scholarly journals Genetic stability of pluripotent stem cells during anti-cancer therapies

2016 ◽  
Vol 11 (3) ◽  
pp. 695-702 ◽  
Author(s):  
WIKTORIA MARIA SUCHORSKA ◽  
EWELINA AUGUSTYNIAK ◽  
MAGDALENA ŁUKJANOW
Keyword(s):  
Stem Cells ◽  
Pluripotent Stem Cells ◽  
Genetic Stability ◽  
Cancer Therapies ◽  
Anti Cancer

Pharmacological targeting of mitochondria in cancer stem cells: An ancient organelle at the crossroad of novel anti-cancer therapies

2019 ◽  
Vol 139 ◽  
pp. 298-313 ◽  
Author(s):  
Jan Skoda ◽  
Karolina Borankova ◽  
Patric J. Jansson ◽  
Michael L.-H. Huang ◽  
Renata Veselska ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Therapies ◽  
Anti Cancer

scholarly journals microRNA: The Impact on Cancer Stemness and Therapeutic Resistance

Cells ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 8 ◽  
Author(s):  
Xueqiao Jiao ◽  
Xianling Qian ◽  
Longyuan Wu ◽  
Bo Li ◽  
Yi Wang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Noncoding Rna ◽  
Tumor Recurrence ◽  
Tumor Promoter ◽  
Therapeutic Resistance ◽  
Cancer Therapies ◽  
Cancer Treatments ◽  
Small Noncoding Rna ◽  
Anti Cancer ◽  
The Impact

Cancer ranks as the second leading cause of death worldwide, causing a large social and economic burden. However, most anti-cancer treatments face the problems of tumor recurrence and metastasis. Therefore, finding an effective cure for cancer needs to be solved urgently. Recently, the discovery of cancer stem cells (CSCs) provides a new orientation for cancer research and therapy. CSCs share main characteristics with stem cells and are able to generate an entire tumor. Besides, CSCs usually escape from current anti-cancer therapies, which is partly responsible for tumor recurrence and poor prognosis. microRNAs (miRNAs) belong to small noncoding RNA and regulate gene post-transcriptional expression. The dysregulation of miRNAs leads to plenty of diseases, including cancer. The aberrant miRNA expression in CSCs enhances stemness maintenance. In this review, we summarize the role of miRNAs on CSCs in the eight most common cancers, hoping to bridge the research of miRNAs and CSCs with clinical applications. We found that miRNAs can act as tumor promoter or suppressor. The dysregulation of miRNAs enhances cell stemness and contributes to tumor metastasis and therapeutic resistance via the formation of feedback loops and constitutive activation of carcinogenic signaling pathways. More importantly, some miRNAs may be potential targets for diagnosis, prognosis, and cancer treatments.

scholarly journals Metabolic Targeting of Cancer Stem Cells

2020 ◽  
Vol 10 ◽  
Author(s):  
Anna Mukha ◽  
Anna Dubrovska
Keyword(s):  
Stem Cells ◽  
Cell Differentiation ◽  
Cancer Stem Cells ◽  
Clonal Evolution ◽  
Cancer Therapies ◽  
Intrinsic Resistance ◽  
Anti Cancer ◽  
Target Tumor Cell ◽  
High Degree ◽  
Metabolic Targeting

Most human tumors possess a high heterogeneity resulting from both clonal evolution and cell differentiation program. The process of cell differentiation is initiated from a population of cancer stem cells (CSCs), which are enriched in tumor‐regenerating and tumor‐propagating activities and responsible for tumor maintenance and regrowth after treatment. Intrinsic resistance to conventional therapies, as well as a high degree of phenotypic plasticity, makes CSCs hard-to-target tumor cell population. Reprogramming of CSC metabolic pathways plays an essential role in tumor progression and metastatic spread. Many of these pathways confer cell adaptation to the microenvironmental stresses, including a shortage of nutrients and anti-cancer therapies. A better understanding of CSC metabolic dependences as well as metabolic communication between CSCs and the tumor microenvironment are of utmost importance for efficient cancer treatment. In this mini-review, we discuss the general characteristics of CSC metabolism and potential metabolic targeting of CSC populations as a potent strategy to enhance the efficacy of conventional treatment approaches.

Research and Findings

2010 ◽  
Vol 14 (02) ◽  
pp. 36-39
Keyword(s):  
Stem Cells ◽  
Vitamin E ◽  
Pluripotent Stem Cells ◽  
Islet Cell ◽  
Malaria Parasite ◽  
Differentiated Cells ◽  
Anti Cancer ◽  
Root Weevils ◽  
Depth Study ◽  
Clover Root

Singapore Scientists Discover New Concoction to Reprogram Differentiated Cells into Pluripotent Stem Cells. NTU Researchers Complete the World's First in-depth Study of the Malaria Parasite Genome. Cause of Islet Cell Rejection Discovered. Scientist Develops Anti-Cancer Derivative of Vitamin E. Destructive Clover Root Weevils Found.

scholarly journals Building Multi-Dimensional Induced Pluripotent Stem Cells-Based Model Platforms to Assess Cardiotoxicity in Cancer Therapies

2021 ◽  
Vol 12 ◽  
Author(s):  
Dilip Thomas ◽  
Sushma Shenoy ◽  
Nazish Sayed
Keyword(s):  
Stem Cells ◽  
Induced Pluripotent Stem Cells ◽  
Pluripotent Stem Cells ◽  
Safety Evaluation ◽  
Cost Effective ◽  
Patient Specific ◽  
Cancer Therapies ◽  
Cardiovascular Risks ◽  
Cardiovascular Cells ◽  
Induced Pluripotent

Cardiovascular disease (CVD) complications have contributed significantly toward poor survival of cancer patients worldwide. These complications that result in myocardial and vascular damage lead to long-term multisystemic disorders. In some patient cohorts, the progression from acute to symptomatic CVD state may be accelerated due to exacerbation of underlying comorbidities such as obesity, diabetes and hypertension. In such situations, cardio-oncologists are often left with a clinical predicament in finding the optimal therapeutic balance to minimize cardiovascular risks and maximize the benefits in treating cancer. Hence, prognostically there is an urgent need for cost-effective, rapid, sensitive and patient-specific screening platform to allow risk-adapted decision making to prevent cancer therapy related cardiotoxicity. In recent years, momentous progress has been made toward the successful derivation of human cardiovascular cells from induced pluripotent stem cells (iPSCs). This technology has not only provided deeper mechanistic insights into basic cardiovascular biology but has also seamlessly integrated within the drug screening and discovery programs for early efficacy and safety evaluation. In this review, we discuss how iPSC-derived cardiovascular cells have been utilized for testing oncotherapeutics to pre-determine patient predisposition to cardiovascular toxicity. Lastly, we highlight the convergence of tissue engineering technologies and precision medicine that can enable patient-specific cardiotoxicity prognosis and treatment on a multi-organ level.

scholarly journals Cell death mechanisms of the anti-cancer drug etoposide on human cardiomyocytes isolated from pluripotent stem cells

2018 ◽  
Vol 92 (4) ◽  
pp. 1507-1524 ◽  
Author(s):  
Harshal Nemade ◽  
Umesh Chaudhari ◽  
Aviseka Acharya ◽  
Jürgen Hescheler ◽  
Jan Georg Hengstler ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Death ◽  
Pluripotent Stem Cells ◽  
Cancer Drug ◽  
Human Cardiomyocytes ◽  
Anti Cancer ◽  
Cell Death Mechanisms

scholarly journals The Role of Cancer Stem Cells in Drug Resistance in Gastroesophageal Junction Adenocarcinoma

2021 ◽  
Vol 8 ◽  
Author(s):  
Kate Dinneen ◽  
Anne-Marie Baird ◽  
Ciara Ryan ◽  
Orla Sheils
Keyword(s):  
Stem Cells ◽  
Drug Resistance ◽  
Cancer Stem Cells ◽  
Current Knowledge ◽  
Gastroesophageal Junction ◽  
Western World ◽  
Specific Cell ◽  
Cancer Therapies ◽  
Mesenchymal Transition ◽  
Anti Cancer

Gastroesophageal junction adenocarcinomas (GEJA) have dramatically increased in incidence in the western world since the mid-20th century. Their prognosis is poor, and conventional anti-cancer therapies do not significantly improve survival outcomes. These tumours are comprised of a heterogenous population of both cancer stem cells (CSC) and non-CSCs, with the former playing a crucial role in tumorigenesis, metastasis and importantly drug resistance. Due to the ability of CSCs to self-replicate indefinitely, their resistance to anti-cancer therapies poses a significant barrier to effective treatment of GEJA. Ongoing drug development programmes aim to target and eradicate CSCs, however their characterisation and thus identification is difficult. CSC regulation is complex, involving an array of signalling pathways, which are in turn influenced by a number of entities including epithelial mesenchymal transition (EMT), microRNAs (miRNAs), the tumour microenvironment and epigenetic modifications. Identification of CSCs commonly relies on the expression of specific cell surface markers, yet these markers vary between different malignancies and indeed are often co-expressed in non-neoplastic tissues. Development of targeted drug therapies against CSCs thus requires an understanding of disease-specific CSC markers and regulatory mechanisms. This review details the current knowledge regarding CSCs in GEJA, with particular emphasis on their role in drug resistance.

scholarly journals Scarless Enriched selection of Genome edited Human Pluripotent Stem Cells Using Induced Drug Resistance

2019 ◽  
Author(s):  
Keun-Tae Kim ◽  
Ju-Chan Park ◽  
Haeseung Lee ◽  
Hyeon-Ki Jang ◽  
Yan Jin ◽  
...  
Keyword(s):  
Stem Cells ◽  
Pluripotent Stem Cells ◽  
Gene Editing ◽  
Human Pluripotent Stem Cells ◽  
Cancer Drug ◽  
Efficient Gene ◽  
Anti Cancer ◽  
Low Efficiency ◽  
High Cytotoxicity ◽  
Selection Of

SummaryAn efficient gene editing technique for use in human pluripotent stem cells (hPSCs) would have great potential value in regenerative medicine, as well as in drug discovery based on isogenic human disease models. However, the extremely low efficiency of gene editing in hPSCs is a major technical hurdle that remains to be resolved. Previously, we demonstrated that YM155, a survivin inhibitor developed as an anti-cancer drug, induces highly selective cell death in undifferentiated hPSCs. In this study, we demonstrated that the high cytotoxicity of YM155 in hPSCs, which is mediated by selective cellular uptake of the drug, is due to high expression of SLC35F2 in these cells. Consistent with this, knockout of SLC35F2 with CRISPR-Cas9 or depletion with siRNAs made hPSCs highly resistant to YM155. Simultaneous gene editing of a gene of interest and transient knockdown of SLC35F2 following YM155 treatment enabled genome-edited hPSCs to survive because YM155 resistance was temporarily induced, thereby achieving enriched selection of genome-edited clonal populations. This precise and efficient genome editing approach took as little as 3 weeks without cell sorting or introduction of additional genes.

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