrated by the intense staining of paraffin‐embedded and frozen tissue sections of normal, benign and malignant tissues, defines the recognized protein as a neuroglandular antigen (NGA). Immunoadsorbents made with the antibodies were used to purify the antigen shed from cultured melanomas. All 6 MAbs recognized this purified antigen while 5 other antimelanoma antibodies did not react with it. On gel electrophoresis this antigen is a highly glycosylated glycoprotein with a protein core of 21 kDa.
Measurements of passive smoking and estimates of lung cancer risk among non‐smoking chinese females
Authors: Koo Linda C. , Ho Ching‐Yee , Ho John H‐C. , Saw Daisy 
Published: February 2007

AbstractLifetime exposures to environmental tobacco smoke from the home or workplace for 88 “never‐smoked” female lung cancer patients and 137 “never‐smoked” district controls were estimated in Hong Kong to assess the possible causal relationship of passive smoking to lung cancer risk. Relative risks based on the husband's smoking habits, or lifetime estimates of total years, total hours, mean hours/day, or total cigarettes/day smoked by each household smoker did not show dose‐response results. Similarly, when such categories as mean hours/day, or earlier age of initial exposure, were combined with years of exposure, there were no apparent increases in relative risk. However, when the data were segregated by histological type and location of the primary tumor, it was seen that peripheral tumors in the middle or lower lobes, or, less strongly, squamous or small‐cell tumors in the middle or lower lobes, had increasing relative risks that might indicate some association with passive smoking exposure.
The plasmin system in human adenocarcinomas and their metastases. A comparative immunofluorescence study
Authors: Burtin P. , Chavanel O. , André‐Bougaran J. , Gentile A. 
Published: February 2007

AbstractComponents of the plasmin system were comparatively studied in lymph node metastases and corresponding primary tumors by immunofluorescence. Primary tumors, all adenocarcinomas, originated from large bowel (N = 12) or breast (N = 10). We used antisera against plasminogen (Pg), plasminogen activators (PA) such as urokinase (UK) and tissue type PA (t‐PA), plasmin inhibitors such as α2 anti‐plasmin (α2AP) and α2 macroglobulin (α2M), plasmin‐α2 anti‐plasmin complex (PAPC). Positivity with anti‐PAPC serum was considered as proving that plasmin was formed by Pg activation. The following results were obtained. 1) Breast adenocarcinomas were more strongly stained than colorectal adenocarcinomas using antisera against Pg, PAPC and PA, while their reactivity was much weaker with antisera against both plasmin inhibitors. 2) Lymph node metastases from colorectal adenocarcinomas were more strongly stained than primary tumors using antisera against PAPC and PA. Reactivity with anti‐Pg was similar, while that with antisera against plasmin inhibitors was much weaker. 3) Metastasis from breast adenocarcinomas, on the average, showed the same type of staining as primary tumors. However, there was a slight decrease in reactivity with anti‐Pg and PAPC in metastases. 4) Tumor cells invading lymphoid areas in metastatic lymph nodes were often strongly labeled using antisera against Pg and UK. Staining was less strong or less frequent using antisera against PAPC and t‐PA. These results favor the role of plasmin in the degradation of basement membrane and connective tissue components, thus implicating it in the invasiveness of tumor cells, at least in most primary tumors and metastases.
HLA studies of endemic african kaposi's sarcoma patients and matched controls: No association with hla‐DR5
Authors: Melbye Mads , Kestens Luc , Gigase Paul L. , Biggar Robert J. , Schreuder Geziena M. T. 
Published: February 2007

AbstractIn the search for a genetic factor involved in the etiology of Kaposi's sarcoma, several studies have recently focused on a significantly increased HLA determinant, DR5, as well as a decreased DR3, among patients with both the classical and the AIDS‐related form of Kaposi's sarcoma. To test the consistency of this phenomenon, we analysed the frequencies of HLA immunogenetic markers in 23 histologically confirmed Kaposi's sarcoma patients from Central Africa, where this tumor is endemic, and a local sex‐ and tribe‐matched control group. No definite association was observed for any of the HLA antigens, including DR5 and DR3. We were not able to support the hypothesis that the same HLA‐associated immune susceptibility factors are involved in all types of Kaposi's sarcoma.
Presence of circulating antibodies against cellular protein p53 in a notable proportion of children with B‐cell lymphoma
Authors: De Fromentel C. Caron , Chandrasekaran K. , May P. , May‐Levin F. , Mouriesse H. , Lemerle J. 
Published: February 2007

AbstractSerum samples taken from children bearing a wide variety of tumors were screened for the presence of circulating antibodies against the cellular tumor antigen p53. There was a significant correlation (p<0.001, n = 119) between the presence of such antibodies and the occurrence of cancer; 12% of the sera tested were positive. These sera were derived from children with a wide range of tumor types. In particular, 21% of the sera obtained from children suffering from a B‐cell lymphoma contained anti‐p53 antibodies. We were not able to establish a correlation between the secretion of p53‐reactive antibodies and any other parameters, such as the age or sex of the child, presence of metastasis, stage or prognosis of disease, or treatment regimen. These results therefore show that the development of p53 immunogenicity is associated with a wide range of neoplastic diseases in children, and in particular with the presence of a B‐cell lymphoma.
Expression of B‐cell‐specific markers in different burkitt lymphoma subgroups
Authors: Ehlin‐Henriksson Barbro , Manneborg‐Sandlund Agneta , Klein George 
Published: February 2007

AbstractForty‐three Burkitt lymphoma (BL) lines were examined for the expression of 5 monoclonal antibody (MAb)‐identified B‐cell‐specific markers and immunoglobulin production. All (13) EBV‐negative BL lines were CALLA+LB‐I‐, whereas 30 EBV‐carrying lines showed a more heterogeneous pattern. In the EBV‐negative lines, the follicle mantle zone markers BA‐I and 35.IC5 were expressed concordantly, at a different level in each line. This coordination was disrupted in EBV‐carrying lines. In the EBV‐negative lines, there was also an inverted correlation between the expression of 35.IC5 and the germinal center marker BLA, suggesting that some etiologically important event, perhaps the translocation, had fixed the cells at different stages of their transition from one zone to the other. This inverted relationship was also disrupted in the EBV‐carrying lines, suggesting that EBV can interfere with the maturation program of the BL cell. This conclusion was also supported by a comparison between 5 EBV‐negative BL lines and their EBV‐converted sublines. All converted lines have undergone marker changes, but the degree and nature of these changes was different for each EBV‐BL line. Both the coordinated expression of BA‐I and 35.1C5 and the inverted relationship between CALLA and LB‐I were disrupted in several other convertants. We have reexamined our previous finding (Ehlin‐Henriksson and Klein, 1984) that the majority of the variant translocation‐carrying BL lines were CALLA‐LB‐I +, in contrast to the majority of the typical translocation carriers that were mostly CALLA+ LB‐I‐. All II EBV‐negative lines were CALLA+ LB‐I‐, irrespective of the type of translocation. Among the EBV‐carrying lines, 4 of 17 typical (8; 14) translocation carriers were CALLA‐LB‐I +, whereas 7 of the 12 variant translocation‐carrying lines were CALLA‐ LB‐I+. The remaining two expressed both antigens to some extent. The difference is statistically significant at the 0.03 level.
The inability of adoptive immunotherapy to eradicate tumor cells in radiation‐induced chimeric mice: The possible down‐regulation of intratumor immune amplification
Authors: Evans Robert , Duffy Theodore M. 
Published: February 2007

AbstractTumors were eradicated following adoptive immunotherapy of (C57BL/6J x DBA/2J) F1 (B6D2F1) hybrid mice bearing the C57B1/6J (B6) sarcoma, MCA/76‐9, by treatment with cyclophosphamide (CY) and adoptively transferred tumor‐sensitized B6D2F1 T cells. Identical treatment of B6→ B6D2F1 or DBA→ B6D2F1 chimeric tumor‐bearing mice resulted in temporary tumor regression only. Immunotherapy in both systems resulted in the appearance at the tumor site of large numbers of T lymphocytes and macrophages, which were shown to be derived from the adoptively transferred donor immune B6D2F1 cells or from the original reconstituting bone marrow respectively. The TAC and TAL isolated from either B6D2F1 or chimeric mice expressed potent toxicity in vitro towards tumor target cells. In addition, TAC from both systems inhibited tumor growth in a Winn assay in an immunologically specific manner. Suppressor cells detected in spleens 8 days after CY injection of normal B6, DBA, B6D2F1 hybrid and chimeric mice and also after adoptive immunotherapy of tumor‐bearing B6, B6D2F1 and chimeric mice and were shown to persist in the spleens of chimeric mice for at least 31 days after adoptive immunotherapy. In contrast, spleen cells taken 31 days after therapy of B6D2F1 mice did not contain detectable suppressor cells and were able to induce tumor eradication when adoptively transferred to CY‐treated tumor‐bearing B6D2F1 mice. The possibility is discussed that two forms of suppressor mechanisms are induced after adoptive immunotherapy of chimeric mice and that they may down‐regulate donor T cell responses at the tumor site.
Generation of activated killer cells in tumor‐bearing hosts
Authors: Ting Chou‐Chik , Hargrove Myrthel E. , Stephany David 
Published: February 2007

AbstractActivated killer (AK) cells were generated in spleen‐cell cultures derived from tumor‐bearing hosts (TS) whereas, under the same conditions, cultured normal spleen cells (NS) gave little cytotoxicity. The AK effectors were primarily Thyl+, AGMI‐ and Lyt2‐ and thus were neither classic cytotoxic T lymphocyts (CTL) nor classic NK cells. These AK cells selectively killed tumor targets of different etiologic origins and did not kill concanavalin‐A‐induced lymphoblasts. The broad target‐cell reactivity of these AK cells was also confirmed by cold target‐inhibition experiments. Generation of AK cell correlated with interleukin‐2 (IL‐2) production, and the levels of AK cells generation paralleled those of IL‐2 production. Furthermore, the generation of AK cells was blocked by the anti‐IL‐2 receptor monoclonal antibody (MAb) (αIL‐2R), indicating that IL‐2 was involved, and thus these AK cells were lymphokine‐activated killer (LAK) cells. We previously showed that the expression of AGMI on LAK precursors disappeared when they differentiated into LAK effectors, indicating that the activated LAK cells lacked AGMI. When examining the serologic phenotype of the LAK precursors in tumor‐bearing hosts, we found that they lacked AGMI, which suggested that these LAK precursors were in an “activated” state. These cells were still Thyl‐, and were thus different from fully activated LAK effectors which were Thyl+ cells, indicating that the full differentiation of LAK cells in vivo was arrested in the tumor‐bearing hosts. We also found that the presence of small amounts of X‐irradiated tumor cells prevented the generation of AK cells. These findings suggest that, in the tumor‐bearing hosts, the presence of tumor cells triggers the activation of AK precursors; however, the same tumor cells may also be immunosuppressive, which prevents the full differentiation of AK precursors into AK effectors.
Characterization of an animal model of metastatic colon carcinoma
Authors: Dunnington Damien J. , Buscarino Charles , Gennaro Doris , Greig Russell , Poste George 
Published: February 2007

AbstractAlthough numerous animal tumor models have been used to study colon carcinoma, few display metastatic properties. We have characterized an animal tumor model that has 3 properties essential for the study of metastasis of colon carcinoma cells: epithelial cell origin; a reproducible pattern of metastatic behavior and the ability to be propagated both in vitro and in vivo to facilitate identification of biochemical correlates of metastasis. The KI2/TR cell line was derived from a transplantable colon carcinoma induced by dimethylhydrazine in the BD‐IX rat strain. Transmission electron microscopy of KI2/TR cells demonstrated junctional complexes, desmosomes and surface microvilli characteristic of gastrointestinal epithelial cells. The epithelial cell origin of KI2/TR was confirmed by demonstrating the presence of keratin, a marker of epithelial cells, but not vimentin, a constituent of mesenchymal cells. Secretion of CEA and Ca19‐9 antigens by KI2/TR cells in vitro was below the sensitivity of the assays (1 ng/ml and 6 U/ml respectively). KI2/TR cells produced tumors following s.c. injection into syngeneic BD‐IX rats, allogeneic RNU/rnuDF rats and xenogeneic CRL:nu/nuBR mice. Macroscopic lung metastases were observed in animals from all 3 groups. Distal lymph node metastases were more frequent in BD‐IX rats than in nude rats or mice. The histological appearances of all tumors and metastases were similar, showing a moderate to poorly differentiated glandular carcinoma. Intrasplenic injections of KI2/TR cells in nude mice resulted in liver colonization. Preferential growth of tumor cells at sites of trauma was also observed. The results show that the KI2/TR system can be used as a model to study metastasis of colon carcinoma cells and may find utility in the testing of chemotherapeutic agents against metastatic lesions.
Studies of skin tumorigenesis in pgk mosaic mice: Many promoter‐independent papillomas and carcinomas do not develop from pre‐existing promoter‐dependent papillomas
Authors: Reddy A. L. , Caldwell Mark , Fialkow Philip J. 
Published: February 2007

AbstractThe induction of mouse skin papillomas in two stages by initiation‐promotion protocols has been studied extensively. On the basis of kinetics of induction and morphological observations of apparent progression to carcinomas, it has been argued that the papillomas sequentially advance to carcinomas through promoter‐dependent and promoter‐independent premalignant stages. Although this hypothesis has been widely accepted, the step‐wise development of the same cell population from papilloma to carcinoma has not been established at the cellular level. We show here that some carcinomas which morphologically appear to result from progression of promoter‐dependent papillomas do not develop from sequential progression of the same cell population as was found in the original papillomas. Other initiated cells also participate during the growth of these tumors and may replace the original papilloma cells. We also present evidence that some tumors develop directly as promoter‐independent papillomas without going through an apparent promoter‐dependent papilloma stage.
Delta agent and the etiology of hepatocellular carcinoma
Authors: Trichopoulos Dimitrios , Tzonou Anastasia , Kaklamani Evangelia , Hatzakis Angelos , Day Nicholas E. , Muñoz Nubia , Hadziyannis Stefanos , Sparos Loukas 
Published: February 2007

AbstractSera from 87 patients with hepatitis B surface antigen (HBsAg)‐positive hepatocellular carcinoma (HCC) and from 29 HBsAg‐positive hospital controls were tested for delta (δ) antigen with an immunoenzymatic procedure and for anti‐δ antibody, hepatitis Be antigen (HBeAg) and antibody to HBeAg (anti‐HBe) by radioimmunoassay. All the sera, from both the HCC cases and the control patients, were negative for δ‐antigen. Among the HCC cases 9 were positive for serum anti‐δ (10%) whereas among the controls none was positive for this antibody (p = 0.067); the anti‐δ‐positive cases were found only among HCC patients negative for HBeAg. The lower prevalence of anti‐δ among HBsAg‐positive HCC patients, as compared to the corresponding prevalence among HBsAg‐positive patients with chronic active hepatitis or cirrhosis (reported in the literature) indicates that the pathogenesis of HCC is frequently independent of the pathogenesis of the other HBsAg‐positive common chronic liver diseases. By contrast, the higher prevalence of anti‐δ among HBsAg‐positive HCC cases than among HBsAg‐positive controls may reflect the longer average duration of the carrier state in HCC patients (until integration is accomplished and the induction period completed). Serum HBeAg was higher among HBsAg‐positive HCC patients with cirrhosis (23%) than among HBsAg‐positive HCC patients without cirrhosis (6%) or HBsAg‐positive controls (3%); thus, the conflicting results in the literature concerning the association of the HBeAg/anti‐HBe system with HCC may be accounted for, in part, by the variable association of HCC with an underlying cirrhosis.
Volatile nitrosamine levels in common foods from tunisia, south china and greenland, high‐risk areas for nasopharyngeal carcinoma (NPC)
Authors: Poirier S. , De‐Thé G. , Hubert A. , Ohshima H. , Bourgade M. C. , Bartsch H. 
Published: February 2007

AbstractOn the basis of anthropological pilot studies on diet in Tunisia, south China and Greenland, food items consumed frequently by these populations at high risk for NPC were analysed for volatile nitrosamines using gas chromatography combined with a thermal energy analyzer. Relatively high levels of N‐nitrosodimethylamine (NDMA), N‐nitrosopyrrolidine (NPYR) and N‐nitrosopiperidine (NPIP) were detected in Tunisian stewing base (“Touklia”) and dried mutton preserved in olive oil (“Qaddid”). NDMA was also detected at levels ranging from trace amounts to 133 μg/kg in several Chinese salted and dried marine fish and in Greenland dried, unsalted fish preparations. NPYR and NPIP were also occasionally detected in several vegetables fermented in brine collected in Tunisia and China. The possible role of nitrosamines in the etiology of NPC is discussed.
Monoclonal antibodies to human colorectal epithelium: Markers for differentiation and tumour characterization
Authors: Richman P. I. , Bodmer W. F. 
Published: February 2007

AbstractA panel of monoclonal antibodies (MAbs) has been obtained, directed against determinants of normal human colorectal epithelium. BALB/c mice were immunized and boosted with mucosal scrapings and cell membrane preparations from normal large intestine. In one case boosting was also performed with HT29 colon carcinoma cells. Hybridoma supernatants were screened immunohistochemically on frozen sections of normal colorectal epithelium, leading to the selection of 12 MAbs which recognized determinants of the major epithelial cell lineages. These antibodies fall into two groups: group I antibodies react with mucus constituents, with or without other cell components; group 2 antibodies react only with non‐mucus components of cells.The normal tissue distribution of the antibody panel has been characterized immunohistochemically. Three of the mucus‐reactive group‐1 antibodies, PR.4D4, PR.5D5 and PR.3A5, and also PR. IA3 of group 2, have a very restricted distribution. In all 4 cases, their reactivity outside the gastrointestinal tract is mainly confined to tracheal epithelium.A series of benign and malignant colorectal tumours has been studied with the antibody panel. The antibodies of group 1, and PR. 1A3 from group 2, show a marked heterogeneity in their reactions with malignant cells and seem to be defining patterns of functional differentiation, independently of standard histological criteria. The reactivity of 6 colorectal carcinoma cell lines has also been assessed with the antibodies. The group‐1 antibodies and PR.1A3 identify those cell lines which have retained some capacity for differentiation.
Sister chromatid exchange induction by benzo(a)pryene in cultured peripheral blood lymphocytes of lung cancer patients and healthy individuals with or without familial history of neoplasms
Authors: Dosaka Hirotoshi , Miyamoto Hiroshi , Kawakami Yoshikazu , Abe Syuiti , Sasaki Motomichi 
Published: February 2007

AbstractThe inducibility of sister chromatid exchanges (SCEs) by benzo(a)pyrene (BP) was studied in cultured peripheral blood lymphocytes of 15 untreated lung cancer patients and 25 healthy persons including 11 high‐ and 14 low‐cancer‐risk individuals tentatively classified by the familial history of lung cancer and other neoplasms. The baseline SCE frequency in cultured lymphocytes was significantly high in lung cancer patients, as compared with all healthy persons or low‐cancer‐risk individuals. Following exposure to BP, the lymphocytes of lung‐cancer patients and high‐cancer‐risk individuals exhibited significantly greater SCE yields than those of persons at low risk, although no significant difference was observed in the lymphocyte SCE yields when the levels of lung cancer patients were compared with those of all healthy persons. A comparison of the net SCE increase (ΔSCE) in BP‐exposed lymphocytes among the study groups, however, revealed a significant difference in ΔSCE values only between high‐ and low‐cancer‐risk individuals. The present findings on both the observed SCE yields and ΔSCE values suggest that lymphocytes of high‐risk individuals may be more susceptible to BP‐induced DNA damage than those of persons at low risk, and that such a chromosomal hypersensitivity to genotoxins may be associated with a high risk of neoplasms.
High incidence of egf receptor hyperproduction in esophageal squamous‐cell carcinomas
Authors: Ozawa Soji , Ueda Masakazu , Ando Nobutoshi , Abe Osahiko , Shimizu Nobuyoshi 
Published: February 2007

AbstractEGF receptor levels were investigated in esophageal squa‐mous‐cell carcinoma tissues from 31 patients. Twenty‐two (71%) of these cancer tissues exhibited significantly higher 125I‐EGF binding activity than normal mucosa in the adjacent noncancerous tissues. These EGF receptor levels were then compared on the basis of pathological findings including lymph‐node metastasis, depth of invasion, differentiation type, vascular invasion, infiltration and location of the lesion. Unlike previous reports on breast and bladder cancers, our study showed no obvious correlation between these pathological characteristics and the EGF receptor levels in esophageal carcinomas. Immunohistochemical staining with the anti‐EGF receptor monoclonal antibody detected EGF receptors in squamous cells of the cancer tissues as well as in the basal cells of nearby normal epithelium. Since the basal cells have proliferative potential in the esophagus, the increase in EGF receptor levels in these cells may possibly be associated with the development of human esophageal squamous‐cell cancer.