Invasion & metastasis最新文献_第8页

Treatment with modified heparins inhibits experimental metastasis formation and leads, in some animals, to long-term survival. 改良肝素治疗可抑制实验性转移的形成，并在一些动物中导致长期生存。

Invasion & metastasis Pub Date : 1996-01-01

T Sciumbata, P Caretto, P Pirovano, P Pozzi, P Cremonesi, G Galimberti, F Leoni, F Marcucci

{"title":"Treatment with modified heparins inhibits experimental metastasis formation and leads, in some animals, to long-term survival.","authors":"T Sciumbata, P Caretto, P Pirovano, P Pozzi, P Cremonesi, G Galimberti, F Leoni, F Marcucci","doi":"","DOIUrl":"","url":null,"abstract":"Two chemically modified heparins with low anticoagulant activity were studied in terms of their antimetastatic activity in the B16-BL6 melanoma model. The two heparins were a very low molecular weight heparin (VLMW-H) and a low molecular weight heparin with 100% succinylation of desulfated N groups (Succ100-LMW-H). Both heparins, VLMW-H more so than Succ100-LMW-H, were highly effective in decreasing the number of lung metastasis on day 21 when administered once subcutaneously 10 min before intravenous injection of melanoma cells or 2 times/week for 3 weeks. When the time of survival was measured, both heparins did not significantly prolong survival when administered once before injection of the tumor cells. When a repeated treatment schedule was adopted over 3 weeks, both heparins led to a slight, yet significant prolongation of survival. When the repeated treatment protocol was continued beyond 3 weeks, a highly significant prolongation of survival was observed with VLMW-H and there were some long-term survivors (20% for VLMW-H and 10% for Succ-LMW-H) that remained disease-free after discontinuation of therapy on day 90. The present results confirm and reinforce the concept that heparins with reduced anticoagulant activity may have interesting therapeutic applications in the prevention of tumor metastasis.","PeriodicalId":14452,"journal":{"name":"Invasion & metastasis","volume":"16 3","pages":"132-43"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20133258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Suppression of metastatic potential of high-metastatic Lewis lung carcinoma cells by vanadate, an inhibitor of tyrosine phosphatase, through inhibiting cell-substrate adhesion. 酪氨酸磷酸酶抑制剂钒酸盐通过抑制细胞-底物粘附抑制高转移性Lewis肺癌细胞的转移潜能。

Invasion & metastasis Pub Date : 1996-01-01

K Takenaga

{"title":"Suppression of metastatic potential of high-metastatic Lewis lung carcinoma cells by vanadate, an inhibitor of tyrosine phosphatase, through inhibiting cell-substrate adhesion.","authors":"K Takenaga","doi":"","DOIUrl":"","url":null,"abstract":"Treatment of high-metastatic Lewis lung carcinoma A11 cells with sodium orthovanadate, a phosphotyrosine phosphatase inhibitor, resulted in a dose- and time-dependent suppression of cell spreading on various extracellular matrix components such as Matrigel, fibronectin, laminin and type IV collagen, while the treatment did not significantly inhibit attachment of the cells to these substrates. Orthovanadate slightly and reversibly inhibited the in vitro cell growth of A11 cells, but the suppression of cell spreading was not directly due to the inhibition of cell growth. Orthovanadate-treated A11 cells showed reduced invasive ability in a reconstituted basement membrane invasion assay and experimental metastatic ability. Protein tyrosine phosphorylation level in A11 cells was elevated after treatment with orthovanadate. The increase in tyrosine phosphorylation level was partially diminished by the tyrosine kinase inhibitor ST638, concomitantly with restoration of the suppressed cell spreading as well as invasive and metastatic abilities. These results suggest that protein tyrosine phosphorylation influences invasive and metastatic potential of tumor cells possibly through regulating cell-substrate adhesion.","PeriodicalId":14452,"journal":{"name":"Invasion & metastasis","volume":"16 2","pages":"97-106"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19988048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Exposure to vinblastine modulates beta 1 integrin expression and in vitro binding to extracellular matrix molecules in a human renal carcinoma cell line. 长春花碱可调节人肾癌细胞系中β 1整合素的表达及其与细胞外基质分子的体外结合。

Invasion & metastasis Pub Date : 1996-01-01

S Duensing, F Brevis Nunez, N Meyer, G Anastassiou, A Nasarek, J Grosse, J Buer, M Probst, A Ganser, J Alzpodien

{"title":"Exposure to vinblastine modulates beta 1 integrin expression and in vitro binding to extracellular matrix molecules in a human renal carcinoma cell line.","authors":"S Duensing, F Brevis Nunez, N Meyer, G Anastassiou, A Nasarek, J Grosse, J Buer, M Probst, A Ganser, J Alzpodien","doi":"","DOIUrl":"","url":null,"abstract":"Solitary stroma-invading tumor cells expressing the ATP-binding cassette transporter P-glycoprotein have been reported to be associated with a significantly higher incidence of vessel invasion and lymph node metastases. In contrast to P-gp-mediated multidrug resistance (MDR) which has become well characterized over the last decade, little is known about further morphological and functional alterations in drug-resistant tumor cells. Binding of malignant cells to components of the extracellular matrix mediated by beta 1 integrins has been suggested to play a substantial role in the metastatic cascade. We studied alterations of beta 1 integrin expression and in vitro adhesiveness to extracellular matrix proteins of the human renal carcinoma line Caki-1 in comparison to the vinblastine resistant sublines Caki-1/V1 and Caki-1/V10 (cultured in the presence of 1 ng/ml and 10 ng/ml vinblastine, respectively). Both VLA-1 and VLA-2 receptors were acquired by the Caki-1/V10 subline, whereas untreated and Caki-1/VI cells lacked surface expression of these antigens. VLA-6 was found to be decreased in the vinblastine-resistant sublines. Attachment of drug-resistant Caki-1/V1 and Caki-1/V10 cells to collagen type I was significantly increased when compared to parental cells (p < or = 0.005). Significant differences in the attachment to type IV collagen were observed between Caki-1/V10 and untreated cells (p < or = 0.045). Both Caki-1/V1 and Caki-1/ V10 cells exhibited increased adhesion to fibronectin when compared to cells of the untreated line (p < or = 0.04). Whether an aberrant expression of beta 1 integrin receptors in resistant cells in combination with altered tumor cell adhesiveness is caused by MDR induction or whether it is an epiphenomenon of cytotoxic stress is unknown. Future studies will be needed to characterize the clinical relevance of MDR-associated changes in tumor cells.","PeriodicalId":14452,"journal":{"name":"Invasion & metastasis","volume":"16 2","pages":"65-72"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19989900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effects of alendronate and taxol on PC-3 ML cell bone metastases in SCID mice. 阿仑膦酸钠和紫杉醇对SCID小鼠pc - 3ml细胞骨转移的影响。

Invasion & metastasis Pub Date : 1996-01-01

M E Stearns, M Wang

{"title":"Effects of alendronate and taxol on PC-3 ML cell bone metastases in SCID mice.","authors":"M E Stearns, M Wang","doi":"","DOIUrl":"","url":null,"abstract":"The combined influence of alendronate, a bisphosphonate compound, and taxol on the establishment and growth of human PC-3 ML subclones injected intravenously via the tail vein in SCID mice was investigated. The pretreatment of SCID mice with alendronate (0.04-0.1 mg/kg twice weekly or 0.1 mg/kg weekly) partially blocked the establishment of bone metastases by human PC-3 ML cells and resulted in tumor formation in the peritoneum and other soft tissues. However, alendronate pretreatment of mice (0.1 mg/kg twice weekly or weekly) and dosing along with taxol (10-50 mg/kg/day, twice weekly, or weekly) blocked the growth of PC-3 ML tumors in the bone marrow and soft tissues in a statistically significant manner and improved survival rates significantly (p < 0.001) by 4-5 weeks. ELISAs and zymography of matrix metalloproteinase production in vitro and in vivo showed that alendronate and taxol alone partially inhibited metalloproteinase production, but that taxol in combination with alendronate totally blocked protease production and release. The combined activities of alendronate and taxol appeared to inhibit the establishment and growth of tumors in SCID mice, perhaps, in part, as a result of inhibition of protease production and release.","PeriodicalId":14452,"journal":{"name":"Invasion & metastasis","volume":"16 3","pages":"116-31"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20133257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Regulation of the steps of angiogenesis by human head and neck squamous cell carcinomas. 人头颈部鳞状细胞癌血管生成过程的调控。

Invasion & metastasis Pub Date : 1996-01-01

J Benefield, G J Petruzzelli, S Fowler, A Taitz, J Kalkanis, M R Young

{"title":"Regulation of the steps of angiogenesis by human head and neck squamous cell carcinomas.","authors":"J Benefield, G J Petruzzelli, S Fowler, A Taitz, J Kalkanis, M R Young","doi":"","DOIUrl":"","url":null,"abstract":"Human head and neck squamous cell carcinoma (HNSCC) cell cultures were established to identify the angiogenic factors they produced and how these factors contribute to two steps of the angiogenic process: endothelial cell proliferation and migration. The HNSCC cells secreted vascular endothelial cell growth factor (VEGF), transforming growth factor-beta (TGF-beta) and prostaglandin E2 (PGE2), but only low levels of basic fibroblast growth factor. Both proliferation-stimulatory and -inhibitory cytokines were produced by the HNSCC cells, with VEGF promoting endothelial cell proliferation, prostaglandins having no effect and TGF-beta downregulating proliferation. Two methods were used to measure endothelial cell migration: migration into a wound in the endothelial cell monolayer and migration across a filter into lower compartments. HNSCC cell supernatants stimulated endothelial cell migration in both migration models. VEGF had no effect on the motility of endothelial cells. However, when TGF-beta activity in the HNSCC supernatants was neutralized with antibody or the production of prostaglandins by HNSCC cells was blocked with indomethacin, the migration-stimulatory activity in the HNSCC cell supernatants was diminished. Adding authentic PGE2 or TGF-beta 1 to endothelial cells mimicked the migration-stimulatory activity of the HNSCC supernatants. Thus, HNSCC-derived VEGF is important in stimulating endothelial cell proliferation, while the antiproliferative effect of TGF-beta and the migration-stimulatory activity of TGF-beta and PGE2 suggest their having a role in the morphogenic processes of angiogenesis.","PeriodicalId":14452,"journal":{"name":"Invasion & metastasis","volume":"16 6","pages":"291-301"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20301704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

E-cadherin mRNA expression in breast carcinomas correlates with overall and disease-free survival. E-cadherin mRNA在乳腺癌中的表达与总生存率和无病生存率相关。

Invasion & metastasis Pub Date : 1996-01-01

N Guriec, L Marcellin, B Gairard, H Caldéroli, A Wilk, R Renaud, J P Bergerat, F Oberling

{"title":"E-cadherin mRNA expression in breast carcinomas correlates with overall and disease-free survival.","authors":"N Guriec, L Marcellin, B Gairard, H Caldéroli, A Wilk, R Renaud, J P Bergerat, F Oberling","doi":"","DOIUrl":"","url":null,"abstract":"E-cadherin (Epithelial-cadherin) is a subclass of the cadherin family that plays a major role in the maintenance of intercellular junctions in epithelial tissues. E-cadherin is also involved in the interactions between epithelial cells and T lymphocytes. In order to explore the relationship between E-cadherin expression, cancer invasion and metastases in vivo, we estimated its expression in normal breast specimens, fibroadenomas, cystic samples and primary breast carcinomas using a semiquantitative reverse transcription-polymerase chain reaction. The relationship between E-cadherin expression, survival and disease-free survival was also investigated. In comparison with normal breasts, 70% of the primary tumors showed reduced expression of E-cadherin suggesting that downregulation of this cell adhesion molecule is a common event in breast carcinoma. Significant correlation was found between E-cadherin expression and the histological classification. Most of the advanced tumors grades (10/13 tumors with grade III) presented decreased E-cadherin expression. No correlation was found between E-cadherin expression, estrogen and progesteron receptors, age and menopausal status at diagnosis. However, disease-free and overall survival was associated with E-cadherin expression. Patients showing poorly expressed E-cadherin in tumor tissue had a worse prognosis. The same results were observed for women without lymph node invasion or metastasis at diagnosis even when they were grouped according to their histological grade for statistical analysis. Therefore, E-cadherin mRNA expression in invasive breast carcinomas might be an early prognostic factor of metastasis.","PeriodicalId":14452,"journal":{"name":"Invasion & metastasis","volume":"16 1","pages":"19-26"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19799076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Micrometastases to the axilla in breast cancer: their size and season of presentation. 乳腺癌腋窝微转移:其大小和出现的季节。

Invasion & metastasis Pub Date : 1996-01-01

F Hartveit

引用次数: 0

Host response in tumor growth and progression. 肿瘤生长和进展中的宿主反应。

Invasion & metastasis Pub Date : 1996-01-01

S Michelson, J T Leith

{"title":"Host response in tumor growth and progression.","authors":"S Michelson, J T Leith","doi":"","DOIUrl":"","url":null,"abstract":"Tumor growth and progression result from complex controls that appear to be facilitated by the growth factors (GFs) which emerge from the tumor and find responsive targets both within the tumor and in the surrounding host. For example, basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) are both angiogenic signals which appear to emerge from upregulated genetic messages in the proliferating rim of a solid tumor in response to tumor-wide hypoxia. If these signals are generated in response to unfavorable environmental conditions, i.e. a tumor-wide decrease in oxygen tension, then the tumor may be playing a role in manipulating its own environment. Two questions are raised in this paper: (1) How does the host respond to such signals? (2) Is there a linkage between the host's response and the ultimate growth of the tumor? To answer these questions, we have idealized these adaptive signals within a mathematical model of tumor growth. The host response is characterized by a function which represents the host's carrying capacity for the tumor. If the function is constant, then environmental control is strictly limited to tumor shape and mitogenic signal processing. However, if we assume that the response of the local stroma to these signals is an increase in the host's ability to support an ever larger tumor, then the model describes a positive feedback controller. In this paper, we summarize our previous results and ask the question: What form of host response is reasonable, and how will it affect ultimate tumor growth? We examine some specific candidate response functions, and analyze them for system stability. In this model, unstable states correspond to 'infinite' tumor growth. We will also discuss countervailing negative feedback signals and their roles in maintaining tumor stability.","PeriodicalId":14452,"journal":{"name":"Invasion & metastasis","volume":"16 4-5","pages":"235-46"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20249796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mathematical models of prevascular spheroid development and catastrophe-theoretic description of rapid metastatic growth/tumor remission. 血管前球体发育的数学模型和快速转移性生长/肿瘤缓解的灾变理论描述。

Invasion & metastasis Pub Date : 1996-01-01

J A Adam

引用次数: 0

Gene amplification in Entamoeba histolytica. 溶组织内阿米巴的基因扩增。

Invasion & metastasis Pub Date : 1996-01-01

M Báez-Camargo, R Gharaibeh, A M Riverón, F de la Cruz Hernández, J P Luna, P Gariglio, P Chávez, E Orozco

{"title":"Gene amplification in Entamoeba histolytica.","authors":"M Báez-Camargo, R Gharaibeh, A M Riverón, F de la Cruz Hernández, J P Luna, P Gariglio, P Chávez, E Orozco","doi":"","DOIUrl":"","url":null,"abstract":"We show here data suggesting that Entamoeba histolytica, the protozoan responsible for human amebiasis, presents DNA amplification in a fashion similar to that described for transformed mammalian cells. By transmission electron microscopy (TEM), we found linear, circular and concentric circular DNA molecules exhibiting the main events of the unscheduled DNA amplification process. Loops were formed after the recombination of two nonadjacent DNA regions, and bubbles appeared from the recombinant strands without involving the looped-out sequences. Bubbles grew up and underwent further replication rounds to produce a nested set of partially replicated circles. Multicircle complexes were also formed from putative replication origin without recombination of distant DNA regions. Clones derived from the strain HM1:IMSS exhibited different DNA contents, suggesting DNA amplification. The parental clone A and its daughter clone C2 differed in rDNA gene copy numbers, but this was observed only when total DNA was separated by pulse field gel electrophoresis, and no significant differences were detected in nuclear DNA. The dissection of the events observed by TEM led us to propose an onion skin model for gene amplification in E. histolytica.","PeriodicalId":14452,"journal":{"name":"Invasion & metastasis","volume":"16 6","pages":"269-79"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20301702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0