Cancer stem cells as markers of bladder cancer recurrence.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e16511-e16511
Author(s):  
Lyubov I. Belyakova ◽  
Aleksandr B. Sagakyants ◽  
Alexey N. Shevchenko ◽  
Elena V. Filatova ◽  
Viktor K. Khvan ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bladder Cancer ◽  
Cancer Stem Cells ◽  
Malignant Tumors ◽  
Cancer Recurrence ◽  
Statistical Processing ◽  
Nonparametric Test ◽  
Disease Recurrence ◽  
Arithmetic Mean ◽  
Significant Deterioration

e16511 Background: Bladder cancer (BC) is an urgent problem of oncology in the world, and without appropriate and timely treatment it can lead to severe disability and a significant deterioration in the quality of life of patients. BC accounts for 4.5% of the total cancer incidence. Cancer stem cells (CSCs) are actively involved in the development of recurrent malignant tumors, and also play an important role in the development of chemotherapy and radioresistance of tumor cells. CSCs in BC are poorly studied. Our purpose was to determine the CSC numbers in patients with non-muscle invasive BC. Methods: The study included 7 patients with newly diagnosed stage I BC, G2, intermediate prognosis according to the EORTC scoring system. All patients underwent transurethral resection of the bladder, and tumor tissues (TT, size up to 1.5 cm) and perifocal tissues (PT, at least 1.0 cm from the tumor) were obtained. The specimens were disintegrated to obtain the cell suspension, and the CSC percentages were determined using the FACS Canto II flow cytometer with monoclonal antibodies to CD45-APC-Cy7, CD24-FITC, and CD133–PE according to the manufacturer's instructions (BD, USA). Numbers of cells with CSC markers (CD24+, CD44+, CD133+, CD24+CD44+, CD44+CD133+) were calculated as the percentage from the total number of CD45--cells. The results of statistical processing were presented as the arithmetic mean and the standard error of the arithmetic mean. The significance of differences between the samples was assessed using the Mann-Whitney’s nonparametric test. Results: The numbers of CD45--cells were similar in TT and PT (61.3±5.8 and 71.8±12.6). The relative numbers of cells with CSC phenotypic markers, such as CD24, CD44, were 77% and 58% higher in TT than in PT: 18.3±3.5 vs. 4.3±2.1 and 15.5±5.3 vs. 6.5±0.8, respectively; p≤0.05. The number of CD133+ cells was 83% higher in PT compared to TT - 41.6±12.1 vs. 22.7±7.6. The numbers of CD44+CD24+ and CD44+CD133+ cells in TT were higher than in PT by 80% and 63%, respectively: 10.3±4.9 vs. 2.1±0.4, 9.0±4.5 vs. 3.3±0.9, p≤0.05. CD44-CD24+ CD133+ cells were not detected in PT. Conclusions: The results indicate the peculiarities of the distribution of CSCs in TT and PT, which can be used to predict the risk of the disease recurrence and/or progression, and also help to evaluate results of the treatment.

scholarly journals The plasticity of pancreatic cancer stem cells: implications in therapeutic resistance

2021 ◽  
Author(s):  
Kalyani Patil ◽  
Farheen B. Khan ◽  
Sabah Akhtar ◽  
Aamir Ahmad ◽  
Shahab Uddin
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Disease Recurrence ◽  
Resistance Mechanisms ◽  
Cytotoxic Agents ◽  
Plastic State ◽  
Metastatic Progression ◽  
Acquired Drug Resistance ◽  
Natural Agents

AbstractThe ever-growing perception of cancer stem cells (CSCs) as a plastic state rather than a hardwired defined entity has evolved our understanding of the functional and biological plasticity of these elusive components in malignancies. Pancreatic cancer (PC), based on its biological features and clinical evolution, is a prototypical example of a CSC-driven disease. Since the discovery of pancreatic CSCs (PCSCs) in 2007, evidence has unraveled their control over many facets of the natural history of PC, including primary tumor growth, metastatic progression, disease recurrence, and acquired drug resistance. Consequently, the current near-ubiquitous treatment regimens for PC using aggressive cytotoxic agents, aimed at ‘‘tumor debulking’’ rather than eradication of CSCs, have proven ineffective in providing clinically convincing improvements in patients with this dreadful disease. Herein, we review the key hallmarks as well as the intrinsic and extrinsic resistance mechanisms of CSCs that mediate treatment failure in PC and enlist the potential CSC-targeting ‘natural agents’ that are gaining popularity in recent years. A better understanding of the molecular and functional landscape of PCSC-intrinsic evasion of chemotherapeutic drugs offers a facile opportunity for treating PC, an intractable cancer with a grim prognosis and in dire need of effective therapeutic advances.

Targeting Bladder Cancer Stem Cells

2016 ◽  
pp. 211-229
Author(s):  
A.V. Kurtova ◽  
K.S. Chan
Keyword(s):  
Stem Cells ◽  
Bladder Cancer ◽  
Cancer Stem Cells

scholarly journals Mitotic quiescence in hepatic cancer stem cells: An incognito mode

2020 ◽  
Vol 14 (1) ◽  
Author(s):  
Kandasamy Ashokachakkaravarthy ◽  
Biju Pottakkat
Keyword(s):  
Hepatocellular Carcinoma ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Immune Evasion ◽  
Immune Surveillance ◽  
Cancer Recurrence ◽  
Tumor Formation ◽  
Proliferating Cells ◽  
Recurrence Rates

Hepatocellular carcinoma represents one of the most aggressive cancers with high recurrence rates. The high recurrence is a major problem in the management of this disease. Cancer stem cells (CSCs) are often regarded as the basis of cancer recurrence. The anti-proliferative therapy kills the proliferating cells but induces mitotic quiescence in CSCs which remain as residual dormant CSCs. Later on, withdrawal of treatment reactivates the residual CSCs from dormancy to produce new cancer cells. The proliferation of these newly formed cancer cells initiates new tumor formation in the liver leading to tumor recurrence. HCC cells evade the immune surveillance via modulating the key immune cells by alpha feto-protein (AFP) secreted from CSCs or hepatic progenitor cells. This AFP mediated immune evasion assists in establishing new tumors by cancer cells in the liver. In this review, we will summarise the CSC mechanisms of recurrence, mitotic quiescence, dormancy and reactivation of CSCs, metastasis and immune evasion of hepatocellular carcinoma.

scholarly journals Cancer Stem Cells and the Ontogeny of Lung Cancer

2008 ◽  
Vol 26 (17) ◽  
pp. 2883-2889 ◽  
Author(s):  
Craig D. Peacock ◽  
D. Neil Watkins
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Progenitor Cell ◽  
Molecular Mechanisms ◽  
Disease Recurrence ◽  
Cancer Death ◽  
Intrinsic Resistance ◽  
The Core ◽  
The World

Lung cancer is the leading cause of cancer death in the world today and is poised to claim approximately 1 billion lives during the 21st century. A major challenge in treating this and other cancers is the intrinsic resistance to conventional therapies demonstrated by the stem/progenitor cell that is responsible for the sustained growth, survival, and invasion of the tumor. Identifying these stem cells in lung cancer and defining the biologic processes necessary for their existence is paramount in developing new clinical approaches with the goal of preventing disease recurrence. This review summarizes our understanding of the cellular and molecular mechanisms operating within the putative cancer-initiating cell at the core of lung neoplasia.

scholarly journals Role of Natural Radiosensitizers and Cancer Cell Radioresistance: An Update

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Arif Malik ◽  
Misbah Sultana ◽  
Aamer Qazi ◽  
Mahmood Husain Qazi ◽  
Gulshan Parveen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Radiation Therapy ◽  
Cancer Stem Cells ◽  
Ionizing Radiation ◽  
Malignant Tumors ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Ros Scavenging

Cancer originates from genetic mutations accumulation. Cancer stem cells have been depicted as tumorigenic cells that can differentiate and self-renew. Cancer stem cells are thought to be resistant to conventional therapy like chemotherapy and radiation therapy. Radiation therapy and chemotherapy damage carcinomic DNA cells. Because of the ability of cancer stem cells to self-renew and reproduce malignant tumors, they are the subject of intensive research. In this review, CSCs radioresistant mechanisms which include DNA damage response and natural radiosensitizers have been summed up. Reactive oxygen species play an important role in different physiological processes. ROS scavenging is responsible for regulation of reactive oxygen species generation. A researcher has proved that microRNAs regulate tumor radiation resistance. Ionizing radiation does not kill the cancer cells; rather, IR just slows down the signs and symptoms. Ionizing radiation damages DNA directly/indirectly. IR is given mostly in combination with other chemo/radiotherapies. We briefly described here the behavior of cancer stem cells and radioresistance therapies in cancer treatment. To overcome radioresistance in treatment of cancer, strategies like fractionation modification, treatment in combination, inflammation modification, and overcoming hypoxic tumor have been practiced. Natural radiosensitizers, for example, curcumin, genistein, and quercetin, are more beneficial than synthetic compounds.

965 CHARACTERIZATION AND PRECLINICAL TARGETING OF HUMAN BLADDER CANCER STEM CELLS

2010 ◽  
Vol 183 (4S) ◽  
Author(s):  
Keith Syson Chan ◽  
Jens-Peter Volkmer ◽  
Mark Chao ◽  
Linda Shortliffe ◽  
Irving Weissman
Keyword(s):  
Stem Cells ◽  
Bladder Cancer ◽  
Cancer Stem Cells ◽  
Human Bladder Cancer ◽  
Human Bladder

scholarly journals Cripto-1 as a Key Factor in Tumor Progression, Epithelial to Mesenchymal Transition and Cancer Stem Cells

2021 ◽  
Vol 22 (17) ◽  
pp. 9280
Author(s):  
Hilal Arnouk ◽  
Gloria Yum ◽  
Dean Shah
Keyword(s):  
Stem Cells ◽  
Wound Healing ◽  
Cancer Stem Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Malignant Tumors ◽  
Lymphatic Vessels ◽  
Mesenchymal Phenotype ◽  
Mesenchymal Transition ◽  
Skin Cancers ◽  
Key Factor

Cripto-1 is an essential protein for human development that plays a key role in the early phase of gastrulation in the differentiation of an embryo as well as assists with wound healing processes. Importantly, Cripto-1 induces epithelial to mesenchymal transition to turn fixed epithelial cells into a more mobile mesenchymal phenotype through the downregulation of epithelial adhesion molecules such as E-cadherin, occludins, and claudins, and the upregulation of mesenchymal, mobile proteins, such as N-cadherin, Snail, and Slug. Consequently, Cripto-1’s role in inducing EMT to promote cell motility is beneficial in embryogenesis, but detrimental in the formation, progression and metastasis of malignant tumors. Indeed, Cripto-1 is found to be upregulated in most cancers, such as breast, lung, gastrointestinal, hepatic, renal, cervical, ovarian, prostate, and skin cancers. Through its role in EMT, Cripto-1 can remodel cancer cells to enable them to travel through the extracellular matrix as well as blood and lymphatic vessels to metastasize to different organs. Additionally, Cripto-1 promotes the survival of cancer stem cells, which can lead to relapse in cancer patients.

Sign in / Sign up

Export Citation Format

Share Document