Transduction of the human deoxycytidine kinase gene in rodent tumor cells induces in vivo growth retardation in syngeneic hosts

2000 ◽  
Vol 156 (2) ◽  
pp. 151-157 ◽  
Author(s):  
K Kawamura
Keyword(s):  
Tumor Cells ◽  
Growth Retardation ◽  
Deoxycytidine Kinase ◽  
Kinase Gene ◽  
In Vivo Growth

scholarly journals The tumor dormant state. Comparison of L5178Y cells used to establish dormancy with those that emerge after its termination.

1979 ◽  
Vol 149 (3) ◽  
pp. 745-757 ◽  
Author(s):  
K J Weinhold ◽  
D A Miller ◽  
E F Wheelock
Keyword(s):  
Tumor Cells ◽  
Antigen Expression ◽  
Cell Subpopulation ◽  
Effector Cells ◽  
Dormant State ◽  
Quantitative Absorption ◽  
Tumor Outgrowth ◽  
In Vivo Growth

The tumor dormant state established in L5178Y immunized and challenged mice is characterized by a prolonged period of clinical normalcy followed by rapid tumor outgrowth. The tumor cells which emerged after termination of the tumor dormant state had abnormal marker chromosomes identical to those in the L5178Y cells used in the original challenge inoculum, indicating that the emergent tumor cells were progeny of the challenge inoculum. Original and emergent L5178Y cells had equivalent in vivo growth rates, when inoculated into normal DBA/2 mice. The emergent L5178Y cells were less susceptible than original cells to in vitro lysis by tumor dormant PC. Original and emergent L5178Y cells expressed common tumor-associated target antigens for cytolytic effector cells. Both modulation and masking of these target antigens were ruled out as mechanisms for decreased susceptibility to cell-mediated cytolysis. Immunofluorescence revealed heterogeneity in tumor-associated antigen expression within both original and emergent cell populations, with a decreased intensity of staining in the emergent population. Both populations were equally susceptible to lysis by alloimmune cells, alloantiserum, and anti-Thy 1.2 serum, but emergent cells were less susceptible to lysis by serum directed against L5178Y TAA. Quantitative absorption revealed that the emergent L5178Y cells expressed eightfold less serologically detectable TAA than the original cells. These findings indicate that the host immune response developing during establishment of the tumor dormant state selects a stable tumor cell subpopulation which expresses decreased amounts of surface tumor-associated target antigens.

Enhanced in vivo growth and resistance to rejection of tumor cells expressing dominant negative IFNγ receptors

Immunity ◽  
1994 ◽  
Vol 1 (6) ◽  
pp. 447-456 ◽  
Author(s):  
Anand S. Dighe ◽  
Elizabeth Richards ◽  
Lloyd J. Old ◽  
Robert D. Schreiber
Keyword(s):  
Tumor Cells ◽  
Dominant Negative ◽  
In Vivo Growth

BRE enhances in vivo growth of tumor cells

2005 ◽  
Vol 326 (2) ◽  
pp. 268-273 ◽  
Author(s):  
Ben Chung-Lap Chan ◽  
Qing Li ◽  
Stephanie Ka-Yee Chow ◽  
Arthur Kar-Keung Ching ◽  
Choong Tsek Liew ◽  
...  
Keyword(s):  
Tumor Cells ◽  
In Vivo Growth ◽  
Growth Of Tumor

scholarly journals Repression of in vivo growth of Myc/Ras transformed tumor cells by Mad1

Oncogene ◽  
2002 ◽  
Vol 21 (3) ◽  
pp. 447-459 ◽  
Author(s):  
Christa Cerni ◽  
Barbara Skrzypek ◽  
Nikita Popov ◽  
Soleman Sasgary ◽  
Gerlinde Schmidt ◽  
...  
Keyword(s):  
Tumor Cells ◽  
In Vivo Growth

Growth of FasL-bearing tumor cells in syngeneic murine host induces apoptosis and toxicity in Fas+ organs

Blood ◽  
2000 ◽  
Vol 95 (6) ◽  
pp. 2111-2117 ◽  
Author(s):  
Ahmet Zeytun ◽  
Mitzi Nagarkatti ◽  
Prakash S. Nagarkatti
Keyword(s):  
Tumor Cells ◽  
Wild Type ◽  
Tissue Destruction ◽  
Tumor Bearing ◽  
Soluble Fasl ◽  
Minimal Damage ◽  
In Vivo Growth ◽  
High Level

Abstract In the current study, we investigated whether the growth of FasL-bearing tumor cells would induce apoptosis and toxicity in organs that express high level of Fas. Sera from C57BL/6 +/+(wild-type) mice injected with syngeneic FasL+ tumors, LSA, or EL-4, showed significantly higher levels of soluble FasL than that from the nontumor-bearing mice. Furthermore, the soluble FasL was functional inasmuch as the sera from tumor-bearing mice were able to induce apoptosis in Fas+ but not Fas−targets. Histopathologic studies and in situ TUNEL assay to detect apoptosis were carried out in C57BL/6 +/+(Fas+) or C57BL/6 lpr/lpr (Fas−) mice injected with syngeneic LSA and EL-4 tumor cells. The morphology of the liver and thymus from tumor bearing C57BL/6 +/+ mice showed marked damage and tissue destruction. In contrast, the liver and thymus from tumor-bearing C57BL/6 lpr/lpr mice showed minimal damage. Furthermore, the tumor-bearing C57BL/6 +/+, but not the C57BL/6 lpr/lpr, mice exhibited significant apoptosis in the liver and thymus. The FasL responsible for toxicity was tumor derived rather than host derived; tumor-bearing C57BL/6 gld/gld(FasL-defective) mice also exhibited significant apoptosis in the liver and thymus. Together, these data suggested that the in vivo growth of FasL-bearing tumor cells can induce significant apoptosis and toxicity in Fas+ tissues of the host. Such toxicity may be mediated by the soluble FasL produced by tumor cells.

scholarly journals Altered expression of a metformin-mediated radiation response in SA-NH and FSa tumor cells treated under in vitro and in vivo growth conditions

2017 ◽  
Vol 93 (7) ◽  
pp. 665-675 ◽  
Author(s):  
Jeffrey S. Murley ◽  
Richard C. Miller ◽  
Raziye Rana Senlik ◽  
Alfred W. Rademaker ◽  
David J. Grdina
Keyword(s):  
Tumor Cells ◽  
Growth Conditions ◽  
Radiation Response ◽  
Altered Expression ◽  
In Vivo Growth

Melatonin modifies tumor hypoxia and metabolism by inhibiting HIF-1α and energy metabolic pathway in the in vitro and in vivo models of breast cancer

2019 ◽  
Vol 2 (4) ◽  
pp. 83-98 ◽  
Author(s):  
André De Lima Mota ◽  
Bruna Vitorasso Jardim-Perassi ◽  
Tialfi Bergamin De Castro ◽  
Jucimara Colombo ◽  
Nathália Martins Sonehara ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Glucose Metabolism ◽  
Tumor Growth ◽  
Tumor Cells ◽  
Carbonic Anhydrases ◽  
In Vivo Models ◽  
Ca Ix ◽  
Gene And Protein Expression

Breast cancer is the most common cancer among women and has a high mortality rate. Adverse conditions in the tumor microenvironment, such as hypoxia and acidosis, may exert selective pressure on the tumor, selecting subpopulations of tumor cells with advantages for survival in this environment. In this context, therapeutic agents that can modify these conditions, and consequently the intratumoral heterogeneity need to be explored. Melatonin, in addition to its physiological effects, exhibits important anti-tumor actions which may associate with modification of hypoxia and Warburg effect. In this study, we have evaluated the action of melatonin on tumor growth and tumor metabolism by different markers of hypoxia and glucose metabolism (HIF-1α, glucose transporters GLUT1 and GLUT3 and carbonic anhydrases CA-IX and CA-XII) in triple negative breast cancer model. In an in vitro study, gene and protein expressions of these markers were evaluated by quantitative real-time PCR and immunocytochemistry, respectively. The effects of melatonin were also tested in a MDA-MB-231 xenograft animal model. Results showed that melatonin treatment reduced the viability of MDA-MB-231 cells and tumor growth in Balb/c nude mice (p <0.05). The treatment significantly decreased HIF-1α gene and protein expression concomitantly with the expression of GLUT1, GLUT3, CA-IX and CA-XII (p <0.05). These results strongly suggest that melatonin down-regulates HIF-1α expression and regulates glucose metabolism in breast tumor cells, therefore, controlling hypoxia and tumor progression. 

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