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Relevant bibliographies by topics / Pancreatic cancer stem cell

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Journal articles

Academic literature on the topic 'Pancreatic cancer stem cell'

Author: Grafiati

Published: 11 March 2023

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Journal articles on the topic "Pancreatic cancer stem cell"

1

Lee, Cheong J., Joseph Dosch, and Diane M. Simeone. "Pancreatic Cancer Stem Cells." Journal of Clinical Oncology 26, no. 17 (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 (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 (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, et al. "Pancreatic stellate cells enhance stem cell-like phenotypes in pancreatic cancer cells." Biochemical and Biophysical Research Communications 421, no. 2 (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 (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 (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, et al. "Alpha-fetoprotein-producing pancreatic cancer cells possess cancer stem cell characteristics." Cancer Letters 308, no. 2 (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 (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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