scholarly journals On a 2D Model of Avascular Tumor with Weak Allee Effect

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Peng Feng ◽  
Zhewei Dai ◽  
Dorothy Wallace
Keyword(s):  
Mathematical Models ◽  
Tumor Cells ◽  
Allee Effect ◽  
Necrotic Core ◽  
Proliferating Cells ◽  
Quiescent Cells ◽  
Three Stages ◽  
Growth Of Tumor ◽  
Avascular Tumor ◽  
2D Model

Recent studies reveal that Allee effect may play important roles in the growth of tumor. We present one of the first mathematical models of avascular tumor that incorporates the weak Allee effect. The model considers the densities of tumor cells in three stages: proliferating cells, quiescent cells, and necrotic cells. We investigate how Allee effect impacts the growth of the avascular tumor. We also investigate the effect of apoptosis of proliferating cells and necrosis of quiescent cells. The system is numerically solved in 2D using different sets of parameters. We show that Allee effect and apoptosis play important roles in the growth of tumor and the formation of necrotic core.

scholarly journals The Role of Glycolysis in the Growth of Tumor Cells

1961 ◽  
Vol 236 (2) ◽  
pp. 285-288
Author(s):  
John Papaconstantinou ◽  
Sidney P. Colowick
Keyword(s):  
Tumor Cells ◽  
Growth Of Tumor

scholarly journals The Role of Glycolysis in the Growth of Tumor Cells

1965 ◽  
Vol 240 (7) ◽  
pp. 2791-2796
Author(s):  
Edward B. Goldberg ◽  
Harold M. Nitowsky ◽  
Sidney P. Colowick
Keyword(s):  
Tumor Cells ◽  
Growth Of Tumor

scholarly journals CBIO-11. NOVEL THERAPY TO TARGET PR-RECURRENT GLIOMA

2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii17-ii18
Author(s):  
Masum Rahman ◽  
Ian E Olson ◽  
Rehan Saber ◽  
Jibo Zhang ◽  
Lucas P Carlstrom ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Tumor Recurrence ◽  
Primary Brain Tumor ◽  
Differential Sensitivity ◽  
Proliferating Cells ◽  
Novel Therapy ◽  
Conventional Radiation ◽  
Long Time ◽  
Radiation Induced

Abstract BACKGROUND Glioblastoma is a fatal infiltrative primary brain tumor, and standard care includes maximal safe surgical resection followed by radiation and Temozolomide (TMZ). Therapy-resistant residual cells persist in a latent state a long time before inevitable recurrence. Conventional radiation and Temozolomide (TMZ) treatment cause oxidative stress and DNA damage resulting senescent-like state of cell-cycle arrest. However, increasing evidence demonstrates escaping senescence leads to tumor recurrence. Thus, the ablation of senescent tumor cells after chemoradiation may be an avenue to limit tumor recurrence. METHODS 100uM TMZ for 7days or 10-20Gy radiation (cesium gamma radiator) was used for senescence induction in human glioblastoma in vitro and confirmed by SA-Beta gal staining and PCR. Replication arrest assessed by automated quantification of cellular confluence (Thermo Scientific Series 8000 WJ Incubator). We evaluated the IC50 for several senolytics targeting multiple SCAPs, including Dasatinib, Quercetin, AMG-232, Fisetin, Onalespib, Navitoclax, and A1331852, and in senescent vs. proliferating cells. RESULTS Among the senolytic tested, the Bcl-XL inhibitors A1331852 and Navitoclax both shown senolytic effect by selectively killing radiated, senescent tumor cells at lower concentrations as compared to 0Gy treated non-senescent cells. Across 12 GBM cell lines, IC50 for senescent cells was 6–500 times lower than non-senescent GBM(p< 0.005). Such differential sensitivity to Bcl-XL inhibition after radiation has also observed by BCL-XL knockdown in radiated glioma. CONCLUSION These findings suggest the potential to harness radiation-induced biology to ablate surviving quiescent cells and demonstrate Bcl-XL dependency as a potential vulnerability of surviving tumor cells after exposure to chemoradiation.

Effect of Garlic, Chinese Medicinal Drugs and Amino Acids on Growth of Erlich Ascites Tumor Cells in Mice

1983 ◽  
Vol 11 (01n04) ◽  
pp. 69-73 ◽  
Author(s):  
Y.M. Choy ◽  
T.T. Kwok ◽  
K.P. Fung ◽  
C.Y. Lee
Keyword(s):  
Amino Acids ◽  
Tumor Cells ◽  
Peritoneal Cavity ◽  
Growth And Development ◽  
Ehrlich Ascites Tumor Cells ◽  
Ascites Tumor ◽  
Tumor Bearing ◽  
Ehrlich Ascites ◽  
Medicinal Drugs ◽  
Growth Of Tumor

A number of food materials or drugs have been screened for the effect on the growth and development of transplantable Ehrlich ascites tumor cells. Growth of tumor-bearing mice was significantly inhibited by feeding garlic as well as some amino acids. These materials significantly reduced the total number of free tumor cells growing in the peritoneal cavity of mice and prolonged significantly the length of time for 50% death of tumor-bearing mice.

A NONLINEAR DELAY MODEL DESCRIBING THE GROWTH OF TUMOR CELLS UNDER IMMUNE SURVEILLANCE AGAINST CANCER AND ITS STABILITY ANALYSIS

2012 ◽  
Vol 05 (03) ◽  
pp. 1260017 ◽  
Author(s):  
LING CHEN ◽  
WANBIAO MA
Keyword(s):  
Stability Analysis ◽  
Hopf Bifurcation ◽  
Periodic Solutions ◽  
Tumor Cells ◽  
Local Stability ◽  
Immune Surveillance ◽  
Delay Model ◽  
Existence Of Periodic Solutions ◽  
Growth Of Tumor ◽  
Nonlinear Delay

In this paper, based on some biological meanings and a model which was proposed by Lefever and Garay (1978), a nonlinear delay model describing the growth of tumor cells under immune surveillance against cancer is given. Then, boundedness of the solutions, local stability of the equilibria and Hopf bifurcation of the model are discussed in details. The existence of periodic solutions explains the restrictive interactions between immune surveillance and the growth of the tumor cells.

scholarly journals Dysregulated circular RNAs in medulloblastoma regulate proliferation and growth of tumor cells via host genes

2018 ◽  
Vol 7 (12) ◽  
pp. 6147-6157 ◽  
Author(s):  
Tao Lv ◽  
Yi-Feng Miao ◽  
Ke Jin ◽  
Shuo Han ◽  
Tian-Qi Xu ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Circular Rnas ◽  
Growth Of Tumor ◽  
Host Genes

scholarly journals Thrombomodulin modulates growth of tumor cells independent of its anticoagulant activity.

1998 ◽  
Vol 101 (7) ◽  
pp. 1301-1309 ◽  
Author(s):  
Y Zhang ◽  
H Weiler-Guettler ◽  
J Chen ◽  
O Wilhelm ◽  
Y Deng ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Anticoagulant Activity ◽  
Growth Of Tumor

scholarly journals Mechanism mediated by a noncoding RNA, nc886, in the cytotoxicity of a DNA-reactive compound

2019 ◽  
Vol 116 (17) ◽  
pp. 8289-8294 ◽  
Author(s):  
Nawapol Kunkeaw ◽  
Yeon-Su Lee ◽  
Wonkyun Ronny Im ◽  
Jiyoung Joan Jang ◽  
Min-Ji Song ◽  
...  
Keyword(s):  
Noncoding Rna ◽  
Short Pulse ◽  
Rna Polymerase Iii ◽  
3D Culture ◽  
Protein Kinase R ◽  
Proliferating Cells ◽  
Quiescent Cells ◽  
3D Culture System ◽  
Reactive Compound ◽  
Pol Iii

DNA-reactive compounds are harnessed for cancer chemotherapy. Their genotoxic effects are considered to be the main mechanism for the cytotoxicity to date. Because this mechanism preferentially affects actively proliferating cells, it is postulated that the cytotoxicity is specific to cancer cells. Nonetheless, they do harm normal quiescent cells, suggesting that there are other cytotoxic mechanisms to be uncovered. By employing doxorubicin as a representative DNA-reactive compound, we have discovered a cytotoxic mechanism that involves a cellular noncoding RNA (ncRNA) nc886 and protein kinase R (PKR) that is a proapoptotic protein. nc886 is transcribed by RNA polymerase III (Pol III), binds to PKR, and prevents it from aberrant activation in most normal cells. We have shown here that doxorubicin evicts Pol III from DNA and, thereby, shuts down nc886 transcription. Consequently, the instantaneous depletion of nc886 provokes PKR and leads to apoptosis. In a short-pulse treatment of doxorubicin, these events are the main cause of cytotoxicity preceding the DNA damage response in a 3D culture system as well as the monolayer cultures. By identifying nc886 as a molecular signal for PKR to sense doxorubicin, we have provided an explanation for the conundrum why DNA-damaging drugs can be cytotoxic to quiescent cells that have the competent nc886/PKR pathway.

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