bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prognosis following locally recurrent soft‐tissue sarcoma. A staging system based on primary and recurrent tumour characteristics
Authors: Choong Peter F. M. , Gustafson Pelle , Willén Helena , Åkerman Måns. , Baldetorp Bo , Fernö Mårten , Alvegård Thor , Rydholm Anders 
Published: February 2007

AbstractWe have shown that the clinical growth rate of local recurrence from soft‐tissue sarcoma could be expressed as a growthrate index (GRI) which was predictive for metastasis, and which was able to identify 2 equal populations of good (80% 2‐year MFS) and poor survivors (33%). We now report the associations between characteristics of the primary and GRI, and combine primary and locally recurrent tumour characteristics in a staging system. We studied 460 adult patients with soft‐tissue sarcomas of the extremities and trunk wall who were diagnosed and treated between 1964 and 1990, of whom 134 developed local recurrences and 151 metastases. The association of primary tumour size, histologic malignancy grade, depth, spontaneous necrosis, intratumoral vascular invasion and S‐phase fraction with local recurrence, GRI and metastasis were examined. High GRI was associated with primary tumours that were larger, deeper, more malignant, underwent spontaneous tumour necrosis, demonstrated intravascular invasion and had a higher S‐phase fraction. The same factors were also strongly associated with the incidence of metastasis. A multivariate analysis found GRI and primary tumour necrosis to be the strongest and most significant prognostic factors. GRI and tumour necrosis were combined in a staging system that identified groups with good survival (79 to 94% 2‐year MFS), intermediate survival (61% 2‐year MFS) and exceptionally poor survival (6% 2‐year MFS). These findings validate our earlier assertion that high GRI reflects highly malignant tumours. A staging system composed of primary tumour necrosis and GRI can identify patients who may be suitable candidates for trials of adjuvant chemotherapy. © 1995 Wiley‐Liss, Inc.
The expression profile of alternatively spliced neuronal c‐src RNA distinguishes between human tumours of the sympatho‐adrenal lineage
Authors: Örtoft Eva , Bjelfman Catarina , Hedborg Fredrik , Grimelius Lars , Påhlman Svcn 
Published: February 2007

AbstractHuman neuronal and neuroendocrine tumour specimens and cell lines were analysed regarding proteins and transcripts coded by the proto‐oncogene c‐src. At the protein level, most of the neuroblastomas and phaeochromocytomas expressed the neuronal c‐src form, pp60c‐srcN. None of the other neuroendocrine tumours, i.e. paragangliomas, neuroendocrine pancreatic tumours, or carcinoid tumours and small‐cell lung carcinomas of different types, appeared to express the neuronal form. In the brain, c‐src is transcribed into 3 differently spliced mRNA variants, c‐src, c‐srcNI, and c‐srcNI + Nll. The expression of these transcripts was analysed by PCR amplification of fragments covering the mini‐exons Nl and Nll of the corresponding cDNAs. The PCR products were analysed by Southern hybridization and characterized by determination of their sequences. Neuroblastomas, paragangliomas, retinoblastomas and the phaeochromocytomas expressed neuronal c‐src splice variants. However, whereas neuroblastomas and retinoblastomas contained all 3 transcripts, the phaeochromocytomas and paragangliomas expressed, with 2 exceptions, only the c‐src and the c‐srcNI + Nll mRNA species. To assess whether neuroblastomas display adrenal chromaffin characteristics, they were analysed regarding expression of the chromaffin marker enzyme, phenylethanolamine‐N‐methyl transferase. Whereas phaeochromocytomas were positive, all neuroblastomas were immunochemically negative for this enzyme. These results and the c‐src expression profile suggest that neuroblastomas, including those with an adrenal location, do not originate from the adrenal chromaffin differentiation lineage. The data further suggest neuronal c‐srcNI mRNA as a marker for sympathetic neuronal cells of the sympatho‐adrenal lineage. © 1995 Wiley‐Liss, Inc.
Chromosome abnormalities in benign hyperproliferative disorders of epithelial and stromal breast tissue
Authors: Dietrich Claudia U. , Pandis Nikos , Teixeira Manuel R. , Bardi Georgia , Gerdes Anne‐Marie , Andersen Johan A. , Heim Sverre 
Published: February 2007

AbstractCytogenetic analysis of short‐term cultures from 15 cases of benign proliferative breast disease (PBD), 10 diffuse PBD and 5 papillomas, and 15 fibroadenomas of the breast revealed clonal chromosome abnormalities in 7 diffuse PBD lesions, 4 papillomas and 5 fibroadenomas. The remaining 14 cases had a normal female chromosome complement. Cytogenetically unrelated abnormal clones were seen in 4 fibroadenomas and 2 PBDs. A single abnormal clone was found in 9 PBDs and I fibroadenoma. Three clonal abnormalities were seen as recurrent changes in 6 cases, namely interstitial deletions of 3p with 3p 12–14 as the minimally common deleted segment (in I papilloma, I diffuse PBD with atypia and I mixed‐pattern lesion with both papilloma and atypical diffuse PBD features), r(9)(p24q34) (in I diffuse PBD and I fibroadenoma), and del(l)(q12) (again in I diffuse PBD and I fibroadenoma). Intriguingly, 6 of the 16 abnormal cases had chromosome changes that have been seen repeatedly as primary abnormalities in breast carcinomas: der(16)t(l;16)(q10;p10), del(3)(p12p14), and del(l)(q12). We conclude that some of the chromosome anomalies frequently found in breast carcinomas are also present in PBD and fibroadenomas. These aberrations may be accepted as early, neoplasia‐relevant mutations. However, they do not seem to be sufficient by themselves to unleash a malignant process. © 1995 Wiley‐Liss, Inc.
nmb, a novel gene, is expressed in low‐metastatic human melanoma cell lines and xenografts
Authors: Weterman Marian A. J. , Ajubi Nasser , van Dinter Irma M. R. , Degen Winfried G. J. , van Muijen Goos N. P. , Ruiter Dirk J. , Bloemers Henri P. J. 
Published: February 2007

AbstractFrom a subtractive cDNA library, we isolated several cDNA clones which showed differential expression between highly and lowly metastatic human melanoma cell lines. One clone, designated nmb, showed preferential expression in the low‐meta‐static cell lines and was chosen for further characterization. Sequence analysis revealed that this clone represents a novel gene, encoding a putative transmembrane glycoprotein which showed the highest homology to the precursor of pMEL17, a melanocyte‐specific protein. nmb RNA expression was absent in most tumor‐cell lines tested and not restricted to the melanocytic lineage. Transfection of a partial nmb cDNA into a highly metastatic melanoma cell line (BLM) resulted, in 2 of 3 transfectants, in slower subcutaneous tumor growth and, in 1 of 3 transfectants, in reduction of the potential for spontaneous metastasis in nude mice. © 1995 Wiley‐Liss, Inc.
Reverse‐zymographic analysis of protease nexin‐II/amyloid β protein precursor of human carcinoma cell lines, with special reference to the grade of differentiation and metastatic phenotype
Authors: Kataoka Hiroaki , Seguchi Kohji , Iwamura Takeshi , Moriyama Takuzou , Nabeshima Kazuki , Koono Masashi 
Published: February 2007

AbstractTrypsin inhibitors in serum‐free conditioned media (SFCM) of various human carcinoma cell lines were analyzed by reverse zymography. Most of the cells secreted high‐molecular‐weight trypsin inhibitors (HMTI) larger than 100 kDa. The cell lines of colorectal carcinoma origin had a tendency to secrete HMTI whose molecular weight was a little higher than that of the other cell lines. Analysis of SFCM of subclones with different histological differentiation and metastatic/invasive potentials derived from a single pancreatic carcinoma cell line SUIT‐2 showed that the HMTI activity in SFCM was correlated to the degree of histological differentiation in vivo and tended to be inversely correlated to their metastatic/invasive capabilities. Immunoblotting analysis revealed that these HMTI were protease nexin‐ll/amyloid β protein precursors (PN‐II/APP). Semi‐quantificative reverse‐transcriptase/polymerase‐chain reaction study for PN‐II/APP mRNAs suggested that the differences in PN‐II/APP activities in SFCM between the subclones might be post‐transcriptional or post‐secretional events. In addition, SFCM of a highly metastatic subclone contained 43‐kDa protein which reacted to anti‐APP monoclonal antibody (MAb) suggesting that the subclone may have APP‐degrading activity. © 1995 Wiley‐Liss, Inc.
Inhibition of aberrant crypt growth by non‐steroidal anti‐inflammatory agents and differentiation agents in the rat colon
Authors: Wargovich Michael J. , Chen Chi Dai , Harris Charles , Yang Eileen , Velasco Marco 
Published: February 2007

AbstractAberrant crypts are aggregates of single to multiple colonic crypts evidencing hallmarks of dysplasia and may be the earliest detectable pathological lesions for colon cancer. The aberrant crypt assay has been developed in 2 protocols. In one, putative chemoprevention agents are tested for inhibitory effects when administered concomitantly with a carcinogen. In the other, the objective of this study, aberrant crypts were induced in F344 rats by parenteral injection of the colon carcinogen azoxymeth‐ane (AOM) and allowed to develop for 4 weeks, when an average of 90‐100 aberrant crypt foci per colon were found in the methylene blue‐stained colon. Then, during the second 4 weeks of the experiment, aberrant crypts were allowed to further develop to a frequency of > 150 foci per colon, a time when multi‐crypt foci were observed. During this time we tested the inhibitory effects of 4 analgesic drugs and 2 differentiation agents for effects of aberrant crypt growth and development. We found the non‐steroidal anti‐inflammatory drugs piroxicam, aspirin and ibuprofen, but not acetaminophen, to be effective in suppressing aberrant crypt formation or the progression to foci of multiple aberrant crypts. Treatment with chemo‐suppressing agents 13‐cis‐retinoic acid (13‐cRA) and 4‐hydroxy‐phenretinamide (4‐HPR), known differentiating agents, however, did suppress expansion of aberrant crypt foci, with 13‐cRA being the much more potent agent.
Catechol interferes with TGF‐β‐induced elimination of transformed cells by normal cells: Implications for the survival of transformed cells during carcinogenesis
Authors: Schaefer Dirk , M. Jürgensmeier Juliane , Bauer Gcorg 
Published: February 2007

AbstractWe have recently shown that TGF‐β‐treated normal fibroblasts are able to induce apoptosis of transformed fibroblasts, leading to their elimination. Here we describe a test system that allows the quantitative analysis of the elimination of G418‐resistant transformed cells by TGF‐β‐treated normal cells. This assay system was used to screen for substances that interfere with the elimination of transformed cells. Catechol and hydro‐quinone, but not resorcinol, were found to represent potent antagonists of TGF‐β‐induced elimination of transformed cells by normal cells. Protection of transformed cells from negative effects derived from their cellular environment defines a hitherto unrecognized crucial mechanism for the survival of transformed cells. The protective effect of catechol as seen in this experimental system may act in concert with its co‐carcinogenic and promoting activities during carcinogenesis.
Tumor‐promoting activity of 2,4‐dinitrofluorobenzene
Authors: Maldve Rcgina E. , Fischer Susan M. 
Published: February 2007

AbstractThe aim of this study was to determine whether the skin‐sensitizing agent 2,4‐dinitrofluorobenzene (DNFB) would elicit the same morphological and biochemical events that are characteristic of 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA). While single applications of 0.1% or 0.2% DNFB produced only mild epidermal hyperplasia, multiple applications produced pronounced hyperplasia. Compared with TPA, a single application of DNFB produced small increases in ODC activity, although a second DNFB treatment produced a greater response. Both DNFB and TPA caused marked induction of ODC, c‐fos and c‐jun mRNA. Vascular permeability increased significantly in response to DNFB, such that after 15 hr the response was quantitatively the same as for TPA. Repeated TPA produced the same response as a single application, but repeated DNFB resulted in a response that was half that of TPA. In contrast to TPA, DNFB failed to activate partially purified protein kinase C (PKC), although it did cause transient down‐regulation of activity 15 hr after treatment. The ability of DNFB to induce ODC activity, however, was unaffected by prior down‐regulation of PKC. DNFB was also shown to promote tumors in initiated SSIN mice. Twice‐weekly applications of 0.1 % or 0.2% DNFB resulted in approximately 65% and 85% of the mice developing an average of 2.0 or 3.2 tumors each, respectively. These results demonstrate that DNFB elicits many of the same changes as TPA and that it does so in a PKC‐independent manner.
Induction of ICAM‐1 and LFA‐3 by Tax1 of human T‐cell leukemia virus type 1 and mechanism of down‐regulation of ICAM‐1 or LFA‐1 in adult‐T‐cell‐leukemia cell lines
Authors: Tanaka Yoshikazu , Fukudome Kenji , Hayashi Masahito , Takagi Shin , Yoshie Osamu 
Published: February 2007

AbstractThe present study was undertaken to determine the role of HTLV‐I TaxI in the up‐regulation of ICAM‐1 and LFA‐3 in human T cells transformed with HTLV‐I and the mechanism of down‐regulation of ICAM‐1 and LFA‐I in ATL‐derived cell lines. Induction of Taxl in a human T‐cell line Jurkat carrying the Taxi gene under the metallothionein promoter led to increases in mRNA and surface expression of ICAM‐1. The response of LFA‐3 to Taxl induction was, on the other hand, relatively slow and weak, and might be indirect. Transactivation of the ICAM‐1 promoter by Taxl was further shown by co‐transfection of a CAT reporter construct with the ICAM‐1 promoter and a plasmid expressing Taxl. The mechanism of down‐regulation of ICAM‐1 or LFA‐1 in 4 ATL cell lines was next examined. ICAM‐1 mRNA was quite low in MT‐1, but no genomic changes were found. The CAT reporter with the ICAM‐1 promoter was inactive in MT‐1. Finally, combined treatment of MT‐1 with 5‐azacytidine and IFN‐γ induced re‐expression of ICAM‐1. Collectively, (a) transcriptional factor(s) necessary for expression of ICAM‐1 gene may be repressed in MT‐1 through DNA methylation. Three other ATL cell lines (TL‐Oml, H582, HuT 102) were found to have little mRNA for the LFA‐1 β chain (CD 18). H582 and HuT 102 were also negative for the LFA‐1 α chain (CDI la) mRNA. No genomic changes were found, and a CAT reporter gene with the CD 18 promoter was inactive in the 3 of them, again suggesting lack of (a) transcriptional factor(s) necessary for CD 18 expression.
Decreased macrophage‐mediated cytotoxicity in mammary‐tumor‐bearing mice is related to alteration of nitric‐oxide production and/or release
Authors: Sotomayor Eduardo M. , Dinapoli Michael R. , Calderón Cesar , Colsky Arthur , Fu Yang‐Xin , Lopez Diana M. 
Published: February 2007

AbstractPeritoneal‐exudate macrophages (PEM) from mammarytumor‐bearing mice have impaired cytotoxic activity against syngeneic and allogeneic tumor targets. The ability of PEM from normal and tumor‐bearing mice to bind tumor targets was found to be similar in the presence or the absence of surrogate receptors, which enhanced the binding but not the killing of tumor targets by PEM from tumor‐bearing mice, suggesting that other mechanisms are involved in their impaired cytolytic activity. Soluble and membrane‐bound TNF‐α, as well as H2O2, were found in higher amounts in PEM from tumor bearers upon stimulation with LPS, as compared with PEM from normal mice. However, tumor‐bearers' macrophages displayed decreased capacity to produce and/or release nitric oxide, which could be reversed by the addition of increasing levels of IFN‐γ. These results indicate that the lack of macrophage cytotoxicity in mammary‐tumor‐bearing mice is related to impaired production and/or release of NO by these effector cells, possibly aggravated by the insufficient IFN‐γ production previously reported in these animals. Moreover, mammary‐tumor progression results in dis‐regulation of synthesis of macrophage‐mediators, with over‐production of molecules to which mammary‐tumor cells are insensitive and deficient production of NO, the crucial molecule to which these cells appear to be highly sensitive.
Clinical characteristics of metachronous colorectal tumors
Authors: Rennert G. , Robinson E. , Rennert H. S. , Neugut A. I. 
Published: February 2007

AbstractA cancerregistrybased study was conducted to investigate the survival patterns associated with metachronous colorectal tumors and to compare the survival of patients with single and metachronous colorectal tumors. The study included all 1,396 White patients with metachronous colorectal tumors diagnosed among 143,283 patients with primary colorectal tumors reported between 1973‐1986 to the SEER program. The influence on survival of age at diagnosis, site of tumor and stage was evaluated by means of multivariate survival analysis, using Cox Proportional Hazards Models. Metachronous tumors developed more often following leftcolon tumors. Stage distribution of the second tumors was better than that of single tumors but 47% of the second tumors were discovered in regionallyadvanced or distantmetastatic stages. Survival from the second tumor diagnosed in the rectum was worse than that of a single tumor in the same stage and site. Only the stage of the second tumor was found to influence survival from metachronous tumors. The relatively high rate of diagnosis of advanced second colorectal tumors may reflect either improper followup after the diagnosis of the first tumor, or more aggressive biological characteristics of the second tumors. © 1995 Wiley‐Liss, Inc.
Possible significance of VLA‐4 (α β1) for hematogenous metastasis of renal‐cell cancer
Authors: Tomita Yoshihiko , Saito Toshihiro , Saito Kazuhide , Oite Takashi , Shimizu Fujio , Sato Shotaro 
Published: February 2007

AbstractVery late antigen‐4 (VLA‐4) composed of α and β, a member of the β ‐integrin subfamily, facilitates cell‐to‐cell interaction with vascular celladhesion molecule‐1 (VCAM‐1) on endothelial cells (EC). Attachment of bloodborne tumor cells to EC is a crucial step for hematogenous metastasis, and VLA‐4‐positive tumor cells can attach to EC by binding to VCAM‐1. Renalcell cancer (RCC) reveals proportionally greater percentages of metastases than other carcinomas at initial diagnosis. We investigated whether VLA‐4 is expressed on RCC, and how such expression on RCC correlates with the metastatic potential of RCC. Immunohistochemical staining on 66 primary and 4 metastatic RCC showed that 4 out of 4 metastatic and 5 out of 8 primary RCC from patients with lung and /or brain metastases expressed α4 and β1 chains. On the other hand, 13 of 58 RCC without metastases expressed α4 chain. α4 and β expressions were also detected on 5 out of 5 human RCC cell lines, ACHN,KRC/Y, A498, Caki1 and Caki2, by flowcytometric analysis. Reversetranscriptasepolymerasechainreaction (RT‐PCR), followed by Southernblot hybridization with cDNA probe for a α4 chain, also confirmed mRNA production in 4 out of 5 RCC cell lines. Furthermore, adhesion of α4‐positive RCC cell lines to human umbilicalvein endothelial cells (HUVEC) was augmented by treatment of HUVEC with tumor necrosis factor‐α (TNF‐α). This adhesion was inhibited by anti‐α4 or anti‐VCAM‐1 antibodies, suggesting that VLA‐4‐VCAM‐1 interaction was involved in the adhesion between RCC cells and HUVEC. Taken together, VLA‐4 on RCC cells might play a crucial role in their hematogenous metastasis. © 1995 Wiley‐Liss. Inc.
Purification and characterization of a new 85‐kDa glycoprotein antigen from human breast tumor
Authors: Pal Saumitra , Sanyal Utpal , Chattopadhyay Utpala 
Published: February 2007

AbstractA new breasttumorassociated antigen (BTAA) was purified and partially characterized from human breast tumor. By DEAE‐cellulose discontinuous NaCl‐gradient chromatography of a crude extract of human malignant breast tumor, 3 major protein peaks were obtained. Circulating antibodies against one of the protein peaks, HF1, was observed in breastcancer patients. The antibodies were absent in patients with carcinoma of the uterine cervix, lung, stomach and liver or with benign breast diseases and in healthy women. Absorption of the sera of breastcancer patients with normal human breast tissue pellet did not remove the HF1‐reactive circulating antibodies. The BTAA was partially purified from HF1 by subjecting the fraction to SDS‐PAGE and eluting the band 3 (HF1‐3). Westernblot analysis confirmed the presence of the BTAA in HF1‐3. Using an affinity column of protein‐A‐Sepharosebound IgG, purified from breastcancer patients' sera, the BTAA was also recovered from HF1. Purification of the BTAA was achieved by subjecting HF1 to sizeexclusion highperformance liquid chromatography (SE‐HPLC). The antigen was characterized as a glycoprotein with MW of approximately 85 kDa and appeared not to be related either to murine mammarytumor virus (MuMTV) structural antigens or to human fetal antigens. The BTAA‐reactive circulating antibodies in the breastcancer patients were of lgG2 subtype, and the level of these antibodies significantly decreased in patients following surgical removal of the breast tumors. © 1995 Wiley‐Liss, Inc.
Interleukin 2 receptor expression and interleukin 2 localisation in human solid tumour cells in situ and in vitro: Evidence for a direct role in the regulation of tumour cell proliferation
Authors: McMillan D. N. , Kernohan N. M. , Flett M. E. , Heys S. D. , Deehan D. J. , Sewell H. F. , Walker F. , Eremin O. 
Published: February 2007

AbstractFrozen sections of 52 human solid tumours (38 malignant and 14 benign) of varied histogenesis were immunohistochemically stained with well characterised monoclonal antibodies (MAbs) to human interleukin 2 (IL‐2) and the α and β chains of its receptor (R). In all malignant specimens, the tumour cells expressed the IL‐2R β subunit (p75) but not the IL‐2R α subunit (CD25). In 36 of 38 malignant tumours examined, there was conspicuous staining for IL‐2 in the tumour cell nuclei/nucleoli and perinuclear cytoplasm. In the human solid tumour cell lines G361 (melanoma), A549 (lung), MCF‐7 (breast) and WiDR (colorectal), both subunits of the IL‐2R appeared to be expressed, although the α subunit only weakly. Exogenous addition of human recombinant (r) interleukin 2 altered cell numbers in 3 of the 4 cell lines (WiDR was refractory). When grown in the absence of exogenously added rIL‐2, IL‐2 staining was observed in all cell lines. The pattern of distribution was similar to that exhibited by the tumour cells in situ (i.e., a nuclear/nucleolar localisation). In G361 melanoma cells, this IL‐2 staining was present in proliferating cells but disappeared as the cultures approached confluence. Addition of an IL‐2R β subunit blocking antibody to growing G361 cultures (grown in the absence of rIL‐2) resulted in a significant reduction in cell numbers. We propose, therefore, that the presence of immunoreactive IL‐2 and IL‐2R expression is characteristic of human malignant cells and that IL‐2 may play a role in the autocrine stimulation of proliferation of malignant cells, such as G361 melanoma cells. © 1995 Wiley‐Liss, Inc.