bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differences in cell surface carbohydrates, and in laminin and fibronectin synthesis, between adherent and non‐adherent ehrlich ascites tumor cells
Authors: Song Zhiwei , Varani James , Goldstein Irwin J. 
Published: February 2007

AbstractDifferences in cell surface carbohydrates and in laminin and fibronectin synthesis between 2 Ehrlich ascites tumor (EAT) cell lines, the adherent and non‐adherent EAT cells, have been studied. The adherent EAT (a‐EAT) cells grow in monolayer in vitro in the presence of fetal bovine serum. The classical, or non‐adherent EAT (na‐EAT), cells grow in suspension in ascites form in the peritoneal cavity of mice, and they do not adhere when cultured in vitro. Both EAT cell lines express surface glycoproteins reactive with Maackia amurensis lectin (MAL) and Griffonia simplicifolia isolectin GS I‐B4. However, only a‐EAT cells react with elderberry (Sambucus nigra) bark lectin (SNA), suggesting that there are some differences in the sialylation of cell surface carbohydrate moieties between these 2 EAT cell lines. Removal of cell surface sialic acid by treating a‐EAT cells with Vibrio cholerae neuraminidase did not abolish the ability of these cells to adhere to laminin‐or fibronectin‐coated plates, indicating that the sialic acid of the cell surface glycoproteins is not essential for their adhesion to these extracellular matrices. Therefore, the difference in sialylation of cell surface glycoproteins is not responsible for the difference in cell adhesion between these 2 lines of EAT cells. Both EAT cell lines express detectable amounts of laminin but not fibronectin on their surfaces; they both secrete fibronectin and entactin into the medium. The na‐EAT cells (but not the a‐EAT cells) also secrete laminin A chain into the culture medium; however, no B chain was detected in the culture medium of either cell line. The laminin isolated from the cell surface of na‐EAT cells reacts with GS 1 and MAL lectins, but not with SNA, whereas the laminin isolated from a‐EAT cells reacts with SNA, as well as GS 1 and MAL.
Prognostic significance of cell DNA content in early‐stage ovarian cancer (figo stages I and II/A) by means of automatic image cytometry
Authors: Wagner T. M. U. , Adler A. , Sevelda P. , Assmann I. , Knepflé C. F. , Czerwenka K. , Heinzl H. , Ploem‐Zaaijer J. J. 
Published: February 2007

AbstractParaffin‐embedded material from 69 patients with epithelial ovarian cancer FIGO stages I and II/A (including 21 patients with borderline carcinoma) was studied with automatic DNA image cytometry. Univariate analysis indicated a significant difference in survival based on the presence of nuclei with high DNA content (higher than 5 C). A group of patients with less than 0.2% cells with high DNA content had a 6‐year survival of 87%, whereas in a group of patients with more than 0.2% of such cells, 6‐year survival was 49%. This parameter remained significant when used in a group of stage I/a and I/b patients. Statistical analysis of diploid vs. non‐diploid tumors also showed significant difference in survival. Separate analysis of 48 invasive ovarian cancers indicated that ploidy, the percentage of cells with high DNA content and tumor stage (stage I/a + b vs. stages I/c + II/a) reached significance for survival, whereas grading did not. In addition, comparison of clinical stage, grading, ploidy and the percentage of cells exceeding 5 C with a threshold at 0.2% by means of a murtivariate analysis (Cox regression model) showed that only the percentage of cells exceeding 5 C remained statistically significant.
The effect of ethnic differences on the pattern of HTLV‐I‐associated T‐cell leukemia/lymphoma (HATL) in the United States
Authors: Levine Paul H. , Manns Angela , Jaffe Elaine S. , Colclough Ginga , Cavallaro Ann , Reddy Gautham , Blattner William A. 
Published: February 2007

AbstractHuman T‐cell lymphotropic virus Type I (HTLV‐I) is the primary etiologic factor for adult T‐cell leukemia/lymphoma (ATL). Although HTLV‐I is endemic in japan and the Caribbean islands, the reported clinical and epidemiologic features of ATL in these 2 parts of the world are quite different. ATL has been diagnosed at a younger age and is reported more frequently as the lymphomatous type rather than the acute type with leukemia in the Caribbean basin as compared with the presentation in Japan. In order to characterize ATL in the United States, a registry has been established at the National Cancer Institute for the purpose of recording all cases originally diagnosed in the United States. This registry was utilized to examine the effect of ethnic differences on age of onset and clinical features of ATL, using the same data base. Clinical and laboratory information was obtained from 177 patients suspected of having ATL, who were treated at the National Institutes of Health, or had biological samples sent for evaluation, or were reported in the literature. Histopathologic review and virologic studies were performed by standardized methods. Of 177 patients registered, 127 were considered as having ATL, according to an algorithm combining clinical, pathologic and laboratory features. Presenting features in the confirmed cases consisted primarily of lymphadenopathy (76.6%), hypercalcemia (72.5%), leukemia (82%), skin involvement (48.2%) and hepatomegaly (53.6%). Patients of Japanese ancestry were generally older (median age 63, range 51 to 73 years) than patients of African‐American descent (median age 39, range 7 to 75 years) and presented more often with leukemia (90 vs. 69%). Of the 103 cases where country of birth was confirmed, 45 (43.7%) were born in the United States. The prognosis was generally poor (median survival 3.24 months), but rare longterm remissions were documented.
Human papillomavirus type 18 E6* MRNA in primary tumors and pelvic lymph nodes of hungarian patients with squamous cervical cancer
Authors: Czégledy J. , Evander M. , Hernádi Z. , Gergely L. , Wadell G. 
Published: February 2007

AbstractSeven biopsy specimens from squamous‐cell carcinomas of the uterine cervix were examined by RT‐PCR for human papilloma‐virus(HPV)‐specific transcripts. With our HPV18 transcription‐specific primer pair (5′ nts 127–149; 3′ nts 587–607), all 7 were shown to contain one strong viral mRNA signal from the early 6/early 7 open reading frames (E6/E7 ORFs). Sequence analysis of the cloned PCR product proved that the transcript was generated by splicing out an intron in E6 from nucleotides 233 to 416, thereby corresponding to the HPV18 E6* spliced mRNA. Nine out of 9 metastatic and 5 of 7 histologically negative lymph nodes from the same patients were also found to be positive for the same mRNA transcript. However, 4 HPV18 unrelated primary tumors and the connected regional pelvic lymph nodes (3 metastatic, 7 histologically negative) were negative for the HPV18 E6* mRNA. Cytokeratin signals indicating tumor cells of epithelial origin were detected in 7 out of the 9 transcript‐positive lymph nodes with histological signs of metastasis and in 2 out of the 5 transcript‐positive histologically negative lymph nodes. This suggests that the dispersion of the epithelial monoclonal tumor cells was lymphogenic in origin.
Risk excess of soft‐tissue sarcoma and thyroid cancer in a community exposed to airborne organochlorinated compound mixtures with a high hexachlorobenzene content
Authors: Grimalt Joan O. , Sunyer Jordi , Moreno Victor , Amaral Osvaldo C. , Sala María , Rosell Antoni , Anto Josep M. , Albaiges Joan 
Published: February 2007

AbstractUnusually high levels of hexachlorobenzene (HCB) were detected in the air and in sera of volunteers of a village located in the vicinity of an organochlorinated‐compounds factory (Flix, Catalonia, Spain). A significant increase for specific causes of death was obtained only for neoplasms of unknown origin. However, an excess of incident cases was observed for thyroid neoplasms, soft‐tissue sarcoma and brain neoplasms in men. These descriptive findings are in agreement with previously reported associations between soft‐tissue sarcoma and human exposure to organochlorinated compounds, as well as with animal experiments relating HCB and thyroid cancer, and add new information on the possible relation between organochlorinated compounds, and particularly HCB, and cancer.
Myeloproliferation in long‐term plasmacytoma‐regressor mice
Authors: Sagi‐Assif Orit , Douer Dan , Shaked Nili , Russell Stephen W. , Witz Isaac P. 
Published: February 2007

AbstractMOPC‐315 plasmacytoma‐bearing BALB/c mice were treated with high doses of melphalan, causing a permanent and complete regression of the tumor. In the present study we analyzed plasmacytoma‐regressor mice (PRM) 3–6 months after plasma‐cytoma regression. A second group of otherwise untreated normal mice was treated with melphalan (M—control group). A third group of mice remained untreated and served as an age‐and sex‐matched control group. PRM were cachectic and had an increased mortality rate compared to the M and the C control groups. Histopathological examination indicated that the spleen of PRM showed pronounced abnormalities, primarily in the red pulp. These abnormalities consisted of extramedullary hematopoiesis and myeloid‐granulocytic hyperplasia. Spleens of M mice showed similar abnormalities but to a much lesser extent. Flow cytometric analysis of cellular surface markers of PRM splenocytes indicated a high number of large MAC‐1‐and GR‐1‐positive cells compared to splenocytes of M or C controls. These large cells also expressed For receptors (FcτRII), stained positively with non‐specific esterase and adhered to plastic dishes; a certain percentage expressed MAC‐2 and MAC‐3 antigens. A quantitative suppression of CD4+ T cells and of B cells was also shown. Circulating levels of TNF were higher in PRM than in M or C mice. The capacity of splenocytes from PRM to secrete factors that stimulated CFU‐GM colony formation in soft agar by bone‐marrow cells from normal mice was significantly up‐regulated compared to that of splenocytes from M or C mice. PRM‐derived splenocytes also reacted significantly better to rIL‐3 and rGM‐CSF than splenocytes from M or C controls. We conclude that the splenic myeloproliferation in PRM was not caused by melphalan chemotherapy alone and is an abnormality related to the primary tumor, possibly in conjunction with chemotherapy. No evidence of a secondary overt malignancy was obtained.
Increased expression of the matrix metalloproteinase 2 in differentiating tera 2 human embryonal carcinoma cells
Authors: Tienari Jukka , Pertovaara Liisa , Saksela Olli , Lehtonen Eero , Vartio Tapio 
Published: February 2007

AbstractSecretion of proteolytic enzymes by cells has been implicated in tissue remodeling during embryonic development as well as in invasive neoplastic diseases. We studied the regulation of type‐IV‐collagenase activity in Tera 2 human embryonal carcinoma cells, which in the undifferentiated state proliferate rapidly and are tumorigenic. The undifferentiated cells produced relatively low levels of matrix‐metalloproteinase‐2 (MMP‐2) activity. This activity was not markedly affected by exogenous basic fibroblast growth factor (bFGF) or 12‐O‐tetradecanoyl‐phorbol‐13‐acetate (TPA), even though the plasminogen activator activity of the cells was increased by these agents. Tera 2 cells can be induced by retinoic acid to differentiate into quiescent cells, of which many express neuronal characteristics. The type‐IV‐collagenase activity of the cells increased markedly during the differentiation. This increase was mainly due to increased expression of MMP‐2. Expression of tissue inhibitors of metalloproteinases (TIMP‐1 and TIMP‐2) was not markedly affected by the differentiation of Tera 2 cells. The results show that in the Tera 2 cell system, increased expression of MMP‐2 is characteristic of the differentiated derivatives. This is in contrast with many other model systems, where increased type‐IV‐collagenase activity is associated with the malignant phenotype. This pattern of regulation may reflect the facts that Tera 2 cells resemble early embryonic cells and that their differentiation mimics related cell‐differentiation processes in the developing embryo.
Changes in perfusion of mouse tumours after photodynamic therapy
Authors: van Geel I. P. J. , Oppelaar H. , Oussoren Y. G. , Stewart F. A. 
Published: February 2007

AbstractThe influence of photodynamic therapy (PDT) on vascular perfusion was investigated in 2 s.c. mouse tumours, a radiation‐induced fibrosarcoma (RIFI) and a squamous‐cell carcinoma (SCCVII). The 86Rb extraction technique was used to measure changes in perfusion relative to cardiac output at various intervals after interstitial PDT. Control groups showed that vascular perfusion in the RIFI tumours decreased with increasing tumour size. For both tumours, of constant size, vascular perfusion decreased to less than 10% of control values within 5 min after high PDT doses. Significant decreases in vascular perfusion were also seen after lower, sub‐curative doses. Thereafter there was slow recovery towards control levels. Photofrin given at shorter intervals before illumination generally resulted in even larger decreases in tumour perfusion, and slower recovery. Comparison of tumour perfusion measurements after PDT with tumour response revealed an inverse correlation with tumour growth delay both for the RIFI and for the SCCVII tumours. PDT with sub‐curative light doses appears to decrease vascular perfusion in the RIFI and SCCVII for a period of at least 24 hr. The most severe reductions in tumour blood flow were associated with the longest regrowth delays, indicating a major role of vascular damage in tumour response to PDT.
Peptide‐antibody conjugates for tumour therapy: A MHC‐class‐II‐restricted tetanus toxin peptide coupled to an anti‐IG light chain antibody can induce cytotoxic lysis of a human B‐cell lymphoma by specific CD4 T cells
Authors: Yu Zhiwei , Healy Frank , Valmori Danila , Escobar Patricia , Corradin Giampietro , Mach Jean‐Pierre 
Published: February 2007

AbstractAnti‐idiotype antibody therapy of B‐cell lymphomas, despite numerous promising experimental and clinical studies, has so far met with limited success. Tailor‐made monoclonal anti‐idiotype antibodies have been injected into a large series of lymphoma patients, with a few impressive complete tumour remissions but a large majority of negative responses. The results presented here suggest that, by coupling to anti‐lymphoma idiotype antibodies a few molecules of the tetanus toxin universal epitope peptide P2 (830–843), one could markedly increase the efficiency of this therapy. We show that after 2‐hr incubation with conjugates consisting of the tetanus toxin peptide P2 coupled by an S‐S bridge to monoclonal antibodies directed to the X light chain of human immunoglobulin, human B‐lymphoma cells can be specifically lysed by a CD4 T‐lymphocyte clone specific for the P2 peptide. Antibody without peptide did not induce B‐cell killing by the CD4 T‐lymphocyte clone. The free cystein‐peptide was also able to induce lysis of the B‐lymphoma target by the T‐lymphocyte clone, but at a molar concentration 500 to 1000 times higher than that of the coupled peptide. Proliferation assays confirmed that the antibody‐peptide conjugate was antigenically active at a much lower concentration than the free peptide. They also showed that antibody‐peptide conjugates required an intact processing function of the B cell for peptide presentation, which could be selectively inhibited by leupeptin and chloroquine. It is reasonable to expect that, in vivo, the anti‐idiotype antibodies will selectively transport the tetanus toxin peptides to the B‐lymphoma cells, which will process the conjugates and present the peptides to the patients' CD4 T‐cell repertoire. Our tetanus‐toxoid‐vaccinated population has T cells specific for the immunogenic peptide and these, in principle, could be further expanded prior to injection of the conjugate.
Effects of nIFN β and rifn γ on growth and morphology of two human melanoma cell lines: Comparison between two‐and three‐dimensional culture
Authors: Görlach A. , Herter P. , Hentschel H. , Frosch P. J. , Acker H. 
Published: February 2007

AbstractWe compared the anti‐proliferative effects of natural inter‐feron β (nIFN β) and recombinant interferon γ (HFN γ) on 2 human melanoma cell lines, IGRI and SK‐Me128, grown in 2‐dimensional monolayer and in 3‐dimensional spheroid culture. In monolayer culture, growth of both lines was inhibited in a dose‐dependent manner by 5‐day treatments with IFN in concentrations ranging between I and 5,000 IU/ml. Incubations with 120 IU/ml nIFN βor 25 IU/ml rIFN γ led to a 50% growth inhibition of IGRI cells. A 50% growth inhibition of SK‐Me128 cells was obtained with 60 IU/ml nIFN β, whereas even 5,000 IU/ml rIFN γ inhibited the growth of this line by only 30%. Growing these melanoma cell lines in 3‐dimensional spheroid culture for 5 days reduced their sensitivity to interferon. Growth inhibition values of 50% were achieved with 3,000 IU/ml rIFN γ or 9,000 IU/ml nIFN β for IGRI spheroids and 10,000 IU/ml nIFN β for SK‐Me128 spheroids, while 10,000 IU/ml rIFN γ reduced the growth of SK‐Me128 spheroids by only 25%. Outgrowth tests showed that the proliferative capacity after 5‐day incubations with IFN was only reduced in IGRI spheroids treated with high doses of nIFN β. The macroscopically observed increased density of interferon‐treated spheroids could be confirmed by light microscopy as corresponding to reduced intercellular space in these spheroids. Scanning electron microscopy furthermore showed variations on the surface of IFN‐treated spheroids as well as in cellular organization and structures between cells, hinting at a possible involvement of extracellular matrix substances in the reaction to interferons. These findings show that the high anti‐proliferative sensitivity of the melanoma cell lines in monolayer culture could not be achieved in spheroid culture. The volume decreases seen in the presence of interferon might be, at least in part, due to an increased packing density in combination with changes in the cellular organization of interferon‐treated spheroids, rather than to direct antiproliferative effects.
Immunoselection of GRP94/endoplasmin from a KNRK cell‐specific λGTLL library using antibodies directed against a putative heparanase amino‐terminal peptide
Authors: de Vouoe Michael W. , Yamazaki Amy , Bennett Steffany A. L. , Chen Jia‐Hua , Shwed Philip S. , Couture Chantal , Birnboim H. Chaim 
Published: February 2007

AbstractInduction of an invasive phenotype by metastatic tumour cells results in part from inappropriate expression of extracellular matrix‐degrading enzymes normally involved in embryonic morphogenesis, tissue remodelling, angiogenesis and wound healing. Such enzymes include endoglycosidases that degrade heparan sulfate (HS) in endothelial basement membrane, as well as better characterized proteases. Heparanase, an endo‐β‐D‐glucuronidase initially detected in B16 melanoma cells, has been described as a Mr 96 000 glycoprotein with pl of 5.2, and has been immunolocalized to the cell surface and cytoplasm. We have utilized a polyacrylamide‐gel‐based HS degradation assay to demonstrate that KNRK, a rat kidney fibroblast cell line transformed by v‐K‐ras, exhibits HS‐degrading activity similar to that of B16F10 mouse melanoma cells. To immuno‐select heparanase‐expressing clones from a KNRK‐cell‐specific λgtII cDNA library, we have also prepared a rabbit anti‐serum directed against a putative amino‐terminal peptide of B16F10 cellular heparanase. Lysogens from one clone expressed a β‐galactosidase fusion protein whose staining with peptide anti‐serum was inhibited by competition with excess peptide. Dideoxy‐mediated sequencing of the insert termini of this reco.mbinant revealed that it represents a rat homologue of Mr94,000 glucose‐regulated protein (GRP94/endoplasmin), a molecular chaperone that contains the exact amino‐terminal sequence previously attributed to heparanase. Our results call into question the specificity of this peptide sequence, as well as previous immunolocalization studies of heparanase carried out using such anti‐sera.
Establishment of human oral‐cancer cell lines (KOSC‐2 and ‐3) carrying p53 and c‐myc abnormalities by geneticin treatment
Authors: Inagaki Toshiro , Matsuwari Satoshi , Takahashi Rei , Shimada Kei‐Kichi , Fujie Kimiko , Maeda Sakan 
Published: February 2007

AbstractTwo cultured cell lines derived from human squamous‐cell carcinomas were established through xenografted tumors in nude mice by „Geneticin”︁ treatment, which allows to eliminate contaminated mouse fibroblasts and obtain enriched tumor cells at the early stage of cultivation. Line KOSC‐2 and KOSC‐3 were each derived from a squamous‐cell carcinoma of the oral floor and of the lower gingiva, respectively. Both lines grew in a cobblestone pattern, demonstrating their epithelial heritage. Ciemsa‐banding patterns by chromosome analysis confirmed that both lines are of human origin. Molecular analysis of cancer‐related genes, including the Ha‐ras, c‐myc and p53 genes, was performed. KOSC‐3 cells showed co‐over‐expression of p53 and c‐myc mRNA, in addition to p53 point mutation at codon 248 with transition from CGG to TGG. However, loss of heterozygosfty (LOH) on chromosome 17 was detected in both lines by Southern blotting. These cell lines provide a model for elucidating the mechanism involving p53 inactivation and c‐myc‐gene over‐expression.
Decreased reactivity to PPD among htlv‐i carriers in relation to virus and hematologic status
Authors: Welles Seth L. , Tachibana Nobuyoshi , Okayama Akihiko , Shioiri Shigemasa , Ishihara Shiro , Murai Koichi , Mueller Nancy E. 
Published: February 2007

AbstractData on human T‐cell lymphotropic‐virus‐type‐1 (HTLV‐I) status and hematology from 528 individuals were analyzed for associations with low reactivity to the purified protein derivative (PPD) of Mycobacterium tuberculosis recall antigen. Subjects were classified as HTLV‐I carriers with abnormal lymphocytes (Ably), carriers without Ably, and seronegatives. All carriers had a significant 2.6‐fold risk of being low responders to PPD compared with the seronegatives, carriers with Ably having the highest relative risk. Carriers with HTLV‐I‐antibody titer 1:256, or with other detectable markers of virus status such as antibody to tax and proviral DNA, had increased risk for low response to PPD similar to the estimate for HTLV‐I seropositivity alone, compared with the seronegatives. Subjects with a low lymphocyte count had 3.5 times the risk for being low responders to PPD, compared with subjects with high counts. Similarly, subjects with a low monocyte count had 2.0 times the risk for low reactivity of those with a moderate to high count. Results were not confounded by age, sex, smoking or alcohol drinking. Using multiple logistic regression, only HTLV‐I seropositivity and low lymphocyte and monocyte counts were predictive of low reactivity to PPD. Analysis indicates that suppression of delayed‐type hypersensitivity is associated with HTLV‐I infection per se, and not with viral replication or load. Furthermore, this effect may occur in part via changes in the number and function of lymphocytes and monocytes. Such a mechanism may involve altered cytokine production in carriers and concomitant changes in cell populations involved in delayed‐type hypersensitivity.