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Journal articles on the topic 'Cancer cells'

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Author: Grafiati

Published: 4 June 2021

Last updated: 28 July 2024

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1

Fernández-Lázaro, Diego, César Ignacio Fernández-Lázaro, and Martínez Alfredo Córdova. "Cell Death: Mechanisms and Pathways in Cancer Cells." Cancer Medicine Journal 1, no. 1 (August 31, 2018): 12–23. http://dx.doi.org/10.46619/cmj.2018.1-1003.

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Programmed cell death is an essential physiological and biological process for the proper development and functioning of the organism. Apoptosis is the term that describes the most frequent form of programmed cell death and derives from the morphological characteristics of this type of death caused by cellular suicide. Apoptosis is highly regulated to maintain homeostasis in the body, since its imbalances by increasing and decreasing lead to different types of diseases. In this review, we aim to describe the mechanisms of cell death and the pathways through apoptosis is initiated, transmitted, regulated, and executed.

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2

Srivastava, A. N., Neema Tiwari, Shailendra Yadav, and Suryakant . "LUNG CANCER STEM CELLS-AN UPDATE." Era's journal of medical research 4, no. 1 (June 1, 2017): 22–31. http://dx.doi.org/10.24041/ejmr2017.4.

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3

Fujimoto, Naohiro, Bin Han, Masayoshi Nomura, and Tetsuro Matsumoto. "WS1-1-1 Nitrogen-Containing Bisphosphonates Inhibit the Growth of Renal Cell Carcinoma Cells(Renal Cell Cancer)." Japanese Journal of Urology 99, no. 2 (2008): 142. http://dx.doi.org/10.5980/jpnjurol.99.142_1.

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4

MAS, Bezerra, Ferreira LAM, Kawasaki-Oyama RS, Nascimento MCA, Cuzziol CI, Castanhole-Nunes MMU, Pavarino EC, Maniglia JM, and Goloni-Bertollo EM. "Effectiveness of Hypoxia-Induced Accumulation of Cancer Stem Cells in Head and Neck Squamous Cell Carcinoma." Cancer Medicine Journal 3, S1 (November 30, 2020): 13–23. http://dx.doi.org/10.46619/cmj.2020.3.s1-1003.

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INTRODUCTION: The small number of cancer stem cells, which correspond to only 0.01% - 0.1% of total tumor cells, has been the biggest obstacle in understanding their biology and role in the origin and maintenance of tumors, their metastatic and recurrence potentials, and resistance to radio-chemotherapy. Therefore, promoting its accumulation will enable further studies and future advances in the diagnosis and treatment of head and neck cancer squamous cell carcinoma. OBJECTIVE: To induce cancer stem cell accumulation in primary cell cultures of head and neck squamous cell carcinoma using a hypoxia chamber. METHODS: Head and neck squamous cell carcinoma samples were cultured and subjected to hypoxia. Oxygen deprivation aimed to induce cancer stem cell accumulation. RESULTS: Immediately after hypoxia, the percentage of O2-deprived cancer stem cells increased 2-fold as compared to control. Surprisingly, new phenotyping performed 45 days after hypoxia showed a 9-fold increase in cancer stem cell percentage in cells that suffered hypoxia. Hypoxic cells showed an increase in spheroid formation when compared to control cells, as well as enhanced abilities in invasion and migration. CONCLUSION: Hypoxia was efficient in cancer stem cell accumulation. As cancer stem cells are a small number of cells within the tumor, promoting their accumulation will enable further studies and future advances in the diagnosis and treatment of head and neck cancer.

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Yin, Wen, Jialing Wang, Linling Jiang, and Y. James Kang. "Cancer and stem cells." Experimental Biology and Medicine 246, no. 16 (April 5, 2021): 1791–801. http://dx.doi.org/10.1177/15353702211005390.

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Being the second leading cause of death globally, cancer has been a long-standing and rapidly evolving focus of biomedical research and practice in the world. A tremendous effort has been made to understand the origin of cancer cells, the formation of cancerous tissues, and the mechanism by which they spread and relapse, but the disease still remains mysterious. Here, we made an attempt to scrutinize evidences that indicate the role of stem cells in tumorigenesis and metastasis, and cancer relapse. We also looked into the influence of cancers on stem cells, which in turn represent a major constituent of tumor microenvironment. Based on current understandings of the properties of (cancer) stem cells and their relation to cancers, we can foresee that novel therapeutic approaches would become the next wave of cancer treatment.

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Pratap, Dr Pushpendra D. "CANCER STEM CELLS IN CERVICAL CANCER AS BENEFICIAL GOALS AND BIOMARKERS: A COMPREHENSIVE." Era's Journal of Medical Research 10, no. 2 (December 2023): 51–55. http://dx.doi.org/10.24041/ejmr2023.36.

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The fourth most prevalent gynaecological malignancy affecting females globally is cervical cancer (CC). HPV (high-risk) infection has been related to the majority of CC cases. Owing to efficient screening through Pap smear and vaccination delivery, the commonness and death rate of CC have significantly decreased. Nevertheless, not all societies have access to this equally. A better therapeutic outcome may be achieved by targeting CSCs, which might play a significant impact in carcinogenesis, metastasis, recurrence, and radio / chemo –resistance of CC. The majority of tumours are made up of a tiny subset of tumour cells called CSCs that have the capability to self-renew and develop into a variety of tumour cell types. Cervical CSCs (CCSC) are challenging to recognise, which has prompted the hunt for other markers. The potential indicators of CSCs in CC are described in the current review. These CCSC indicators might be used as molecular goals to improve the effectiveness and lessen the negative effects of chemotherapy in HR-HPV-positive CC.

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7

Moorthy, Rajesh Kannan, Chandhru Srinivasan, Sridharan Jayamohan, Mahesh Kumar Kannan, Siva Sankari Thirugnanam, Janaki Sankar Ganesh, and Antony Joseph Velanganni Arockiam. "Knockdown of microRNA-375 suppresses cell proliferation and promotes apoptosis in human breast cancer cells." Indian Journal of Science and Technology 14, no. 43 (November 12, 2021): 3199–209. http://dx.doi.org/10.17485/ijst/v14i43.1719.

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8

Lee, Cheong J., Joseph Dosch, and Diane M. Simeone. "Pancreatic Cancer Stem Cells." Journal of Clinical Oncology 26, no. 17 (June 10, 2008): 2806–12. http://dx.doi.org/10.1200/jco.2008.16.6702.

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Cellular heterogeneity in cancer was observed decades ago by studies in mice which showed that distinct subpopulations of cells within a tumor mass are capable of driving tumorigenesis. Conceptualized from this finding was the stem-cell hypothesis for cancer, which suggests that only a specific subset of cancer cells within each tumor is responsible for tumor initiation and propagation, termed tumor initiating cells or cancer stem cells (CSCs). Recent data has been provided to support the existence of CSCs in human blood cell–derived cancers and solid organ tumors of the breast, brain, prostate, colon, and skin. Study of human pancreatic cancers has also revealed a specific subpopulation of cancer cells that possess the characteristics of CSCs. These pancreatic cancer stem cells express the cell surface markers CD44, CD24, and epithelial-specific antigen, and represent 0.5% to 1.0% of all pancreatic cancer cells. Along with the properties of self-renewal and multilineage differentiation, pancreatic CSCs display upregulation of important developmental genes that maintain self-renewal in normal stem cells, including Sonic hedgehog (SHH) and BMI-1. Signaling cascades that are integral in tumor metastasis are also upregulated in the pancreatic CSC. Understanding the biologic behavior and the molecular pathways that regulate growth, survival, and metastasis of pancreatic CSCs will help to identify novel therapeutic approaches to treat this dismal disease.

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9

Elgaly, Maher E., Mohamed E. El Ghareeb, and Farha El shennawy. "Cord Blood Mesenchymal Stem Cells Conditioned Media Suppress Epithelial Ovarian Cancer Cells in Vitro." International Journal of Trend in Scientific Research and Development Volume-2, Issue-5 (August 31, 2018): 1783–88. http://dx.doi.org/10.31142/ijtsrd18182.

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10

SK, Deshmukh. "Immune Cells in the Tumor Microenvironment and Cancer Stem Cells: Interplay for Tumor Progression." Journal of Embryology & Stem Cell Research 2, no. 2 (2018): 1–2. http://dx.doi.org/10.23880/jes-16000109.

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11

Inderberg, Else Marit, and Sébastien Wälchli. "T cells successfully fighting cancer." Open Access Government 43, no. 1 (July 8, 2024): 84–85. http://dx.doi.org/10.56367/oag-043-11536.

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T cells successfully fighting cancer Else Marit Inderberg and Sébastien Wälchli from Oslo University Hospital explore what we need to know about T cells successfully fighting cancer. Cell-based immunotherapy uses the patient’s own immune cells to target and kill cancer cells in a specific manner. Lymphocytes called T cells are mainly used for this type of therapy, and to target them more efficiently against cancer cells, they are genetically modified to express chimeric antigen receptors (CAR) or T cell receptors (TCR) that bind proteins or peptides presented on the surface of cancer cells. There are currently six CAR T cell therapies approved for the treatment of blood cancers. However, none of these cellular therapies are yet available outside clinical studies for solid cancers.

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12

KOCHIN, Vitaly, Takayuki KANASEKI, Daiichi MOROOKA, Akari TAKAYA, Yoshihiko HIROHASHI, Yasuo KOKAI, Toshihiko TORIGOE, and Noriyuki SATO. "P4-006 Natural peptidome presented by HLA-A24 of cancer and cancer stem cells." Japanese Journal of Clinical Immunology 37, no. 4 (2014): 348b. http://dx.doi.org/10.2177/jsci.37.348b.

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13

Logtenberg, Meike E. W., and Johannes Boonstra. "Cancer stem cells and addicted cancer cells." Oncology Discovery 1, no. 1 (2013): 7. http://dx.doi.org/10.7243/2052-6199-1-7.

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14

Reya, Tannishtha, Sean J. Morrison, Michael F. Clarke, and Irving L. Weissman. "Stem cells, cancer, and cancer stem cells." Nature 414, no. 6859 (November 2001): 105–11. http://dx.doi.org/10.1038/35102167.

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15

Pecqueur, Claire, Lisa Oliver, Kristell Oizel, Lisenn Lalier, and François M. Vallette. "Targeting Metabolism to Induce Cell Death in Cancer Cells and Cancer Stem Cells." International Journal of Cell Biology 2013 (2013): 1–13. http://dx.doi.org/10.1155/2013/805975.

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Abnormal metabolism and the evasion of apoptosis are considered hallmarks of cancers. Accumulating evidence shows that cancer stem cells are key drivers of tumor formation, progression, and recurrence. A successful therapy must therefore eliminate these cells known to be highly resistant to apoptosis. In this paper, we describe the metabolic changes as well as the mechanisms of resistance to apoptosis occurring in cancer cells and cancer stem cells, underlying the connection between these two processes.

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16

S, Tanabe. "Molecular Markers and Networks for Cancer and Stem Cells." Journal of Embryology & Stem Cell Research 1, no. 1 (2017): 1–13. http://dx.doi.org/10.23880/jes-16000101.

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17

Takaishi, Shigeo, Tomoyuki Okumura, and Timothy C. Wang. "Gastric Cancer Stem Cells." Journal of Clinical Oncology 26, no. 17 (June 10, 2008): 2876–82. http://dx.doi.org/10.1200/jco.2007.15.2603.

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Cancer stem cells are defined as the unique subpopulation in the tumors that possess the ability to initiate tumor growth and sustain self-renewal as well as metastatic potential. Accumulating evidence in recent years strongly indicate the existence of cancer stem cells in solid tumors of a wide variety of organs. In this review, we will discuss the possible existence of a gastric cancer stem cell. Our recent data suggest that a subpopulation with a defined marker shows spheroid colony formation in serum-free media in vitro, as well as tumorigenic ability in immunodeficient mice in vivo. We will also discuss the possible origins of the gastric cancer stem cell from an organ-specific stem cell versus a recently recognized new candidate bone marrow–derived cell (BMDC). We have previously shown that BMDC contributed to malignant epithelial cells in the mouse model of Helicobacter-associated gastric cancer. On the basis of these findings from animal model, we propose that a similar phenomenon may also occur in human cancer biology, particularly in the cancer origin of other inflammation-associated cancers. The expanding research field of cancer stem-cell biology may offer a novel clinical apparatus to the diagnosis and treatment of cancer.

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18

Kiberstis, P. A. "CANCER: Reprogramming Cancer Cells." Science 305, no. 5688 (August 27, 2004): 1214a. http://dx.doi.org/10.1126/science.305.5688.1214a.

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19

Afify, Chen, Yan, Calle, Nair, Murakami, Zahra, et al. "Method to Convert Stem Cells into Cancer Stem Cells." Methods and Protocols 2, no. 3 (August 16, 2019): 71. http://dx.doi.org/10.3390/mps2030071.

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The cancer stem cell (CSC) hypothesis suggests that tumors are sustained exclusively by a small population of the cells with stem cell properties. CSCs have been identified in most tumors and are responsible for the initiation, recurrence, and resistance of different cancers. In vitro CSC models will be of great help in revisiting the mechanism of cancer development, as well as the tumor microenvironment and the heterogeneity of cancer and metastasis. Our group recently described the generation of CSCs from induced pluripotent stem cells (iPSCs), which were reprogrammed from normal cells, and/or embryonic stem cells (ESCs). This procedure will improve the understanding of the essential niche involved in cancer initiation. The composition of this cancer-inducing niche, if identified, will let us know how normal cells convert to malignant in the body and how, in turn, cancer prevention could be achieved. Further, once developed, CSCs demonstrate the ability to differentiate into endothelial cells, cancer-associated fibroblasts, and other phenotypes establishing the CSC niche. These will be good materials for developing novel cancer treatments. In this protocol, we describe how to handle mouse iPSCs/ESCs and how to choose the critical time for starting the conversion into CSCs. This CSC generation protocol is essential for understanding the role of CSC in cancer initiation and progress.

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20

Michor, Franziska. "Mathematical Models of Cancer Stem Cells." Journal of Clinical Oncology 26, no. 17 (June 10, 2008): 2854–61. http://dx.doi.org/10.1200/jco.2007.15.2421.

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Human cancers are thought to be sustained in their growth by a pathologic counterpart of normal adult stem cells: cancer stem cells. This concept was first developed in human myeloid leukemias and is today being extended to solid tumors such as breast and brain cancers. A quantitative understanding of cancer stem cells requires a mathematical framework to describe the dynamics of cancer initiation and progression, the response to treatment, and the evolution of resistance. In this review, I use chronic myeloid leukemia as an example to discuss how mathematical and computational techniques have been used to gain insights into the biology of cancer stem cells.

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21

Balzanelli, Mario G., Pietro Distratis, Rita Lazzaro, Van Hung Pham, Raffaele Del Prete, Adriana Mosca, Francesco Inchingolo, et al. "From Pathogens to Cancer: Are Cancer Cells Evolved Mitochondrial Super Cells?" Diagnostics 13, no. 4 (February 20, 2023): 813. http://dx.doi.org/10.3390/diagnostics13040813.

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Life is based on a highly specific combination of atoms, metabolism, and genetics which eventually reflects the chemistry of the Universe which is composed of hydrogen, oxygen, nitrogen, sulfur, phosphorus, and carbon. The interaction of atomic, metabolic, and genetic cycles results in the organization and de-organization of chemical information of that which we consider as living entities, including cancer cells. In order to approach the problem of the origin of cancer it is therefore reasonable to start from the assumption that the sub-molecular level, the atomic structure, should be the considered starting point on which metabolism, genetics, and external insults eventually emanate. Second, it is crucial to characterize which of the entities and parts composing human cells may live a separate life; certainly, this theoretical standpoint would consider mitochondria, an organelle of “bacteria” origin embedded in conditions favorable for the onset of both. This organelle has not only been tolerated by immunity but has also been placed as a central regulator of cell defense. Virus, bacteria, and mitochondria are also similar in the light of genetic and metabolic elements; they share not only equivalent DNA and RNA features but also many basic biological activities. Thus, it is important to finalize that once the cellular integrity has been constantly broken down, the mitochondria like any other virus or bacteria return to their original autonomy to simply survive. The Warburg’s law that states the ability of cancers to ferment glucose in the presence of oxygen, indicates mitochondria respiration abnormalities may be the underlying cause of this transformation towards super cancer cells. Though genetic events play a key part in altering biochemical metabolism, inducing aerobic glycolysis, this is not enough to impair mitochondrial function since mitochondrial biogenesis and quality control are constantly upregulated in cancers. While some cancers have mutations in the nuclear-encoded mitochondrial tricarboxylic acid (TCA) cycle, enzymes that produce oncogenic metabolites, there is also a bio-physic pathway for pathogenic mitochondrial genome mutations. The atomic level of all biological activities can be considered the very beginning, marked by the electron abnormal behavior that consequently affects DNA of both cells and mitochondria. Whilst the cell’s nucleus DNA after a certain number of errors and defection tends to gradually switch off, the mitochondria DNA starts adopting several escape strategies, switching-on a few important genes that belong back at their original roots as independent beings. The ability to adopt this survival trick, by becoming completely immune to current life-threatening events, is probably the beginning of a differentiation process towards a “super-power cell”, the cancer cells that remind many pathogens, including virus, bacteria, and fungi. Thus, here, we present a hypothesis regarding those changes that first begin at the mitochondria atomic level to steadily involve molecular, tissue and organ levels in response to the virus or bacteria constant insults that drive a mitochondria itself to become an “immortal cancer cell”. Improved insights into this interplay between these pathogens and mitochondria progression may disclose newly epistemological paradigms as well as innovative procedures in targeting cancer cell progressive invasion.

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22

Liu, Suling, and Max S. Wicha. "Targeting Breast Cancer Stem Cells." Journal of Clinical Oncology 28, no. 25 (September 1, 2010): 4006–12. http://dx.doi.org/10.1200/jco.2009.27.5388.

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There is increasing evidence that many cancers, including breast cancer, contain populations of cells that display stem-cell properties. These breast cancer stem cells, by virtue of their relative resistance to radiation and cytotoxic chemotherapy, may contribute to treatment resistance and relapse. The elucidation of pathways that regulate these cells has led to the identification of potential therapeutic targets. A number of agents capable of targeting breast cancer stem cells in preclinical models are currently entering clinical trials. Assessment of the efficacy of the agents will require development of innovative clinical trial designs with appropriate biologic and clinical end points. The effective targeting of breast cancer stem cells has the potential to significantly improve outcome for women with both early-stage and advanced breast cancer.

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23

Gedye, Craig, Adee-Jonathan Davidson, Martin R. Elmes, Jonathan Cebon, Damien Bolton, and Ian D. Davis. "Cancer stem cells in urologic cancers." Urologic Oncology: Seminars and Original Investigations 28, no. 6 (November 2010): 585–90. http://dx.doi.org/10.1016/j.urolonc.2009.06.010.

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24

Tavartkiladze, Alexandre, Revaz Turmanidze, Gaiane Simonia, Margalita Gogoladze, Pati Revazishvili, George Dundua, and Irine Andronikashvili. "Circulating Tumor Cells and cfDNA: Key Predictive Biomarkers in Non - Small Cell Lung Cancer Progression and Treatment." International Journal of Science and Research (IJSR) 12, no. 10 (October 5, 2023): 1078–81. http://dx.doi.org/10.21275/sr231013031834.

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25

Dyall, Sheetal, Simon A. Gayther, and Dimitra Dafou. "Cancer Stem Cells and Epithelial Ovarian Cancer." Journal of Oncology 2010 (2010): 1–9. http://dx.doi.org/10.1155/2010/105269.

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The cancer stem cell hypothesis is becoming more widely accepted as a model for carcinogenesis. Tumours are heterogeneous both at the molecular and cellular level, containing a small population of cells that possess highly tumourigenic “stem-cell” properties. Cancer stem cells (CSCs), or tumour-initiating cells, have the ability to self-renew, generate xenografts reminiscent of the primary tumour that they were derived from, and are chemoresistant. The characterisation of the CSC population within a tumour that drives its growth could provide novel target therapeutics against these cells specifically, eradicating the cancer completely. There have been several reports describing the isolation of putative cancer stem cell populations in several cancers; however, no defined set of markers has been identified that conclusively characterises “stem-like” cancer cells. This paper highlights the current experimental approaches that have been used in the field and discusses their limitations, with specific emphasis on the identification and characterisation of the CSC population in epithelial ovarian cancer.

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26

Krishnamurthy, S., and J. E. Nör. "Head and Neck Cancer Stem Cells." Journal of Dental Research 91, no. 4 (September 20, 2011): 334–40. http://dx.doi.org/10.1177/0022034511423393.

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Most cancers contain a small sub-population of cells that are endowed with self-renewal, multipotency, and a unique potential for tumor initiation. These properties are considered hallmarks of cancer stem cells. Here, we provide an overview of the field of cancer stem cells with a focus on head and neck cancers. Cancer stem cells are located in the invasive fronts of head and neck squamous cell carcinomas (HNSCC) close to blood vessels (perivascular niche). Endothelial cell-initiated signaling events are critical for the survival and self-renewal of these stem cells. Markers such as aldehyde dehydrogenase (ALDH), CD133, and CD44 have been successfully used to identify highly tumorigenic cancer stem cells in HNSCC. This review briefly describes the orosphere assay, a method for in vitro culture of undifferentiated head and neck cancer stem cells under low attachment conditions. Notably, recent evidence suggests that cancer stem cells are exquisitely resistant to conventional therapy and are the “drivers” of local recurrence and metastatic spread. The emerging understanding of the role of cancer stem cells in the pathobiology of head and neck squamous cell carcinomas might have a profound impact on the treatment paradigms for this malignancy.

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Runel, Gaël, Noémie Lopez-Ramirez, Julien Chlasta, and Ingrid Masse. "Biomechanical Properties of Cancer Cells." Cells 10, no. 4 (April 13, 2021): 887. http://dx.doi.org/10.3390/cells10040887.

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Since the crucial role of the microenvironment has been highlighted, many studies have been focused on the role of biomechanics in cancer cell growth and the invasion of the surrounding environment. Despite the search in recent years for molecular biomarkers to try to classify and stratify cancers, much effort needs to be made to take account of morphological and nanomechanical parameters that could provide supplementary information concerning tissue complexity adaptation during cancer development. The biomechanical properties of cancer cells and their surrounding extracellular matrix have actually been proposed as promising biomarkers for cancer diagnosis and prognosis. The present review first describes the main methods used to study the mechanical properties of cancer cells. Then, we address the nanomechanical description of cultured cancer cells and the crucial role of the cytoskeleton for biomechanics linked with cell morphology. Finally, we depict how studying interaction of tumor cells with their surrounding microenvironment is crucial to integrating biomechanical properties in our understanding of tumor growth and local invasion.

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Kadhim, Shahd Abdulamer. "Purpose of Intracellular Communication Connexin 43 in Breast Cancer Cells." International Journal of Psychosocial Rehabilitation 24, no. 4 (February 28, 2020): 3910–15. http://dx.doi.org/10.37200/ijpr/v24i4/pr201503.

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29

Nunes, Toni, Diaddin Hamdan, Christophe Leboeuf, Morad El Bouchtaoui, Guillaume Gapihan, Thi Nguyen, Solveig Meles, et al. "Targeting Cancer Stem Cells to Overcome Chemoresistance." International Journal of Molecular Sciences 19, no. 12 (December 13, 2018): 4036. http://dx.doi.org/10.3390/ijms19124036.

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Cancers are heterogeneous at the cell level, and the mechanisms leading to cancer heterogeneity could be clonal evolution or cancer stem cells. Cancer stem cells are resistant to most anti-cancer treatments and could be preferential targets to reverse this resistance, either targeting stemness pathways or cancer stem cell surface markers. Gold nanoparticles have emerged as innovative tools, particularly for photo-thermal therapy since they can be excited by laser to induce hyperthermia. Gold nanoparticles can be functionalized with antibodies to specifically target cancer stem cells. Preclinical studies using photo-thermal therapy have demonstrated the feasibility of targeting chemo-resistant cancer cells to reverse clinical chemoresistance. Here, we review the data linking cancer stem cells and chemoresistance and discuss the way to target them to reverse resistance. We particularly focus on the use of functionalized gold nanoparticles in the treatment of chemo-resistant metastatic cancers.

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Papaccio, Federica, Francesca Paino, Tarik Regad, Gianpaolo Papaccio, Vincenzo Desiderio, and Virginia Tirino. "Concise Review: Cancer Cells, Cancer Stem Cells, and Mesenchymal Stem Cells: Influence in Cancer Development." STEM CELLS Translational Medicine 6, no. 12 (October 26, 2017): 2115–25. http://dx.doi.org/10.1002/sctm.17-0138.

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31

Ding, Shijie, Chunbao Li, Ninghui Cheng, Xiaojiang Cui, Xinglian Xu, and Guanghong Zhou. "Redox Regulation in Cancer Stem Cells." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/750798.

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Reactive oxygen species (ROS) and ROS-dependent (redox regulation) signaling pathways and transcriptional activities are thought to be critical in stem cell self-renewal and differentiation during growth and organogenesis. Aberrant ROS burst and dysregulation of those ROS-dependent cellular processes are strongly associated with human diseases including many cancers. ROS levels are elevated in cancer cells partially due to their higher metabolism rate. In the past 15 years, the concept of cancer stem cells (CSCs) has been gaining ground as the subpopulation of cancer cells with stem cell-like properties and characteristics have been identified in various cancers. CSCs possess low levels of ROS and are responsible for cancer recurrence after chemotherapy or radiotherapy. Unfortunately, how CSCs control ROS production and scavenging and how ROS-dependent signaling pathways contribute to CSCs function remain poorly understood. This review focuses on the role of redox balance, especially in ROS-dependent cellular processes in cancer stem cells (CSCs). We updated recent advances in our understanding of ROS generation and elimination in CSCs and their effects on CSC self-renewal and differentiation through modulating signaling pathways and transcriptional activities. The review concludes that targeting CSCs by manipulating ROS metabolism/dependent pathways may be an effective approach for improving cancer treatment.

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Zecchin, Annalisa, Gitte Borgers, and Peter Carmeliet. "Endothelial cells and cancer cells." Current Opinion in Hematology 22, no. 3 (May 2015): 234–42. http://dx.doi.org/10.1097/moh.0000000000000138.

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Yue, Fengming, Kanji Hirashima, Daihachiro Tomotsune, Sakiko Takizawa-Shirasawa, Tadayuki Yokoyama, and Katsunori Sasaki. "Reprogramming of retinoblastoma cancer cells into cancer stem cells." Biochemical and Biophysical Research Communications 482, no. 4 (January 2017): 549–55. http://dx.doi.org/10.1016/j.bbrc.2016.11.072.

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34

Sucharitha, Are. "An Overview of Cancer." Advances in Cancer Chemotherapy and Pharmacology 1, no. 1 (2023): 1–8. http://dx.doi.org/10.23880/accp-16000102.

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Cancer is defined as one of the large groups of diseases characterized by the development of abnormal cells that grow beyond their boundaries, which can invade adjoining tissues via circulation, and spread to other organs in the body. Cancer can be initiated anywhere in the body, where damaged cells grow and multiply where they shouldn't. These cells form tumors, also called neoplasm- an abnormal mass of cells. Tumors can be non-cancerous (benign) and cancerous (malignant). Cancers are grouped according to their origin of tissue or organ. Four major types of cancers- • Carcinomas – are malignancies that begin in the epithelial cells, which make up the skin , and tissues that line other internal organs. Examples of carcinomas involved are prostate cancer, breast cancer, lung cancer, and colorectal cancer. • Sarcomas- sarcoma is a type of cancer that starts in tissues like bone or soft tissues and connective tissues . • Leukemias- leukemias are cancer of the white blood cells, which begins in the bone marrow as the bone marrow produces an excessive amount of abnormal white blood cells, that do not function properly. There are 4 major types of leukemia - acute lymphocytic leukemia, chronic lymphocytic leukemia, acute myelogenous leukemia, and chronic myelogenous leukemia . • Lymphoma- a cancer that begins in the lymphatic system, the lymphatic system includes the lymph nodes, spleen, thymus gland, and other network of vessels. There are main types of lymphomas- Hodgkin’s lymphoma and non-Hodgkin's lymphomas. • And there are also other types of cancer • In overview, cancer is a condition where cells multiply abnormally over time. The cells divide and grow rebelliously, they invade surrounding tissues and spread to distant parts of the body. In the course of time, the mass of the cancer cells can get massive enough to make lumps(tumors) that can be felt or seen. But not all tumors are cancer.

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Møller, Trine, Jaslin P. James, Kim Holmstrøm, Flemming B. Sørensen, Jan Lindebjerg, and Boye S. Nielsen. "Co-Detection of miR-21 and TNF-α mRNA in Budding Cancer Cells in Colorectal Cancer." International Journal of Molecular Sciences 20, no. 8 (April 17, 2019): 1907. http://dx.doi.org/10.3390/ijms20081907.

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MicroRNA-21 (miR-21) is upregulated in many cancers including colon cancers and is a prognostic indicator of recurrence and poor prognosis. In colon cancers, miR-21 is highly expressed in stromal fibroblastic cells and more weakly in a subset of cancer cells, particularly budding cancer cells. Exploration of the expression of inflammatory markers in colon cancers revealed tumor necrosis factor alpha (TNF-α) mRNA expression at the invasive front of colon cancers. Surprisingly, a majority of the TNF-α mRNA expressing cells were found to be cancer cells and not inflammatory cells. Because miR-21 is positively involved in cell survival and TNF-α promotes necrosis, we found it interesting to analyze the presence of miR-21 in areas of TNF-α mRNA expression at the invasive front of colon cancers. For this purpose, we developed an automated procedure for the co-staining of miR-21, TNF-α mRNA and the cancer cell marker cytokeratin based on analysis of frozen colon cancer tissue samples (n = 4) with evident cancer cell budding. In all four cases, TNF-α mRNA was seen in a small subset of cancer cells at the invasive front. Evaluation of miR-21 and TNF-α mRNA expression was performed on digital slides obtained by confocal slide scanning microscopy. Both co-expression and lack of co-expression with miR-21 in the budding cancer cells was noted, suggesting non-correlated expression. miR-21 was more often seen in cancer cells than TNF-α mRNA. In conclusion, we report that miR-21 is not linked to expression of the pro-inflammatory cytokine TNF-α mRNA, but that miR-21 and TNF-α both take part in the cancer expansion at the invasive front of colon cancers. We hypothesize that miR-21 may protect both fibroblasts and cancer cells from cell death directed by TNF-α paracrine and autocrine activity.

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Aguilar-Gallardo, Cristóbal, and Carlos Simón. "Cells, Stem Cells, and Cancer Stem Cells." Seminars in Reproductive Medicine 31, no. 01 (January 17, 2013): 005–13. http://dx.doi.org/10.1055/s-0032-1331792.

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Shang, Zhiyang, Yingxin Xu, Wentao Liang, Kai Liang, Xiang Hu, Lei Wang, Zhenyu Zou, and Yue Ma. "Isolation of cancer progenitor cells from cancer stem cells in gastric cancer." Molecular Medicine Reports 15, no. 6 (April 3, 2017): 3637–43. http://dx.doi.org/10.3892/mmr.2017.6423.

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Subramaniam, Dharmalingam, Gaurav Kaushik, Prasad Dandawate, and Shrikant Anant. "Targeting Cancer Stem Cells for Chemoprevention of Pancreatic Cancer." Current Medicinal Chemistry 25, no. 22 (July 4, 2018): 2585–94. http://dx.doi.org/10.2174/0929867324666170127095832.

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Pancreatic ductal adenocarcinoma is one of the deadliest cancers worldwide and the fourth leading cause of cancer-related deaths in United States. Regardless of the advances in molecular pathogenesis and consequential efforts to suppress the disease, this cancer remains a major health problem in United States. By 2030, the projection is that pancreatic cancer will be climb up to be the second leading cause of cancer-related deaths in the United States. Pancreatic cancer is a rapidly invasive and highly metastatic cancer, and does not respond to standard therapies. Emerging evidence supports that the presence of a unique population of cells called cancer stem cells (CSCs) as potential cancer inducing cells and efforts are underway to develop therapeutic strategies targeting these cells. CSCs are rare quiescent cells, and with the capacity to self-renew through asymmetric/symmetric cell division, as well as differentiate into various lineages of cells in the cancer. Studies have been shown that CSCs are highly resistant to standard therapy and also responsible for drug resistance, cancer recurrence and metastasis. To overcome this problem, we need novel preventive agents that target these CSCs. Natural compounds or phytochemicals have ability to target these CSCs and their signaling pathways. Therefore, in the present review article, we summarize our current understanding of pancreatic CSCs and their signaling pathways, and the phytochemicals that target these cells including curcumin, resveratrol, tea polyphenol EGCG (epigallocatechin- 3-gallate), crocetinic acid, sulforaphane, genistein, indole-3-carbinol, vitamin E δ- tocotrienol, Plumbagin, quercetin, triptolide, Licofelene and Quinomycin. These natural compounds or phytochemicals, which inhibit cancer stem cells may prove to be promising agents for the prevention and treatment of pancreatic cancers.

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Li, Sha, Yan Li, Xun Qu, Xiaolin Liu, and Jing Liang. "Detection and significance of TregFoxP3+ and Th17 cells in peripheral blood of non-small cell lung cancer patients." Archives of Medical Science 2 (2014): 232–39. http://dx.doi.org/10.5114/aoms.2014.42573.

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Apriani, Riza, and Fajar Fauzi Abdullah. "Cytotoxic Activity of Ethyl-para-methoxycinnamate from Kaempferia galanga L. on A549 Lung Cancer and B16 Melanoma Cancer Cells." Jurnal Kimia Sains dan Aplikasi 24, no. 1 (February 28, 2020): 22–28. http://dx.doi.org/10.14710/jksa.24.1.22-28.

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Kaempferia galanga L. belongs to the family of Zingiberaceae, an endangered medicinal plant with pharmacology activities. Ethyl-p-methoxycinnamate (EPMC) is an essential phytoconstituent of K. galanga rhizomes. Several studies have reported that EPMC has anticancer activities in several cancer cells, including CL-6 gallbladder cancer cells, HepG2liver cancer cells, MCF-7 breast cancer cells, and Raji lymphoma cancer cells. However, studies on A549 lung cancer and B16 melanoma cancer cells have not been reported. This study aimed to determine the anticancer activity of EPMC against A549 lung cancer and B16 melanoma cancer cells. EPMC was obtained by extraction using n-hexane, then recrystallized with chloroform. The isolate was then analyzed by thin-layer chromatography (TLC), and the structure was characterized by Fourier Transform Infrared (FTIR) and Nuclear Magnetic Resonance (NMR) spectroscopy. Cytotoxic activity was determined under Presto Blue assay. Based on the result, EPMC from K. galanga showed the cytotoxic effect on B16 cells with an IC50 value of 97.09 μg/mL, whereas EPMC showed no significant cytotoxic effect on A549 with an IC50 value of 1407.75 μg/mL. It was concluded that EPMC has potential cytotoxic on B16 melanoma cancer cells, but it showed inactive activity against A549 lung cancer cells. Further molecular mechanism underlying EPMC cytotoxic activity needs to be conducted.

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Barbato, Luisa, Marco Bocchetti, Anna Di Biase, and Tarik Regad. "Cancer Stem Cells and Targeting Strategies." Cells 8, no. 8 (August 18, 2019): 926. http://dx.doi.org/10.3390/cells8080926.

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Chemoresistance is a major problem in cancer therapy as cancer cells develop mechanisms that counteract the effect of chemotherapeutic compounds, leading to relapse and the development of more aggressive cancers that contribute to poor prognosis and survival rates of treated patients. Cancer stem cells (CSCs) play a key role in this event. Apart from their slow proliferative property, CSCs have developed a range of cellular processes that involve drug efflux, drug enzymatic inactivation and other mechanisms. In addition, the microenvironment where CSCs evolve (CSC niche), effectively contributes to their role in cancer initiation, progression and chemoresistance. In the CSC niche, immune cells, mesenchymal stem cells (MSCs), endothelial cells and cancer associated fibroblasts (CAFs) contribute to the maintenance of CSC malignancy via the secretion of factors that promote cancer progression and resistance to chemotherapy. Due to these factors that hinder successful cancer therapies, CSCs are a subject of intense research that aims at better understanding of CSC behaviour and at developing efficient targeting therapies. In this review, we provide an overview of cancer stem cells, their role in cancer initiation, progression and chemoresistance, and discuss the progress that has been made in the development of CSC targeted therapies.

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Caneba, Christine A., Nadège Bellance, Lifeng Yang, Lisa Pabst, and Deepak Nagrath. "Pyruvate uptake is increased in highly invasive ovarian cancer cells under anoikis conditions for anaplerosis, mitochondrial function, and migration." American Journal of Physiology-Endocrinology and Metabolism 303, no. 8 (October 15, 2012): E1036—E1052. http://dx.doi.org/10.1152/ajpendo.00151.2012.

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Anoikis resistance, or the ability for cells to live detached from the extracellular matrix, is a property of epithelial cancers. The “Warburg effect,” or the preference of cancer cells for glycolysis for their energy production even in the presence of oxygen, has been shown to be evident in various tumors. Since a cancer cell's metastatic ability depends on microenvironmental conditions (nutrients, stromal cells, and vascularization) and is highly variable for different organs, their cellular metabolic fluxes and nutrient demand may show considerable differences. Moreover, a cancer cell's metastatic ability, which is dependent on the stage of cancer, may further create metabolic alterations depending on its microenvironment. Although recent studies have aimed to elucidate cancer cell metabolism under detached conditions, the nutrient demand and metabolic activity of cancer cells under nonadherent conditions remain poorly understood. Additionally, less is known about metabolic alterations in ovarian cancer cells with varying invasive capability under anoikis conditions. We hypothesized that the metabolism of highly invasive ovarian cancer cells in detachment would differ from less invasive ovarian cancer cells and that ovarian cancer cells will have altered metabolism in detached vs. attached conditions. To assess these metabolic differences, we integrated a secretomics-based metabolic footprinting (MFP) approach with mitochondrial bioenergetics. Interestingly, MFP revealed higher pyruvate uptake and oxygen consumption in more invasive ovarian cancer cells than their less invasive counterparts. Furthermore, ATP production was higher in more invasive vs. less invasive ovarian cancer cells in detachment. We found that pyruvate has an effect on highly invasive ovarian cancer cells' migration ability. Our results are the first to demonstrate that higher mitochondrial activity is related to higher ovarian cancer invasiveness under detached conditions. Importantly, our results bring insights regarding the metabolism of cancer cells under nonadherent conditions and could lead to the development of therapies for modulating cancer cell invasiveness.

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Kobayashi, Hisataka, Aki Furusawa, Adrian Rosenberg, and Peter L. Choyke. "Near-infrared photoimmunotherapy of cancer: a new approach that kills cancer cells and enhances anti-cancer host immunity." International Immunology 33, no. 1 (June 4, 2020): 7–15. http://dx.doi.org/10.1093/intimm/dxaa037.

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Abstract Near-infrared photoimmunotherapy (NIR-PIT) is a recently developed hybrid cancer therapy that directly kills cancer cells as well as producing a therapeutic host immune response. Conventional immunotherapies, such as immune-activating cytokine therapy, checkpoint inhibition, engineered T cells and suppressor cell depletion, do not directly destroy cancer cells, but rely exclusively on activating the immune system. NIR-PIT selectively destroys cancer cells, leading to immunogenic cell death that initiates local immune reactions to released cancer antigens from dying cancer cells. These are characterized by rapid maturation of dendritic cells and priming of multi-clonal cancer-specific cytotoxic T cells that kill cells that escaped the initial direct effects of NIR-PIT. The NIR-PIT can be applied to a wide variety of cancers either as monotherapy or in combination with conventional immune therapies to further activate anti-cancer immunity. A global Phase 3 clinical trial (https://clinicaltrials.gov/ct2/show/NCT03769506) of NIR-PIT targeting the epidermal growth factor receptor (EGFR) in patients with recurrent head and neck cancer is underway, employing RM1929/ASP1929, a conjugate of anti-EGFR antibody (cetuximab) plus the photo-absorber IRDye700DX (IR700). NIR-PIT has been given fast-track recognition by regulators in the USA and Japan. A variety of imaging methods, including direct IR700 fluorescence imaging, can be used to monitor NIR-PIT. As experience with NIR-PIT grows, additional antibodies will be employed to target additional antigens on other cancers or to target immune-suppressor cells to enhance host immunity. NIR-PIT will be particularly important in patients with localized and locally advanced cancers and may help such patients avoid side-effects associated with surgery, radiation and chemotherapy.

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Munro, Matthew J., Susrutha K. Wickremesekera, Lifeng Peng, Swee T. Tan, and Tinte Itinteang. "Cancer stem cells in colorectal cancer: a review." Journal of Clinical Pathology 71, no. 2 (September 23, 2017): 110–16. http://dx.doi.org/10.1136/jclinpath-2017-204739.

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Colorectal cancer (CRC) is the second most common cancer in women and the third most common in men. Adenocarcinoma accounts for 90% of CRC cases. There has been accumulating evidence in support of the cancer stem cell (CSC) concept of cancer which proposes that CSCs are central in the initiation of cancer. CSCs have been the focus of study in a range of cancers, including CRC. This has led to the identification and understanding of genes involved in the induction and maintenance of pluripotency of stem cells, and markers for CSCs, including those investigated specifically in CRC. Knowledge of the expression pattern of CSCs in CRC has been increasing in recent years, revealing a heterogeneous population of cells within CRC ranging from pluripotent to differentiated cells, with overlapping and sometimes unique combinations of markers. This review summarises current literature on the understanding of CSCs in CRC, including evidence of the presence of CSC subpopulations, and the stem cell markers currently used to identify and localise these CSC subpopulations. Future research into this field may lead to improved methods for early detection of CRC, novel therapy and monitoring of treatment for CRC and other cancer types.

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HARAGUCHI, Naotsugu, Hiroshi INOUE, Fumiaki TANAKA, Koshi MIMORI, Tohru UTSUNOMIYA, Atsushi SASAKI, and Masaki MORI. "Cancer stem cells in human gastrointestinal cancers." Human Cell 19, no. 1 (February 2006): 24–29. http://dx.doi.org/10.1111/j.1749-0774.2005.00004.x.

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Walter, Karolin, Kanishka Tiwary, Marija Trajkovic-Arsic, Ana Hidalgo-Sastre, Laura Dierichs, Sven T. Liffers, Jiangning Gu, et al. "MEK Inhibition Targets Cancer Stem Cells and Impedes Migration of Pancreatic Cancer Cells In Vitro and In Vivo." Stem Cells International 2019 (June 2, 2019): 1–11. http://dx.doi.org/10.1155/2019/8475389.

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Pancreatic ductal adenocarcinoma (PDAC) remains a devastating disease with a very poor prognosis. At the same time, its incidence is on the rise, and PDAC is expected to become the second leading cause of cancer-related death by 2030. Despite extensive work on new therapeutic approaches, the median overall survival is only 6-12 months after diagnosis and the 5-year survival is less than 7%. While pancreatic cancer is particularly difficult to treat, patients usually succumb not to the growth of the primary tumor, but to extensive metastasis; therefore, strategies to reduce the migratory and metastatic capacity of pancreatic cancer cells merit close attention. The vast majority of pancreatic cancers harbor RAS mutations. The outstanding relevance of the RAS/MEK/ERK pathway in pancreatic cancer biology has been extensively shown previously. Due to their high dependency on Ras mutations, pancreatic cancers might be particularly sensitive to inhibitors acting downstream of Ras. Herein, we use a genetically engineered mouse model of pancreatic cancer and primary pancreatic cancer cells were derived from this model to demonstrate that small-molecule MEK inhibitors functionally abrogate cancer stem cell populations as demonstrated by reduced sphere and organoid formation capacity. Furthermore, we demonstrate that MEK inhibition suppresses TGFβ-induced epithelial-to-mesenchymal transition and migration in vitro and ultimately results in a highly significant reduction in circulating tumor cells in mice.

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Horak, I. R., N. V. Latyshko, and O. O. Hudkova. "Adaptor protein Ruk/CIN85 affects redox balance in breast cancer cells." Ukrainian Biochemical Journal 92, no. 4 (September 10, 2020): 24–34. http://dx.doi.org/10.15407/ubj92.04.024.

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Garrepalli, Saritha. "Potentiation of Natural Killer Cells in Cancer Immunology and Reproductive Medicine." Cancer Research and Cellular Therapeutics 1, no. 2 (September 4, 2017): 01–02. http://dx.doi.org/10.31579/2640-1053/008.

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Peacock, Craig D., and D. Neil Watkins. "Cancer Stem Cells and the Ontogeny of Lung Cancer." Journal of Clinical Oncology 26, no. 17 (June 10, 2008): 2883–89. http://dx.doi.org/10.1200/jco.2007.15.2702.

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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.

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Laura Howes. "Copulating cancer cells." C&EN Global Enterprise 99, no. 3 (January 25, 2021): 8. http://dx.doi.org/10.1021/cen-09903-scicon11.

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