bluuebunny/crossref_metadata_2025_split huggingface dataset:
Influence of an anti‐angiogenic treatment on 9L gliosarcoma: Oxygenation and response to cytotoxic therapy
Authors: Teicher Beverly A. , Holden Sylvia A. , Ara Gulshan , Dupuis Norman P. , Liu Fang , Yuan Jia , Ikebe Masahiko , Kakeji Yoshihiro 
Published: February 2007

AbstractTissue oxygen tensions were measured in subcutaneously growing rat 9L gliosarcoma under normal air and carbogen breathing conditions prior to and after i.v. administration of a perflubron emulsion. When these animals were treated with the anti‐angiogenic agents TNP‐470 and minocycline for 5 days prior to oxygen measurement, tumor hypoxia was decreased compared with untreated tumors. Hypoxia, defined as the percent of pO2 readings ≤5 mm Hg, was decreased from 71% in untreated air‐breathing controls to 34% in animals treated with the anti‐angiogenic agents, the perflubron emulsion and carbogen breathing. These effects were manifest in the increased response of the tumor to single‐dose (10, 20 and 30 Gy) radiation therapy. Twenty‐four hours after treatment with BCNU oxygenation of the tumors was not altered; however, 24 hr after administration of adriamycin oxygenation of the tumors was increased such that hypoxia in adriamycin‐treated tumors in animals receiving the perflubron emulsion and carbogen was reduced to 21%. Tumor growth delay in the s.c. tumors was increased by the addition of treatment with the anti‐angiogenic agents from day 4 through day 18 post‐tumor cell implantation along with BCNU or adriamycin on days 7–11. Administration of the perflubron emulsion and carbogen breathing resulted in increased tumor growth delay with the chemotherapeutic agents alone and in combination with the anti‐angiogenic agents. Life span in animals bearing intracranially implanted 9L gliosarcoma progressively increased with administration of the anti‐angiogenic agents and then the anti‐angiogenic agents and perflubron emulsion/carbogen compared to treatment with BCNU or adriamycin. © 1995 Wiley‐Liss, Inc.
Evidence of a chromatin basis for increased mutagen sensitivity associated with multiple primary malignancies of the head and neck
Authors: Pandita Tej K. , Hittelman Walter N. 
Published: February 2007

AbstractIndividuals at increased risk for cancer development have been reported to exhibit increased mutagen sensitivity as detected by the G2 phase chromosome breakage assay. To better understand the basis for such chromosome sensitivity, we examined 4 lymphoblastoid cell lines derived from 4 head and neck cancer patients, 2 of whom were previously shown to have normal bleomycin sensitivity and 2 high bleomycin sensitivity (and multiple primary tumors). These cell lines were studied for cell survival and initial damage and repair at both the DNA and chromosome levels, and the results compared to a normal control cell line and 3 ataxia telangiectasia homozygote cell lines. While all cell lines exhibited nearly equal levels of initial DNA damage and repair throughout the cell cycle, both the ataxia telangiectasia homozygote cell lines and 2 cell lines derived from individuals with multiple head and neck primary tumors showed increased levels of initial chromosome damage (detected by premature chromosome condensation), a reduced fast repair component and higher residual chromosome damage. Our results suggest that one component of the enhanced mutagen sensitivity phenotype observed in cancer‐prone individuals may involve an inherent chromatin alteration that allows a more efficient translation of DNA damage into chromosome damage following mutagen exposure. The degree of such an alteration might then be associated with an increased risk for second primary tumors in other carcinogen‐exposed sites. © 1995 Wiley‐Liss, Inc.
Substance‐P receptors in human primary neoplasms: Tumoral and vascular localization
Authors: Hennig Ivo M. , Laissue Jean A. , Horisberger Ulla , Reubi Jean‐Claude 
Published: February 2007

AbstractPrimary human neoplasms were examined for the presence of substance‐P receptors by receptor autoradiography with 125I‐labelled Bolton‐Hunter substance P. Substance‐P receptors were localized and characterized in the neoplastic cells of 9/12 astrocytomas, 10/10 glioblastomas, 10/12 medullary thyroid carcinomas, 8/16 breast carcinomas and 4/5 ganglioneuroblastomas. Conversely, substance‐P receptors were not or only rarely identified on non‐small‐cell carcinomas of the lung (1/16), neuroblastomas (0/8), adenocarcinomas of the colon (1/21) or the pancreas (1/9), or on malignant lymphomas (3/18). However, in the great majority of the investigated tumours, substance‐P receptors were found on intra‐ and peritumoral blood vessels. All substance‐P receptors detected had the pharmacological characteristics of the neurokinin‐I receptor sub‐type. In addition, the expression of somatostatin receptors was examined in all the neoplastic tissues mentioned above. Both substance‐P and somatostatin receptors were present in astrocytomas and in ganglioneuroblastomas, whereas little or no receptor was found in pancreatic and non‐small‐cell lung carcinomas. The extent of somatostatin‐receptor expression was inversely correlated to that of the substance‐P receptors in glioblastomas, neuroblastomas and non‐Hodgkin's lymphomas. The tumoral and vascular localization of substance‐P receptors in tumours may have clinical implications. The use of radiolabelled substance P for in vivo scintigraphy may supplement the current set of diagnostic tools. Substance‐P antagonists might be used in the treatment of tumours, as their binding to vascular receptors may decrease tumoral blood supply and drainage. © 1995 Wiley‐Liss, Inc.
Inhibition of 3′‐methyl‐4‐dimethylaminoazobenzene‐induced hepatocarcinogenesis in rat by dietary β‐carotene: Changes in hepatic anti‐oxidant defense enzyme levels
Authors: Sarkar Alok , Mukherjee Biswajit , Chatterjee Malay 
Published: February 2007

AbstractThe dietary administration of β‐carotene (BC) daily has been found to be highly effective in reducing hepatocarcinogenesis in male Sprague‐Dawley rats fed 3′‐methyl‐4‐dimethylaminoazo‐benzene (3′‐Met‐DAB). The anti‐cancer efficacy of BC was evaluated by estimating some possible pre‐neoplastic and neo‐plastic hepatic anti‐oxidant markers such as glutathione (GSH) and related enzymes, namely glutathione S‐transferases (GSHT, with varying substrate specificities), γ‐glutamyl transpeptidase (GGT), glutathione peroxidase (GPX) and reductase. BC proved to be an effective anti‐neoplastic substance in long‐term treatment. Furthermore, BC limited the exponential increase of GSH, GGT, GSH‐T and GPX both in the hyperplastic nodules (HNs) and surrounding liver (NNSP) areas compared with carcinogen control (3′‐Met‐DAB) rats during long‐term treatment. Early marginal changes in GSH, GGT and GSHT (with 1‐chloro‐2,4‐dinitrobenzene as a substrate) activities in BC‐treated groups for 10 days compared with carcinogen (3′‐Met‐DAB once) control rats entail the participation of BC in the initial stages of hepatocarcinogenesis. A decrease in the number of hyperplastic nodules and the total liver parenchyma they occupy was observed in BC‐treated groups. HNs and NNSP liver areas are directly correlated with hepatic BC and vitamin A content and with rates and patterns of hepatic anti‐oxidant defense enzymes. Our results confirm that BC is protective in limiting the action of 3′‐Met‐DAB during the initiation phase of hepatocarcinogenesis. © 1995 Wiley‐Liss, Inc.
Vitamin‐D3 derivatives and breast‐tumor cell growth: Effect on intracellular calcium and apoptosis
Authors: Vandewalle Brigitte , Hornez Louis , Wattez Nicole , Revillion Françoise , Lefebvre Jean 
Published: February 2007

AbstractVitamin‐D3 derivatives are now well‐recognized growth inhibitors of numerous tumoral cells and in particular breast‐cancer cells. However, the mechanisms by which they operate are not well established. Among the wide range of physiological and biological functions of vitamin‐D3 derivatives, the best described include their action on calcium homeostasis. In this study, we sought to establish whether the effects of vitamin‐D3 derivatives on breast‐cancer cell growth may be in part related to intracellular calcium modulation and induction of apoptosis. To address these questions, we used, in addition to 1,25(OH)2D3, the active metabolite of vitamin D3, a non‐calcemic 1,25(OH)2D3 derivative: Ro 23‐7553 [16‐ene‐23‐yne‐1,25(OH)2D3], which in our hands was more potent than the parent compound in inhibiting breast‐cancer cell growth. We showed that the efficiency of both compounds in growth inhibition was higher in the estradiol‐receptor‐positive‐breast‐tumor MCF‐7 cells than in the estradiol‐receptor‐negative MDA‐MB 231 cells. In MCF‐7 cells in particular, important modifications of intracellular calcium related to the emptying of intracellular pools were observed. The depletion of Ca++ from intracellular stores was followed by the induction of apoptosis. Such a phenomenon was never observed in MDA‐MB 231 cells. Our results suggest that the action of vitamin‐D3 derivatives on the depletion of calcium stores, which was more significant in MCF‐7 than in MDA‐MB 231 cells, may induce apoptosis in the former cells and account for the high efficiency of vitamin‐D3 derivatives on growth inhibition of MCF‐7 breast‐tumor cells. © 1995 Wiley‐Liss, Inc.
Presence of the bcl‐2 protein and apoptosis in non‐hodgkin lymphomas with diffuse growth pattern
Authors: Leoncini Lorenzo , Del Vecchio Maria T. , Spina Donatella , Megha Tiziana , Barbini Paolo , Sabattini Elena , Pileri Stefano , Tosi Piero , Kraft Rainer , Laissue Jean A. , Cottier Hans 
Published: February 2007

AbstractIn an attempt to further clarify the role of the apoptosis‐counteracting protein bcl‐2, non‐Hodgkin lymphomas (NHL, n = 170) were examined immunohistochemically, across the boundaries of histologic classification, for the presence of this oncoprotein, in comparison with apoptotic indices (AI) and percentages of Ki‐67+ cells (growth fraction). The results of this retrospective study revealed a highly significant inverse relationship (“mirror image”) between the proportion of bcl‐2+ cells and the AI per case. Both these parameters, although variable, clearly distinguished low‐ from high‐grade‐malignancy lymphomas according to the Kiel classification. Cluster analysis detected 2 separate groups of high‐grade NHL, one with rather high AI and low percentages of bcl‐2+ cells, comprising most anaplastic large‐cell lymphomas, the other group with reverse characteristics. We found no correlation between the percentage of bcl‐2+ cells per case and overall survival. © 1995 Wiley‐Liss, Inc.
Colon goblet cells lose proliferative response to TGFα as they differentiate
Authors: Sauma Samir , Huang Fei , Winawer Sidney , Friedman Eileen 
Published: February 2007

AbstractTwo cell line models for colon goblet cells expressed 6‐ to 14‐fold elevated levels of the EGF receptor, 3‐ to 5‐fold levels of TGFα and 11‐ to 15‐fold levels of amphiregulin compared with 2 cell lines which model colon enterocytic differentiation, suggesting a role for the EGF receptor and its ligands in goblet cell growth control. Two HT29 colon carcinoma sublines were used to model normal goblet cells at different stages of maturation. TGFα induced a 2‐fold increase in growth of the HD8 subline but inhibited the growth of the more differentiated HD6 subline by 40%. EGF receptors were activated in each line by ligand, but signal transduction varied sharply. Both MAP kinase isoforms, p44 and p42, were markedly activated in HD8 cells for at least 20 min, while only a marginal activation was seen in HD6 cells. In contrast, the more differentiated HD6 cells showed an increase in 105 kDa MBP kinase activity with EGF treatment, while HD8 cells displayed constitutively elevated levels of this kinase. Thus, activated EGF receptors initiated different signalling pathways in model cell lines for colon goblet cells at different stages of maturation. TGFα protein levels have been shown by other investigators to be restricted to the top of the cylinder‐like colonic crypt, where cells terminally differentiate and cease division, an unexpected location for an epithelial cell mitogen. Our data with model cell lines imply that normal colon goblet cells lose proliferative response to TGFα as they differentiate and the elevated levels of TGFα at the top of the colonic crypt in vivo serve to inhibit goblet cell growth. © 1995 Wiley‐Liss, Inc.
Susceptibility of colorectal‐carcinoma cells to natural‐killer‐mediated lysis: Relationship to CEA expression and degree of differentiation
Authors: Prado Ivete B. , Laudanna Antonio A. , Carneiro Célia R. W. 
Published: February 2007

AbstractThis study addresses the relevance of colorectal‐carcinoma‐cell (CRC) CEA expression and degree of differentiation in natural‐killer(NK)‐mediated lysis susceptibility. A 51Cr‐release cytotoxicity assay performed with 5 human CRC lines demonstrated that CRC CEA expression was related to resistance to NK lysis. Moreover, the addition of anti‐CEA Fab fragments to the assay led to a significant increase of lysability of high‐CEA‐producing and NK‐resistant cells (LS 174‐T), whereas purified CEA drastically reduced lysis of low‐CEA‐producing and NK‐susceptible cells (LISP‐1) in a dose‐dependent manner. These results strongly suggest that CEA plays a causal role in CRC resistance to NK lysis. Nevertheless, our data did not demonstrate CEA binding to effector cell surface, suggesting that CEA expression can protect CRC, possibly by preventing NK‐tumor‐cell adhesion to occur. Our results also show that CRC susceptibility to NK lysis was related to a less differentiated phenotype. HCT‐8, which are poorly differentiated and low‐CEA‐producing cells, were cultured in vitro in the presence of the differentiation agent sodium butyrate. Treated cells became less susceptible to NK lysis as they progressed towards a more differentiated phenotype. However, CEA production was not altered upon differentiation. Our study thus demonstrates that both features, CEA expression and degree of cellular differentiation, may individually influence CRC susceptibility to NK lysis. © 1995 Wiley‐Liss, Inc.
Expression of acid cysteine proteinase inhibitor (acpi) in the normal human prostate, benign prostatic hyperplasia and adenocarcinoma
Authors: Söderström Karl‐Ove , Laato Matti , Wu Ping , Hopsu‐Havu Väinä K. , Nurmi Martti , Rinne Ari 
Published: February 2007

AbstractAcid cysteine proteinase inhibitor (ACPI or cystatin A) is a protein (12 kDa) which inhibits the action of several cysteine proteinases, e.g. cathepsins B, H, L and S. In this study the cellular location of ACPI has been immunohistochemically investigated in the normal human prostate, in benign prostatic hyperplasia (BPH) and in adenocarcinoma. ACPI was found in the basal epithelial cells of the normal prostate. The secretory epithelial cells did not express ACPI. In the hyperplastic prostate, the expression of ACPI was decreased and it was also expressed more focally in the basal cells. Hyperplastic basal cells also expressed ACPI. In prostatic adenocarcinoma, no ACPI expression was found. The absence of ACPI expression was obvious and if the sections contained both benign and malignant cells, only the benign glandular structures always expressed ACPI. The results suggest that expression of ACPI might be related to prostatic epithelial cell proliferation and differentiation. Possibly the detection of ACPI in tissue sections might be helpful in identifying prostatic adenocarcinoma, especially in cases with small carcinomatous foci. © 1995 Wiley‐Liss Inc.
Human and viral interleukin‐10 in Hodgkin's disease, and its influence on CD4+ and CD8+ T lymphocytes
Authors: Ohshima Koichi , Suzumiya Junji , Akamatu Minoru , Takeshjta Morishige , Kikuchi Masahiro 
Published: February 2007

AbstractThe Epstein‐Barr virus (EBV) is closely related to Hodgkin's disease (HD), while the BCRF‐I (viral [v] IL‐10) gene of the EBV is highly homologous to the human interleukin‐10 (h IL‐10) gene. To investigate the relationship of IL‐10 and HD, we performed both immunostaining and in situ hybridization (ISH) in 30 cases of HD. The presence of EBV in Hodgkin (H) and Reed‐Sternberg (RS) cells was seen in 16 of the 30 cases, by ISH of the EBV EBER‐I region and/or immunostaining of latent membrane protein (LMP‐I). Of the 16 EBV‐positive cases, 12 also showed IL‐10 antigen (Ag) in H and RS cells by immunostaining, 5 of the 16 demonstrated hIL‐10 RNA by ISH and 14 of the 16 showed vIL‐10 RNA. But only 2 of the 14 EBV‐negative cases showed IL‐10 Ag, and one of them showed hIL‐10 RNA, while none demonstrated vIL‐10 RNA. The T cells in the HD‐involved tissues were found to be mainly CD4‐positive T cells, and had no association with EBV infection. However, the lymphocytes surrounding H and RS cells were more frequently CD4 cells and rarely CD8 cells in the EBV‐positive cases, in contrast with the EBV‐negative cases. The above results indicate that an EBV infection influenced both cytokine synthesis and the response of T cells in HD. © 1995 Wiley‐Liss Inc.
Second primary cancers in patients with carcinoma in situ of the uterine cervix. The norwegian experience 1970–1992
Authors: Bjørge Tone , Hennig Elin M. , Skare Gry B. , Søreide Odd , Thoresen Steinar Ø. 
Published: February 2007

AbstractMultiple primary cancers in the same individual occur rarely. Consequently, a large number of cancer patients have to be followed for long periods to obtain adequate information about their risk of subsequent tumour development. Studies of multiple malignancies are of interest, since they may provide information on common or opposite risk factors. In the present study, the risk of second primary cancers following carcinoma in situ of the uterine cervix diagnosed in Norway in the period 1970–1992 was examined and quantified. Altogether, 37,001 patients with carcinoma m situ were followed from the date of diagnosis until 31 December 1992. The follow‐up period was divided into 5‐year intervals. The results were expressed as standardized incidence ratios (SIR = O/E), and their 95% confidence intervals were given. A total of 1,037 second primary cancers in 989 individuals were identified. There was no overall excess of second primary cancers. However, there were differences depending on the site: cancers of the oesophagus, nose, nasal cavities, trachea, bronchus, lung, vulva, vagina, bladder and other urinary organs, and other skin cancers, excluding basal‐cell carcinoma, occurred more frequently. A lower risk than expected was noted for cancer of the cervix uteri and cancer of the corpus uteri. There was a rising trend with time in the observed/expected ratio for cancer of urinary organs. In the group of patients evaluated, the likelihood of subsequent tumour development was no greater than in the general female population. Nevertheless, cancer sites of higher and of lower risk than expected were identified among the carcinoma‐In situ patients. © 1995 Wiley‐Liss Inc.
A novel human monoclonal antibody, TONO‐1, reactive with T‐lymphocytic leukemia cells
Authors: Numasaki Muneo , Fukuoka Yoshihiro , Kudo Toshio , Saeki Hisaaki , Tachibana Takehiko , Motomiya Masakichi , Nukiwa Toshihiro 
Published: February 2007

AbstractMononuclear cells from the peripheral blood of patients with systemic lupus erythematosus (SLE) were transformed with the Epstein‐Barr virus (EBV) and the resultant polyclonal B‐lymphoblastoid cell lines were tested for antibody activity to membrane antigens of certain T‐cell lines. B lymphoblastoid cell lines secreting specific antibodies were fused with (mouse x human) heteromyeloma SHM‐D33 cells. Among the large number of hybridomas generated, one which produced a human monoclonal antibody (MAb) TONO‐I (1gM, λ) was selected. MAb TONO‐I proved to be reactive with 4 human T‐cell lines, HPB‐MLT, L‐MAT, MOLT‐3 and MOLT‐4F, but not with B‐leukemia, Burkitt's lymphoma, myelomonocytic leukemia, erythroleukemia or non‐hematopoietic malignant cell lines. MAb TONO‐I reacted positively with fresh leukemia cells from 2 of 7 patients with acute T‐lymphocytic leukemia, but no reaction was observed in non‐T‐cell leukemia cases. Normal lymphocytes, monocytes, granulocytes, red blood cells and platelets in the peripheral blood did not demonstrate remarkable binding. Neither thymocytes nor bone‐marrow cells from healthy volunteers were reactive. The antigens defined by MAb TONO‐I were polypeptides of 57 kDa and 68 kDa. Immunohistological studies revealed no staining of thymocytes in the thymus of a 6‐month‐old child, but showed epithelial reticular cells and Hassall's corpuscles to stain positively. These results suggest that MAb TONO‐I is directed to T‐leukemic cells and some components of thymus tissue. © 1995 Wiley‐Liss Inc.
Sequence specificity on the growth suppression and induction of apoptosis of chronic myeloid leukemia cells by BCR‐ABL anti‐sense oligodeoxynucleoside phosphorothioates
Authors: Maekawa Taira , Kimura Shinya , Hirakawa Kouichi , Murakami Akira , Zon Gerald , Abe Tatsuo 
Published: February 2007

AbstractSequence specificity of inhibitory effects of various BCR‐ABL anti‐sense oligodeoxynucleoside phosphorothioates (AS PS‐ODN) on the proliferation of the chronic myeloid‐leukemia cell line BV173 was examined. We confirmed that 26,18, and 16mer B2A2 AS PS‐ODN had strong inhibitory effects on the proliferation of BV173 cells with B2A2 mRNA expression, and that B3A2 AS PS‐ODN were equally inhibitory when cultures were initiated at lower cell concentrations. However, at higher cell concentrations, the inhibitory effects by B3A2 AS PS‐ODN were reduced and B2A2 AS PS‐ODNs could suppress the proliferation of BV173 cells with much more relative sequence specificity. The 26mer B2A2 AS PS‐ODN induced apoptosis of BV173 cells following reduction of BCR‐ABL mRNA expression and p210 protein synthesis. Various sense (S), reverse order, and random sequences had no inhibitory effects except 16mer B2A2 S and B3A2 S that revealed significant suppressive effects. Furthermore, 26mer B3A2 AS also reduced B2A2 mRNA expression and p210 protein synthesis, while 16mer S sequences did not. These results suggest that B2A2 AS may be cross‐reactive with B3A2 AS on the growth suppression of CML cells under certain culture conditions, possibly due to their partial hybridization to the ABL portion of the target mRNA, although other non‐sequence‐specific mechanisms are also possible. © 1995 Wiley‐Liss Inc.