scholarly journals Target discovery of acivicin in cancer cells elucidates its mechanism of growth inhibition

2015 ◽  
Vol 6 (1) ◽  
pp. 237-245 ◽  
Author(s):  
Johannes Kreuzer ◽  
Nina C. Bach ◽  
Daniel Forler ◽  
Stephan A. Sieber
Keyword(s):  
Cell Growth ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Mechanistic Explanation ◽  
Cancer Cell Growth ◽  
Target Discovery ◽  
Mechanism Of Growth

Using a chemical proteomic strategy we analyzed the targets of acivicin and provided a mechanistic explanation for its inhibition of cancer cell growth.

The Cephalostatins. 24. Isolation, Structure, and Cancer Cell Growth Inhibition of Cephalostatin 20

2015 ◽  
Vol 78 (6) ◽  
pp. 1446-1450 ◽  
Author(s):  
George R. Pettit ◽  
Jun-Ping Xu ◽  
Jean-Charles Chapuis ◽  
Noeleen Melody
Keyword(s):  
Cell Growth ◽  
Growth Inhibition ◽  
Cancer Cell ◽  
Cell Growth Inhibition ◽  
Cancer Cell Growth

Cancer-associated fibroblasts (CAFs) in thyroid papillary carcinoma: molecular networks and interactions

2021 ◽  
pp. jclinpath-2020-207357
Author(s):  
Jeehoon Ham ◽  
Bin Wang ◽  
Joseph William Po ◽  
Amandeep Singh ◽  
Navin Niles ◽  
...  
Keyword(s):  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Stromal Cells ◽  
Cancer Metastasis ◽  
Current Knowledge ◽  
Molecular Networks ◽  
Cancer Cell Growth ◽  
Molecular Events

In 1989, Stephen Paget proposed the ‘seed and soil’ theory of cancer metastasis. This theory has led to previous researchers focusing on the role of a tumour as a cancer seed and antiangiogenesis agents as cancer soil fumigant; for the latter to be effective, it is important for them to be able to distinguish cancer cells from stromal cells. However, antiangiogenesis agents have not produced dramatic survival benefits in vivo. This may be related to their inability to destroy the supporting stroma that promote cancer cell growth. Therefore, in order to effectively arrest cancer cell growth for therapeutic purposes, a paradigm shift is required in our fundamental approach to decipher the molecular events and networks in the stromal environment that cancer cells can thrive and proliferate. The pathogenesis of cancer is a multidimensional process of pathological molecular and cellular pathways, influencing different stromal properties and achieving a mutually negotiated crosstalk between cancer cells and stromal cells. This review summarises the clinical presentation of current knowledge of classical papillary thyroid carcinoma (PTC), emerging molecular diagnostics and future directions of classical PTC research.

Fibrin and Cancer Cell Growth: Problems in the Evaluation of Experimental Models

1979 ◽  
Author(s):  
Andreina Poggi
Keyword(s):  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Primary Tumour ◽  
Antiplatelet Agent ◽  
Experimental Models ◽  
Surgical Removal ◽  
Antiinflammatory Drugs ◽  
Cancer Cell Growth ◽  
Lung Carcinoma Cells

Studies on the role of fibrin in experimental cancer growth should take into account the following problems: 1) during growth and dissemination of experimental tumours, haemostatic changes may occur which vary depending on the route of inoculation of cancer cells and on the tissue wherethe tumour grows. Thrombocytopenia, haemolytic microangiopathic anaemia and decreased survival of fibrinogen were observed during spontaneous dissemination to the lung of i.m. implanted Lewis Lung Carcinoma cells, not when metastatic growth occurred after surgical removal of the primary tumour or lung nodules developed following i.v. injection of the same cells. 2) Treatment of experimental tumours with drugs active on the haemostatic system may have different effects depending on the stage of growth of the tumour. This observation (which we have made with both warfarin and a defibrinating enzyme in murine metastasizing tumours) could suggest that fibrin may play different roles at different phases of cancer cell growth. 3) The supposed antiturooral activity of drugs active on the haemostatic system may be also influenced by other factors, such as a direct activity on cancer cells or on the host’s immune system or on blood supply to the tumour. As an example, non steroidal antiinflammatory drugs may act not only as antiplatelet agent but also as inhibitors of prostaglandin synthesis by cancer cells and some snake venoms may influence cancer cell growth not only through defibrination, but also with their iinnu-nodepressant properties. (Supported by Italian CNR and NIM. MCI, USA).

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