bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sensitive detection of numerical and structural aberrations of chromosome 1 in neuroblastoma by interphase fluorescence in situ hybridization. comparison with restriction fragment length polymorphism and conventional cytogenetic analyses
Authors: Combaret Valérie , Turc‐Carel Claude , Thiesse Philippe , Rebillard Anne‐Catherine , Frappaz Didier , Haus Odile , Philip Thierry , Favrot Marie C. 
Published: February 2007

AbstractChromosome 1 abnormalities are indicators of prognosis in neuroblastoma (NB) but are not yet routinely exploited because conventional methods are technically demanding. We evaluated the pertinence of interphase cytogenetics fluorescence in situ hybridization (FISH) for the analysis of chromosome 1 in NB, compared with conventional methods. Deletion of 1p was detected in 8 of 9 cell lines analyzed by both FISH and restriction fragment length polymorphism (RFLP), but was evidenced in only 2 cases by conventional cytogenetics, painting analysis being required to reveal the other cases. The chromosome 1 number evaluated by FISH reflected the total chromosome modal number obtained by cytogenetics. Twenty‐eight specimens obtained from ultrasound‐guided punctures, surgical biopsies of the primary tumor and bone‐marrow aspirates were studied by FISH on frozen cytocentrifuged smears; 12 had a chromosome 1 trisomy and 16 a disomy. Requirements for a reliable control analysis of 1p deletion by RFLP were met in only 23 cases. The retention of 2 alleles was observed in 15 cases and 1p deletion in 7, by both techniques. In one case, an interstitial deletion of 1p was evidenced only by RFLP, and one of 5 cases analyzed only by FISH had a 1p deletion. Although FISH might be improved by using additional probes, it presents major advantages for routine exploitation. Determining 1p deletion in individual cells makes it possible to analyze small and heterogeneous tumoral specimens; the technique requires only a few hours and can easily be standardized in non‐specialized laboratories. The number of chromosome 1 homologues per cell might serve as a rapid screening for ploidy. © 1995 Wiley‐Liss, Inc.
Direct tumorigenic conversion of human gallbladder carcinoma cells by v‐src but not by activated c‐H‐ras oncogene
Authors: Tatsumoto Takashi , Nakano Shuji , Shimizu Kenji , Ono Mayumi , Esaki Taito , Ohshima Koh‐Ichi , Niho Yoshiyuki 
Published: February 2007

AbstractThe roles of activated ras and src oncogene products in the acquisition of fully neoplastic phenotype by human gallbladder adenocarcinoma cells were investigated by co‐transfecting non‐tumorigenic HAG‐1 human gallbladder carcinoma cells with the pSV2neo plasmid and a plasmid carrying either activated c‐H‐ras or v‐src oncogene. G‐418‐resistant clones were isolated and assessed for the acquisition of anchorage‐independent growth potential. Neither the 10 established clones transfected with pSV2neo alone nor the 17 clones transfected with activated c‐H‐ras, including 4 clones expressing the mutated p21H‐ras protein, could form colonies in soft agar. By contrast, out of 10 clones transfected with v‐src, 2 formed colonies in soft agar and produced tumors in athymic nude mice, the resulting progressive neoplasms being poorly differentiated adenocarcinomas. These tumorigenic clones were shown to have v‐src DNA and mRNA levels with p60v‐src protein, but there were no significant chromosomal alterations following tumorigenic conversion. Moreover, herbimycin A, a selective src‐kinase inhibitor, markedly reduced clonogenic growth of these cells in soft agar rather than monolayer growth, suggesting that anchorage‐independent growth of the v‐src‐transformed HAG‐1 cells might be driven directly by p60v‐src kinase activity. Taken together, our data suggest that the fully neoplastic conversion of HAG‐1 cells depends on src‐related tyrosine‐kinase activity, but not solely on the function mediated by activated ras, thus providing evidence of an src‐related signaling pathway for the acquisition of tumorigenic potential by human gallbladder adenocarcinoma cells. © 1995 Wiley‐Liss, Inc.
Hypergastrinemia in rats with azoxymethane‐induced colon cancers
Authors: D'Agostino Luciano , Pignata Sandro , Tritto Giovanni , D'Adamo Giuseppe , Contegiacomo Alma , Daniele Bruno , Calderopoli Rita , Pizzi Claudia , Squame Giovanni , Mazzacca Gabriele 
Published: February 2007

AbstractGastrin has been suggested to be involved in the promotion and progression of colon cancer. Mice colon cancers and colon‐carcinoma cell lines are stimulated to grow by gastrin, and gastrin receptors have been found in the majority of human colon‐tumor specimens. High serum gastrin levels have been reported in patients with colon polyps and cancers, together with increased ornithine decarboxylase (ODC) activity. Since gastrin stimulates ornithine decarboxylase in colon cancer cells in vitro it has been suggested that increased synthesis of intracellular polyamines is one of the mechanisms activated by the hormone. In order to confirm the presence of hypergastrinemia in colon cancer and to investigate the relationship between plasma gastrin and tumor growth, we used an animal model of colon carcinogenesis that minimizes the possible bias of human studies, related to varying diet, age and environmental factors. We evaluated blood gastrin levels in 35 rats with colon cancer induced by the carcinogen azoxymethane (AOM), and we correlated gastrinemia with tumor proliferation, assessed by thymidine‐labeling index (TLI) and ODC activity; 6 animals constituted the control group. Gastrin levels in rats with AOM‐induced tumors were significantly higher than in controls. Significantly higher TLI and ODC activity were found in the tumors of hypergastrinemic rats than in neoplasms of animals with normal gastrin levels. Our data provide additional evidence of a role for gastrin as trophic hormone for colon neoplastic cells. © 1995 Wiley‐Liss, Inc.
Glycoconjugate profile and cd44 expression in human melanoma cell lines with different metastatic capacity
Authors: Van Muijen Goos N. P. , Danen Erik H. J. , Veerkamp Jacques H. , Ruiter Dirk J. , Lesley Jayne , Van Den Heuvel Lambert P. W. J. 
Published: February 2007

AbstractChanges in glycoconjugate production have been reported for tumor cells. In this study, we investigated the glycoconjugate expression pattern in normal human melanocytes and in a panel of 6 human melanoma cell lines with different metastatic capacity after s.c. inoculation into nude mice. Glycoconjugates were labeled in vitro with [35S] sulphate and [3H] glucosamine, purified from cells and culture medium by column chromatography and identified by treatment with specific glycosidases. Characterization of the purified glycoconjugate fractions as well as alcian‐blue staining of xenograft lesions revealed that hyaluronic acid (HA) is the main glycoconjugate produced by all cell lines. Highly metastatic cell lines expressed higher levels of HA than melanocytes and than weakly metastatic or non‐metastatic cell lines. In addition, a shift in dominance from chondroitin‐sulphate proteoglycan to heparan‐sulphate proteoglycan was observed with increasing metastatic capacity. We also studied the expression and binding activity of the HA receptor CD44. Immunoprecipitation experiments indicated high CD44 synthesis only in highly metastatic cell lines, but FACS analysis demonstrated approximately the same surface expression in melanocytes as in all cell lines. Adhesion assays to immobilized HA showed that CD44 can be present in an inactive or an active conformation. Our data suggest that a combination of increased HA production and the expression of CD44 on the cell surface may be associated with high metastatic potential of human melanoma cell lines in nude mice. © 1995 Wiley‐Liss, Inc.
Rejection of mouse melanoma elicited by local secretion of interleukin‐2: Implicating macrophages without T cells or natural killer cells in tumor rejection
Authors: Hara Isao , Nguyen Hai , Takechi Yoshizumi , Gansbacher Bernd , Chapman Paul B. , Houghton Alan N. 
Published: February 2007

AbstractTumor cells transduced with cytokine genes provide a model to study host‐effector mechanisms involved in tumor rejection. Local IL‐2 production within a tumor site mimics a specific helper‐T‐cell response, bypassing an immunization phase. Growth of mouse B16F10 melanomas transduced with interleukin‐2 (IL‐2) in syngeneic hosts were significantly delayed. IL‐2‐producing B16F10 cells were super‐transduced with inter‐feron‐γ to up‐regulate expression of major‐histocompatibility‐complex (MHC) antigens. Expression of class‐1‐ or class‐11‐MHC molecules did not augment tumor rejection of IL‐2‐secreting tumor cells. Rejection of IL‐2‐transduced B16F10 cells in syngeneic mice was unaffected by depletion of CD8+ T‐cell and NK1.1+ natural‐killer (NK) cell populations. Tumor rejection occurred in SCID mice even after depletion of NK1.1+ cells, confirming that T cells and NK cells were not required for tumor rejection. Histologic examination of sites of tumor rejection showed inflammation, characterized by infiltrates of macrophages, occasional neutrophils, and areas of necrosis. When mice were treated systemically with macrophage‐colony‐stimulating factor to expand monocyte pools, tumor rejection was significantly augmented further. This study shows that in situ IL‐2 production can result in tumor rejection mediated by inflammatory events, possibly involving macrophages, and mimicking a delayed‐type hypersensitivity (DTH) response even in the absence of T cells and NK cells. Furthermore, tumor rejection can be enhanced by systemic administration of a cytokine to expand potential inflammatory cell populations. © 1995 Wiley‐Liss, Inc.
Differential regulation of glycosphingolipid biosynthesis in phenotypically distinct Burkitt's lymphoma cell lines
Authors: Taga Samir , Mangeney Marianne , Tursz Thomas , Wiels Joëlle 
Published: February 2007

AbstractEarlier studies have shown that Burkitt's lymphoma (BL) cell lines can be divided into 2 major groups: group I, which retain the original BL biopsy phenotype with expression of CD 10 and CD77 antigens and lack of B‐cell activation markers, and group III, which, after several in vitro passages, progress toward an “LCL‐like” phenotype with loss of CD 10 and CD77 expression and up‐regulation of B‐cell activation antigens. In previous studies we have shown that several glycolipid molecules constitute stage‐specific antigens for B cells and that sequential shifts in the 3 major glycolipid series are observed during B‐cell differentiation, these changes being mostly due to sequential activations of the corresponding glycosyltransferases. In the present work, 10 BL cell lines with group I or group III phenotype have been examined for cell surface expression of 5 glycolipid antigens (LacCer, GM3, Gb3/CD77, Gb4 and GM2), total glycolipid content and enzymatic activities of 4 glycosyl‐transferases (GM3, Gb3, Gb4 and GM2 synthetases). We now report that group I and group III BL cells differ in their glycolipid metabolism and express either mostly globoseries or ganglio‐series compounds. Indeed, Gb3 is the major glycolipid of group I cells, whereas GM3 and GM2 are the 2 major components of group III cells, and these phenotypic differences are mainly due to differential activities of the corresponding glycosyltransfer‐ases: group I cells have high Gb3 synthetase activities and low or no GM3 and GM2 synthetase activities, whereas group III cells have high GM3 and GM2 synthetase activities and low Gb3 synthetase activities. Finally, we also show that, unlike LCL, group III BL cells do not synthesize Gb4. © 1995 Wiley‐Liss, Inc.
Establishment of human acute myelogenous leukemia lines secreting interleukin‐1β in SCID mice
Authors: Giavazzi Raffaella , Berardino Cristina Di , Garofalo Angela , Motta Teresio , Gobbi Alberto , Scanziani Eugenio , Giudici Giovanni , Galli Monica , Mayo Joseph G. , Barbui Tiziano , Biondi Andrea , Rambaldi Alessandro 
Published: February 2007

AbstractA reproducible in vivo model of human acute myelogeneous leukemia (AML) was established in severe combined immunodeficient (SCID) mice. The AML‐CL and AML‐PS lines were originated from leukemic blasts purified respectively from the peripheral blood of a 27‐year‐old woman with previously untreated hyperleukocytotic AML and from the bone marrow of a 61‐year‐old man during the third leukemic relapse. The 2 lines were maintained and serially transplanted i.p. in SCID mice. AML‐PS and AML‐CL produced ascitogenous gross tumors after approximately 4 and 6 weeks, respectively, and all mice died within 6‐8 weeks. Microscopic evaluation of different organs at autopsy showed massive involvement of bone marrow, liver and spleen, though with differences in the tumor burdens for the 2 lines (AML‐CL > AML‐PS). Flow cytometric analysis documented the spread of leukemic cells to bone marrow, peripheral blood and spleen. AML‐PS and AML‐CL cells show an immunophenotypic profile (CDI3+, CD33+) and cytogenetic findings similar to freshly isolated blasts. Interleukin‐1β (1L‐1β) gene expression was observed by Northern blot analysis in leukemic cells from AML‐CL and AML‐PS SCID mice. After 24 hr of culture both lines released IL‐1β in culture supernatants. High levels of circulating IL‐1β were secreted in plasma of tumor‐bearing mice. This AML‐SCID murine model could contribute to an understanding of the mechanisms of AML growth in vivo and the possible role of the autocrine production of IL‐1β in promoting cell growth. © 1995 Wiley‐Liss, Inc.
Cancer survival in Khon Kaen province, Thailand
Authors: Sriamporn Supannee , Black Roger J. , Sankaranarayanan Rengaswamy , Kamsa‐ad Supot , Parkin D. Maxwell , Vatanasapt Vanchai 
Published: February 2007

AbstractThailand is one of the few developing countries for which population‐based cancer survival data are available. Using clinical follow‐up information and reply‐paid postal enquiries, 10,333 residents of Khon Kaen province registered with cancer in the period 1985–1992 were followed‐up to the end of 1993. The sites of the most common cancers in the province were liver (5‐year relative survival rate 9.2%), cervix (60.1%), lung (15.4%), breast (48.1%) and large bowel (41.9%). Results for Khon Kaen were compared with age‐standardized survival data for the US and Scotland. Survival was consistently higher for US whites compared to Khon Kaen residents for those cancers whose prognosis is associated with early diagnosis (breast, cervix and large bowel) or the availability of intensive therapy (leukaemia and lymphoma). The main implication of these results for cancer control in Thailand is that the interventions of greatest potential benefit are those designed to promote early detection. More than one‐third of all cancers in Thailand are liver tumours: primary prevention through control of hepatitis‐B infection and liver fluke infestation is the only effective strategy for their control. © 1995 Wiley‐Liss, Inc.
Changes in biological markers after primary chemotherapy for breast cancers
Authors: Daidone Maria Grazia , Silvestrini Rosella , Luisi Antonella , Mastore Marinella , Benini Elvira , Veneroni Silvia , Brambilla Cristina , Ferrari Laura , Greco Marco , Andreola Salvatore , Veronesi Umberto 
Published: February 2007

AbstractThe profiles of functional (proliferative rate and cell distribution in the cell cycle) and phenotypic (nuclear DNA content and hormone receptor status) biological markers and the expression of P53 and Bcl‐2 proteins were prospectively evaluated in breast cancers before and after different regimens of primary chemotherapy. Overall, changes induced on the 2 proliferation indices (3H‐thymidine labelling index, 3H‐dT LI, and flow‐cytometric S‐phase fraction, FCM‐S) mainly consisted of a decrease for rapidly proliferating tumours and an increase or no change for slowly proliferating tumours. However, when considered as a function of treatment type, changes of 3H‐dT LI and FCM‐S were superimposable in rapidly proliferating tumours, regardless of the type of treatment, and in slowly proliferating tumours only after anthracycline‐including regimens. Conversely, following CMF, FCM‐S was increased in 90% of the cases and 3H‐dT LI in only 50%. Our data imply that the 2 proliferation indices could reflect different phenomena: an actual variation of proliferative activity by 3H‐dT LI and an accumulation of cells in the S‐phase by FCM‐S. In addition, a higher accumulation of cells in G2‐M phases could be detected by FCM after anthracycline‐including regimens than after CMF. The fraction of P53‐positive cells was reduced by primary chemotherapy in about 50% of P53‐positive tumours, whereas Bcl‐2 expression was only marginally affected. DNA ploidy and hormone receptor status did not change in about 75% of cases, regardless of the chemotherapeutic regimen. © 1995 Wiley‐Liss, Inc.
Mutations clustered in exon 5 of the p53 gene in primary nasopharyngeal carcinomas from Southeastern Asia
Authors: Chakrani Fatima , Armand Jean‐Pierre , Lenoir Gilbert , Ju Li‐Ya , Liang Jian‐Ping , May Evelyne , May Pierre 
Published: February 2007

AbstractMutations in the p53 tumor suppressor gene play an important role in the development of many common human malignancies. In nasopharyngeal carcinomas (NPC), p53 gene mutations were not detected in primary tumors, with one exception for a primary tumor displaying a p53 mutation at codon 280, whereas p53 mutations were identified in some metastatic and nude mouse‐passaged NPC specimens. In the present report, 41 NPC primary tumors of the undifferentiated carcinoma nasopharyngeal type (UCNT; 21 from Hong Kong and 20 from Guangxi, southeastern China) were studied. Four point mutations that result in amino acid substitutions were identified by PCR amplification of exons 2–9 and direct DNA sequencing, combined with PCR‐singfe‐strand conformation polymorphism analysis. The 4 mutations detected were clustered within the DNA stretch from codon 175 to 177. Our data, taken together with those of others, suggest that mutation in p53 may occur in NPC at various points during tumorigenesis. Alternative mechanisms of p53 inactivation in NPC are also possible. © 1995 Wiley‐Liss, Inc.
HPV infection in cervical‐cancer cases in Russia
Authors: Samoylova Ella V. , Shaikhaiev Gadji O. , Petrov Semjon V. , Kisseljova Natalia P. , Kisseljov Fjodor L. 
Published: February 2007

AbstractThe presence of human papillomavirus (HPV) sequences in 21 biopsies from cervical carcinomas, II specimens of tissues adjacent to tumours, 2 specimens of cervical tissues with radiation fibrosis from patients after radiation therapy of cervical cancer and 7 normal epithelial tissues from the patients with other genital tumours were examined by polymerase chain reaction (PCR) and Southern‐blot analysis. All tumours were HPV‐positive by type‐specific PCR and 86% by Southern‐blot analysis. In normal epithelial and adjacent tissues, HPV sequences were detected in 20% of samples by Southern‐blot analysis and in 70% of samples by PCR, including 2 cases of tissues after radiation therapy. HPV 16 was the most prevalent type in tumours (18/21) as well as in normal epithelial tissues (5/7). One HPV‐positive tumour contained HPV18 DNA and 2 were doubly infected with HPVs 16 and 18 (2/21). The persistence of exclusively episomal HPV16 DNA was observed in 5 out of 11 tumours examined: 3 cases of squamous‐cell carcinomas on the early stage of tumour progression and 2 advanced tumours (squamous‐cell carcinoma and adenocarcinoma). The integration of HPV16 genome was detected in 6 out of 11 tumours, but most of them contained episomal forms of viral DNA simultaneously (5 out of 6). The integrative HPV18 genome was found in 2 tumours examined, and the persistence of episomal forms was also observed in one of them. Our data demonstrate that cervical tumours are associated invariably with high‐risk types of HPV in Russia. © 1995 Wiley‐Liss, Inc.
Effects of interferon‐α on human b cells: Repression of apoptosis and prevention of cell growth are independent responses of burkitt lymphoma lines
Authors: Milner Anne E. , Grand Roger J. A. , Gregory Christopher D. 
Published: February 2007

AbstractWe have previously shown that interferon‐α (IFN‐α) can repress apoptosis in Burkitt lymphoma (BL) cells. In this study, we have compared this protective response with a further, well‐established effect of IFN‐α on BL cells, that of growth arrest. Of a panel of BL lines comprising (i) EBV‐positive and ‐negative lines that retain the phenotype of the parental tumour cells and (ii) the prototype IFN‐α‐growth‐inhibited line, Daudi, only Daudi cells were found to undergo substantial growth inhibition in response to the cytokine. By contrast, all lines, with the notable exception of Daudi, were protected by IFN‐α from high‐rate apoptosis initiated by the Ca2+ ionophore ionomycin. lonomycin failed to elicit an IFN‐α‐repressible apoptotic response in either wild‐type Daudi cells or IFN‐resistant sublines that were refractory to the growth‐arresting effects of the cytokine. Analysis of c‐myc protein levels confirmed previous observations that repression of apoptosis in IFN‐α‐rescuable BL cells was associated with an early inhibition of myc that was followed by a return to high‐level expression. Significantly, ionomycin alone induced a comparable transient inhibition of myc protein in Daudi cells. In Daudi cells, but not in IFN‐α‐rescuable BL cells, renewed expression of myc observed after the early, transient down‐regulation was followed by sustained down‐regulation of the protein, which paralleled growth arrest. Our results indicate that long‐term growth arrest and repression of apoptosis in BL are distinct cellular responses to IFN‐α. © 1995 Wiley‐Liss, Inc.
Induction of CD44 expression by the epstein‐barr virus latent membrane protein LMP1 is associated with lymphoma dissemination
Authors: Walter Jürgen , Schirrmacher Volker , Mosier Donald 
Published: February 2007

AbstractEpstein‐Barr Virus (EBV) is implicated in the pathogenesis of endemic Burkitt's lymphoma (BL), B‐cell lymphomas occuring under immunosuppression, nasopharyngeal carcinoma and Hodgkin's disease. Two distinct patterns of latent EBV gene expression occur in EBV‐associated lymphomas. BLs typically display expression of the nuclear antigen EBNAI only, whereas EBV‐associated, non‐Burkitt B‐cell lymphomas express at least 9 latent viral genes (6 EBNAs and 3 latent membrane proteins), reminiscent of in vitro EBV‐immortalized lymphoblastoid cell lines (LCL). BLs are characterized by local, extra‐nodal growth, whereas EBV‐associated B‐cell lymphomas often disseminate to peripheral lymphoid tissue. We show here that BL cells forming local tumors after xenotransplantation into SCID mice disseminate to lymphoid tissue following introduction of the latent membrane protein 1 (LMP1) gene. Introduction of LMP1 into BL cells induced expression of CD44 on the cell surface, a molecule implicated in enhanced lymphoid tumor growth and dissemination. Introduction of CD44 into LMP1‐/CD44‐BL cells was observed to confer the disseminated tumor growth pattern associated with LMP1 expression. Taken together our results show that expression of LMP1 may regulate expression of CD44 and play an important role in the behavior of EBV‐based lymphomas. © 1995 Wiley‐Liss, Inc.