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Готові списки джерел за темами / Pancreatic cancer stem cell / Статті в журналах

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Статті в журналах з теми "Pancreatic cancer stem cell"

Автор: Grafiati

Опубліковано: 11 березня 2023

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1

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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2

Nishiyama, T., K. Shimizu, K. Uenoyama, C. Yamasaki, and Y. Hori. "Oncogene-mediated mouse pancreatic stem cell shows pancreatic cancer stem cell phenotype." Pancreatology 16, no. 1 (January 2016): S5. http://dx.doi.org/10.1016/j.pan.2015.12.023.

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3

GursesCila, Hacer E., Muradiye Acar, Furkan B. Barut, Mehmet Gunduz, Reidar Grenman, and Esra Gunduz. "Investigation of the expression of RIF1 gene on head and neck, pancreatic and brain cancer and cancer stem cells." Clinical & Investigative Medicine 39, no. 6 (December 1, 2016): 43. http://dx.doi.org/10.25011/cim.v39i6.27500.

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Purpose: Recent studies have shown that cancer stem cells are resistant to chemotherapy. The aim of this study was to compare RIF1 gene expression in head and neck, pancreatic cancer and glioma cell lines and the cancer stem cells isolated from these cell lines. Methods: UT-SCC-74 from Turku University and UT-SCC-74B primary tumor metastasis and neck cancer cell lines, YKG-1 glioma cancer cell line from RIKEN, pancreatic cancer cell lines and ASPC-1 cells from ATCC were grown in cell culture. To isolate cancer stem cells, ALDH-1 for UT-SCC-74 and UT-SCC-74B cell line, CD-133 for YKG-1 cell line and CD-24 for ASPC-1 cell line, were used as markers of cancer stem cells. RNA isolation was performed for both cancer lines and cancer stem cells. RNAs were converted to cDNA. RIF1 gene expression was performed by qRT-PCR analysis. RIF1 gene expression was compared with cancer cell lines and cancer stem cells isolated from these cell lines. The possible effect of RIF1 gene was evaluated. Results: In the pancreatic cells, RIF1 gene expression in the stem cell-positive cell line was 256 time that seen in the stem cell-negative cell line. Conclusion: Considering the importance of RIF1 in NHEJ and of NHEJ in pancreatic cancer, RIF1 may be one of the genes that plays an important role in the diagnoses and therapeutic treatment of pancreatic cancer. The results of head and neck and brain cancers are inconclusive and further studies are required to elucidate the connection between RIF1 gene and these other types of cancers.

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4

Hamada, Shin, Atsushi Masamune, Tetsuya Takikawa, Noriaki Suzuki, Kazuhiro Kikuta, Morihisa Hirota, Hirofumi Hamada, Masayoshi Kobune, Kennichi Satoh, and Tooru Shimosegawa. "Pancreatic stellate cells enhance stem cell-like phenotypes in pancreatic cancer cells." Biochemical and Biophysical Research Communications 421, no. 2 (May 2012): 349–54. http://dx.doi.org/10.1016/j.bbrc.2012.04.014.

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5

Herreros-Villanueva, Marta. "Embryonic stem cell factors and pancreatic cancer." World Journal of Gastroenterology 20, no. 9 (2014): 2247. http://dx.doi.org/10.3748/wjg.v20.i9.2247.

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6

Kumar, Rachit, Avani Dholakia, and Zeshaan Rasheed. "Stem cell–directed therapies in pancreatic cancer." Current Problems in Cancer 37, no. 5 (September 2013): 280–86. http://dx.doi.org/10.1016/j.currproblcancer.2013.10.005.

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7

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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8

Sasaki, Naoya, Takamichi Ishii, Ryo Kamimura, Masatoshi Kajiwara, Takafumi Machimoto, Norio Nakatsuji, Hirofumi Suemori, Iwao Ikai, Kentaro Yasuchika, and Shinji Uemoto. "Alpha-fetoprotein-producing pancreatic cancer cells possess cancer stem cell characteristics." Cancer Letters 308, no. 2 (September 2011): 152–61. http://dx.doi.org/10.1016/j.canlet.2011.04.023.

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9

Xia, Pu, and Da-Hua Liu. "Cancer stem cell markers for liver cancer and pancreatic cancer." Stem Cell Research 60 (April 2022): 102701. http://dx.doi.org/10.1016/j.scr.2022.102701.

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10

Huang, Ling, and Senthil Muthuswamy. "Abstract A068: Investigation of changes in epithelial cell states in pancreatic cancer using human organoids." Cancer Research 82, no. 22_Supplement (November 15, 2022): A068. http://dx.doi.org/10.1158/1538-7445.panca22-a068.

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Abstract Pancreatic cancer is among the deadliest cancers in the US. The low survival rates of pancreatic cancer are mainly due to late diagnosis and a lack of effective treatments. To improve the clinical management of pancreatic cancer, we need better understand the biological mechanisms underlying the initiation and progression of this disease. With a focus on elucidating pancreatic cancer biology in human patients, we have developed organoid models for pancreatic normal physiology and malignancy using pluripotent stem cells or patient tumor tissues. Using stem cell-derived organoids, we investigated the interactions between pancreatic epithelial cell states, oncogenic signaling pathways, and cytokines. In this study, we discovered that human acinar organoids, compared to ductal organoids, were more sensitive to KRasG12D oncogenic signaling in vitro and in vivo, which supported acinar cells as the main cell of origin for pancreatic cancer in human patients. We have also developed working pipelines using organoid models to identify biomarkers and predict patient drug responses. Based on those successful studies, we now focus on investigating biological principles underlying racial disparities in pancreatic cancer using human cell models. Citation Format: Ling Huang, Senthil Muthuswamy. Investigation of changes in epithelial cell states in pancreatic cancer using human organoids [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer; 2022 Sep 13-16; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2022;82(22 Suppl):Abstract nr A068.

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11

Choudhury, Sangeeta, Neha Chopra, Kriti Jain, Poonam Yadav, Surinder P. Singh, and Yashika Charla. "Abstract B081: Synergistic paracrine action of Vitamin D and mesenchymal stem cell secretome in targeting pancreatic cancer stem cells." Cancer Research 82, no. 22_Supplement (November 15, 2022): B081. http://dx.doi.org/10.1158/1538-7445.panca22-b081.

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Abstract The knowledge of immunomodulatory and reparative properties of Mesenchymal Stem cells (MSCs) are rapidly advancing and could be best suited as a therapeutic option for inflammatory or adverse immunological conditions such as cancer. In the last decade, Mesenchymal stem cells have attracted significant attention because of their accessibility, tumor-oriented homing capacity and the transplantation feasibility. Until date, MSC-based therapy for pancreatic cancer has not been demonstrated. As per the current understanding of the potentials of MSCs in regenerative medicine, we hypothesized their inhibitory influence on pancreatic cancer cells. For experimentation purposes, we have used human Wharton’s jelly derived MSCs (hWJ-MSCs) and pancreatic cell line models. Our findings show that secretion of soluble biologically active factors from hWJ-MSCs (secretome) had a greater impact on induction of anergy and apoptosis of pancreatic tumor cells. The mechanistic approach directed to influence the tumor microenvironment appear to be two pronged: one, via modulation of tumor glycoproteins (MUC-1 and EpCAM) and second, via GSK3β/Stat3/HIF1-α axis. Treatment with calcitriol, an analogue of Vitamin D known to regulate cell cycle, cell differentiation ca also reduce side effects of chemo-drugs, one of the mainstay of therapy in pancreatic cancer. Yet, the potential mechanism to exert anti-cancer effect remains underexplored. We attempted to elicit the involvement of VitD in one of the crucial stem-cell related embryonic pathway, the Sonic Hedgehog (SHH) pathway. Our data showed enhanced apoptosis of calcitirol treated-pCSCs cells when treated with salinomycin (SHH inhibitor). Further combinatorial treatment with secretome + VitD decreased copy numbers of transcription factors C-myc, SMO, PTCH1, PTCH2, and hypoxia-induced factor (HIF1-α) demonstrating the potential mechanism of action. In conclusion, our experimental evidence postulates a potential mechanism by which VitD-analogue regulate sHH-mTOR axis and in combination with mesenchymal stem cell secretome can affect the proliferation and migratory (oncogenic) capabilities of pancreatic cancer stem cells. So, what next? Do we have the evidence to suggest secretome as a novel cell-free therapeutic candidate!! Citation Format: Sangeeta Choudhury, Neha Chopra, Kriti Jain, Poonam Yadav, Surinder P. Singh, Yashika Charla. Synergistic paracrine action of Vitamin D and mesenchymal stem cell secretome in targeting pancreatic cancer stem cells [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer; 2022 Sep 13-16; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2022;82(22 Suppl):Abstract nr B081.

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12

Bao, Qi, Yue Zhao, Andrea Renner, Hanno Niess, Hendrik Seeliger, Karl-Walter Jauch, and Christiane J. Bruns. "Cancer Stem Cells in Pancreatic Cancer." Cancers 2, no. 3 (August 19, 2010): 1629–41. http://dx.doi.org/10.3390/cancers2031629.

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13

Li, Jiahui, Christopher Betzler, Philipp Lohneis, Marie Christine Popp, Jiwei Qin, Thomas Kalinski, Thomas Wartmann, Christiane J. Bruns, Yue Zhao, and Felix C. Popp. "The IL-17A/IL-17RA Axis Is Not Related to Overall Survival and Cancer Stem Cell Modulation in Pancreatic Cancer." International Journal of Molecular Sciences 21, no. 6 (March 23, 2020): 2215. http://dx.doi.org/10.3390/ijms21062215.

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(1) Background: IL-17A accelerates pancreatic intraepithelial neoplasia (PanIN) progression. In this study, we examined whether IL-17A/IL-17RA promotes pancreatic ductal adenocarcinoma (PDAC) aggressiveness in terms of survival and cancer stem cell modulation. (2) Methods: In vitro, the wound-healing assay, the sphere formation assay, and flow cytometry were applied to assess cancer stem cell features. In vivo, pancreatic tumors were induced in C57BL/6 mice using electroporation with oncogenic plasmids (P53-/- R172H; KrasG12V). Anti-IL-17 antibodies were administered as immunotherapy. We analyzed IL-17A/IL-17RA related survival using publicly available transcriptomic data (n = 903). (3) Results: IL-17A/IL-17RA expression was not related to survival in PDAC patients. IL-17A neither induces stem cell markers nor increases sphere formation and cell motility in vitro. Blocking the IL-17A/IL-17RA axis in a murine pancreatic cancer model did not improve the survival of mice, but reduced the tumor burden slightly. (4) Conclusions: IL-17A does not promote stem cell expansion in PDAC cell lines. Blocking IL-17A/IL-17RA signaling does not interfere with pancreatic cancer development and progression and may not be considered as a promising monotherapy for PDAC.

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14

Aksoy, F., E. Kaya, U. Egeli, H. Z. Dundar, P. Tasar, S. A. Aksoy, Y. Ozen, B. Tunca, G. Cecener, and O. Yerci. "Cancer stem cell markers in pancreatic ductal adenocarcinoma." Annals of Oncology 29 (October 2018): viii54. http://dx.doi.org/10.1093/annonc/mdy269.170.

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15

Malaer, Joseph D., and Porunelloor A. Mathew. "Cancer stem cells inhibit NK cell effector function via PCNA-NKp44 interaction." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 134.12. http://dx.doi.org/10.4049/jimmunol.202.supp.134.12.

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Abstract NK cells participate in the innate immune response against infection and cancer without prior sensitization. NK cell function depends on a balance of signals transmitted from activating and inhibitory receptors interacting with ligands on the surface of cells. Cancer cells may evade NK-mediated killing by expressing ligands for inhibitory receptors. Proliferating cell nuclear antigen (PCNA) associates with MHC I and forms the inhibitory ligand for NKp44, resulting in the inhibition of NK function. Cancer stem cells (CSC), a unique subset of tumor cells, possess a stem-cell-like phenotype and are thought to facilitate metastasis by escaping NK cell effector function. Pancreatic and colon CSC can be identified by co-expression of surface markers CD44 and CD133. In both cell lines, Panc-1 and HCT 116, cell surface PCNA is associated with co-expression of CD44 and CD133 as well as increased CSC transcription factor expression (NANOG, SOX2, and Oct-4). Blocking the interaction of NKp44 and PCNA enhanced the specific lysis of cells by NK cells. Collectively these data demonstrate that surface PCNA, CD44, and CD133 co-expression is a marker of pancreatic and colon CSC. Our research implicates that blocking NKp44-PCNA interaction may provide a novel immunotherapeutic target for pancreatic and colon cancer stem cells and prevent metastasis.

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16

García-Silva, Susana, Javier Frias-Aldeguer, and Christopher Heeschen. "Stem cells & pancreatic cancer." Pancreatology 13, no. 2 (March 2013): 110–13. http://dx.doi.org/10.1016/j.pan.2012.12.003.

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17

Heeschen, Christopher. "Targeting pancreatic cancer stem cells." Pancreatology 16, no. 3 (June 2016): S5. http://dx.doi.org/10.1016/j.pan.2016.04.021.

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18

Zhao, Jiangang, Jiahui Li, Hans A. Schlößer, Felix Popp, Marie Christine Popp, Hakan Alakus, Karl-Walter Jauch, Christiane J. Bruns, and Yue Zhao. "Targeting Cancer Stem Cells and Their Niche: Current Therapeutic Implications and Challenges in Pancreatic Cancer." Stem Cells International 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/6012810.

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Cancer stem cells (CSCs) have been identified as a subpopulation of stem-like cancer cells with the ability of self-renewal and differentiation in hematological malignancies and solid tumors. Pancreatic cancer is one of the most lethal cancers worldwide. CSCs are thought to be responsible for cancer initiation, progression, metastasis, chemoresistance, and recurrence in pancreatic cancer. In this review, we summarize the characteristics of pancreatic CSCs and discuss the mechanisms involved in resistance to chemotherapy, the interactions with the niche, and the potential role in cancer immunoediting. We propose that immunotherapy targeting pancreatic CSCs, in combination with targeting the niche components, may provide a novel treatment strategy to eradicate pancreatic CSCs and hence improve outcomes in pancreatic cancer.

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19

Rangwala, Fatima, Alessia Omenetti, and Anna Mae Diehl. "Cancer Stem Cells: Repair Gone Awry?" Journal of Oncology 2011 (2011): 1–11. http://dx.doi.org/10.1155/2011/465343.

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Because cell turnover occurs in all adult organs, stem/progenitor cells within the stem-cell niche of each tissue must be appropriately mobilized and differentiated to maintain normal organ structure and function. Tissue injury increases the demands on this process, and thus may unmask defective regulation of pathways, such as Hedgehog (Hh), that modulate progenitor cell fate. Hh pathway dysregulation has been demonstrated in many types of cancer, including pancreatic and liver cancers, in which defective Hh signaling has been linked to outgrowth of Hh-responsive cancer stem-initiating cells and stromal elements. Hence, the Hh pathway might be a therapeutic target in such tumors.

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20

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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21

Rao, M. Sambasiva, and Janardan K. Reddy. "Pancreatic Stem Cells: Differentiation Options." Stem Cell Reviews 1, no. 3 (2005): 265–72. http://dx.doi.org/10.1385/scr:1:3:265.

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22

May, Randal, Sripathi M. Sureban, Stan A. Lightfoot, Aimee B. Hoskins, Daniel J. Brackett, Russell G. Postier, Rama Ramanujam, et al. "Identification of a novel putative pancreatic stem/progenitor cell marker DCAMKL-1 in normal mouse pancreas." American Journal of Physiology-Gastrointestinal and Liver Physiology 299, no. 2 (August 2010): G303—G310. http://dx.doi.org/10.1152/ajpgi.00146.2010.

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Stem cells are critical in maintaining adult homeostasis and have been proposed to be the origin of many solid tumors, including pancreatic cancer. Here we demonstrate the expression patterns of the putative intestinal stem cell marker DCAMKL-1 in the pancreas of uninjured C57BL/6 mice compared with other pancreatic stem/progenitor cell markers. We then determined the viability of isolated pancreatic stem/progenitor cells in isotransplantation assays following DCAMKL-1 antibody-based cell sorting. Sorted cells were grown in suspension culture and injected into the flanks of athymic nude mice. Here we report that DCAMKL-1 is expressed in the main pancreatic duct epithelia and islets, but not within acinar cells. Coexpression was observed with somatostatin, NGN3, and nestin, but not glucagon or insulin. Isolated DCAMKL-1+ cells formed spheroids in suspension culture and induced nodule formation in isotransplantation assays. Analysis of nodules demonstrated markers of early pancreatic development (PDX-1), glandular epithelium (cytokeratin-14 and Ep-CAM), and isletlike structures (somatostatin and secretin). These data taken together suggest that DCAMKL-1 is a novel putative stem/progenitor marker, can be used to isolate normal pancreatic stem/progenitors, and potentially regenerates pancreatic tissues. This may represent a novel tool for regenerative medicine and a target for anti-stem cell-based therapeutics in pancreatic cancer.

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23

Hohwieler, Meike, Martin Müller, Pierre-Olivier Frappart, and Sandra Heller. "Pancreatic Progenitors and Organoids as a Prerequisite to Model Pancreatic Diseases and Cancer." Stem Cells International 2019 (February 25, 2019): 1–11. http://dx.doi.org/10.1155/2019/9301382.

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Embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) are characterized by their unique capacity to stepwise differentiate towards any particular cell type in an adult organism. Pluripotent stem cells provide a beneficial platform to model hereditary diseases and even cancer development. While the incidence of pancreatic diseases such as diabetes and pancreatitis is increasing, the understanding of the underlying pathogenesis of particular diseases remains limited. Only a few recent publications have contributed to the characterization of human pancreatic development in the fetal stage. Hence, most knowledge of pancreatic specification is based on murine embryology. Optimizing and understanding current in vitro protocols for pancreatic differentiation of ESCs and iPSCs constitutes a prerequisite to generate functional pancreatic cells for better disease modeling and drug discovery. Moreover, human pancreatic organoids derived from pluripotent stem cells, organ-restricted stem cells, and tumor samples provide a powerful technology to model carcinogenesis and hereditary diseases independent of genetically engineered mouse models. Herein, we summarize recent advances in directed differentiation of pancreatic organoids comprising endocrine cell types. Beyond that, we illustrate up-and-coming applications for organoid-based platforms.

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24

Al-Assar, Osama, Fevzi Demiciorglu, Serena Lunardi, Maria Manuela Gaspar-Carvalho, William Gillies McKenna, Ruth M. Muschel, and Thomas B. Brunner. "Contextual regulation of pancreatic cancer stem cell phenotype and radioresistance by pancreatic stellate cells." Radiotherapy and Oncology 111, no. 2 (May 2014): 243–51. http://dx.doi.org/10.1016/j.radonc.2014.03.014.

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25

Das, Jayanta Kumar, Madhumita Das, Mayur Doke, Stanislaw Wnuk, Rosy Mary Stiffin, Marco Ruiz, and Jonathan P. Celli. "A small molecule inhibits pancreatic cancer stem cells." International Journal of Experimental Research and Review 26 (December 30, 2021): 1–15. http://dx.doi.org/10.52756/ijerr.2021.v26.001.

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Pancreatic cancer is the fourth highest cause of cancer-related deaths in the United States, with a projected 60,430 new cases diagnosed and 48,220 patients dying in 2021. We employed a small chemical, N-(6-Chloro-2-enzothiazolyl)-3, 4-dimethoxy-benzene propanamide (KY-02111), to target suppression of tumori-sphero-genesis of PANC1ORGRCD19+31+45+133+, to propose a novel therapeutic strategy against drug registrant pancreatic cancer stem cells (PANC1ORGRCD19+31+45+133+). According to our findings, the pancreatic stem cell indicators (CD19+31+45+133+) are found to be more strongly expressed in pancreatic cancer tissues than in normal pancreatic tissues.The flow cytometry, immunoblot and immunofluorescence analysis showed that the expression ofthese markers (CD19+31+45+133+) in PANC1ORGR spheroid cells was lowered by treatment of our new therapeutic approach. Therefore, this study identified the significant relationship of inhibition of tumori-sphero-genesis of PANC1ORGR with associated novel biomarkers (CD19+31+45+133+) which could be target candidates in designing drugs against pancreatic cancer. Further investigation and funding areneeded to find the molecular mechanism of inhibition of tumori-sphero-genesis by this small molecule. This work was partly used the financial support from award money of 2017 Translational Research Award, Society of Toxicology and 2018 AACR Minority and Minority-Serving Institution Faculty Scholar award of Dr. Jayanta K. Das.

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26

Bednar, Filip, and Diane M. Simeone. "Pancreatic cancer stem cells and relevance to cancer treatments." Journal of Cellular Biochemistry 107, no. 1 (May 1, 2009): 40–45. http://dx.doi.org/10.1002/jcb.22093.

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27

van der Kooy, Derek. "O16. Pancreatic stem cells." Differentiation 80 (November 2010): S11. http://dx.doi.org/10.1016/j.diff.2010.09.159.

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28

Valle, Sandra, Laura Martin-Hijano, Sonia Alcalá, Marta Alonso-Nocelo, and Bruno Sainz Jr. "The Ever-Evolving Concept of the Cancer Stem Cell in Pancreatic Cancer." Cancers 10, no. 2 (January 26, 2018): 33. http://dx.doi.org/10.3390/cancers10020033.

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Pancreatic ductal adenocarcinoma (PDAC), the most common type of pancreatic cancer, is the 4th most frequent cause of cancer-related death worldwide, primarily due to the inherent chemoresistant nature and metastatic capacity of this tumor. The latter is believed to be mainly due to the existence of a subpopulation of highly plastic “stem”-like cells within the tumor, known as cancer stem cells (CSCs), which have been shown to have unique metabolic, autophagic, invasive, and chemoresistance properties that allow them to continuously self-renew and escape chemo-therapeutic elimination. As such, current treatments for the majority of PDAC patients are not effective and do not significantly impact overall patient survival (<7 months) as they do not affect the pancreatic CSC (PaCSC) population. In this context, it is important to highlight the need to better understand the characteristics of the PaCSC population in order to develop new therapies to target these cells. In this review, we will provide the latest updates and knowledge on the inherent characteristics of PaCSCs, particularly their unique biological properties including chemoresistance, epithelial to mesenchymal transition, plasticity, metabolism and autophagy.

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Celik, Feyzi, and Tugce Duran. "Effects of Fentanyl on pancreatic cancer cell proliferation and cancer stem cell differentiation." Cellular and Molecular Biology 65, no. 7 (September 30, 2019): 21. http://dx.doi.org/10.14715/cmb/2019.65.7.5.

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Bimonte, Sabrina, Antonio Barbieri, Maddalena Leongito, Giuseppe Palma, Vitale del Vecchio, Michela Falco, Raffaele Palaia, et al. "The Role of miRNAs in the Regulation of Pancreatic Cancer Stem Cells." Stem Cells International 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/8352684.

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Pancreatic ductal adenocarcinoma is currently one of the deadliest cancers with low overall survival rate. This disease leads to an aggressive local invasion and early metastases and is poorly responsive to treatment with chemotherapy or chemoradiotherapy. Several studies have shown that pancreatic cancer stem cells (PCSCs) play different roles in the regulation of drug resistance and recurrence in pancreatic cancer. MicroRNA (miRNA), a class of newly emerging small noncoding RNAs, is involved in the modulation of several biological activities ranging from invasion to metastases development, as well as drug resistance of pancreatic cancer. In this review, we synthesize the latest findings on the role of miRNAs in regulating different biological properties of pancreatic cancer stem cells.

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Kennedy, Timothy J., Xianzhong Ding, and Richard H. Bell. "Evidence for stem cell origin of human pancreatic cancer." Gastroenterology 124, no. 4 (April 2003): A350. http://dx.doi.org/10.1016/s0016-5085(03)81768-7.

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Bednar, Filip, and Diane M. Simeone. "Pancreatic cancer stem cell biology and its therapeutic implications." Journal of Gastroenterology 46, no. 12 (November 3, 2011): 1345–52. http://dx.doi.org/10.1007/s00535-011-0494-7.

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LUO, GUOPEI, JIANG LONG, XIAOBO CUI, ZHIWEN XIAO, ZUQIANG LIU, SI SHI, LIANG LIU, et al. "Highly lymphatic metastatic pancreatic cancer cells possess stem cell-like properties." International Journal of Oncology 42, no. 3 (January 18, 2013): 979–84. http://dx.doi.org/10.3892/ijo.2013.1780.

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Ise, Yuuki, Kazuya Shimizu, Kyohei Uenoyama, Satoshi Nishiyama, Yuka Tsuchida, and Yuichi Hori. "Oncogene-mediated mouse pancreatic progenitor cells show cancer stem cell phenotype." Pancreatology 16, no. 4 (August 2016): S143. http://dx.doi.org/10.1016/j.pan.2016.06.514.

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Herreros-Villanueva, Marta, Tze-Kiong Er, and Luis Bujanda. "Retinoic Acid Reduces Stem Cell–Like Features in Pancreatic Cancer Cells." Pancreas 44, no. 6 (August 2015): 918–24. http://dx.doi.org/10.1097/mpa.0000000000000373.

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Ai, Jiaoyu, Sonja M. Wörmann, Kıvanç Görgülü, Mireia Vallespinos, Sladjana Zagorac, Sonia Alcala, Nan Wu, et al. "Bcl3 Couples Cancer Stem Cell Enrichment With Pancreatic Cancer Molecular Subtypes." Gastroenterology 161, no. 1 (July 2021): 318–32. http://dx.doi.org/10.1053/j.gastro.2021.03.051.

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Xu, Lantao. "Cancer stem cell in the progression and therapy of pancreatic cancer." Frontiers in Bioscience 18, no. 3 (2013): 795. http://dx.doi.org/10.2741/4143.

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Matsuda, Yoko, Shoko Kure, and Toshiyuki Ishiwata. "Nestin and other putative cancer stem cell markers in pancreatic cancer." Medical Molecular Morphology 45, no. 2 (June 2012): 59–65. http://dx.doi.org/10.1007/s00795-012-0571-x.

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Sorescu, George P., Lora W. Forman та Douglas V. Faller. "Effect of inhibition of protein kinase C delta (PKCδ) on pancreatic cancer cells." Journal of Clinical Oncology 30, № 15_suppl (20 травня 2012): e14591-e14591. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e14591.

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e14591 Background: 93% of pancreatic cancers have activating mutations in the K-Ras gene. We have previously shown that mutated, constitutively-activated Ras is lethal to cells if an essential Ras-driven survival pathway is disrupted by suppression of PKCδ. PKCδ has various cellular functions, but is not required for the survival of normal cells and its inhibition in vitro or in vivo has no known adverse effects. Signal transducer and activator of transcription 3 (STAT3) is constitutive driver of many solid cancers, including pancreatic cancers. STAT3 requires phosphorylation of Tyr 705 for activation and, once activated translocates to the nucleus, where it controls genes involved in cell survival or death. Methods: Human pancreatic cancer cell lines PancI, MIAPACA and primary human pancreatic cancer stem cells were studied. shRNA-mediated knockdown of PKCδ, with scrambled shRNA as a control, was used to validate PKCδ as a target. Rottlerin and KAM1 were used as relatively specific PKCδ inhibitors. For inhibition of STAT3, specific shRNA against STAT3 versus scrambled shRNA were employed for knock-downs. For cytotoxicity analyses, MTS assays were used to assess cell growth. Z-vad-FMK was used as a pan-caspase inhibitor. Immunoblotting was used to verify knock-down of PKCδ or STAT3 and to quantify the phosphorylation status of STAT3 phospho-Tyr 705. Results: PKCδ inhibition by either shRNA knock-down or inhibitor led to dephosphorylation of STAT3 at Tyr 705, extensive cytotoxicity of pancreatic cancer cells and dramatic reductions in tumor clonogenic capacity. Knock down of STAT3 was equally cytotoxic to pancreatic cancer cells. Cytotoxicity following PKCδ inhibition was not prevented by a pan-caspase inhibitor. Conclusions: Activated STAT3 and survival in pancreatic cancer cells requires PKCδ. Inhibition of PKCδ, and subsequent suppression of STAT3 activation, is cytotoxic for pancreatic cancer cells through a mechanism independent of caspase activation or apoptosis. Small molecule inhibitors of PKCδ have potential as targeted therapeutic agents against pancreatic tumors, pancreatic cancer stem cells, and other human tumors with mutational activation of Ras.

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Sunami, Yoshiaki, Johanna Häußler, and Jörg Kleeff. "Cellular Heterogeneity of Pancreatic Stellate Cells, Mesenchymal Stem Cells, and Cancer-Associated Fibroblasts in Pancreatic Cancer." Cancers 12, no. 12 (December 15, 2020): 3770. http://dx.doi.org/10.3390/cancers12123770.

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Pancreatic cancer is projected to become the second deadliest cancer by 2030 in the United States, and the overall five-year survival rate stands still at around 9%. The stroma compartment can make up more than 90% of the pancreatic tumor mass, contributing to the hypoxic tumor microenvironment. The dense stroma with extracellular matrix proteins can be a physical and metabolic barrier reducing therapeutic efficacy. Cancer-associated fibroblasts are a source of extracellular matrix proteins. Therefore, targeting these cells, or extracellular matrix proteins, have been considered as therapeutic strategies. However, several studies show that deletion of cancer-associated fibroblasts may have tumor-promoting effects. Cancer-associated fibroblasts are derived from a variety of different cell types, such as pancreatic stellate cells and mesenchymal stem cells, and constitute a diverse cell population consisting of several functionally heterogeneous subtypes. Several subtypes of cancer-associated fibroblasts exhibit a tumor-restraining function. This review article summarizes recent findings regarding origin and functional heterogeneity of tumor-promoting as well as tumor-restraining cancer-associated fibroblasts. A better understanding of cancer-associated fibroblast heterogeneity could provide more specific and personalized therapies for pancreatic cancer patients in the future.

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Li, Chenwei, David G. Heidt, Piero Dalerba, Charles F. Burant, Lanjing Zhang, Volkan Adsay, Max Wicha, Michael F. Clarke, and Diane M. Simeone. "Identification of Pancreatic Cancer Stem Cells." Cancer Research 67, no. 3 (February 1, 2007): 1030–37. http://dx.doi.org/10.1158/0008-5472.can-06-2030.

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Li, C., D. G. Heidt, N. Mollenberg, M. Clarke, and D. M. Simeone. "IDENTIFICATION OF PANCREATIC CANCER STEM CELLS." Pancreas 31, no. 4 (November 2005): 452. http://dx.doi.org/10.1097/01.mpa.0000193704.00116.c2.

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Yao, Wantong, and Anirban Maitra. "Hear Pancreatic Cancer Stem Cells ROR." Cell 177, no. 3 (April 2019): 516–18. http://dx.doi.org/10.1016/j.cell.2019.04.002.

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Heidt, D. G., C. Li, N. Mollenberg, M. F. Clarke, and D. Simeone. "Identification of pancreatic cancer stem cells." Journal of Surgical Research 130, no. 2 (February 2006): 194–95. http://dx.doi.org/10.1016/j.jss.2005.11.093.

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45

a Kim, Sun, Soo Been Park, and Si Young Song. "GLRX3, a novel secretory biomarker of pancreatic cancer based on pancreatic cancer stem cell characteristics." Pancreatology 13, no. 4 (July 2013): S3. http://dx.doi.org/10.1016/j.pan.2013.07.070.

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Kim, Sun a., Soo Been Park, and Si Young Song. "PAUF (Pancreatic adenocarcinoma upregulating factor), role as a cancer stem cell marker of pancreatic cancer." Pancreatology 13, no. 4 (July 2013): S54. http://dx.doi.org/10.1016/j.pan.2013.07.208.

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Hsieh, Mei Jen, Tai-Jan Chiu, Yu Chun Lin, Ching-Chieh Weng, Yu-Ting Weng, Chang-Chun Hsiao, and Kuang-hung Cheng. "Inactivation of APC Induces CD34 Upregulation to Promote Epithelial-Mesenchymal Transition and Cancer Stem Cell Traits in Pancreatic Cancer." International Journal of Molecular Sciences 21, no. 12 (June 23, 2020): 4473. http://dx.doi.org/10.3390/ijms21124473.

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Pancreatic cancer (PC) is a highly lethal malignancy due to the cancer routinely being diagnosed late and having a limited response to chemotherapy. Pancreatic ductal adenocarcinoma (PDAC) is the most common form of pancreatic malignant tumor, representing more than 85% of all pancreatic cancers. In the present study, we characterized the phenotypes of concomitant P53 and APC mutations in pancreatic neoplasms driven by the oncogene KRAS in genetically modified mice (GEMM). In this GEMM setting, APC haploinsufficiency coupled with P53 deletion and KRASG12D activation resulted in an earlier appearance of pancreatic intraepithelial neoplasia (PanIN) lesions and progressed rapidly to highly invasive and metastatic PDAC. Through a microarray analysis of murine PDAC cells derived from our APC-deficient PDAC model, we observed that APC loss leads to upregulated CD34 expression in PDAC. CD34 is a member of a family of single-pass transmembrane proteins and is selectively expressed in hematopoietic progenitor cells, vascular endothelial cells, interstitial precursor cells, and various interstitial tumor cells. However, the functional roles of CD34 in pancreatic cancer remain unclear. Thus, in this study, we explored the mechanisms regarding how CD34 promotes the deterioration of pancreatic malignancy. Our results demonstrated that the increased expression of CD34 induced by APC inactivation promotes the invasion and migration of PDAC cells, which may relate to PDAC metastasis in vivo. Collectively, our study provides first-line evidence to delineate the association between CD34 and the APC/Wnt pathway in PDAC, and reveals the potential roles of CD34 in PDAC progression.

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Calmeiro, J., M. Carrascal, L. Mendes, IF Duarte, C. Gomes, J. Serra, A. Falcão, MT Cruz, and BM Neves. "P04.01 Dendritic-cell based immunotherapy targeting pancreatic and NSCLC cancer stem cells." Journal for ImmunoTherapy of Cancer 8, Suppl 2 (October 2020): A36. http://dx.doi.org/10.1136/jitc-2020-itoc7.70.

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BackgroundThe field of cancer immunotherapy is growing at a fast pace, with new developments in this field leading to a change in cancer therapy. Dendritic cells (DCs) are one of the central tools in cellular anti-tumour immunotherapy and the production of clinical grade monocyte-derived DCs (Mo-DCs) is the most frequent approach for antitumor vaccines production. However, there is a large space for improvement of protocols and a clear need for the establishment of clinical standard operating procedures (CSOP). Cancer stem cells (CSCs) are a recently identified small cell population present in the tumour, resistant to radio/chemotherapy and known to be responsible for disease recurrence. Here, we aim to contribute to the standardization of CSOPs and to target and eradicate CSCs by developing a DC-based immunotherapy vaccine for pancreatic and non-small cells lung cancer (NSCLC), comparing DC loading with CSCs vs. classical tumour lysates.Materials and MethodsCSCs from PANC-1 (pancreatic cancer) and A549 (NSCLC) cell lines were isolated and characterized by RT-PCR and flow citometry. CSCs resistance to chemotherapy was also assessed. In vitro anti-tumour cytotoxicity assays were performed. We also defined and compared the effect of 4 culture media during human Mo-DCs production. Three Good Manufacturing Practice (GMP) serum-free culture media for clinical use were tested - DendriMACS, AIM-V and X-VIVO 15. RPMI was used as a comparative term given that it is largely used in pre-clinical research. We characterized DC viability, differentiation, maturation, internalization of tumour lysates, cytokines production and autologous T cell stimulatory capacity, as well as metabolomic profiles by Nuclear Magnetic Resonance (NMR) spectroscopy.ResultsCSCs from PANC-1 and A549 cell lines were successfully isolated and overexpressed the stem-like markers NANOG, OCT4, SOX2 and CD133, with resistance to gemcitabine. In terms of differentiation, maturation, antigen uptake capacity and metabolic profiles, AIM-V and X-VIVO 15 present similar results. However, the use of X-VIVO 15 shows an enhanced DC production of IL-12. DCs cultured in X-VIVO 15 and AIM-V media are able to induce a superior stimulation of T cells (CTLs and Th1 responses) while DCs cultured in DendriMACS are more prone to induce Treg polarization. Our data show that X-VIVO 15 and AIM-V culture media are preferable to support the differentiation of DCs to be used in immunostimulatory approaches such as in cancer immunotherapy.ConclusionsOverall, our results demonstrate that blood monocytic precursors present considerable plasticity allowing a tailored differentiation of DCs just by changing the nutritive support. This highlights the need of critically defining the culture medium to be used in DC cancer immunotherapy, attaining the desired cell characteristics and consequent robust clinical responses. We are now assessing in vitro anti-tumour cytotoxicity to evaluate if DC loading with CSC antigens can be an efficient immunotherapy strategy to target and eliminate this specific and resistant cancer cell population.FundingImmunoDCs@CancerStemCells: Cellular Immunotherapy towards the elimination of cancer stem cells (Ref.: POCI-01-0247-FEDER-033532), co-funded by FEDER, COMPETE2020 and University of Coimbra.Disclosure InformationJ. Calmeiro: None. M. Carrascal: A. Employment (full or part-time); Significant; Tecnimede Group. L. Mendes: None. I.F. Duarte: None. C. Gomes: None. J. Serra: A. Employment (full or part-time); Significant; Tecnimede Group. A. Falcão: None. M.T. Cruz: None. B.M. Neves: None.

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Andrikou, Kalliopi, Luca Faloppi, Cristian Loretelli, Alessandra Mandolesi, Italo Bearzi, and Stefano Cascinu. "Expression of stem cell markers in pancreatic ductal adenocarcinoma and clinical relevance." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e15058-e15058. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e15058.

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e15058 Background: Emerging evidence has suggested that malignant tumors are heterogeneous and that are composed of a small subset of distinct cancer cells (usually defined by cell surface marker expression) that are responsible for tumor initiation and propagation, termed cancer stem cells. These cancer stem cells (CSCs), or tumor-initiating cells (TICs), exhibit properties of normal stem cells and are associated with resistance to current therapies. It was found that human pancreatic cancer has shown a population of cancer stem cells that have aberrantly activated developmental signaling pathways, are resistant to standard chemotherapy and radiation, and have up-regulated signaling cascades that are integral for tumor metastasis. The aim of our study is to investigate the prognostic implication of cancer stem cell markers in pancreatic ductal adenocarcinoma. Methods: In 43 histological samples of pancreatic ductal adenocarcinoma were performed molecular biology assessment of CD 24, CD44, CD133, CD166, OCT3/4, LGR5. Results: At univariate analysis patients with an overexpression of CD44, CD133, OCT3/4 showed a worse prognosis in terms of overall survival (respectively: p=0.031; p=0.014; p=0.001). At multivariate analysis OCT3/4 resulted to be independent factor influencing outcome (HR=0.23). Patients with overexpression of all factors seem to have a worse OS compared to patients expressing only two, one or none (8.6 vs. 15.6 vs. 18.0 vs. 59.9 mts; p=0.006). Conclusions: Our data suggest that the presence of cancer stem cells could be linked with tumor aggressiveness and patients’ survival. This finding could drive therapeutic decision towards less or more intensive treatment.

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Liu, Yang, Peng Qin, Rong Wu, Lianfang Du, and Fan Li. "ERas regulates cell proliferation and epithelial–mesenchymal transition by affecting Erk/Akt signaling pathway in pancreatic cancer." Human Cell 33, no. 4 (July 22, 2020): 1186–96. http://dx.doi.org/10.1007/s13577-020-00401-2.

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Abstract Pancreatic cancer is the fourth most common lethal malignancy with an overall 5-year survival rate of less than 5%. ERas, a novel Ras family member, was first identified in murine embryonic stem cells and is upregulated in various cancers. However, the expression and potential role of ERas in pancreatic cancer have not been investigated. In this study, we found that ERas mRNA and protein were upregulated in pancreatic cancer tissues and cells compared with controls. Knockdown of ERas in pancreatic cancer cells by siRNA significantly decreased cell proliferation, colony formation, migration, and invasion and promoted cell apoptosis in vitro. Epithelial–mesenchymal transition (EMT) is closely related to tumor progression. We observed a significant decrease in N-cadherin expression in pancreatic cancer cells in response to ERas gene silencing by immunofluorescence assay and western blot. Furthermore, tumor growth and EMT were inhibited in xenografts derived from pancreatic cancer cells with ERas downregulation. We further investigated the regulatory mechanisms of ERas in pancreatic cancer and found that ERas may activate the Erk/Akt signaling pathway. Moreover, Erk inhibitor decreased pancreatic cancer cells proliferation and colony formation activities. Our data suggest that targeting ERas and its relevant signaling pathways might represent a novel therapeutic approach for the treatment of pancreatic cancer.

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