Effect of cisplatin on primary tumour growth and liver metastases in the M 5076 reticulum sarcoma: implication for new screening modalities

1993 ◽  
Vol 119 (6) ◽  
pp. 312-314
Author(s):  
Michael Schirner ◽  
Martin R. Schneider
Keyword(s):  
Liver Metastases ◽  
Tumour Growth ◽  
Primary Tumour ◽  
Primary Tumour Growth

CYCLO-OXYGENASE INHIBITION ATTENUATES ENDOTOXIN INDUCED PRIMARY TUMOUR GROWTH AND METASTASIS.

Shock ◽  
2002 ◽  
Vol 18 (Supplement) ◽  
pp. 22
Author(s):  
G Roche-Nagle ◽  
J H Harmey ◽  
R Casey ◽  
J Kelly ◽  
D Bouchier-Hayes
Keyword(s):  
Tumour Growth ◽  
Primary Tumour ◽  
Primary Tumour Growth

The α2β1 binding domain of chondroadherin inhibits breast cancer-induced bone metastases and impairs primary tumour growth: A preclinical study

2015 ◽  
Vol 358 (1) ◽  
pp. 67-75 ◽  
Author(s):  
Nadia Rucci ◽  
Mattia Capulli ◽  
Ole K. Olstad ◽  
Patrik Önnerfjord ◽  
Viveka Tillgren ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Bone Metastases ◽  
Tumour Growth ◽  
Primary Tumour ◽  
Preclinical Study ◽  
Binding Domain ◽  
Primary Tumour Growth

scholarly journals Genexol inhibits primary tumour growth and metastases in gemcitabine-resistant pancreatic ductal adenocarcinoma

HPB ◽  
2011 ◽  
Vol 13 (3) ◽  
pp. 153-157 ◽  
Author(s):  
Jill E. Shea ◽  
Kweon-Ho Nam ◽  
Natalya Rapoport ◽  
Courtney L. Scaife
Keyword(s):  
Pancreatic Ductal Adenocarcinoma ◽  
Tumour Growth ◽  
Primary Tumour ◽  
Ductal Adenocarcinoma ◽  
Primary Tumour Growth

Suppression of rat breast cancer metastasis and reduction of primary tumour growth by the small synthetic urokinase inhibitor WX-UK1

2005 ◽  
Vol 93 (04) ◽  
pp. 779-786 ◽  
Author(s):  
Buddy Setyono-Han ◽  
Jörg Stürzebecher ◽  
Wolfgang Schmalix ◽  
Bernd Muehlenweg ◽  
Anieta Sieuwerts ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumour Growth ◽  
Cancer Metastasis ◽  
Primary Tumour ◽  
Single Agent ◽  
Subcutaneous Administration ◽  
Axillary Lymph ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Primary Tumour Growth

SummaryThe serine protease uPA (urokinase-type plasminogen activator) and its receptor uPAR (CD87) are often elevated in malignant tumours, hence, inhibition of this tumour-associated plasminogen activation system provides an attractive target for therapeutic strategies. WX-UK1, a derivative of 3-aminophenylalanine in the L-conformation with inhibitory antiproteolytic properties, was tested for its specificity spectrum using specific chromogenic paranitroanilide peptide substrates. The corresponding D-enantiomer of WX-UK1 was used as a control. The anti-tumour and anti-metastatic (number of lung foci and weight of the axillary lymph nodes) properties were studied by subcutaneous administration of WX-UK1 to Brown Norwegian (BN) rats carrying orthotopically transplanted BN472 rat breast tumours. WX-UK1 selectively inhibited tumour-related proteases from rats and humans such as uPA, plasmin, or thrombin in the sub or low micromolar range. The activity was stereoselective as the D-enantiomer of WX-UK1 inhibited uPA and plas-min at approximately 70-fold higher Ki values than the active L-form. Chronical administration of the L-enantiomer of WXUK1 impaired primary tumour growth and metastasis of BN472 rat breast cancer in a dose-dependent manner. The minimum inhibitory dosage with maximal effect was between 0.15 and 0.3 mg/kg/day. The inactive D-enatiomer of WX-UK1 was not active in this respect. Daily treatment with WX-UK1 for up to 35 days was well tolerated as judged by the unchanged body and organ weight development. In conclusion, our results provide evidence that WX-UK1 as a single agent inhibits breast tumour growth and metastasis in vivo, and thus is a promising candidate drug to treat human cancer.

scholarly journals A mathematical model of tumour self-seeding reveals secondary metastatic deposits as drivers of primary tumour growth

2013 ◽  
Vol 10 (82) ◽  
pp. 20130011 ◽  
Author(s):  
Jacob G. Scott ◽  
David Basanta ◽  
Alexander R. A. Anderson ◽  
Philip Gerlee
Keyword(s):  
Mathematical Model ◽  
Tumour Growth ◽  
Experimental Validation ◽  
Primary Tumour ◽  
Accelerate Growth ◽  
Secondary Tissue ◽  
Circulating Tumour Cell ◽  
Capillary Bed ◽  
Metastatic Process ◽  
Primary Tumour Growth

Two models of circulating tumour cell (CTC) dynamics have been proposed to explain the phenomenon of tumour ‘self-seeding’, whereby CTCs repopulate the primary tumour and accelerate growth: primary seeding, where cells from a primary tumour shed into the vasculature and return back to the primary themselves; and secondary seeding, where cells from the primary first metastasize into a secondary tissue and form microscopic secondary deposits, which then shed cells into the vasculature returning to the primary. These two models are difficult to distinguish experimentally, yet the differences between them is of great importance to both our understanding of the metastatic process and also for designing methods of intervention. Therefore, we developed a mathematical model to test the relative likelihood of these two phenomena in the subset of tumours whose shed CTCs first encounter the lung capillary bed, and show that secondary seeding is several orders of magnitude more likely than primary seeding. We suggest how this difference could affect tumour evolution, progression and therapy, and propose several possible methods of experimental validation.

scholarly journals Primary tumour growth in an orthotopic osteosarcoma mouse model is not influenced by analgesic treatment with buprenorphine and meloxicam

2015 ◽  
Vol 49 (4) ◽  
pp. 284-293 ◽  
Author(s):  
K Husmann ◽  
M J E Arlt ◽  
P Jirkof ◽  
M Arras ◽  
W Born ◽  
...  
Keyword(s):  
Mouse Model ◽  
Tumour Growth ◽  
Primary Tumour ◽  
Analgesic Treatment ◽  
Primary Tumour Growth

scholarly journals Differential roles of the Drosophila EMT-inducing transcription factors Snail and Serpent in driving primary tumour growth

PLoS Genetics ◽  
2018 ◽  
Vol 14 (2) ◽  
pp. e1007167 ◽  
Author(s):  
Kyra Campbell ◽  
Gaëlle Lebreton ◽  
Xavier Franch-Marro ◽  
Jordi Casanova
Keyword(s):  
Transcription Factors ◽  
Tumour Growth ◽  
Primary Tumour ◽  
Primary Tumour Growth
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