scholarly journals Antibiotics that target mitochondria effectively eradicate cancer stem cells, across multiple tumor types: Treating cancer like an infectious disease

Oncotarget ◽  
2015 ◽  
Vol 6 (7) ◽  
pp. 4569-4584 ◽  
Author(s):  
Rebecca Lamb ◽  
Bela Ozsvari ◽  
Camilla L. Lisanti ◽  
Herbert B. Tanowitz ◽  
Anthony Howell ◽  
...  
Keyword(s):  
Infectious Disease ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Multiple Tumor ◽  
Tumor Types

scholarly journals Graphene oxide selectively targets cancer stem cells, across multiple tumor types: Implications for non-toxic cancer treatment, via “differentiation-based nano-therapy”

Oncotarget ◽  
2015 ◽  
Vol 6 (6) ◽  
pp. 3553-3562 ◽  
Author(s):  
Marco Fiorillo ◽  
Andrea F. Verre ◽  
Maria Iliut ◽  
Maria Peiris-Pagés ◽  
Bela Ozsvari ◽  
...  
Keyword(s):  
Stem Cells ◽  
Graphene Oxide ◽  
Cancer Stem Cells ◽  
Cancer Treatment ◽  
Multiple Tumor ◽  
Tumor Types

scholarly journals Current Strategies for Identification of Glioma Stem Cells: Adequate or Unsatisfactory?

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Paola Brescia ◽  
Cristina Richichi ◽  
Giuliana Pelicci
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Cancer Stem Cells ◽  
Large Scale ◽  
Molecular Mechanisms ◽  
Cell Phenotype ◽  
Multiple Tumor ◽  
Early Results ◽  
Tumorigenic Potential ◽  
Tumor Types

Cancer stem cells (CSCs) were isolated in multiple tumor types, including human glioblastomas, and although the presence of surface markers selectively expressed on CSCs can be used to isolate them, no marker/pattern of markers are sufficiently robust to definitively identify stem cells in tumors. Several markers were evaluated for their prognostic value with promising early results, however none of them was proven to be clinically useful in large-scale studies, leading to outstanding efforts to identify new markers. Given the heterogeneity of human glioblastomas further investigations are necessary to identify both cancer stem cell-specific markers and the molecular mechanisms sustaining the tumorigenic potential of these cells to develop tailored treatments. Markers for glioblastoma stem cells such as CD133, CD15, integrin-α6, L1CAM might be informative to identify these cells but cannot be conclusively linked to a stem cell phenotype. Overlap of expression, functional state and morphology of different subpopulations lead to carefully consider the techniques employed so far to isolate these cells. Due to a dearth of methods and markers reliably identifying the candidate cancer stem cells, the isolation/enrichment of cancer stem cells to be therapeutically targeted remains a major challenge.

scholarly journals Targeting Signaling Pathways in Cancer Stem Cells for Cancer Treatment

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Jeffrey Koury ◽  
Li Zhong ◽  
Jijun Hao
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Treatment ◽  
Signaling Pathways ◽  
Small Subset ◽  
Self Renewal ◽  
Multiple Tumor ◽  
Notch Pathways ◽  
Tumor Types ◽  
Heterogeneous Tumor

The Wnt, Hedgehog, and Notch pathways are inherent signaling pathways in normal embryogenesis, development, and hemostasis. However, dysfunctions of these pathways are evident in multiple tumor types and malignancies. Specifically, aberrant activation of these pathways is implicated in modulation of cancer stem cells (CSCs), a small subset of cancer cells capable of self-renewal and differentiation into heterogeneous tumor cells. The CSCs are accountable for tumor initiation, growth, and recurrence. In this review, we focus on roles of Wnt, Hedgehog, and Notch pathways in CSCs’ stemness and functions and summarize therapeutic studies targeting these pathways to eliminate CSCs and improve overall cancer treatment outcomes.

Targeting Nodal and Cripto-1: Perspectives Inside Dual Potential Theranostic Cancer Biomarkers

2019 ◽  
Vol 26 (11) ◽  
pp. 1994-2050 ◽  
Author(s):  
Annamaria Sandomenico ◽  
Menotti Ruvo
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Normal Development ◽  
Cancer Biomarkers ◽  
Normal Tissues ◽  
Tumor Relapse ◽  
Developmental Factors ◽  
Theranostic Agents ◽  
Tumor Types ◽  
Embryonic Signaling

Background:Elucidating the mechanisms of recurrence of embryonic signaling pathways in tumorigenesis has led to the discovery of onco-fetal players which have physiological roles during normal development but result aberrantly re-activated in tumors. In this context, Nodal and Cripto-1 are recognized as onco-developmental factors, which are absent in normal tissues but are overexpressed in several solid tumors where they can serve as theranostic agents.Objective:To collect, review and discuss the most relevant papers related to the involvement of Nodal and Cripto-1 in the development, progression, recurrence and metastasis of several tumors where they are over-expressed, with a particular attention to their occurrence on the surface of the corresponding sub-populations of cancer stem cells (CSC).Results:We have gathered, rationalized and discussed the most interesting findings extracted from some 370 papers related to the involvement of Cripto-1 and Nodal in all tumor types where they have been detected. Data demonstrate the clear connection between Nodal and Cripto-1 presence and their multiple oncogenic activities across different tumors. We have also reviewed and highlighted the potential of targeting Nodal, Cripto-1 and the complexes that they form on the surface of tumor cells, especially of CSC, as an innovative approach to detect and suppress tumors with molecules that block one or more mechanisms that they regulate.Conclusion:Overall, Nodal and Cripto-1 represent two innovative and effective biomarkers for developing potential theranostic anti-tumor agents that target normal as well as CSC subpopulations and overcome both pharmacological resistance and tumor relapse.

scholarly journals Cancer stem cells: a new approach to tumor development

2015 ◽  
Vol 61 (1) ◽  
pp. 86-93 ◽  
Author(s):  
Natália Cristina Ciufa Kobayashi ◽  
Samuel Marcos Ribeiro de Noronha
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Cancer Stem Cells ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Cell Cancer ◽  
Tumor Development ◽  
New Approach ◽  
Tumor Types ◽  
Immunosuppressed Mice

Many theories have been proposed to explain the origins of cancer. Currently, evidences show that not every tumor cell is capable of initiating a tumor. Only a small part of the cancer cells, called cancer stem cells (CSCs), can generate a tumor identical to the original one, when removed from human tumors and transplanted into immunosuppressed mice. The name given to these cells comes from the resemblance to normal stem cells, except for the fact that their ability to divide is infinite. These cells are also affected by their microenvironment. Many of the signaling pathways, such as Wnt, Notch and Hedgehog, are altered in this tumoral subpopulation, which also contributes to abnormal proliferation. Researchers have found several markers for CSCs; however, much remains to be studied, or perhaps a universal marker does not even exist, since they vary among tumor types and even from patient to patient. It was also found that cancer stem cells are resistant to radiotherapy and chemotherapy. This may explain the re-emergence of the disease, since they are not completely eliminated and minimal amounts of CSCs can repopulate a tumor. Once the diagnosis in the early stages greatly increases the chances of curing cancer, identifying CSCs in tumors is a goal for the development of more effective treatments. The objective of this article is to discuss the origin of cancer according to the theory of stem cell cancer, as well as its markers and therapies used for treatment.

Clinical Experience With Hedgehog Pathway Inhibitors

2010 ◽  
Vol 28 (36) ◽  
pp. 5321-5326 ◽  
Author(s):  
Jennifer A. Low ◽  
Frederic J. de Sauvage
Keyword(s):  
Stem Cells ◽  
Cell Growth ◽  
Cancer Stem Cells ◽  
Basal Cell Carcinoma ◽  
Myelogenous Leukemia ◽  
Molecule Inhibitor ◽  
Cell Growth And Differentiation ◽  
Hh Signaling ◽  
Tumor Types

The Hedgehog (Hh) signaling pathway is critical for cell growth and differentiation during embryogenesis and early development. While it is mostly quiescent in adults, inappropriate reactivation of the Hh pathway has been shown to be involved in the development of cancer. A number of tumor types rely on overexpression of Hh ligands to activate the pathway in a paracrine manner from the tumor to the surrounding stroma. Alternatively, Hh ligands may act on cancer stem cells in some hematopoietic cancers, such as chronic myelogenous leukemia. However, the role of the Hh pathway is best established in tumors, such as basal cell carcinoma and medulloblastoma, where the pathway is activated via mutations. Understanding the contribution of Hh signaling in these various tumor types will be critical to the development and use of agents targeting this pathway in the clinic. We review here the activity of clinical inhibitors of the Hh pathway, including GDC-0449, a small molecule inhibitor of Smoothened (SMO).

scholarly journals Estimating stem cell fractions in hierarchically organized tumors

2015 ◽  
Author(s):  
Benjamin Werner ◽  
Jacob G Scott ◽  
Andrea Sottoriva ◽  
Alexander RA Anderson ◽  
Arne Traulsen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Cancer Stem Cells ◽  
Tumor Growth ◽  
Treatment Strategies ◽  
Exact Result ◽  
Growth Patterns ◽  
Cell Fractions ◽  
Tumor Types

Cancers arise as a result of genetic and epigenetic alterations. These accumulate in cells during the processes of tissue development, homeostasis and repair. Many tumor types are hierarchically organized and driven by a sub-population of cells often called cancer stem cells. Cancer stem cells are uniquely capable of recapitulating the tumor and can be highly resistant to radio- and chemotherapy treatment. We investigate tumor growth patterns from a theoretical standpoint and show how significant changes in pre- and post-therapy tumor dynamics are tied to the dynamics of cancer stem cells. We identify two characteristic growth regimes of a tumor population that can be leveraged to estimate cancer stem cell fractions in vivo using simple linear regression. Our method is a mathematically exact result, parameter free and does not require any microscopic knowledge of the tumor properties. A more accurate quantification of the direct link between the sub-population driving tumor growth and treatment response promises new ways to individualize treatment strategies.

scholarly journals Different Shades of L1CAM in the Pathophysiology of Cancer Stem Cells

2020 ◽  
Vol 9 (5) ◽  
pp. 1502 ◽  
Author(s):  
Marco Giordano ◽  
Ugo Cavallaro
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Epithelial Mesenchymal Transition ◽  
Therapy Resistance ◽  
Biological Properties ◽  
Cytotoxic Agents ◽  
Tumor Initiating Cells ◽  
Mesenchymal Transition ◽  
Tumor Types

L1 cell adhesion molecule (L1CAM) is aberrantly expressed in several tumor types where it is causally linked to malignancy and therapy resistance, acting also as a poor prognosis factor. Accordingly, several approaches have been developed to interfere with L1CAM function or to deliver cytotoxic agents to L1CAM-expressing tumors. Metastatic dissemination, tumor relapse and drug resistance can be fueled by a subpopulation of neoplastic cells endowed with peculiar biological properties that include self-renewal, efficient DNA repair, drug efflux machineries, quiescence, and immune evasion. These cells, known as cancer stem cells (CSC) or tumor-initiating cells, represent, therefore, an ideal target for tumor eradication. However, the molecular and functional traits of CSC have been unveiled only to a limited extent. In this context, it appears that L1CAM is expressed in the CSC compartment of certain tumors, where it plays a causal role in stemness itself and/or in biological processes intimately associated with CSC (e.g., epithelial-mesenchymal transition (EMT) and chemoresistance). This review summarizes the role of L1CAM in cancer focusing on its functional contribution to CSC pathophysiology. We also discuss the clinical usefulness of therapeutic strategies aimed at targeting L1CAM in the context of anti-CSC treatments.

scholarly journals Deubiquitinating Enzyme-Mediated Signaling Networks in Cancer Stem Cells

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3253
Author(s):  
Kamini Kaushal ◽  
Suresh Ramakrishna
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Cancer Stem Cells ◽  
Signaling Pathways ◽  
Cell Fate ◽  
Deubiquitinating Enzymes ◽  
Self Renewal ◽  
Stem Cell Fate ◽  
Multiple Tumor ◽  
Cell Fate Decisions

Cancer stem cells (CSCs) have both the capacity for self-renewal and the potential to differentiate and contribute to multiple tumor properties, such as recurrence, metastasis, heterogeneity, multidrug resistance, and radiation resistance. Thus, CSCs are considered to be promising therapeutic targets for cancer therapy. The function of CSCs can be regulated by ubiquitination and deubiquitination of proteins related to the specific stemness of the cells executing various stem cell fate choices. To regulate the balance between ubiquitination and deubiquitination processes, the disassembly of ubiquitin chains from specific substrates by deubiquitinating enzymes (DUBs) is crucial. Several key developmental and signaling pathways have been shown to play essential roles in this regulation. Growing evidence suggests that overactive or abnormal signaling within and among these pathways may contribute to the survival of CSCs. These signaling pathways have been experimentally shown to mediate various stem cell properties, such as self-renewal, cell fate decisions, survival, proliferation, and differentiation. In this review, we focus on the DUBs involved in CSCs signaling pathways, which are vital in regulating their stem-cell fate determination.

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