scholarly journals Cancer Stem Cells as Mediators of Treatment Resistance in Brain Tumors: Status and Controversies

Neoplasia ◽  
2007 ◽  
Vol 9 (11) ◽  
pp. 882-892 ◽  
Author(s):  
Per Ø. Sakariassen ◽  
Heike Immervoll ◽  
Martha Chekenya
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Brain Tumors ◽  
Treatment Resistance

Therapeutic potency of oncolytic virotherapy–induced cancer stem cells targeting in brain tumors, current status, and perspectives

2018 ◽  
Vol 120 (3) ◽  
pp. 2766-2773 ◽  
Author(s):  
Amirhossein Bahreyni ◽  
Elnaz Ghorbani ◽  
Hamid Fuji ◽  
Mikhail Ryzhikov ◽  
Majid Khazaei ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Brain Tumors ◽  
Current Status ◽  
Oncolytic Virotherapy

Cancer stem cells

2019 ◽  
pp. 283-300
Author(s):  
Connor Sweeney ◽  
Lynn Quek ◽  
Betty Gration ◽  
Paresh Vyas
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Experimental Studies ◽  
Treatment Resistance ◽  
Experimental Models ◽  
Self Renewal ◽  
Multipotent Stem Cells ◽  
Anticancer Chemotherapy ◽  
Normal Tissues ◽  
Oncogenic Mutation

The concept of cancer stem cells (CSCs) emerged from our understanding of the way in which normal tissues are generated from multipotent stem cells. Regenerative tissues exhibit a cellular hierarchy of differentiation, which is maintained by stem cells. Evidence from experimental models has indicated that a similar hierarchy is seen in at least some cancers, where CSCs give rise to disordered and dysfunctional tissues, leading to disease. The CSC model proposes that tumours can be divided into at least two distinct populations. The stem cells are a specialized population of cancer cells with the unique property of long-term self-renewal that maintain the growth of the cancerous clone. These stem cells give rise to the second population of cells, which form the bulk of the tumour, and lack indefinite self-renewal. Recently, our understanding of CSCs has been refined through combining genetic, epigenetic, and functional models of tumorigenesis. Malignant transformation occurs as the result of sequential acquisition of genetic mutations. Capacity for self-renewal is essential for a clone to survive and progress to become cancerous. If an oncogenic mutation occurs in a cell that is incapable of self-renewal, the clone will become exhausted through differentiation. CSCs may survive anticancer chemotherapy and increasing evidence indicates their role in mediating treatment resistance and relapse. Therefore, strategies to eradicate cancers must effectively target the stem cells that maintain their growth. CSC-directed therapeutic strategies are currently being explored in experimental studies and clinical trials but reducing toxicity to normal tissue stem cells represents a significant challenge.

P3.68. Cancer stem cells as mediators of treatment resistance in squamous cell carcinoma of the head and neck

2009 ◽  
Vol 3 (1) ◽  
pp. 224
Author(s):  
A. Okamoto ◽  
K. Chikamatsu ◽  
K. Sakakura ◽  
K. Hatsushika ◽  
G. Takahashi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Squamous Cell Carcinoma ◽  
Cancer Stem Cells ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Treatment Resistance

Abstract 832: Evaluation of relevance of genes expressed in cancer stem cells and under hypoxia in astrocytic brain tumors

2010 ◽  
Author(s):  
Philipp Lehmann ◽  
Muna N. Awad-Masalmeh ◽  
Sandra Sampl ◽  
Johannes Hainfellner ◽  
Matthias Preusser ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Brain Tumors

Drug repurposing towards targeting cancer stem cells in pediatric brain tumors

2020 ◽  
Vol 39 (1) ◽  
pp. 127-148 ◽  
Author(s):  
Hisham F. Bahmad ◽  
Mohamad K. Elajami ◽  
Talal El Zarif ◽  
Jolie Bou-Gharios ◽  
Tamara Abou-Antoun ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Brain Tumors ◽  
Drug Repurposing ◽  
Pediatric Brain Tumors ◽  
Pediatric Brain

Association of ALDH-expressing cancer stem cells with survival in patients with resected pancreatic adenocarcinoma treated with adjuvant chemoradiation.

2014 ◽  
Vol 32 (3_suppl) ◽  
pp. 262-262
Author(s):  
Rachit Kumar ◽  
Avani Satish Dholakia ◽  
Joseph M. Herman ◽  
Anirban Maitra ◽  
William H. Matsui ◽  
...  
Keyword(s):  
Stem Cells ◽  
Overall Survival ◽  
Cancer Stem Cells ◽  
Pancreatic Adenocarcinoma ◽  
Treatment Resistance ◽  
Progression Free Survival ◽  
Distant Metastases ◽  
Tumor Grade ◽  
Tumor Initiating Cells ◽  
Radiology Reports

262 Background: We and others have identified aldehyde dehydrogenase (ALDH) activity as a marker of pancreatic cancer stem cells (or tumor-initiating cells). The presence of cancer stem cells (CSCs) has been associated with decreased survival and treatment resistance in pancreatic adenocarcinoma. We investigate the role of ALDH expression in predicting survival and patterns of disease recurrence in patients treated with chemoradiation (CRT) following pancreatectomy. Methods: Tissue microarrays using surgical specimens from 1998 to 2002 were stained for ALDH1 and scored as ALDH-positive or ALDH-negative by two expert pancreatic pathologists blinded to patient outcomes. Physician documentation and radiology reports were used to determine follow-up information. Time to local failure (TLF), time to distant metastases (TDM), progression-free survival (PFS), and overall survival (OS) were analyzed using SPSS software. Results: Previously we found that ALDH expression was associated with worse OS in a cohort of 269 patients with resected pancreatic adenocarcinoma (Rasheed, JNCI 2009). From this cohort, adjuvant treatment information was available for 87 patients with ALDH-negative tumors (48.6%) and 41 patients with ALDH-positive tumors (45.6%). In patients treated with adjuvant CRT, median overall survival was superior in the ALDH-negative cohort vs. the ALDH-positive cohort, 26.3 months vs. 18.2 months (p=0.011). Further, in patients treated with adjuvant CRT, ALDH-negative patients had statistically greater TLF, TDM, and PFS than their ALDH-positive counterparts (see table). On multivariate analysis, ALDH positive tumor staining (HR 1.94, p=0.004) and tumor grade (HR 1.54, p=0.041) predicted lower OS, and ALDH positive tumor staining (HR 1.83, p=0.008), tumor grade (HR 1.52, p=0.038), and tumor size >3 cm (HR 1.65, p=0.023) predicted decreased PFS. Conclusions: This study suggests that adjuvant CRT improves TLF, TDM, PFS, and OS in patients with localized pancreatic adenocarcinoma not enriched with ALDH-expressing CSCs. Laboratory studies will help elucidate the mechanisms of treatment resistance in ALDH expressing CSCs.

scholarly journals Norcantharidin, Derivative of Cantharidin, for Cancer Stem Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Chen-Hsi Hsieh ◽  
K. S. Clifford Chao ◽  
Hui-Fen Liao ◽  
Yu-Jen Chen
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Treatment ◽  
Treatment Resistance ◽  
Notch Signaling Pathway ◽  
Chemotherapeutic Agents ◽  
Water Soluble ◽  
Self Renewal ◽  
Active Efflux ◽  
Effective Strategies

Cancer stem cells (CSCs) existing in human cancers have been demonstrated to be a major cause of cancer treatment resistance, invasion, metastasis, and relapse. Self-renewal pathways, Wnt/β-catenin, Sonic hedgehog (Shh), and the Notch signaling pathway play critical roles in developing CSCs and lead to angiogenesis, migration, invasion, and metastasis. Multidrug resistance (MDR) is an unfavorable factor causing the failure of treatments against cancer cells. The most important and thoroughly studied mechanism involved in MDR is the active efflux of chemotherapeutic agents through membrane drug transporters. There is growing evidence that Norcantharidin (NCTD), a water-soluble synthetic small molecule derivative of naturally occurring cantharidin from the medicinal insect blister beetle (Mylabris phalerataPallas), is capable of chemoprevention and tumor inhibition. We summarize investigations into the modulation of self-renewal pathways and MDR in CSCs by NCTD. This review may aid in further investigation of using NCTD to develop more effective strategies for cancer treatment to reduce resistance and recurrence.

scholarly journals Stemness, Inflammation and Epithelial–Mesenchymal Transition in Colorectal Carcinoma: The Intricate Network

2021 ◽  
Vol 22 (23) ◽  
pp. 12891
Author(s):  
Inese Briede ◽  
Dainis Balodis ◽  
Janis Gardovskis ◽  
Ilze Strumfa
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Colorectal Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Treatment Resistance ◽  
Resistance Mechanisms ◽  
Mesenchymal Transition ◽  
Cancer Statistics ◽  
Screening Programs ◽  
A Minor

In global cancer statistics, colorectal carcinoma (CRC) ranks third by incidence and second by mortality, causing 10.0% of new cancer cases and 9.4% of oncological deaths worldwide. Despite the development of screening programs and preventive measures, there are still high numbers of advanced cases. Multiple problems compromise the treatment of metastatic colorectal cancer, one of these being cancer stem cells—a minor fraction of pluripotent, self-renewing malignant cells capable of maintaining steady, low proliferation and exhibiting an intriguing arsenal of treatment resistance mechanisms. Currently, there is an increasing body of evidence for intricate associations between inflammation, epithelial–mesenchymal transition and cancer stem cells. In this review, we focus on inflammation and its role in CRC stemness development through epithelial–mesenchymal transition.

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