bluuebunny/crossref_metadata_2025_split huggingface dataset:
Role of MHC class‐i antigens and the CD3 complex in the lysis of autologous human tumours by T‐cell clones
Authors: Roberts T. E. , Shipton U. , Moore M. 
Published: February 2007

AbstractPeripheral blood lymphocytes (PBL) of 4 patients with malignant effusions were stimulated for 6 days with purified autologous tumour cells, before isolation of the lymphoblasts and cloning by limiting dilution in interleukin‐2 (IL‐2). Fortyfive clones were analyzed for cytotoxicity (CTX) against autologous, allogeneic tumour and erythromyeloid K562 cells of known status with respect to expression of major histocompatibility complex (MHC) antigens, estimated by reaction with the W6/32 (anti HLA, ‐A, ‐B, ‐C monomorphic) and TDR 31.1 (anti HLA‐DR) monoclonal antibodies (MAb). All 45 clones were CD3+. Twenty‐five (56%) of them were cytotoxic for at least one target; 24 were autoreactive (restricted in 7); 17 were alloreactive; 16 were K562 reactive. Under comparable conditions autoreactivity was partially blocked by W6/32 in 12/20 effectoratarget combinations; alloreactivity in 8/13 and K562 reactivity in 0/14. Modulation of effector cell surface CD3 antigens by OKT3 monitored by flow cytometry reduced autoreactivity in 9/14 combinations, alloreactivity in 2/6 and K562 reactivity in 0/4. W6/32 blocking and T3 modulation of cytotoxicity were almost invariably concordant against the same target. The data suggest that, to accomplish lysis of autologous and allogeneic tumour targets, certain clones require MHC recognition and a functional CD3 complex, while for others with similar target cell repertoires, there is no such requirement. It is possible that T‐cell clones responding to a tumour‐associated antigen (TAA) in the context of self MHC antigens can also respond to an allogeneic class‐I product in the absence of TAA, and/or that aberrant class‐I antigen expression on autologous tumours accounts for the alloreactivity.
Evaluation of monoclonal antibodies for the detection of exfoliative nasopharyngeal carcinoma cells
Authors: Chan K. H. , Yip T. C. , Choy Damon , Chan C. W. , Zeng Y. , Ng M. H. 
Published: February 2007

AbstractExfoliative cells were aspirated from 15 patients suspected of having nasopharyngeal carcinoma (NPC) and showing the presence of lesions or other abnormalities in the nasopharynx. They were tested for binding with a 125I monoclonal antibody (MAb) (MA6) which is selectively reactive against human B lymphocytes and a variety of carcinomas. A positive result was obtained from 6/9 patients with, and from 0/5 patients without, histologically confirmed disease. One patient with eskimoma also gave a negative binding result. Cytology was specific but less sensitive, tumour cells being detected in 3 of the patients with confirmed disease. Immunocytology using MA6 was limited, like cytology, by poor recovery of the tumour cells and the results were in complete concordance with cytology. The other MAbs used were raised against carcinoembryonic antigen (CEA) and a carcinoma cell line (Ca2), respectively. The latter was not reactive against the NPC tumour cells while the CEA antibody was not sufficiently selective to be useful.
Dissociation between thromboxane generation and metastatic potential in cells from a murine fibrosarcoma. Studies with a selective thromboxane synthase inhibitor
Authors: Vicenzi Elisa , Lampugnani Maria Grazia , Dalessandro Anna Paola Bolognese , Niewiarowska Anna , De Gaetano Giovanni , Donati Maria Benedetta 
Published: February 2007

AbstractSince the highly metastatic variant M4 of the mFS6 fibrosarcoma has the peculiar feature of generating larger amounts of immunoreactive thromboxane B2 (TxB2) than the nonmetastatic variant (M9), we used the thromboxane synthase inhibitor dazmegrel (UK‐38,485) in an effort to influence its metastatic potential. TxB2 formation by tumor cells freshly harvested from the primary tumor could be completely inhibited by drug addition in vitro. TxB2 generation was inhibited with a dose‐response curve, 2 μm being the lowest dazmegrel concentration giving 100% inhibition. Chronic treatment of tumor‐bearing mice with dazmegrel (150 mg/kg b.w. twice daily by gavage) from the day of tumor‐cell implantation until killing of the animals caused a more than 10‐fold reduction in serum TxB2 formation; TxB2 generation by tumor cells was also significantly depressed. This treatment, however, did not significantly modify either primary tumor weight or metastasis formation. Our data suggest that selective inhibition of thromboxane generation in either blood or tumor cells does not prevent spontaneous metastasis formation in the murine model studied.
A highly leukemogenic radiation leukemia virus isolate is a thymotropic, immunosuppressive retrovirus with a unique rna structure
Authors: David Ya'acob Ben , Kotler Moshe , Yefenof Eitan 
Published: February 2007

AbstractClones of N‐, B‐ and NB‐fibrotropic viruses were isolated from weakly (D‐RadLV) and strongly (A‐RadLV) leukomogenic RadLV preparations. A highly leukemogenic, thymotropic virus (TV) was isolated by ex‐vivo infection of thymocytes with A‐RadLV. This virus could not be isolated from D‐RadLV. Two‐dimensional fingerprint analysis suggested that TV recombines unique RNA sequences with RNA genomic material derived from a B‐tropic endogenous virus. C57BL/6 (B6) mice injected with B‐ or NB‐fibrotropic clones, but not with TV or N‐tropic viral clones, developed reactive T lymphocytes (Tr), capable of differentiating into anti‐tumor cytotoxic cells. The N‐tropic virus isolates were non‐immunogenic in B6 mice whereas the TV isolate induced suppressor T lymphocytes (Ts) that abrogated a potential Tr response. These results suggest that emergence of highly leukemogenic RadLV involves activation of endogenous fibrotropic virus which is immunogenic in its natural host strain (B6). This virus can further recombine with other retroviral genetic sequences, resulting in a suppressogenic and thymotropic, highly leukemogenic virus.
Cultured mammary carcinoma cells contain gonadotropin‐releasing hormone‐like immunoreactivity, gnrh binding sites and chorionic gonadotropin
Authors: Bützow R. , Huhtaniemi I. , Clayton R. , Wahlström T. , Andersson L. C. , Seppälä M. 
Published: February 2007

AbstractImmunoperoxidase staining and radioimmunoassay were used to identify gonadotropin‐releasing hormone (GnRH) and chorionic gonadotropin (hCG) in 4 mammary carcinoma cell lines. GnRH‐like immunoreactivity was found in all cell lines; 2 lines also contained hCG. Binding of a GnRH agonist was demonstrated by radioreceptor assay in cultured mammary carcinoma cells. In cell column perfusion of the same cells, exogenous GnRH did not stimulate release of hCG.
Establishment and characterization of a T‐lymphoblastoid cell line MDCC‐MTB1 derived from chick lymphocytes infected in vitro with marek's disease virus serotype 1
Authors: Ikuta Kazuyoshi , Nakajima Kazuhiro , Kanamori Akihiro , Maotani Kumiko , Mah Jum Sool , Ueda Shigeharu , Kato Shiro , Yoshida Mariko , Nii Shiro , Naito Matao , Nishida‐Umehara Chizuko , Sasaki Motomichi , Hirai Kanji 
Published: February 2007

AbstractContinuously proliferating T‐lymphoblastoid cells, named MDCC‐MTB1, were obtained by infection of chick embryo lymphocytes with Marek's disease virus serotype 1 (MDV1) in culture and subsequent cultivation in the presence of human interleukin 2 (IL‐2). The MTB1 cells have now been growing well for at least 4 months with a doubling time of about 10 hr, irrespective of the presence of IL‐2. The MTB1 cells show lymphoblastoid morphology, and carry T‐lymphocyte marker surface antigens and a karyotype of female chick origin with several abnormal chromosomes. Southern blot hybridization showed that they contain about 10 virus genome equivalents/cell of almost the whole MDV genome. Infectious virus could not be rescued from MTB1 cells by co‐cultivation of these with chick embryo fibroblasts. In addition, no virus particles were found in thin‐sectioned MTB1 cells by electron microscopy. An immunofluorescence test with monoclonal antibody (MAb) to MDV‐specific phosphorylated proteins showed that MTB1 cells expressed the MDV‐specific antigen in the cytoplasm only after the cells had been treated with 5‐iodo‐2‐deoxyuridine for 48 hr at 41 °C. MTB1 cells can form colonies in 0.33% soft agar, and can be transplanted into chicks by i.p. injection. Thus, continuously growing lymphoblastoid cells were obtained by in vitro infection of chick embryo lymphocytes with oncogenic MDV1 and cultivation of the cells in the presence of human IL‐2 during the transformation step. These cells appear to show a similar phenotype to an MD lymphoma‐derived cell line.
Trisomy 15 as a regular finding in chemically induced murine t‐cell leukemogenesis
Authors: Carbonell F. , Eul J. , Anselstetter V. , Hameister H. , Seidel H. J. , Kreja L. 
Published: February 2007

AbstractTrisomy 15 is described as a common finding in all T‐cell leukemias induced by a single dose of methylnitrosourea (MNU) in BDF1 mice and in the leukemias induced by 7 doses of benzo(a)pyrene. Additional trisomies were found in about half of the leukemias. The organ distribution suggests that the leukemic cells with trisomy 15 originate in the thymus. Trisomy 15 was detected in the thymus as early as 6 weeks after the application of MNU, i.e. during the latency period.
Aflatoxin exposure, hepatitis b virus infection and liver cancer in swaziland
Authors: Peers Frank , Bosch Xavier , Kaldor John , Linsell Allen , Pluijmen Mathieu 
Published: February 2007

AbstractA study was carried out in Swaziland to assess the relationship between aflatoxin exposure, hepatitis B infection, and the incidence of liver‐cell carcinoma, which is the most commonly occurring malignancy among males in Swaziland. Levels of aflatoxin intake were evaluated in dietary samples from households across the country, and crop samples taken from representative farms. Prevalence of hepatitis B markers was estimated from the serum of blood donors, and liver cancer incidence was recorded for the years 1979–83 through a national system of cancer registration. Across 4 broad geographic regions, there was a more than 5‐fold variation in the estimated daily intake of aflatoxin, ranging from 3.1 to 17.5 μg. The proportion of HBV‐exposed individuals was very high (86% in men), but varied relatively little by geographic region; the prevalence of carriers of the surface antigen was 23% in men, and varied from 21 to 28%. Liver cancer incidence varied over a 5‐fold range, and was strongly associated with estimated levels of aflatoxin. In an analysis involving 10 smaller subregions, aflatoxin exposure emerged as a more important determinant of the variation in liver cancer incidence than the prevalence of hepatitis infection. Aflatoxin estimates from crop samples appeared to be a reasonable surrogate for dietary measurements. A comparison with dietary aflatoxin levels measured in an earlier survey in Swaziland suggested that programmes aimed at reducing contamination levels had had some success.
Second malignancies following testicular cancer, ovarian cancer and hodgkin's disease: An international collaborative study among cancer registries
Authors: Kaldor J. M. , Day N. E. , Band P. , Choi N. W. , Clarke E. A. , Coleman M. P. , Hakama M. , Koch M. , Langmark F. , Neal F. E. , Pettersson F. , Pompe‐Kirn V. , Prior P. , Storm H. H. 
Published: February 2007

AbstractEleven population‐based cancer registries tabulated second cancers among 133,411 patients diagnosed with testicular cancer, ovarian cancer or Hodgkin's disease between 1945 and 1984. Overall, 3,157 second cancers were observed, as compared with 2,420 expected at least one year after the first cancer. Survivors of testicular and ovarian cancer experienced 30% and 20% more cancers respectively than the general population comparison group, and patients previously diagnosed with Hodgkin's disease had an 80% excess of cancer. No information was available either on treatment for the first cancer, or other risk factors. However, temporal patterns in the risk of specific second cancers were analysed, with particular reference to the possible role of therapy for the first cancer. Leukaemia of the acute or non‐lymphatic type, which has been previously linked to alkylating agent therapy, occurred in excess following all 3 first cancers, as did non‐Hodgkin's lymphoma (overall relative risks of 6.1 and 1.8 respectively, with considerably higher relative risks following Hodgkin's disease). Other cancers for which important and plausibly therapy‐induced excesses occurred were lung cancer following Hodgkin's disease (relative risk 1.9), breast cancer following Hodgkin's disease (relative risk 1.4) and bladder cancer following ovarian cancer and Hodgkin's disease (relative risks 1.7 and 2.2 in women, respectively). Rarer sites at which striking excesses occurred were the salivary gland, thyroid, bone and connective tissue. There were smaller, but clear excesses for cancers of the rectum and colon following ovarian cancer and testicular cancer, skin cancer following Hodgkin's disease, and kidney cancer following ovarian cancer. Over‐diagnosis, misclassification of metastases and confounding by other risk factors were all considered as explanations of observed excesses. Nonetheless, it appeared that there are clear excess risks for cancers other than acute leukaemia which must be ascribed to therapy for the first cancer, especially in view of the possible under‐reporting in registry material. Case‐control studies are under way to provide information on the role of specific aspects of therapy.
The activation‐associated antigen 4f2 predicts patient survival in low‐grade b‐cell lymphomas
Authors: Holte Harald , Davies Catharina De L. , Kvaløy Stein , Smeland Erlend B. , Foss‐Abrahamsen Arne , Kaalhus Olav , Marton Per F. , Godal Tore 
Published: February 2007

AbstractExpression of the activation‐associated 4F2 antigen, transferrin receptor and interleukin‐2 (IL‐2) receptor on suspended cells from 75 biopsied low‐grade non‐Hodgkin lymphomas (L‐NHL) of B‐cell origin was correlated to patient survival, clinical prognostic parameters and estimated DNA synthesis. 4F2 antigen expression correlated significantly with poor patient survival, high DNA synthesis and transferrin receptor expression. Transferrin receptor expression was associated with high DNA synthesis and treatment response, but not with patient survival. On the other hand, IL‐2 receptor was correlated neither to patient survival nor to other studied markers for cell activation, but seemed to be expressed on certain subsets of lymphomas. We suggest that monoclonal antibody (MAb) against the activation‐associated 4F2 antigen could be used to select patients with L‐NHL for aggressive chemotherapy.
Antibody protein dose and radioimmunodetection of gw‐39 human colon tumor xenografts
Authors: Sharkey Robert M. , Primus F. James , Goldenberg David M. 
Published: February 2007

AbstractThis study investigates the influence of antibody protein dose on the radioimmunodetection of a CEA‐producing, human colonic tumor xenograft (GW‐39) using affinity‐purified goat anti‐carcinoembryonic antigen (CEA) antibody and a murine monoclonal anti‐CEA antibody (NP‐2). Hamsters bearing GW‐39 tumors were given an equal mixture of 131I‐labelled antibody and 125l‐labelled irrelevant IgG at doses varying from 0.01 to 1.0 mg (0.1 to 10 mg/kg body weight) for each antibody preparation. No differences were found in the percentage of antibody in the tumor or the clearance rate from the blood as the antibody dose was increased. The concentration of antibody in the tumor increased proportionally with the antibody dose and maintained a linear relationship with increasing dose, indicating that antigenic sites in the tumor were not saturated with antibody. The concentration of irrelevant IgG in the tumor also increased proportionally as the dose was increased, but the concentration of irrelevant IgG in the tumor was less than the antibody and was removed more rapidly from the tumor than the antibody. By considering the amount of irrelevant IgG in the tumor as a measure of the amount of antibody non‐specifically bound, we determined that there was no change in the amount of antibody in the tumor between days 3 and 7, and the amount of antibody increased uniformly for both the tumor and non‐tumor tissues, resulting in no improvement in the tumor/non‐tumor ratios with increasing antibody dose. External scintigraphy verified that the dose of the antibody did not influence tumor imaging. Thus, tumor accretion of antibody in this model is not dependent principally on the antibody protein dose, and other factors such as accessibility to antigen and antibody metabolism may play important roles in regulating the uptake of antibody in tumor.
A new animal model for human colon cancer metastasis
Authors: Bresalier Robert S. , Raper Steven E. , Hujanen Erkki S. , Kim Young S. 
Published: February 2007

AbstractAn animal model for human colon cancer metastasis is described in which spontaneously metastasizing colonic tumors are formed after injection of human colon cancer cells into the cecal wall of young athymic nude mice. Lymphatic and vascular invasion were demonstrated histologically after injection of both well‐ and poorly‐differentiated cell lines, and metastases were found in a pattern similar to that of naturally occurring human colonic cancer. In contrast, little or no visceral organ involvement could be demonstrated after s.c. injection. Cells with increased liver‐metastasizing potential were obtained by serial selection in this system. These cells had an enhanced ability to penetrate a reconstituted basement membrane in the presence of partially purified liver extract when compared to lung or brain extracts in a modified Boyden chamber assay. These results demonstrate the ability of human epithelial tumor cells to metastasize reproducibly in an animal model system, which may be useful for studying many aspects of the pathogenesis of cancer metastasis. In addition, it is suggested that local invasion by colon cancer cells may be influenced in part by tissue‐specific factors.
W‐7, a calmodulin inhibitor, potentiates dacarbazine cytotoxicity in human neoplastic cells
Authors: Lönn Ulf , Lönn Sigrid 
Published: February 2007

AbstractDacarbazine induces damage in replicative DNA, with a maximum level at 24 hr after treatment. Repair of these lesions does not occur when cells are post‐treated with the calmodulin inhibitor W‐7. In parallel cell cytotoxicity increases. The augmentation effect of W‐7 is prevented by simultaneous incubation of cells with high levels of calmodulin and does not occur in cells pre‐treated with aphidicolin (to stop DNA synthesis). Furthermore, W‐5, an analogue of W‐7 with a less inhibitory effect on calmodulin, does not interfere with DNA repair. The results show that calmodulin and/or calmodulin‐regulated proteins are involved in the repair process of dacarbazine‐induced DNA lesions.
Lipomas have characteristic structural chromosomal rearrangements of 12q13‐q14
Authors: Mandahl N. , Heim S. , Johansson B. , Bennet K. , Mertens F. , Olsson G. , Rööser B. , Rydholm A. , Willén H. , Mitelman F. 
Published: February 2007

AbstractCytogenetic analysis was performed in 10 consecutive lipomas; 6 had typical benign histology whereas four had foci of atypia. Three tumors had supernumerary ring chromosomes, 6 had different balanced rearrangements, and one had a normal karyotype. Chromosome 12 was involved in 5 of the balanced rearrangements and, although less certainly, in all the ring chromosomes, with breakpoints localized to 12q13 or q14. The other rearranged chromosomes were numbers 2,3,7,8,11,17 and 22. These results demonstrate the non‐random involvement of chromosomal region 12q13‐q14 in benign lipogenic tumors. The combined data from this and previous studies on benign and malignant lipogenic tumors indicate that different levels of cytogenetic specificity exist within this group of neoplasms. We suggest that myxoid liposarcoma development requires the recombination of 2 specific chromosomal bands (12q13 and 16q11), whereas for some types of benign lipogenic tumors structural changes in 12q13‐q14 may be sufficient for neoplastic growth.
Glycoproteic nature of surface molecules of effector cells with lymphokine‐activated killer (LAK) activity. Evidence that T11, T8 or T3 molecules are not involved in tumor‐cell lysis by LAK effector T cells
Authors: Bagnasco Marcello , Mingari Maria Cristina , Pende Daniela , Venuti Daniela , Canonica Giorgio Walter , Moretta Lorenzo 
Published: February 2007

AbstractHuman peripheral blood mononuclear cells cultured in the presence of interleukin‐2 (IL‐2) acquire the capability of lysing NK‐resistant fresh tumor target cells. In an attempt to delineate the surface structure(s) present on the effector cells, the latter were first treated with different amounts of pronase and neuraminidase. The effect of the enzymes on cytolytic activity against fresh melanoma cells was evaluated and compared with the NK‐like activity against K562 target cells of the same effector population. At a pronase concentration of 0.01 mg/ml, no inhibition of NK‐like activity was detected, whereas LAK activity was inhibited by more than 75%. In addition, neuraminidase had no effect on NK‐like activity, even at I U/ml, whereas as little as 0.03 U/ml inhibited LAK activity by more than 75%. Metabolic inhibition of N‐linked glycosylation with Tunicamycin prevented the generation of LAK activity, even when added late (18 hr before termination of the culture). Tunicamycin, on the other hand, had no effect on the boost of NK activity induced by IL‐2. Provided that LAK activity can also be generated in T‐cell (E‐rosetting) populations, in the presence of adherent cells, we analyzed the inhibitory activity of monoclonal antibodies (MAbs) to T11, T3 and T8 molecules. While all these MAbs strongly inhibited the specific target cell lysis by alloreactive CTLs, they had no effect on the LAK activity.
Hot maté drinking and precancerous lesions of the oesophagus: An endoscopic survey in southern brazil
Authors: Muñoz Nubia , Victora Cesar G. , Crespi Massimo , Saul Carlos , Braga Noris M. , Correa Pelayo 
Published: February 2007

AbstractThermal injury resulting from drinking very hot beverages has been incriminated as a risk factor for oesophageal cancer, although no information is available on the lesions caused by this injury in human or experimental animals. The drinking of hot mate tea is very common in areas of moderately high incidence of oesophageal cancer in south‐eastern areas of South America. This study investigated the prevalence of precancerous lesions of the oesophagus in 60 unskilled male workers, of whom half were daily maté drinkers and the remainder were non‐maté drinkers. These 2 groups were matched for age, smoking and alcohol intake. Maté drinkers were 2.2 times more likely (p = 0.046) to develop histologically confirmed oesophagitis than non‐maté drinkers.