Cancer stem cells and clonal evolution in bone sarcomas

2022 ◽  
pp. 371-391
Author(s):  
René Rodríguez ◽  
Jiri Hatina ◽  
Stefano Gambera ◽  
Sofía T. Menéndez ◽  
Javier García-Castro
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Clonal Evolution ◽  
Bone Sarcomas

scholarly journals Lung Cancer Stem Cells—Origin, Diagnostic Techniques and Perspective for Therapies

Cancers ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2996
Author(s):  
Agata Raniszewska ◽  
Iwona Kwiecień ◽  
Elżbieta Rutkowska ◽  
Piotr Rzepecki ◽  
Joanna Domagała-Kulawik
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Early Recognition ◽  
Human Life ◽  
Clonal Evolution ◽  
Diagnostic Techniques ◽  
Complex Processes ◽  
Age Related ◽  
Lung Cancer Stem Cells

Lung cancer remains one of the most aggressive solid tumors with an overall poor prognosis. Molecular studies carried out on lung tumors during treatment have shown the phenomenon of clonal evolution, thereby promoting the occurrence of a temporal heterogeneity of the tumor. Therefore, the biology of lung cancer is interesting. Cancer stem cells (CSCs) are involved in tumor initiation and metastasis. Aging is still the most important risk factor for lung cancer development. Spontaneously occurring mutations accumulate in normal stem cells or/and progenitor cells by human life resulting in the formation of CSCs. Deepening knowledge of these complex processes and improving early recognition and markers of predictive value are of utmost importance. In this paper, we discuss the CSC hypothesis with an emphasis on age-related changes that initiate carcinogenesis. We analyze the current literature in the field, describe our own experience in CSC investigation and discuss the technical challenges with special emphasis on liquid biopsy.

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.

scholarly journals Breast Tumor Heterogeneity: Cancer Stem Cells or Clonal Evolution?

Cell Cycle ◽  
2007 ◽  
Vol 6 (19) ◽  
pp. 2332-2338 ◽  
Author(s):  
Lauren L. Campbell ◽  
Kornelia Polyak
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Breast Tumor ◽  
Tumor Heterogeneity ◽  
Clonal Evolution

scholarly journals Targeting Aldehyde Dehydrogenases to Eliminate Cancer Stem Cells in Gynecologic Malignancies

Cancers ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 961 ◽  
Author(s):  
Vaishnavi Muralikrishnan ◽  
Thomas D. Hurley ◽  
Kenneth P. Nephew
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Clonal Evolution ◽  
Gynecologic Malignancies ◽  
Gynecologic Cancers ◽  
Aldehyde Dehydrogenases ◽  
Functional Roles ◽  
Clinical Scenarios ◽  
Attractive Therapeutic Target ◽  
Reduce Tumor Growth

Gynecologic cancers cause over 600,000 deaths annually in women worldwide. The development of chemoresistance after initial rounds of chemotherapy contributes to tumor relapse and death due to gynecologic malignancies. In this regard, cancer stem cells (CSCs), a subpopulation of stem cells with the ability to undergo self-renewal and clonal evolution, play a key role in tumor progression and drug resistance. Aldehyde dehydrogenases (ALDH) are a group of enzymes shown to be robust CSC markers in gynecologic and other malignancies. These enzymes also play functional roles in CSCs, including detoxification of aldehydes, scavenging of reactive oxygen species (ROS), and retinoic acid (RA) signaling, making ALDH an attractive therapeutic target in various clinical scenarios. In this review, we discuss the critical roles of the ALDH in driving stemness in different gynecologic malignancies. We review inhibitors of ALDH, both general and isoform-specific, which have been used to target CSCs in gynecologic cancers. Many of these inhibitors have been shown to be effective in preclinical models of gynecologic malignancies, supporting further development in the clinic. Furthermore, ALDH inhibitors, including 673A and CM037, synergize with chemotherapy to reduce tumor growth. Thus, ALDH-targeted therapies hold promise for improving patient outcomes in gynecologic malignancies.

Human primary bone sarcomas contain CD133 + cancer stem cells displaying high tumorigenicity in vivo

2011 ◽  
Vol 25 (6) ◽  
pp. 2022-2030 ◽  
Author(s):  
Virginia Tirino ◽  
Vincenzo Desiderio ◽  
Francesca Paino ◽  
Alfredo De Rosa ◽  
Federica Papaccio ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Bone Sarcomas ◽  
Primary Bone

Cancer stem cells: A product of clonal evolution?

2016 ◽  
Vol 140 (5) ◽  
pp. 993-999 ◽  
Author(s):  
Gustav van Niekerk ◽  
Lester M. Davids ◽  
Suzèl M. Hattingh ◽  
Anna-Mart Engelbrecht
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Clonal Evolution

scholarly journals Cancer Stem Cells and Nucleolin as Drivers of Carcinogenesis

2021 ◽  
Vol 14 (1) ◽  
pp. 60
Author(s):  
Laura Sofia Carvalho ◽  
Nélio Gonçalves ◽  
Nuno André Fonseca ◽  
João Nuno Moreira
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Clonal Evolution ◽  
Therapy Resistance ◽  
Cellular Heterogeneity ◽  
Multifunctional Protein ◽  
Mesenchymal Transition ◽  
Cancer Hallmarks

Cancer, one of the most mortal diseases worldwide, is characterized by the gain of specific features and cellular heterogeneity. Clonal evolution is an established theory to explain heterogeneity, but the discovery of cancer stem cells expanded the concept to include the hierarchical growth and plasticity of cancer cells. The activation of epithelial-to-mesenchymal transition and its molecular players are widely correlated with the presence of cancer stem cells in tumors. Moreover, the acquisition of certain oncological features may be partially attributed to alterations in the levels, location or function of nucleolin, a multifunctional protein involved in several cellular processes. This review aims at integrating the established hallmarks of cancer with the plasticity of cancer cells as an emerging hallmark; responsible for tumor heterogeneity; therapy resistance and relapse. The discussion will contextualize the involvement of nucleolin in the establishment of cancer hallmarks and its application as a marker protein for targeted anticancer therapies

scholarly journals Ovarian Cancers: Genetic Abnormalities, Tumor Heterogeneity and Progression, Clonal Evolution and Cancer Stem Cells

Medicines ◽  
2018 ◽  
Vol 5 (1) ◽  
pp. 16 ◽  
Author(s):  
Ugo Testa ◽  
Eleonora Petrucci ◽  
Luca Pasquini ◽  
Germana Castelli ◽  
Elvira Pelosi
Keyword(s):  
Ovarian Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Clonal Evolution ◽  
Cell Subpopulation ◽  
Ovarian Cancer Cells ◽  
High Grade ◽  
Histological Subtypes ◽  
Ovarian Cancer Stem Cells ◽  
Ovarian Cancers

Four main histological subtypes of ovarian cancer exist: serous (the most frequent), endometrioid, mucinous and clear cell; in each subtype, low and high grade. The large majority of ovarian cancers are diagnosed as high-grade serous ovarian cancers (HGS-OvCas). TP53 is the most frequently mutated gene in HGS-OvCas; about 50% of these tumors displayed defective homologous recombination due to germline and somatic BRCA mutations, epigenetic inactivation of BRCA and abnormalities of DNA repair genes; somatic copy number alterations are frequent in these tumors and some of them are associated with prognosis; defective NOTCH, RAS/MEK, PI3K and FOXM1 pathway signaling is frequent. Other histological subtypes were characterized by a different mutational spectrum: LGS-OvCas have increased frequency of BRAF and RAS mutations; mucinous cancers have mutation in ARID1A, PIK3CA, PTEN, CTNNB1 and RAS. Intensive research was focused to characterize ovarian cancer stem cells, based on positivity for some markers, including CD133, CD44, CD117, CD24, EpCAM, LY6A, ALDH1. Ovarian cancer cells have an intrinsic plasticity, thus explaining that in a single tumor more than one cell subpopulation, may exhibit tumor-initiating capacity. The improvements in our understanding of the molecular and cellular basis of ovarian cancers should lead to more efficacious treatments.

scholarly journals Androgen receptor and prostate cancer stem cells: biological mechanisms and clinical implications

2015 ◽  
Vol 22 (6) ◽  
pp. T209-T220 ◽  
Author(s):  
Qu Deng ◽  
Dean G Tang
Keyword(s):  
Prostate Cancer ◽  
Stem Cells ◽  
Androgen Receptor ◽  
Cancer Stem Cells ◽  
Clonal Evolution ◽  
Population Level ◽  
Cell Types ◽  
Therapy Resistance ◽  
Cellular Heterogeneity ◽  
Prostate Cancer Stem Cells

Prostate cancer (PCa) contains phenotypically and functionally distinct cells, and this cellular heterogeneity poses clinical challenges as the distinct cell types likely respond differently to various therapies. Clonal evolution, driven by genetic instability, and intraclonal cancer cell diversification, driven by cancer stem cells (CSCs), together create tumor cell heterogeneity. In this review, we first discuss PCa stem cells (PCSCs) and heterogeneity of androgen receptor (AR) expression in primary, metastatic, and treatment-failed PCa. Based on literature reports and our own studies, we hypothesize that, whereas PCSCs in primary and untreated tumors and models are mainly AR−, PCSCs in CRPCs could be either AR+or AR−/lo. We illustrate the potential mechanisms AR+and AR−PCSCs may employ to propagate PCa at the population level, mediate therapy resistance, and metastasize. As a result, targeting AR alone may not achieve long-lasting therapeutic efficacy. Elucidating the roles of AR and PCSCs should provide important clues to designing novel personalized combinatorial therapeutic protocols targeting both AR+and AR−PCa cells.

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