Log in

Relevant bibliographies by topics / Tumor initiating cells (CICs) / Journal articles

To see the other types of publications on this topic, follow the link: Tumor initiating cells (CICs).

Journal articles on the topic 'Tumor initiating cells (CICs)'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Tumor initiating cells (CICs).'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Ravindran, Shilpa, Saad Rasool, and Cristina Maccalli. "The Cross Talk between Cancer Stem Cells/Cancer Initiating Cells and Tumor Microenvironment: The Missing Piece of the Puzzle for the Efficient Targeting of these Cells with Immunotherapy." Cancer Microenvironment 12, no. 2-3 (2019): 133–48. http://dx.doi.org/10.1007/s12307-019-00233-1.

Full text

Abstract:

AbstractCancer Stem Cells/Cancer Initiating Cells (CSCs/CICs) is a rare sub-population within a tumor that is responsible for tumor formation, progression and resistance to therapies. The interaction between CSCs/CICs and tumor microenvironment (TME) can sustain “stemness” properties and promote their survival and plasticity. This cross-talk is also pivotal in regulating and modulating CSC/CIC properties. This review will provide an overview of the mechanisms underlying the mutual interaction between CSCs/CICs and TME. Particular focus will be dedicated to the immunological profile of CSCs/CICs and its role in orchestrating cancer immunosurveillance. Moreover, the available immunotherapy strategies that can target CSCs/CICs and of their possible implementation will be discussed. Overall, the dissection of the mechanisms regulating the CSC/CIC-TME interaction is warranted to understand the plasticity and immunoregulatory properties of stem-like tumor cells and to achieve complete eradications of tumors through the optimization of immunotherapy.

APA, Harvard, Vancouver, ISO, and other styles

2

Tomei, Sara, Ola Ibnaof, Shilpa Ravindran, Soldano Ferrone, and Cristina Maccalli. "Cancer Stem Cells Are Possible Key Players in Regulating Anti-Tumor Immune Responses: The Role of Immunomodulating Molecules and MicroRNAs." Cancers 13, no. 7 (2021): 1674. http://dx.doi.org/10.3390/cancers13071674.

Full text

Abstract:

Cancer cells endowed with stemness properties and representing a rare population of cells within malignant lesions have been isolated from tumors with different histological origins. These cells, denominated as cancer stem cells (CSCs) or cancer initiating cells (CICs), are responsible for tumor initiation, progression and resistance to therapies, including immunotherapy. The dynamic crosstalk of CSCs/CICs with the tumor microenvironment orchestrates their fate and plasticity as well as their immunogenicity. CSCs/CICs, as observed in multiple studies, display either the aberrant expression of immunomodulatory molecules or suboptimal levels of molecules involved in antigen processing and presentation, leading to immune evasion. MicroRNAs (miRNAs) that can regulate either stemness properties or their immunological profile, with in some cases dual functions, can provide insights into these mechanisms and possible interventions to develop novel therapeutic strategies targeting CSCs/CICs and reverting their immunogenicity. In this review, we provide an overview of the immunoregulatory features of CSCs/CICs including miRNA profiles involved in the regulation of the interplay between stemness and immunological properties.

APA, Harvard, Vancouver, ISO, and other styles

3

Lotti, Fiorenza, Awad M. Jarrar, Rish K. Pai, et al. "Chemotherapy activates cancer-associated fibroblasts to maintain colorectal cancer-initiating cells by IL-17A." Journal of Experimental Medicine 210, no. 13 (2013): 2851–72. http://dx.doi.org/10.1084/jem.20131195.

Full text

Abstract:

Many solid cancers display cellular hierarchies with self-renewing, tumorigenic stemlike cells, or cancer-initiating cells (CICs) at the apex. Whereas CICs often exhibit relative resistance to conventional cancer therapies, they also receive critical maintenance cues from supportive stromal elements that also respond to cytotoxic therapies. To interrogate the interplay between chemotherapy and CICs, we investigated cellular heterogeneity in human colorectal cancers. Colorectal CICs were resistant to conventional chemotherapy in cell-autonomous assays, but CIC chemoresistance was also increased by cancer-associated fibroblasts (CAFs). Comparative analysis of matched colorectal cancer specimens from patients before and after cytotoxic treatment revealed a significant increase in CAFs. Chemotherapy-treated human CAFs promoted CIC self-renewal and in vivo tumor growth associated with increased secretion of specific cytokines and chemokines, including interleukin-17A (IL-17A). Exogenous IL-17A increased CIC self-renewal and invasion, and targeting IL-17A signaling impaired CIC growth. Notably, IL-17A was overexpressed by colorectal CAFs in response to chemotherapy with expression validated directly in patient-derived specimens without culture. These data suggest that chemotherapy induces remodeling of the tumor microenvironment to support the tumor cellular hierarchy through secreted factors. Incorporating simultaneous disruption of CIC mechanisms and interplay with the tumor microenvironment could optimize therapeutic targeting of cancer.

APA, Harvard, Vancouver, ISO, and other styles

4

Ghatak, Shibnath, Vincent C. Hascall, Roger R. Markwald, and Suniti Misra. "FOLFOX Therapy Induces Feedback Upregulation of CD44v6 through YB-1 to Maintain Stemness in Colon Initiating Cells." International Journal of Molecular Sciences 22, no. 2 (2021): 753. http://dx.doi.org/10.3390/ijms22020753.

Full text

Abstract:

Cancer initiating cells (CICs) drive tumor formation and drug-resistance, but how they develop drug-resistance characteristics is not well understood. In this study, we demonstrate that chemotherapeutic agent FOLFOX, commonly used for drug-resistant/metastatic colorectal cancer (CRC) treatment, induces overexpression of CD44v6, MDR1, and oncogenic transcription/translation factor Y-box-binding protein-1 (YB-1). Our study revealed that CD44v6, a receptor for hyaluronan, increased the YB-1 expression through PGE2/EP1-mTOR pathway. Deleting CD44v6, and YB-1 by the CRISPR/Cas9 system attenuates the in vitro and in vivo tumor growth of CICs from FOLFOX resistant cells. The results of DNA:CD44v6 immunoprecipitated complexes by ChIP (chromatin-immunoprecipitation) assay showed that CD44v6 maintained the stemness traits by promoting several antiapoptotic and stemness genes, including cyclin-D1,BCL2,FZD1,GINS-1, and MMP9. Further, computer-based analysis of the clones obtained from the DNA:CD44v6 complex revealed the presence of various consensus binding sites for core stemness-associated transcription factors “CTOS” (c-Myc, TWIST1, OCT4, and SOX2). Simultaneous expressions of CD44v6 and CTOS in CD44v6 knockout CICs reverted differentiated CD44v6-knockout CICs into CICs. Finally, this study for the first time describes a positive feedback loop that couples YB-1 induction and CD44 alternative splicing to sustain the MDR1 and CD44v6 expressions, and CD44v6 is required for the reversion of differentiated tumor cells into CICs.

APA, Harvard, Vancouver, ISO, and other styles

5

Holgado, Esther, Maria Cortes Semperes, Olga Pernia, et al. "Insulin analogues to stimulate cell growth in human cancer initiating cells (CICs)." Journal of Clinical Oncology 31, no. 15_suppl (2013): 1575. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.1575.

Full text

Abstract:

1575 Background: Conflicting epidemiologic studies have suggested insulin and their analogues currently used in the management of type 2 diabetes to be involved in tumor progression and development. Surprisingly, time of exposure to insulin analogs reported in those retrospective studies is too short for be a carcinogen. We hypothesized that differential affinity that insulin analogs display for insulin receptor and IGF-1R at CICs may account for this possibility. [AspB10]insulin (X10) is a long-acting insulin analog that displays greater affinity for IGF1R than either the long-acting insulin analog GLA or human insulin (HI) in vitro. X10 is tumorigenic in animal models whereas GLA is not. GLA is rapidly metabolized to the metabolites, M1 and M2 that exhibit metabolic and mitogenic profiles similar to that of HI in vitro. CICs are cancer cells with self-renewing, stem cell-like properties with the ability to proliferate and differentiate into specific cells found in tumor types and thus they are able to maintain tumor bulk. Many cancers are thought to be initiated by CICs, and there is evidence that they cause cancer recurrence, metastatic progression and resistance to therapies. Our aim was to compare the mitogenic activity of HI, GLA, X10, M1 and M2 on human CICs in vitro. Methods: CICs derived from 10 human cell lines including glioma, lung, breast, colon, and prostatic cancers were isolated and grown in defined growth medium (no serum) with either HI, GLA, X10, M1 or M2. Growth was estimated using the MTS colorimetric assay. Results: HI, GLA and X10 stimulated CIC growth to a similar extend, whereas M1 and M2 had growth promoting activity similar to medium without HI. Similar results were obtained when measuring diametric sphere growth. Additionally, AKT phosphorylation levels were increased 2-fold after stimulation with HI, GLA or X10, whereas stimulation with M1 or M2 did not produce a significant increase. Conclusions: This is the first study that has explored the biology of CICs treated with insulin analogs. The data show that GLA displays a mitogenic profile comparable to that of human insulin for all CIC lines tested, whereas M1, has even less growth promoting activity.

APA, Harvard, Vancouver, ISO, and other styles

6

Kato, S., M. F. Liberona, J. Cerda-Infante, et al. "Simvastatin interferes with cancer ‘stem-cell’ plasticity reducing metastasis in ovarian cancer." Endocrine-Related Cancer 25, no. 10 (2018): 821–36. http://dx.doi.org/10.1530/erc-18-0132.

Full text

Abstract:

Cell plasticity of ‘stem-like’ cancer-initiating cells (CICs) is a hallmark of cancer, allowing metastasis and cancer progression. Here, we studied whether simvastatin, a lipophilic statin, could impair the metastatic potential of CICs in high-grade serous ovarian cancer (HGS-ovC), the most lethal among the gynecologic malignancies. qPCR, immunoblotting and immunohistochemistry were used to assess simvastatin effects on proteins involved in stemness and epithelial-mesenchymal cell plasticity (EMT). Its effects on tumor growth and metastasis were evaluated using different models (e.g., spheroid formation and migration assays, matrigel invasion assays, 3D-mesomimetic models and cancer xenografts). We explored also the clinical benefit of statins by comparing survival outcomes among statin users vs non-users. Herein, we demonstrated that simvastatin modifies the stemness and EMT marker expression patterns (both in mRNA and protein levels) and severely impairs the spheroid assembly of CICs. Consequently, CICs become less metastatic in 3D-mesomimetic models and show fewer ascites/tumor burden in HGS-ovC xenografts. The principal mechanism behind statin-mediated effects involves the inactivation of the Hippo/YAP/RhoA pathway in a mevalonate synthesis-dependent manner. From a clinical perspective, statin users seem to experience better survival and quality of life when compared with non-users. Considering the high cost and the low response rates obtained with many of the current therapies, the use of orally or intraperitoneally administered simvastatin offers a cost/effective and safe alternative to treat and potentially prevent recurrent HGS-ovCs.

APA, Harvard, Vancouver, ISO, and other styles

7

Wang, Dongqing, Haitao Zhu, Yanfang Liu, et al. "The Low Chamber Pancreatic Cancer Cells Had Stem-Like Characteristics in Modified Transwell System: Is It a Novel Method to Identify and Enrich Cancer Stem-Like Cells?" BioMed Research International 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/760303.

Full text

Abstract:

Cancer stem cells (CSCs) or cancer-initiating cells (CICs) play an important role in tumor initiation, progression, metastasis, chemoresistance, and recurrence. It is important to construct an effective method to identify and isolate CSCs for biotherapy of cancer. During the past years, many researchers had paid more attention to it; however, this method was still on seeking. Therefore, compared to the former methods that were used to isolate the cancer stem cell, in the present study, we tried to use modified transwell system to isolate and enrich CSCs from human pancreatic cancer cell lines (Panc-1). Our results clearly showed that the lower chamber cells in modified transwell system were easily forming spheres; furthermore, these spheres expressed high levels of stem cell markers (CD133/CD44/CD24/Oct-4/ESA) and exhibited chemoresistance, underwent epithelial-to-mesenchymal transition (EMT), and possessed the properties of self-renewalin vitroand tumorigenicityin vivo. Therefore, we speculated that modified transwell assay system, as a rapid and effective method, can be used to isolate and enrich CSCs.

APA, Harvard, Vancouver, ISO, and other styles

8

Li, Lingyu, Jiuwei Cui, Chang Wang, et al. "Adoptive transfer of NK cells in combination with chemotherapy to improve outcomes of patients with locally advanced colon carcinoma." Journal of Clinical Oncology 35, no. 15_suppl (2017): e15038-e15038. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e15038.

Full text

Abstract:

e15038 Background: The prognosis of advanced colon cancer (CC) patients remains disappointing, partly due to their greater proportion of CC-initiating cells (CICs), which is responsible for cancer drug-resistance and immune escape. Immunotherapies by harnessing the immune system to eliminate tumors have attracted broad attention. This study was to detect whether chemotherapy could enhance cytotoxicity of natural killer (NK) cells to CC cells (CCs), especially for CICs in vitro, and further evaluate the efficacy and safety of NK-cell therapy combined with chemotherapy in patients with local advanced CC. Methods: We observed that cytotoxicity of NK cells to CCs and CICs pretreated with 5-Fu or oxaliplatin. Then, an open-label pilot cohort study was conducted with local advanced CC patients who had received surgical excision. 60 patients elected to receive either NK-cell therapy combined with chemotherapy (NK-cell group, 27 patients) or pure chemotherapy (control group, 33 patients). Progression-free survival (PFS), overall survival (OS) and adverse effects were investigated. Results: Chemotherapy sensitized CCs and CICs to NK cell lysis through upregulation of their NK cell activating ligands and reducing inhibitory ligands. Poorly differentiated CCs were more susceptible to NK-cell than well-differentiated CCs, and CICs were more easily to be killed by NK cell than their differentiated CCs. In the cohort study, the 5-year PFS and OS rates in the NK-cell group were significantly higher than those in the control group (51.1% vs. 34.9%, p= 0.043; 73% vs. 51.3%, p= 0.038, respectively).Among patients with poorly differentiated carcinomas or low expression of HLA-1, median PFS in the NK-cell group vs. the control group was 23.5 vs. 11.5 months ( p= 0.047), and median OS was 30 vs. 15 months ( p= 0.043), respectively. No significant adverse reaction was found during NK-cell therapy. Conclusions: NK-cell therapy in combination with chemotherapy in locally advanced CC prevented recurrence and prolonged survival with acceptable adverse effects, especially for poorly differentiated carcinomas.

APA, Harvard, Vancouver, ISO, and other styles

9

Ishigaki, Tomohiro, Seiichiro Kobayashi, Nobuhiro Ohno, et al. "Comprehensive Analysis of Surface Antigens on Adult T-Cell Leukemia/Lymphoma (ATL) Cells and Search for ATL-Initiating Cell Markers." Blood 124, no. 21 (2014): 1674. http://dx.doi.org/10.1182/blood.v124.21.1674.1674.

Full text

Abstract:

Abstract Adult T-cell leukemia/lymphoma (ATL) is highly aggressive malignancy caused by human T-cell leukemia virus type 1 (HTLV1). Intensive combination chemotherapy can initially reduce ATL cells, but relapses are common. Today many kinds of tumors are considered to be organized in a hierarchy of heterogeneous cell populations, with only a small proportion of cancer initiating cells (CICs) capable of sustaining tumor formation and growth. Even if most of tumor cells are killed, remaining chemo-resistant CICs can be causes of relapses. However, CICs of ATL have not been identified yet. Our first goal is to identify ATL-initiating cells using in-vitro and in-vivo models. Because co-culture of HTLV1-infected ATL cells and normal lymphocytes results in extraordinarily high HTLV1 integration into normal lymphocytes, which is not seen in the bodies of patients, purification of ATL cells is necessary for evaluation of tumor-specific proliferation. We reported that HTLV1-infected ATL cells could be specifically enriched in the CD4+CADM1+ fraction, while the HTLV-1 basic leucine zipper (HBZ) gene was not detected in CD4+CADM1- cells by PCR analysis. To purify ATL cells, CD4+CADM1+ gating was used. First, we performed comprehensive analysis of surface antigens specifically on ATL cells. Peripheral blood mononuclear cells (PBMCs) were isolated from typical acute-type ATL patients and healthy volunteers. Using flow cytometry and gating, surface expression of 105 antigens, including activated T-cell markers, cell adhesive molecules, and lineage markers, was analyzed. The expression on ATL cells was compared with other CD4-positive non-ATL lymphocytes. Statistical hierarchical clustering analysis of 10 sample groups showed that ATL cells were all grouped into the same cluster, and markers specific for acute-type ATL cells were therefore picked up as candidate markers. Second, CD4+CADM1+ cells were classified by differences in expression of those candidate markers and sorted using 12-color flow cytometry. Although growing primary ATL cells in vitro is very difficult, it was reported that only a small proportion of ATL cells can survive and proliferate on the murine MS-5 stromal cell line, which also allows the proliferation of some ALL and hematopoietic progenitor cells. We repeated these 14-days in-vitro assays and tried to identify the cells capable of surviving and proliferating on MS-5, which we consider to be ATL-initiating cells. Although most of picked-up markers didn't have any impacts on survival and proliferation of ATL cells, several surface antigens affected the results. After confirmation and prioritization, CD25+ and CD71- fractions were finally picked up. Combining these two fractions, we found that CD71-CD25+CD4+CADM1+ cells could survive and proliferate on MS-5, while other CD4+CADM1+ cells died off in many cases. Even in a case where CD71-CD25+ cells accounted only for 1.1% among the CD4+CADM1+ fraction, CD71-CD25+ cells exclusively survived and proliferated in vitro (figure 1). Moreover, CD71-CD25+ cells could generate CD71+ and CD25- cells on MS-5. In serial culture models, the CD71-CD25+ cells could serially generate other CD4+CADM1+ cells in vitro. Then, we focused on the clinical course of actual ATL patients, and followed up the CD71-CD25+ ATL cells before and after chemotherapy. After chemotherapy, the frequency of CD71-CD25+ cells among CD4+CADM1+ cells became obviously higher, and they therefore seemed to be resistant to chemotherapy. In a case where robust reduction of ATL cells was achieved, more than 90% of remaining ATL cells were in the CD71-CD25+ fraction. Lastly, we compared the in-vivo proliferation of CD71-CD25+ ATL cells and other CD4+CADM1+ cells. Both cells were transplanted intravenously into neonatal NOD/Shi-scid/IL-2Rγnull (NOG) mice within 48 hours from birth. CD71-CD25+CD4+CADM1+ cells could proliferate in vivo while others couldn't as far as we tried. Moreover, flow cytometric analysis of murine peripheral blood in 70 days after transplantation showed that CD71-CD25+CD4+CADM1+ cells could generate ATL cells with other phenotype seen in primary ATL patients. In summary, we successfully found that CD71-CD25+CD4+CADM1+ cells could generate other ATL cells in vitro and in vivo. This research suggested ATL-initiating cells could be in the CD71-CD25+CD4+CADM1+ fraction. Figure 1. Flow cytometric gating of ATL cells and CD71-CD25+CD4+CADM1+ cells Figure 1. Flow cytometric gating of ATL cells and CD71-CD25+CD4+CADM1+ cells Disclosures Tojo: Novartis: Research Funding, Speakers Bureau.

APA, Harvard, Vancouver, ISO, and other styles

10

Chang, Ching-Wen, Chien-Chih Chen, Meng-Ju Wu, et al. "Active Component ofAntrodia cinnamomeaMycelia Targeting Head and Neck Cancer Initiating Cells through Exaggerated Autophagic Cell Death." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–15. http://dx.doi.org/10.1155/2013/946451.

Full text

Abstract:

Head and neck squamous cell carcinoma (HNSCC) is a highly lethal cancer. Previously, we identify head and neck cancer initiating cells (HN-CICs), which are highly tumorigenic and resistant to conventional therapy. Therefore, development of drug candidates that effectively target HN-CICs would benefit future head and neck cancer therapy. In this study, we first successfully screened for an active component, named YMGKI-1, from natural products ofAntrodia cinnamomeaMycelia (ACM), which can target the stemness properties of HNSCC. Treatment of YMGKI-1 significantly downregulated the aldehyde dehydrogenase (ALDH) activity, one of the characteristics of CIC in HNSCC cells. Additionally, the tumorigenic properties of HNSCC cells were attenuated by YMGKI-1 treatmentin vivo. Further, the stemness properties of HN-CICs, which are responsible for the malignancy of HNSCC, were also diminished by YMGKI-1 treatment. Strikingly, YMGKI-1 also effectively suppressed the cell viability of HN-CICs but not normal stem cells. Finally, YMGKI-1 induces the cell death of HN-CICs by dysregulating the exaggerated autophagic signaling pathways. Together, our results indicate that YMGKI-1 successfully lessens stemness properties and tumorigenicity of HN-CICs. These findings provide a new drug candidate from purified components of ACM as an alternative therapy for head and neck cancer in the future.

APA, Harvard, Vancouver, ISO, and other styles

11

Bansal, Nitu, and Debabrata Banerjee. "Tumor Initiating Cells." Current Pharmaceutical Biotechnology 10, no. 2 (2009): 192–96. http://dx.doi.org/10.2174/138920109787315015.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Zhang, Li-Zhi, Chang-Qing Zhang, Zhen-Yu Yan, Qing-Cheng Yang, Yao Jiang, and Bing-Fang Zeng. "Tumor-initiating cells and tumor vascularization." Pediatric Blood & Cancer 56, no. 3 (2010): 335–40. http://dx.doi.org/10.1002/pbc.22886.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

Xie, Qi, Qiulian Wu, Stephen C. Mack, et al. "CDC20 maintains tumor initiating cells." Oncotarget 6, no. 15 (2015): 13241–54. http://dx.doi.org/10.18632/oncotarget.3676.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Lin, Tao, Lingjun Meng, Yi Li, and Robert Y. L. Tsai. "Tumor-Initiating Function of Nucleostemin-Enriched Mammary Tumor Cells." Cancer Research 70, no. 22 (2010): 9444–52. http://dx.doi.org/10.1158/0008-5472.can-10-2159.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Chen, Jingyu, Chien-Yu Chen, Christopher Nguyen, Lulu Chen, Kangmin Lee, and Bangyan L. Stiles. "Emerging signals regulating liver tumor initiating cells." Liver Research 2, no. 2 (2018): 73–80. http://dx.doi.org/10.1016/j.livres.2018.08.003.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Hansford, Loen M., and David R. Kaplan. "Tumor-Initiating Cells in Childhood Neuroblastoma—Response." Cancer Research 72, no. 3 (2012): 823–24. http://dx.doi.org/10.1158/0008-5472.can-11-3548.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Kim, Youngmi, Qiulian Wu, Petra Hamerlik, et al. "Aptamer Identification of Brain Tumor–Initiating Cells." Cancer Research 73, no. 15 (2013): 4923–36. http://dx.doi.org/10.1158/0008-5472.can-12-4556.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Wu, Jian. "Epigenetic regulation of hepatic tumor-initiating cells." Frontiers in Bioscience 20, no. 6 (2015): 946–63. http://dx.doi.org/10.2741/4349.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Yi, Shan Yong, and Ke Jun Nan. "Tumor-initiating stem cells in liver cancer." Cancer Biology & Therapy 7, no. 3 (2008): 325–30. http://dx.doi.org/10.4161/cbt.7.3.5527.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Rajan, Prithi, and Roopa Srinivasan. "Immunotherapies Towards Tumor Initiating Cells and Cancer Stem Cells." Open Cancer Immunology Journal 1, no. 1 (2008): 1–6. http://dx.doi.org/10.2174/1876401000801010001.

Full text

Abstract:

Active immunotherapy of cancer is a promising treatment modality by inducing long lived tumor reactive immune effector cells. Several vaccine trials have indicated that its effectiveness is probably best when the tumor burden is low. An attractive population of cells to target by this approach may be tumor initiating cells (TICs). Recent research suggests that such types of cells may be precursors to cancer possibly giving rise to metastatic disease. Although more work is being done to characterize appropriate phenotypic and functional markers, this population of cells would make an ideal target for active immunotherapy in high risk patients, so as to achieve remission over much longer periods of time. This review gives an overview of the potential of immunotherapy and how it may target TICs as a potential treatment option for cancer patients.

APA, Harvard, Vancouver, ISO, and other styles

21

Bellamkonda, K., S. Savari, N. Chandrashekar, and A. Sjolander. "899: Identifying genes involved in the colon cancer initiating cells (CICs) survivability against montelukast treatment in xenograft model." European Journal of Cancer 50 (July 2014): S220. http://dx.doi.org/10.1016/s0959-8049(14)50799-x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Lu, Jie, Alexander Ksendzovsky, Chunzhang Yang та ін. "CNTF receptor subunit α as a marker for glioma tumor-initiating cells and tumor grade". Journal of Neurosurgery 117, № 6 (2012): 1022–31. http://dx.doi.org/10.3171/2012.9.jns1212.

Full text

Abstract:

Object Tumor-initiating cells are uniquely resilient to current treatment modalities and play an important role in tumor resistance and recurrence. The lack of specific tumor-initiating cell markers to identify and target these cells presents a major obstacle to effective directed therapy. Methods To identify tumor-initiating cell markers in primary brain tumors, the authors compared the proteomes of glioma tumor-initiating cells to their differentiated progeny using a novel, nongel/shotgun-based, multidimensional liquid-chromatography protein separation technique. An in vivo xenograft model was used to demonstrate the tumorigenic and stem cell properties of these cells. Western blot and immunofluorescence analyses were used to confirm findings of upregulated ciliary neurotrophic factor receptor subunit–α (CNTFRα) in undifferentiated tumor-initiating cells and gliomas of increasing tumor grade. Sequencing of the CNTFRα coding regions was performed for mutation analysis. Finally, antibody-dependent cell-mediated cytotoxicity was used to establish the role of CNTFRα as a potential immunotherapeutic target. Results Ciliary neurotrophic factor receptor subunit–α expression was increased in tumor-initiating cells and was decreased in the cells' differentiated progeny, and expression levels increased with glioma grade. Mutations of CNTFRα are not common in gliomas. Functional studies using CNTF treatment in glioma tumor-initiating cells showed induction of differentiation through the CNTFRα pathway. Treatment with anti-CNTFRα antibody resulted in increased antibody-dependent cell-mediated cytotoxicity in CNTFRα expressing DAOY cells but not in cell lines that lack CNTFRα. Conclusions These data indicate that CNTFRα plays a role in the formation or maintenance of tumor-initiating cells in gliomas, is a marker that correlates with histological grade, may underlie treatment resistance in some cases, and is a potential therapeutic target.

APA, Harvard, Vancouver, ISO, and other styles

23

Mu, Lei, Kaiyu Huang, Yibing Hu, et al. "Small-sized colorectal cancer cells harbor metastatic tumor-initiating cells." Oncotarget 8, no. 64 (2017): 107907–19. http://dx.doi.org/10.18632/oncotarget.22392.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Kwon, Mi, and Young Shin. "Regulation of Ovarian Cancer Stem Cells or Tumor-Initiating Cells." International Journal of Molecular Sciences 14, no. 4 (2013): 6624–48. http://dx.doi.org/10.3390/ijms14046624.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Timaner, Michael, Nitzan Letko-Khait, Ruslana Kotsofruk, et al. "Therapy-Educated Mesenchymal Stem Cells Enrich for Tumor-Initiating Cells." Cancer Research 78, no. 5 (2018): 1253–65. http://dx.doi.org/10.1158/0008-5472.can-17-1547.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Morii, Eiichi. "Heterogeneity of tumor cells in terms of cancer-initiating cells." Journal of Toxicologic Pathology 30, no. 1 (2017): 1–6. http://dx.doi.org/10.1293/tox.2016-0056.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Richard, Vinitha, Madhumathy G. Nair, T. R. Santhosh Kumar, and M. Radhakrishna Pillai. "Side Population Cells as Prototype of Chemoresistant, Tumor-Initiating Cells." BioMed Research International 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/517237.

Full text

Abstract:

Classically, isolation of CSCs from tumors exploits the detection of cell surface markers associated with normal stem cells. Invariable expression of these cell surface markers in almost all proliferating tumor cells that albeit impart specific functionality, the universality, and clinical credibility of CSC phenotype based on markers is still dubious. Side Population (SP) cells, as defined by Hoechst dye exclusion in flow cytometry, have been identified in many solid tumors and cell lines and the SP phenotype can be considered as an enriched source of stem cells as well as an alternative source for the isolation of cancer stem cells especially when molecular markers for stem cells are unknown. SP cells may be responsible for the maintenance and propagation of tumors and the proportion of SP cells may be a predictor of patient outcome. Several of these markers used in cell sorting have emerged as prognostic markers of disease progression though it is seen that the development of new CSC-targeted strategies is often hindered by poor understanding of their regulatory networks and functions. This review intends to appraise the experimental progress towards enhanced isolation and drug screening based on property of acquired chemoresistance of cancer stem cells.

APA, Harvard, Vancouver, ISO, and other styles

28

Anderson, Angela S., Paul C. Roberts, Madlyn I. Frisard, Matthew W. Hulver, and Eva M. Schmelz. "Ovarian tumor-initiating cells display a flexible metabolism." Experimental Cell Research 328, no. 1 (2014): 44–57. http://dx.doi.org/10.1016/j.yexcr.2014.08.028.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Han, Dan, Veronica Rodriguez-Bravo, Elizabeth Charytonowicz, et al. "Targeting sarcoma tumor-initiating cells through differentiation therapy." Stem Cell Research 21 (May 2017): 117–23. http://dx.doi.org/10.1016/j.scr.2017.04.004.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Koshkin, Vasilij, Burton B. Yang, and Sergey N. Krylov. "Kinetics of MDR Transport in Tumor-Initiating Cells." PLoS ONE 8, no. 11 (2013): e79222. http://dx.doi.org/10.1371/journal.pone.0079222.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Zhang, Mei, Rachel L. Atkinson, and Jeffrey M. Rosen. "Selective targeting of radiation-resistant tumor-initiating cells." Proceedings of the National Academy of Sciences 107, no. 8 (2010): 3522–27. http://dx.doi.org/10.1073/pnas.0910179107.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Blough, M. D., M. R. Westgate, D. Beauchamp, et al. "Sensitivity to temozolomide in brain tumor initiating cells." Neuro-Oncology 12, no. 7 (2010): 756–60. http://dx.doi.org/10.1093/neuonc/noq032.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Cermeño, Efraín A., and Andrés J. García. "Tumor-Initiating Cells: Emerging Biophysical Methods of Isolation." Current Stem Cell Reports 2, no. 1 (2016): 21–32. http://dx.doi.org/10.1007/s40778-016-0036-6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Hansford, L., K. Smith, A. Datti, et al. "[ST5]: Tumor initiating cells from neuroblastoma, a neural crest‐derived tumor." International Journal of Developmental Neuroscience 24, no. 8 (2006): 489. http://dx.doi.org/10.1016/j.ijdevneu.2006.09.047.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

Jeon, Hye-Min, Sung-Hak Kim, Xun Jin, et al. "Crosstalk between Glioma-Initiating Cells and Endothelial Cells Drives Tumor Progression." Cancer Research 74, no. 16 (2014): 4482–92. http://dx.doi.org/10.1158/0008-5472.can-13-1597.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Emmink, Benjamin L., Winan J. Van Houdt, Robert G. Vries, et al. "Differentiated Human Colorectal Cancer Cells Protect Tumor-Initiating Cells From Irinotecan." Gastroenterology 141, no. 1 (2011): 269–78. http://dx.doi.org/10.1053/j.gastro.2011.03.052.

Full text

APA, Harvard, Vancouver, ISO, and other styles

37

Thieu, Khanh, Marlon E. Ruiz, and David M. Owens. "Cells of origin and tumor-initiating cells for nonmelanoma skin cancers." Cancer Letters 338, no. 1 (2013): 82–88. http://dx.doi.org/10.1016/j.canlet.2012.05.008.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Ishizawa, Kota, Zeshaan A. Rasheed, Robert Karisch, et al. "Tumor-Initiating Cells Are Rare in Many Human Tumors." Cell Stem Cell 7, no. 3 (2010): 279–82. http://dx.doi.org/10.1016/j.stem.2010.08.009.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Wang, Xiuxing, Zhi Huang, Qiulian Wu, et al. "MYC-Regulated Mevalonate Metabolism Maintains Brain Tumor–Initiating Cells." Cancer Research 77, no. 18 (2017): 4947–60. http://dx.doi.org/10.1158/0008-5472.can-17-0114.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Markant, Shirley, Lourdes Adriana Esparza, Kelly Barton, Jesse Sun, and Robert Wechsler-Reya. "Abstract CN07-02: Targeting tumor-initiating cells in medulloblastoma." Cancer Prevention Research 5, no. 11 Supplement (2012): CN07–02—CN07–02. http://dx.doi.org/10.1158/1940-6207.prev-12-cn07-02.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Yo, Yi-Te, Ya-Wen Lin, Yu-Chi Wang, et al. "Growth Inhibition of Ovarian Tumor–Initiating Cells by Niclosamide." Molecular Cancer Therapeutics 11, no. 8 (2012): 1703–12. http://dx.doi.org/10.1158/1535-7163.mct-12-0002.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Wang, Ying-Jie, and Meenhard Herlyn. "The emerging roles of Oct4 in tumor-initiating cells." American Journal of Physiology-Cell Physiology 309, no. 11 (2015): C709—C718. http://dx.doi.org/10.1152/ajpcell.00212.2015.

Full text

Abstract:

Octamer-binding transcription factor 4 (Oct4), a homeodomain transcription factor, is well established as a master factor controlling the self-renewal and pluripotency of pluripotent stem cells. Also, a large body of research has documented the detection of Oct4 in tumor cells and tissues and has indicated its enrichment in a subpopulation of undifferentiated tumor-initiating cells (TICs) that critically account for tumor initiation, metastasis, and resistance to anticancer therapies. There is circumstantial evidence for low-level expression of Oct4 in cancer cells and TICs, and the participation of Oct4 in various TIC functions such as its self-renewal and survival, epithelial-mesenchymal transition (EMT) and metastasis, and drug resistance development is implicated from considerable Oct4 knockdown and overexpression-based studies. In a few studies, efforts have been made to identify Oct4 target genes in TICs of different sources. Based on such information, Oct4 in TICs appears to act via mechanisms quite distinct from those in pluripotent stem cells, and a main challenge for future studies is to unravel the molecular mechanisms of action of Oct4, particularly to address the question on how such low levels of Oct4 may exert its functions in TICs. Acquiring cells from their native microenvironment that are of high enough quantity and purity is the key to reliably analyze Oct4 functions and its target genes in TICs, and the information gained may greatly facilitate targeting and eradicating those cells.

APA, Harvard, Vancouver, ISO, and other styles

43

Mohlin, Sofie, Alexander Pietras, Caroline Wigerup, et al. "Tumor-Initiating Cells in Childhood Neuroblastoma—Letter: Figure 1." Cancer Research 72, no. 3 (2012): 821–22. http://dx.doi.org/10.1158/0008-5472.can-11-1761.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Borcherding, Nicholas, David Kusner, Ryan Kolb, et al. "Paracrine WNT5A Signaling Inhibits Expansion of Tumor-Initiating Cells." Cancer Research 75, no. 10 (2015): 1972–82. http://dx.doi.org/10.1158/0008-5472.can-14-2761.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

James, C. D. "Tumor-Initiating Cells: An Influential Paradigm for Xenograft Research." Neuro-Oncology 12, no. 6 (2010): 519. http://dx.doi.org/10.1093/neuonc/noq053.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

Adhikari, Amit, S. "Metastatic potential of tumor-initiating cells in solid tumors." Frontiers in Bioscience 16, no. 1 (2011): 1927. http://dx.doi.org/10.2741/3831.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Bezuidenhout and Shoshan. "A Shifty Target: Tumor-Initiating Cells and Their Metabolism." International Journal of Molecular Sciences 20, no. 21 (2019): 5370. http://dx.doi.org/10.3390/ijms20215370.

Full text

Abstract:

Tumor-initiating cells (TICs), or cancer stem cells, constitute highly chemoresistant, asymmetrically dividing, and tumor-initiating populations in cancer and are thought to play a key role in metastatic and chemoresistant disease. Tumor-initiating cells are isolated from cell lines and clinical samples based on features such as sphere formation in stem cell medium and expression of TIC markers, typically a set of outer membrane proteins and certain transcription factors. Although both bulk tumor cells and TICs show an adaptive metabolic plasticity, TIC metabolism is thought to differ and likely in a tumor-specific and growth condition-dependent pattern. In the context of some common solid tumor diseases, we here review reports on how TIC isolation methods and markers associate with metabolic features, with some focus on oxidative metabolism, including fatty acid and lipid metabolism. These have emerged as significant factors in TIC phenotypes, and in tumor biology as a whole. Other sections address mitochondrial biogenesis and dynamics in TICs, and the influence of the tumor microenvironment. Further elucidation of the complex biology of TICs and their metabolism will require advanced methodologies.

APA, Harvard, Vancouver, ISO, and other styles

48

Feng, Weiguo, Andrew Gentles, Ramesh V. Nair, et al. "Targeting Unique Metabolic Properties of Breast Tumor Initiating Cells." STEM CELLS 32, no. 7 (2014): 1734–45. http://dx.doi.org/10.1002/stem.1662.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Imrich, Sannia, Matthias Hachmeister, and Olivier Gires. "EpCAM and its potential role in tumor-initiating cells." Cell Adhesion & Migration 6, no. 1 (2012): 30–38. http://dx.doi.org/10.4161/cam.18953.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Xie, Qi, Qiulian Wu, Craig M. Horbinski, et al. "Mitochondrial control by DRP1 in brain tumor initiating cells." Nature Neuroscience 18, no. 4 (2015): 501–10. http://dx.doi.org/10.1038/nn.3960.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!