Molecular pathology of tumor metastasis III

Tı́már, József; Ladányi, Andrea; Peták, István; Jeney, A.; Kopper, László

doi:10.1007/bf03033715

Cited by 11 publications

(4 citation statements)

References 170 publications

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“…Recent advances in molecular cancer research have clarified a variety of therapeutic targets, some of which are being tested in clinical trials (10). Very recently, the relationship between tumor metastasis and MAPKs has been investigated (11,12).…”

Section: Mice Platelets Of P38␣mentioning

confidence: 99%

Involvement of p38α Mitogen-activated Protein Kinase in Lung Metastasis of Tumor Cells

Matsuo

Amano

Furuya

et al. 2006

Journal of Biological Chemistry

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To study the role of p38 mitogen-activated protein kinase (p38) activity during the process of metastasis, p38␣؉/؊ mice were subjected to an in vivo metastasis assay. The number of lung colonies of tumor cells intravenously injected in p38␣ ؉/؊ mice was markedly decreased compared with that in wild-type (WT) mice. On the other hand, the time-dependent increase in tumor volume after subcutaneous tumor cells transplantation was comparable between WT and p38␣ mice. Platelets of p38␣؉/؊ mice were poorly bound to tumor cells in vitro and in vivo compared with those of WT mice. Eand P-selectin mRNAs were markedly induced in the lung after intravenous injection of tumor cells. However, the induction of these selectin mRNAs in p38␣ ؉/؊ mice was weaker than that in WT mice. Furthermore, the resting expression levels of E-selectin in lung endothelial cells and P-selectin in platelets of p38␣

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Section: Mice Platelets Of P38␣mentioning

confidence: 99%

Involvement of p38α Mitogen-activated Protein Kinase in Lung Metastasis of Tumor Cells

Matsuo

Amano

Furuya

et al. 2006

Journal of Biological Chemistry

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“…Morphologic observations show tumor cells closely associated with platelets after vascular arrest (10,11). A variety of platelet factors contribute to this binding including the glycoproteins, integrin ␣ IIb ␤ 3 (12)(13)(14). P-selectin has also been shown to facilitate metastasis of tumor cells bearing P-selectin ligand (15).…”

Section: Introductionmentioning

confidence: 99%

Coagulation Facilitates Tumor Cell Spreading in the Pulmonary Vasculature during Early Metastatic Colony Formation

Im¹,

Fu²,

Wang³

et al. 2004

Cancer Research

266

210

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Coagulation has long been known to facilitate metastasis. To pinpoint the steps where coagulation might play a role in the metastasis, we used three-dimensional visualization of direct infusion of fluorescence labeled antibody to observe the interaction of tumor cells with platelets and fibrinogen in isolated lung preparations. Tumor cells arrested in the pulmonary vasculature were associated with a clot composed of both platelets and fibrin(ogen). Initially, the cells attached to the pulmonary vessels were rounded. Over the next 2 to 6 hours, they spread on the vessel surface. The associated clot was lysed coincident with tumor cell spreading. To assess the importance of clot formation, we inhibited coagulation with hirudin, a potent inhibitor of thrombin. The number of tumor cells initially arrested in the lung of hirudin-treated mice was essentially the same as in control mice. However, tumor cell spreading and subsequent retention of the tumor cells in the lung was markedly inhibited in the anticoagulated mice. These associations of the tumor cells with platelets were independent of tumor cell expression of P-selectin ligands. This work identifies tumor cell spreading onto the vascular surface as an important component of the metastatic cascade and implicates coagulation in this process.

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“…The answer is probably no; for cytotoxicity against a tumour cell, mostly higher drug doses are needed, than for the inhibition of endothelial cell production and vasculature proliferation [36]. Therefore, it seems to be a logical idea to combine cytotoxic and antiangiogenic agents.…”

Section: Anticancer Agents Of the Intercellular Spacementioning

confidence: 97%

Novel Agents in Anticancer Drug Therapy I (Antiangiogenic Agents, Egfr Inhibitors)

Eckhardt¹

2005

MCRO

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This report is the first part of an updated review of a previous survey published in this journal (2002,2,. Since the discovery of the Human Genome Project dramatically increased our knowledge in regard of the mutated cancer cell, it is worthy to follow up those findings, that have brought progress in the therapy of malignant diseases. The molecular targeted drug therapy with transtuzumab or imatinib produced great initial success and several other candidate agents are now available for cancer treatment.This review summarises the antitumour effect of compounds under clinical testing. In the extracellular space, antiangiogenic molecules inhibit the metastasis production. Anti-MMP-s currently investigated are listed, followed by drugs designed to block endothelial proliferation. Membrane receptor blockers, signal transduction inhibitors, DNA replication inactivators, revertants and apoptosis inducers act in the intracellular space. Amongst these, proteasome inhibitors are of particular interest.This part of the review deals only with antiangiogenic products and the membrane receptor inhibitors. All other agents will be reviewed in the next part of this publication.

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Molecular pathology of tumor metastasis III

Cited by 11 publications

References 170 publications

Involvement of p38α Mitogen-activated Protein Kinase in Lung Metastasis of Tumor Cells

Involvement of p38α Mitogen-activated Protein Kinase in Lung Metastasis of Tumor Cells

Coagulation Facilitates Tumor Cell Spreading in the Pulmonary Vasculature during Early Metastatic Colony Formation

Novel Agents in Anticancer Drug Therapy I (Antiangiogenic Agents, Egfr Inhibitors)

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