Investigation of the Effect of Adding Stem Cells-as an Therapeutic Suggestion-on the Immune System's Response to the Cancerous Cells: A Mathematical Approach

Author(s):  
Zahra Veisi ◽  
Samin Ravanshadi ◽  
Heydar Khadem ◽  
Zahra Veisi ◽  
Samin Ravanshadi ◽  
...  
2012 ◽  
Vol 198 (3) ◽  
pp. 281-293 ◽  
Author(s):  
Irène Baccelli ◽  
Andreas Trumpp

The cancer stem cell (CSC) concept, which arose more than a decade ago, proposed that tumor growth is sustained by a subpopulation of highly malignant cancerous cells. These cells, termed CSCs, comprise the top of the tumor cell hierarchy and have been isolated from many leukemias and solid tumors. Recent work has discovered that this hierarchy is embedded within a genetically heterogeneous tumor, in which various related but distinct subclones compete within the tumor mass. Thus, genetically distinct CSCs exist on top of each subclone, revealing a highly complex cellular composition of tumors. The CSC concept has therefore evolved to better model the complex and highly dynamic processes of tumorigenesis, tumor relapse, and metastasis.


Author(s):  
Zahra VEISI ◽  
Heydar KHADEM ◽  
Samin RAVANSHADI

Background: Immunotherapy is a recently developed method of cancer therapy, aiming to strengthen a patient’s immune system in different ways to fight cancer. One of these ways is to add stem cells into the patient’s body. Methods: The study was conducted in Kermanshah, western Iran, 2016-2017. We first modeled the interaction between cancerous and healthy cells using the concept of evolutionary game theory. System dynamics were analyzed employing replicator equations and control theory notions. We categorized the system into separate cases based on the value of the parameters. For cases in which the system converged to undesired equilibrium points, “stem-cell injection” was employed as a therapeutic suggestion. The effect of stem cells on the model was considered by reforming the replicator equations as well as adding some new parameters to the system. Results: By adjusting stem cell-related parameters, the system converged to desired equilibrium points, i.e., points with no or a scanty level of cancerous cells. In addition to the theoretical analysis, our simulation results suggested solutions were effective in eliminating cancerous cells. Conclusion: This model could be applicable to different types of cancer, so we did not restrict it to a specific type of cancer. In fact, we were seeking a flexible mathematical framework that could cover different types of cancer by adjusting the system parameters.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Luan Nguyen ◽  
Myrthe Jager ◽  
Ruby Lieshout ◽  
Petra E. de Ruiter ◽  
Mauro D. Locati ◽  
...  

AbstractInflammatory liver disease increases the risk of developing primary liver cancer. The mechanism through which liver disease induces tumorigenesis remains unclear, but is thought to occur via increased mutagenesis. Here, we performed whole-genome sequencing on clonally expanded single liver stem cells cultured as intrahepatic cholangiocyte organoids (ICOs) from patients with alcoholic cirrhosis, non-alcoholic steatohepatitis (NASH), and primary sclerosing cholangitis (PSC). Surprisingly, we find that these precancerous liver disease conditions do not result in a detectable increased accumulation of mutations, nor altered mutation types in individual liver stem cells. This finding contrasts with the mutational load and typical mutational signatures reported for liver tumors, and argues against the hypothesis that liver disease drives tumorigenesis via a direct mechanism of induced mutagenesis. Disease conditions in the liver may thus act through indirect mechanisms to drive the transition from healthy to cancerous cells, such as changes to the microenvironment that favor the outgrowth of precancerous cells.


2009 ◽  
Vol 42 (4) ◽  
pp. 529-540 ◽  
Author(s):  
C. Turner ◽  
A. R. Stinchcombe ◽  
M. Kohandel ◽  
S. Singh ◽  
S. Sivaloganathan

Drug Research ◽  
2019 ◽  
Vol 69 (09) ◽  
pp. 471-478 ◽  
Author(s):  
Mohammed Hawash

AbstractCancer is the second leading cause of death in worldwide, because of that we need a great effort to discover, determine and understand the main pathways and mechanism of action of new novel anticancer drugs, which highly selective on the cancerous cells over the normal cells. The traditional approaches to the treat cancer depend on surgery, radiotherapy, and chemotherapy, according to the medicinal reports the chemotherapy is still the main procedure in the cancer cure or treatment till nowadays, and it is one of the main factors that drops the mortality of cancer in the last years. In the past decades the chemotherapeutic agents were used in the cancer treatment without clear understand on which target, protein, or enzyme that is working, and it was making the inhibition on the whole family of enzymes or receptors which lead to high toxicity and side effects, but nowadays the anticancer agents work with high selectivity on specific subtype of clear targets, and these targets usually present in high percentage in the cancerous cells. In this review article we will summarize some of these specific targets for anticancer drugs like Cyclin-dependent kinases (CDKs), epidermal growth factor receptors (EGFR), Ras protein, and Cancer stem cells, finally, we will mention some anticancer drugs which approved by FDA in 2018 which work on specific targets.


2020 ◽  
Vol 21 (22) ◽  
pp. 8599 ◽  
Author(s):  
Jin Seok ◽  
Sujin Jun ◽  
Jung Ok Lee ◽  
Gi Jin Kim

Mitochondrial dynamics are involved in many cellular events, including the proliferation, differentiation, and invasion/migration of normal as well as cancerous cells. Human placenta-derived mesenchymal stem cells (PD-MSCs) were known to regulate the invasion activity of trophoblasts. However, the effects of PD-MSCs on mitochondrial function in trophoblasts are still insufficiently understood. Therefore, the objectives of this study are to analyze the factors related to mitochondrial function and investigate the correlation between trophoblast invasion and mitophagy via PD-MSC cocultivation. We assess invasion ability and mitochondrial function in invasive trophoblasts according to PD-MSC cocultivation by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and extracellular flux (XF) assay. Under PD-MSCs co-cultivation, invasion activity of a trophoblast is increased via activation of the Rho signaling pathway as well as Matrix metalloproteinases (MMPs). Additionally, the expression of mitochondrial function (e.g., reactive oxygen species (ROS), calcium, and adenosine triphosphate (ATP) synthesis) in trophoblasts are increased via PD-MSCs co-cultivation. Finally, PD-MSCs regulate mitochondrial autophagy factors in invasive trophoblasts via regulating the balance between PTEN-induced putative kinase 1 (PINK1) and parkin RBR E3 ubiquitin protein ligase (PARKIN) expression. Taken together, these results demonstrate that PD-MSCs enhance the invasion ability of trophoblasts via altering mitochondrial dynamics. These results support the fundamental mechanism of trophoblast invasion via mitochondrial function and provide a new stem cell therapy for infertility.


2010 ◽  
Vol 30 (6) ◽  
pp. 455-455 ◽  
Author(s):  
Dongyan Shi ◽  
Dan Ma ◽  
Feiqing Dong ◽  
Chen Zong ◽  
Liyue Liu ◽  
...  

2010 ◽  
Vol 34 (8) ◽  
pp. S39-S39
Author(s):  
Dewu Liu ◽  
Honglan Xiong ◽  
Yuangui Mao ◽  
Peixin Huang ◽  
Jianping Chen ◽  
...  

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