Tumor Cell Population Kinetics Following Noncurative Treatment1

2015 ◽  
pp. 148-156 ◽  
Author(s):  
L. M. Schiffer ◽  
P. G. Braunschweiger ◽  
J. J. Stragand
Keyword(s):  
Tumor Cell ◽  
Cell Population ◽  
Tumor Cell Population ◽  
Population Kinetics

PD-0835 Bone-tropic circulating tumor cell population in mCRPC patients under ablative radiotherapy

2021 ◽  
Vol 161 ◽  
pp. S670-S671
Author(s):  
D. Klusa ◽  
F. Lohaus ◽  
H. Neubauer ◽  
A. Franken ◽  
M. Rivandi ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Population ◽  
Circulating Tumor Cell ◽  
Tumor Cell Population

scholarly journals The Chemokine Receptor CXCR3 Isoform B Drives Breast Cancer Stem Cells

2019 ◽  
Vol 13 ◽  
pp. 117822341987362 ◽  
Author(s):  
Namita Kundu ◽  
Xinrong Ma ◽  
Regine Brox ◽  
Xiaoxuan Fan ◽  
Tyler Kochel ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Tumor Cell ◽  
Cell Population ◽  
Chemokine Receptor ◽  
Migration And Invasion ◽  
Breast Cancer Cell Lines ◽  
Tumor Cell Population ◽  
Isoform B

We are seeking to identify molecular targets that are relevant to breast cancer cells with stem-like properties. There is growing evidence that cancer stem cells (CSCs) are supported by inflammatory mediators expressed in the tumor microenvironment. The chemokine receptor CXCR3 binds the interferon-γ-inducible, ELR-negative CXC chemokines CXCL9, CXCL10, and CXCL11 and malignant cells have co-opted this receptor to promote tumor cell migration and invasion. There are 2 major isoforms of CXCR3: CXCR3A and CXCR3B. The latter is generated from alternative splicing and results in a protein with a longer N-terminal domain. CXCR3 isoform A is generally considered to play a major role in tumor metastasis. When the entire tumor cell population is examined, CXCR3 isoform B is usually detected at much lower levels than CXCR3A and for this, and other reasons, was not considered to drive tumor progression. We have shown that CXCR3B is significantly upregulated in the subpopulation of breast CSCs in comparison with the bulk tumor cell population in 3 independent breast cancer cell lines (MDA-MB-231, SUM159, and T47D). Modulation of CXCR3B levels by knock in strategies increases CSC populations identified by aldehyde dehydrogenase activity or CD44+CD24− phenotype as well as tumorsphere-forming capacity. The reverse is seen when CXCR3B is gene-silenced. CXCL11 and CXCL10 directly induce CSC. We also report that novel CXCR3 allosteric modulators BD064 and BD103 prevent the induction of CSCs. BD103 inhibited experimental metastasis. This protective effect is associated with the reversal of CXCR3 ligand-mediated activation of STAT3, ERK1/2, CREB, and NOTCH1 pathways. We propose that CXCR3B, expressed on CSC, should be explored further as a novel therapeutic target.

TUMOR CELL POPULATION OF THE EHRLICH ASCITES TUMORS

1968 ◽  
Vol 10 (3) ◽  
pp. 723-746 ◽  
Author(s):  
Narsingh D. Agnish ◽  
Sergey Fedoroff
Keyword(s):  
Tumor Cell ◽  
Cell Population ◽  
Tumor Cell Population ◽  
Ehrlich Ascites ◽  
Ascites Tumors

scholarly journals Establishment and characterization of a primary calcifying epithelial odontogenic tumor cell population

2013 ◽  
Vol 43 (3) ◽  
pp. 183-190 ◽  
Author(s):  
Hope M. Amm ◽  
Douglas L. Rollins ◽  
Changchun Ren ◽  
Juan Dong ◽  
Patricia DeVilliers ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Population ◽  
Odontogenic Tumor ◽  
Calcifying Epithelial Odontogenic Tumor ◽  
Tumor Cell Population ◽  
Epithelial Odontogenic Tumor

MODELING TUMOR CELL POPULATION DYNAMICS BASED ON MOLECULAR ADHESION ASSUMPTIONS

2004 ◽  
Vol 12 (03) ◽  
pp. 273-288 ◽  
Author(s):  
WIESLAW GRYGIERZEC ◽  
ANDREAS DEUTSCH ◽  
WALTER SCHUBERT ◽  
MANUELA FRIEDENBERGER ◽  
LARS PHILIPSEN
Keyword(s):  
Population Dynamics ◽  
Tumor Cell ◽  
Cell Population ◽  
Adhesion Forces ◽  
Protein Patterns ◽  
Cell Population Dynamics ◽  
Tumor Cell Population ◽  
Molecular Adhesion ◽  
Ca Model ◽  
Adhesion Process

A model of cell population dynamics based on molecular adhesion is explained and discussed in this paper. We consider cancer cells experiencing interactions due to adhesion forces. In the cells' membranes there are proteins directly involved in adhesion. These proteins in the membrane are assembled in complex patterns called Combinatorial Protein Patterns (CPP). The goal of this work is to understand the mechanisms governing the adhesion process — in particular distinguishing CPPs involved in interactions. On the basis of experimental observation we have constructed an asynchronous cellular automaton (CA) model that simulates protein network dynamics in a population of cells.

scholarly journals The Effect of p53 Status on Radio-Sensitivity of Quiescent Tumor Cell Population Irradiated With γ-Rays at Various Dose Rates

2018 ◽  
Vol 10 (11) ◽  
pp. 815-821 ◽  
Author(s):  
Shin-ichiro Masunaga ◽  
Junya Kobayashi ◽  
Keizo Tano ◽  
Yu Sanada ◽  
Minoru Suzuki ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Population ◽  
Tumor Cell Population ◽  
Dose Rates ◽  
P53 Status ◽  
Γ Rays ◽  
Radio Sensitivity

Patient-specific biomathematical model to predict benefit of resection in human gliomas.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e13017-e13017
Author(s):  
Anne Baldock ◽  
Russell Rockne ◽  
Sunyoung Ahn ◽  
Maxwell Neal ◽  
David Corwin ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Population ◽  
Survival Benefit ◽  
Cost Benefit Analysis ◽  
Glioma Cells ◽  
Cost Benefit ◽  
Residual Tumor ◽  
Patient Specific ◽  
Tumor Cell Population ◽  
Tumor Invasiveness

e13017 Background: Gliomas are incurable, primary brain tumors noted for their invasion of brain parenchyma. Our goal was to apply a biomathematical model to estimate the overall tumor invasiveness on an individual basis and determine whether the estimated number of residual glioma cells after resection of any extent is predictive of survival. Methods: Estimates of net rates of proliferation (ρ) and diffusion (D) of glioma cells, based on a biomathematical model of cell density, yield a ratio describing relative invasiveness (ρ/D). This metric was derived for 185 contrast enhancing gliomas from pretreatment MRIs. The residual MRI-detectable volume was combined with the ρ/D tuned to each patient's tumor to allow estimation of the number of glioma cells remaining post-resection. The patients were split into three cohorts by ρ/D values. Within each cohort, all possible cut-off values were considered as a possible threshold between low and high residual patient groups. Log-rank tests were performed for each possible threshold to determine if the Kaplan-Meyer curves were significantly different. Results: We demonstrate that for low ρ/D tumors there was no threshold of residual tumor cell population observed that could yield a significant survival benefit. Both the mid ρ/D and high ρ/D had robust thresholds of residual tumor cell population, below which patients saw significantly higher survival than patients with similar invasiveness and more residual tumor. Conclusions: These results suggest that our patient-specific biomathematical model-based estimates of tumor invasiveness and residual tumor cells have clinical utility in driving neurosurgical decision making. Given the physicians understanding of patient-specific risk factors such as tumor location, age, and physical health, an understanding of the differential surgical benefit allows for more informed cost-benefit analysis and improved quality of life. This metric enables physicians to identify a subset of patients who do not see a survival benefit from resection, making the operation potentially not worth the risks.

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