Relevant bibliographies by topics / Pancreatic CSC

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Pancreatic CSC'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Pancreatic CSC"

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Yang, Zhiyong, Ning Zhao, Jing Cui, Heshui Wu, Jiongxin Xiong, and Tao Peng. "Exosomes derived from cancer stem cells of gemcitabine-resistant pancreatic cancer cells enhance drug resistance by delivering miR-210." Cellular Oncology 43, no. 1 (November 12, 2019): 123–36. http://dx.doi.org/10.1007/s13402-019-00476-6.

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Abstract Purpose Gemcitabine (GEM)-based chemotherapy is the first-line treatment for locally advanced pancreatic cancer. GEM resistance, however, remains a significant clinical challenge. Here, we investigated whether exosomes derived from GEM-resistant pancreatic cancer stem cells (CSCs) mediate cell-cell communication between cells that are sensitive or resistant to GEM and, by doing so, regulate drug resistance. Methods GEM-sensitive BxPC-3-derived BxS and PANC-1 pancreatic cancer cells were cultured with exosomes extracted from CSCs isolated from GEM-resistant BxPC-3-derived BxR cells (BxR-CSC). The effect of exosomes on drug resistance, cell cycle progression, apoptosis and miRNA expression was evaluated in BxS and PANC-1 cells. Relevant miRNAs associated with GEM resistance were identified and the role of miR-210 in conferring drug resistance was examined in vitro and in vivo. Results BxR-CSC-derived exosomes induced GEM resistance, inhibited GEM-induced cell cycle arrest, antagonized GEM-induced apoptosis, and promoted tube formation and cell migration in BxS and PANC-1 cells. Elevated miR-210 expression levels were detected in BxR-CSCs and BxR-CSC-derived exosomes compared to those in BxS-CSCs and BxS-CSC-derived exosomes. In addition, increased expression levels of miR-210 were observed in BxS and PANC-1 cells cultured with BxR-CSC-derived exosomes upon exposure to GEM in a dose-dependent manner. Also, a series of biological changes was observed in BxS cells after transfection with miR-210 mimics, including activation of the mammalian target of rapamycin (mTOR) signaling pathway, and these changes were similar to those triggered by BxR-CSC-derived exosomes. Conclusions Our findings suggest that exosomes derived from GEM-resistant pancreatic cancer stem cells mediate the horizontal transfer of drug-resistant traits to GEM-sensitive pancreatic cancer cells by delivering miR-210.
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Walter, Karolin, Eva Rodriguez-Aznar, Monica S. Ventura Ferreira, Pierre-Olivier Frappart, Tabea Dittrich, Kanishka Tiwary, Sabine Meessen, et al. "Telomerase and Pluripotency Factors Jointly Regulate Stemness in Pancreatic Cancer Stem Cells." Cancers 13, no. 13 (June 23, 2021): 3145. http://dx.doi.org/10.3390/cancers13133145.

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To assess the role of telomerase activity and telomere length in pancreatic CSCs we used different CSC enrichment methods (CD133, ALDH, sphere formation) in primary patient-derived pancreatic cancer cells. We show that CSCs have higher telomerase activity and longer telomeres than bulk tumor cells. Inhibition of telomerase activity, using genetic knockdown or pharmacological inhibitor (BIBR1532), resulted in CSC marker depletion, abrogation of sphere formation in vitro and reduced tumorigenicity in vivo. Furthermore, we identify a positive feedback loop between stemness factors (NANOG, OCT3/4, SOX2, KLF4) and telomerase, which is essential for the self-renewal of CSCs. Disruption of the balance between telomerase activity and stemness factors eliminates CSCs via induction of DNA damage and apoptosis in primary patient-derived pancreatic cancer samples, opening future perspectives to avoid CSC-driven tumor relapse. In the present study, we demonstrate that telomerase regulation is critical for the “stemness” maintenance in pancreatic CSCs and examine the effects of telomerase inhibition as a potential treatment option of pancreatic cancer. This may significantly promote our understanding of PDAC tumor biology and may result in improved treatment for pancreatic cancer patients.
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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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Smith, Ebony, and Tuan Tran. "Recurrence of Pancreatic Cancer Presenting as Choroidal Metastasis: A Case Report." Case Reports in Ophthalmology 12, no. 3 (October 25, 2021): 854–58. http://dx.doi.org/10.1159/000519689.

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A patient initially diagnosed as having central serous chorioretinopathy (CSC) presented to a clinic with recurrence of pancreatic cancer manifesting as choroidal metastasis. He was initially diagnosed with CSC by a local ophthalmologist 8 weeks earlier and subsequently presented to our clinic for second opinion after further loss of vision. His medical history was significant for locally advanced pancreatic cancer that was resected by pancreaticoduodenectomy and was treated with adjuvant Folfirinox chemotherapy that was completed 12 months earlier. On examination, there was a large serous retinal detachment overlying a large pale ill-defined elevated choroidal lesion. A diagnosis of choroidal metastasis from recurrence of his pancreatic cancer was made. The diagnosis of choroidal metastasis of his pancreatic cancer represented recurrence of his pancreatic cancer that is associated with high mortality. Early recognition by clinical assessment may allow timely management with chemotherapy and radiation, and potentially prolong survival.
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Chen, Yu-Jen, Yu-Chuen Huang, Tung-Hu Tsai, and Hui-Fen Liao. "Effect of Wasabi Component 6-(Methylsulfinyl)hexyl Isothiocyanate and Derivatives on Human Pancreatic Cancer Cells." Evidence-Based Complementary and Alternative Medicine 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/494739.

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The naturally occurring compound 6-(methylsulfinyl)hexyl isothiocyanate (6-MITC) was isolated fromWasabia japonica(Wasabi), a pungent spice used in Japanese food worldwide. The synthetic derivatives 6-(methylsulfenyl)hexyl isothiocyanate (I7447) and 6-(methylsulfonyl)hexyl isothiocyanate (I7557) are small molecule compounds derived from 6-MITC. This study aimed to evaluate the effect of these compounds on human pancreatic cancer cells. Human pancreatic cancer cell lines PANC-1 and BxPC-3 were used to perform an MTT assay for cell viability and Liu’s stain for morphological observation. The cell cycle was analyzed by DNA histogram. Aldehyde dehydrogenase (ALDH) activity was used as a marker for cancer stem cells (CSC). Western blotting was performed for the expression of proteins related to CSC signaling. The results showed that compounds 6-MITC and I7557, but not I7447, inhibited viability of both PANC-1 and BxPC-3 cells. Morphological observation showed mitotic arrest and apoptosis in 6-MITC- and I7557-treated cells. These two compounds induced G2/M phase arrest and hypoploid population. Percentages of ALDH-positive PANC-1 cells were markedly reduced by 6-MITC and I7557 treatment. The expression of CSC signaling molecule SOX2, but not NOTCH1, ABCG2, Sonic hedgehog, or OCT4, was inhibited by 6-MITC and I7557. In conclusion, wasabi compounds 6-MITC and I7557 may possess activity against the growth and CSC phenotypes of human pancreatic cancer cells.
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Malaer, Joseph D., and Porunelloor A. Mathew. "Pancreatic and colon cancer stem cells escape NK cell effector function via PCNA–NKp44 interaction." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 88.16. http://dx.doi.org/10.4049/jimmunol.204.supp.88.16.

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Abstract Natural killer (NK) cells play an important role in the innate immune response against cancer. Unlike B or T lymphocytes, NK cells do not require prior sensitization and can immediately respond to target cells. 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 escape NK-mediated responses by expressing inhibitory ligands. Proliferating cell nuclear antigen (PCNA), in association MHC I, forms the inhibitory ligand for NKp44. 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. CSC can be identified by a variety of markers such as surface co-expression of CD44 and CD133. In both Panc-1 and HCT 116 cell lines, surface PCNA is associated with co-expression of CD44 and CD133. Triple positive (PCNA+CD44+CD133+) cells have increased CSC transcription factor (NANOG, SOX2, and Oct-4) expression compared to double positive (PCNA−CD44+CD133+) or negative cells. Additionally, blocking the PCNA–NKp44 interaction alters IFN-g secretion and increases specific lysis of cancer cells by NK cells. Taken together, these data suggest that surface co-expression of PCNA, CD44, and CD133 are markers of pancreatic and colon CSC and blocking the PCNA–NKp44 interaction may provide an immunotherapeutic approach to target pancreatic and colon CSC and prevent metastasis.
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Sasaki, Norihiko, Kazumi Hirano, Yuuki Shichi, Fujiya Gomi, Hisashi Yoshimura, Akira Matsushita, Masashi Toyoda, and Toshiyuki Ishiwata. "Gp130-Mediated STAT3 Activation Contributes to the Aggressiveness of Pancreatic Cancer through H19 Long Non-Coding RNA Expression." Cancers 14, no. 9 (April 19, 2022): 2055. http://dx.doi.org/10.3390/cancers14092055.

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Signaling pathways involving signal transducer and activator of transcription 3 (STAT3) play key roles in the aggressiveness of pancreatic ductal adenocarcinoma (PDAC), including their tumorigenesis, invasion, and metastasis. Cancer stem cells (CSCs) have been correlated with PDAC aggressiveness, and activation of STAT3 is involved in the regulation of CSC properties. Here, we investigated the involvement of interleukin-6 (IL-6) or the leukemia inhibitory factor (LIF)/glycoprotein 130 (gp130)/STAT3 pathway and their role in pancreatic CSCs. In PDAC CSC-like cells formed by culturing on a low attachment plate, autocrine/paracrine IL-6 or LIF contributes to gp130/STAT3 pathway activation. Using a gp130 inhibitor, we determined that the gp130/STAT3 pathway contributes to the maintenance of stemness features, the expression of membrane-type 1 matrix metalloproteinase (MT1-MMP), and the invasion of PDAC CSC-like cells. The gp130/STAT3 pathway also modulates the transforming growth factor (TGF)-β1/Smad pathway required for epithelial-mesenchymal transition induction through regulation of TGFβ-RII expression in PDAC CSC-like cells. Furthermore, chromatin immunoprecipitation assays revealed that p-STAT3 can access the active promoter region of H19 to influence this metastasis-related long non-coding RNA and contribute to its transcription in PDAC CSC-like cells. Therefore, the autocrine/paracrine IL-6 or LIF/gp130/STAT3 pathway in PDAC CSC-like cells may eventually facilitate invasion and metastasis, two hallmarks of malignancy. We propose that inhibition of the gp130/STAT3 pathway provides a promising strategy for targeting CSCs for the treatment of PDAC.
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Alcalá, Sonia, Paola Martinelli, Patrick C. Hermann, Christopher Heeschen, and Bruno Sainz. "The Anthrax Toxin Receptor 1 (ANTXR1) Is Enriched in Pancreatic Cancer Stem Cells Derived from Primary Tumor Cultures." Stem Cells International 2019 (May 2, 2019): 1–13. http://dx.doi.org/10.1155/2019/1378639.

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Pancreatic ductal adenocarcinoma (PDAC) is currently the fourth leading cause of cancer-related mortality. Cancer stem cells (CSCs) have been shown to be the drivers of pancreatic tumor growth, metastasis, and chemoresistance, but our understanding of these cells is still limited by our inability to efficiently identify and isolate them. While a number of markers capable of identifying pancreatic CSCs (PaCSCs) have been discovered since 2007, there is no doubt that more markers are still needed. The anthrax toxin receptor 1 (ANTXR1) was identified as a functional biomarker of triple-negative breast CSCs, and PDAC patients stratified based on ANTXR1 expression levels showed increased mortality and enrichment of pathways known to be necessary for CSC biology, including TGF-β, NOTCH, Wnt/β-catenin, and IL-6/JAK/STAT3 signaling and epithelial to mesenchymal transition, suggesting that ANTXR1 may represent a putative PaCSC marker. In this study, we show that ANTXR1+ cells are not only detectable across a panel of 7 PDAC patient-derived xenograft primary cultures but ANTXR1 expression significantly increased in CSC-enriched 3D sphere cultures. Importantly, ANTXR1+ cells also coexpressed other known PaCSC markers such as CD44, CD133, and autofluorescence, and ANTXR1+ cells displayed enhanced CSC functional and molecular properties, including increased self-renewal and expression of pluripotency-associated genes, compared to ANTXR1- cells. Thus, this study validates ANTXR1 as a new PaCSC marker and we propose its use in identifying CSCs in this tumor type and its exploitation in the development of CSC-targeted therapies for PDAC.
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Cash, Timothy P., Sonia Alcalá, María del Rosario Rico-Ferreira, Elena Hernández-Encinas, Jennifer García, María Isabel Albarrán, Sandra Valle, et al. "Induction of Lysosome Membrane Permeabilization as a Therapeutic Strategy to Target Pancreatic Cancer Stem Cells." Cancers 12, no. 7 (July 4, 2020): 1790. http://dx.doi.org/10.3390/cancers12071790.

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Despite significant efforts to improve pancreatic ductal adenocarcinoma (PDAC) clinical outcomes, overall survival remains dismal. The poor response to current therapies is partly due to the existence of pancreatic cancer stem cells (PaCSCs), which are efficient drivers of PDAC tumorigenesis, metastasis and relapse. To find new therapeutic agents that could efficiently kill PaCSCs, we screened a chemical library of 680 compounds for candidate small molecules with anti-CSC activity, and identified two compounds of a specific chemical series with potent activity in vitro and in vivo against patient-derived xenograft (PDX) cultures. The anti-CSC mechanism of action of this specific chemical series was found to rely on induction of lysosomal membrane permeabilization (LMP), which is likely associated with the increased lysosomal mass observed in PaCSCs. Using the well characterized LMP-inducer siramesine as a tool molecule, we show elimination of the PaCSC population in mice implanted with tumors from two PDX models. Collectively, our approach identified lysosomal disruption as a promising anti-CSC therapeutic strategy for PDAC.
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Guo, Yichen, Yinan Jiang, J. Bart Rose, Ganji Purnachandra Nagaraju, Renata Jaskula-Sztul, Anita B. Hjelmeland, Adam W. Beck, Herbert Chen, and Bin Ren. "Protein Kinase D1 Signaling in Cancer Stem Cells with Epithelial-Mesenchymal Plasticity." Cells 11, no. 23 (December 1, 2022): 3885. http://dx.doi.org/10.3390/cells11233885.

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Pancreatic neuroendocrine tumors (pNETs) are extremely diverse and highly vascularized neoplasms that arise from endocrine cells in the pancreas. The pNETs harbor a subpopulation of stem cell-like malignant cells, known as cancer stem cells (CSCs), which contribute to intratumoral heterogeneity and promote tumor maintenance and recurrence. In this study, we demonstrate that CSCs in human pNETs co-express protein kinase PKD1 and CD44. We further identify PKD1 signaling as a critical pathway in the control of CSC maintenance in pNET cells. PKD1 signaling regulates the expression of a CSC- and EMT-related gene signature and promotes CSC self-renewal, likely leading to the preservation of a subpopulation of CSCs at an intermediate EMT state. This suggests that the PKD1 signaling pathway may be required for the development of a unique CSC phenotype with plasticity and partial EMT. Given that the signaling networks connected with CSC maintenance and EMT are complex, and extend through multiple levels of regulation, this study provides insight into signaling regulation of CSC plasticity and partial EMT in determining the fate of CSCs. Inhibition of the PKD1 pathway may facilitate the elimination of specific CSC subsets, thereby curbing tumor progression and metastasis.
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Dissertations / Theses on the topic "Pancreatic CSC"

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RITELLI, Rossana. "Generating a pancreatic cancer mouse model: from Cancer Stem Cells to in vivo imaging strategies." Doctoral thesis, Università degli Studi di Verona, 2010. http://hdl.handle.net/11562/344615.

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Presupposti: nonostante gli enormi sforzi della ricerca per lo studio del carcinoma del pancreas, a tutt’oggi questo tumore aggressivo rimane incurabile e necessita di terapie mirate che garantiscano un miglioramento concreto della qualità della vita dei pazienti. Pertanto, è forte il bisogno di creare un sistema efficace e mirato all’identificazione di nuovi composti per la cura del cancro del pancreas. Scopo: lo scopo di questo lavoro è quello di contribuire alla generazione di un sistema che porti selezione di nuovi composti per il trattamento del carcinoma pancreatico. Questo sistema include tecniche, protocolli e un modello cellulare e animale di tumore del pancreas indispensabili per testare in vitro un alto numero di composti e per la successiva validazione in vivo dei composti selezionati. Risultati: nel corso di questo lavoro, abbiamo innanzitutto completato la caratterizzazione delle Panc1-sfere, che sono cellule tumorali presentanti caratteristiche di staminalità, precedentemente isolate nel nostro laboratorio dalla linea cellulare Panc1. Tali cellule coincidono con la subpopolazione cellulare più chemoresistente a numerosi composti già in uso clinico, pertanto sono ritenute essere il modello cellulare più indicato per la selezione di nuovi farmaci sia in vitro che in vivo. Al fine di studiare il comportamento in vivo delle Panc1-sfere, dapprima abbiamo inoculato queste cellule in sede orto topica in topi immunodeficienti e seguito la crescita tumorale ortotopici tramite Risonanza Magnetica (RMI). I nostri risultati hanno dimostrato che le Panc1-sfere rappresentano la subpopolazione più aggressiva perché crescono più velocemente rispetto alla controparte aderente, metastatizzano con maggiore frequenza e sono positive ai markers mesenchimali. Inoltre, abbiamo osservato che la RMI non è in grado di rilevare masse che poi sono state trovate nel corso delle necropsie, pertanto abbiamo effettuato un secondo esperimento, utilizzando due tecniche di Imaging in più: l’ecografia e l’Imaging Ottico. I risultati dimostrano che l’utilizzo contemporaneo di più tecniche di Imaging è estremamente utile perché fornisce informazioni complementari garantendo una maggiore precisione soprattutto per seguire in vivo gli effetti dei composti che saranno selezionati dallo screening in vitro. Conclusione: i nostri risultati dimostrano che il tumore ortotopico generato inoculando le Panc1- sfere è un buon modello che può essere usato nello validazione in vivo di nuovi composti potenzialmente in grado di curare questa malattia. Inoltre, proponiamo un protocollo combinato delle tre metodiche di Imaging che, considerando i limiti e i vantaggi di ciascuna, garantisce di monitorare la crescita tumorale in ogni sua fase, sempre nelle migliori condizioni.
Background: Pancreatic cancer remains a highly aggressive and not curable cancer in spite of the ample research in the last decades. Since conventional treatment approaches have not satisfactory effects because they don’t result in a significant improvement of the disease outcome, an effective research system is still strongly needed, in order to accurately predict the clinical efficacy of novel compounds developed for pancreatic cancer treatment. Aim: the aim of the current study is to contribute to the generation of a complete and straightforward system useful for the identification and pre-clinic screening of novel drug for the treatment pancreatic cancer. This system should provide the techniques, the protocols and a pancreatic cancer model suitable firstly for in vitro high-throughput compounds screening and then for in vivo validation of the selected molecules. Results: findings previously obtained in our laboratory have already demonstrate potential stemlike behavior of Panc-1 cells growing as 3-dimensional spheres (Panc1-spheres), isolated from adherent Panc-1 cell line. In this study we continued with the in vivo characterization of Panc-1 spheres because we used them as pancreatic cancer cell line model in the compounds screening system we are generating. So, we performed subcutaneus and orthotopical injections in nude mice with adherent Panc1 and Panc1-spheres cells. Tumor growths were followed using MRI. In order to deepen the characterization of Panc1-spheres, we also studied EMT on tumors derived from this experiment such as in vitro in both cell lines. Moreover, we observed that an improvement of imaging strategies was actually needed, in order to better control above all the formation of small masses as metastasis and early primary tumors, since MRI was not sufficient when used alone. For this reason, we also decided to focus our attention to the most important non-invasive small animalimaging modalities available today, in particular MRI, Micro-Ultrasound (US) and In Vivo Optical Imaging. Then, we correlated these techniques, arriving to the point to have an “imaging protocol”, able to offset some of the limitation of each modality when used alone, to be used in the compounds screening system we would like to generate. Conclusion: Our findings have demonstrated that the pancreatic cancer spheres are more than just cancer stem-like cells. Our mouse model, established with Sphere-growing cells, may be used for the testing of novel compounds specifically designed to target this stem-like compartment, resistant to standard chemotherapies. A combined imaging approach, with combine MRI, Optical imaging and US, in this contest become extremely important, in order to follow primary tumor sizes and metastasis detection before and after the treatment with novel compounds.
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D'AGOSTO, SABRINA LUIGIA. "EVALUATION OF CANCER-STEM CELLS IN DIFFERENT MODELS OF PANCREATIC DUCTAL ADENOCARCINOMA." Doctoral thesis, 2017. http://hdl.handle.net/11562/960930.

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Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease, mainly due to late diagnosis and its intrinsic resistance to available treatments. Similarly to many solid cancers, PDAC contains a rare population of highly tumorigenic ‘stem-like’ cells (CSC, cancer-stem cells), which have been shown to possess distinct features as compared to more differentiated cells composing the bulk of a tumour. While more differentiated cells are thought to succumb to the effects of chemotherapy, CSCs survive drug treatments and cause relapses by rapidly repopulating tumours. However, CSCs represent only a small fraction (1-5%) of neoplastic cells in tumour, which makes their study challenging. Previous studies have shown that pancreatic CSCs can be enriched in vitro as anchorage-independent spherical colonies expressing stem cell markers (e.g., CD133 and autofluorescence). In vitro three-dimensional (3D) cultures, including organoids, are emerging as novel systems to study tissue development and organogenesis. Here, we report the characterization of CSCs in pancreatic tumour cultures established from patient derived xenograft (PDX) of PDAC. We established organoid cultures from four PDX-tumours and showed that they are epithelial cultures enriched for cells expressing stem cell markers (e.g., autofluorescence) and displaying high expression of pluripotency-associated genes as compared to their corresponding more differentiated monolayer cell cultures. Most importantly, following transplantation in immunodeficient mice, organoids were capable of recapitulating the morphological heterogeneity of the parental tumour. Our results highlight the enhanced stemness potential of PDAC organoids and their potential value as an in vitro model system to study CSCs. 3D systems have recently emerged as advanced drug screening platforms as, unlike the 2D cell cultures, organoids more adequately mimic the cell and tissue architecture observed in vivo. Our preliminary data show that PDAC organoids are more resistant than conventional monolayer cell cultures to standard chemotherapy with gemcitabine and abraxane aligning them with the resistance/sensitivity profile usually observed in vivo. Thus, pancreatic organoids can be used to model PDAC and as drug screening platforms to predict clinical responses and personalised cancer treatments.
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Book chapters on the topic "Pancreatic CSC"

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Alvina, Fidelia B., Arvin M. Gouw, and Anne Le. "Cancer Stem Cell Metabolism." In The Heterogeneity of Cancer Metabolism, 161–72. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_12.

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AbstractCancer stem cells (CSCs), also known as tumorinitiating cells (TICs), are a group of cells found within cancer cells. Like normal stem cells, CSCs can proliferate, engage in self-renewal, and are often implicated in the recurrence of tumors after therapy [1, 2]. The existence of CSCs in various types of cancer has been proven, such as in acute myeloid leukemia (AML) [3], breast [4], pancreatic [5], and lung cancers [6], to name a few. There are two theories regarding the origin of CSCs. First, CSCs may have arisen from normal stem/progenitor cells that experienced changes in their environment or genetic mutations. On the other hand, CSCs may also have originated from differentiated cells that underwent genetic and/or heterotypic modifications [7]. Either way, CSCs reprogram their metabolism in order to support tumorigenesis.
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Y. Liu, Alvin, Tatjana Crnogorac-Jurcevic, James J. Lai, and Hung-Ming Lam. "Antibody Therapy Targeting Cancer-Specific Cell Surface Antigen AGR2." In Advances in Precision Medicine Oncology. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96492.

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For anterior gradient 2 (AGR2), normal cells express the intracellular form iAGR2 localized to the endoplasmic reticulum while cancer cells express the extracellular form eAGR2 localized on the cell surface and secreted. Antibodies targeting eAGR2+ cancer cells for eradication will spare normal cells. Two AGR2 monoclonal antibodies, P1G4 and P3A5, were shown to recognize specifically eAGR2+ pancreatic tumors implanted in mice. In addition, P1G4 showed enhancement in drug inhibition of tumor growth. Human:mouse chimeric antibodies of IgG1, IgG2, IgG4 were generated for both antibodies. These human IgG were shown to lyse eAGR2+ prostate cancer cells in vitro with human serum. AGR2 has an important function in distal spread of cancer cells, and is highly expressed in prostate, pancreatic, bladder metastases. Therefore, immunotherapy based on AGR2 antibody-mediated ADCC and CDC is highly promising. Cancer specificity of eAGR2 predicts possibly minimal collateral damage to healthy tissues and organs. Moreover, AGR2 therapy, once fully developed and approved, can be used to treat other solid tumors since AGR2 is an adenocarcinoma antigen found in many common malignancies.
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Tüysüz, Umut. "Choledochal Cysts." In Biliary Tract - Review and Recent Progress [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.109023.

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Choledochal cysts are congenital dilatations of the intra- and extrahepatic biliary tract that cause various pancreatic and hepatobiliary disorders. Pancreaticobiliary maljunction (PBM) results in choledochal cysts. PBM is a congenital pancreatic and bile duct juncture anomaly. It is widely accepted that the clinical presence of PBM is an etiological factor in the pathogenesis of biliary carcinogenesis in patients with choledochal cysts. For definitive diagnosis, ultrasonography sometimes shows the relationship with the biliary tract. If USG findings cannot rule out other causes, ideally MRI should be performed together with MRCP. CT may be the initial test for undiagnosed common bile duct malformations. In rare cases where conventional imaging results are uncertain, nuclear hepatobiliary iminodiacetic acid (HIDA) scanning enables the evaluation of radiological trace of involvement and accumulation in cystic structures associated with the biliary system. Todani added five anomalies and organized the most commonly used classification system. There are five subtypes. A type I cyst, A choledochal diverticulum (Todani type II), Choledochoceles (Todani type III), type IV cyst, Caroli disease (Todani type V). Surgical treatment should be based on the extent of biliary involvement based on the widely used Todani classification and anatomical findings and the presence or absence of PBM. The standard treatment in most CCs is the resection of the bile duct up to the lobar bifurcation. Residual postoperative intrapancreatic choledochal cyst may also lead to secondary carcinogenesis and associated morbidity. The localization of the pancreatic cyst is inside the head of the pancreas, close to the neck and to the left of the bile duct. Surgical treatment options include laparoscopic treatment. Its main advantages include excellent visualization and low blood loss.
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Conference papers on the topic "Pancreatic CSC"

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Arima, Kota, Takatsugu Ishimoto, Hirohisa Okabe, Yuki Kitano, Risa Inoue, Kensuke Yamamura, Takayoshi Kaida, et al. "Abstract 3350: Verification of mechanism that CSC markers are implicated in poor prognosis for pancreatic ductal adenocarcinoma." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3350.

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Avan, Amir, Karl Quint, Francesco Nicolini, Mina Maftouh, Niccola Funel, Godefridus J. Peters, and Elisa Giovannetti. "Abstract A46: c-MET as a potential therapeutic target in pancreatic cancer: Implications in cancer-stem-like cell (CSC) population and gemcitabine resistance in pancreatic cancer." In Abstracts: AACR Special Conference on Pancreatic Cancer: Progress and Challenges; June 18-21, 2012; Lake Tahoe, NV. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.panca2012-a46.

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Bossard, Carine, Nathalia Cruz, Brian Eastman, Chi-Ching Mak, Sunil KC, Betty Tam, Timothy Phalen, and Steven Cha. "Abstract C08: SM08502, a novel, small-molecule CDC-like kinase (CLK) inhibitor, demonstrates activity against cancer stem cell (CSC)-enriched pancreatic cancer cells and suppresses stemness in vitro." In Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; September 6-9, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.panca19-c08.

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Kim, Edward J., Gazala N. Khan, Kent Griffith, Joel Greenson, Naoko Takebe, Mark Zalupski, and Diane Simeone. "Abstract A40: Cancer stem cells (CSC) and inhibition of hedgehog (Hh) pathway signaling in advanced pancreatic cancer: GDC-0449 in combination with gemcitabine (Gem)." In Abstracts: AACR Special Conference on Pancreatic Cancer: Progress and Challenges; June 18-21, 2012; Lake Tahoe, NV. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.panca2012-a40.

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Li, Rui, and Yaolong Qi. "Network-based analysis of important subnetworks during pancreatic cancer development." In 2016 35th Chinese Control Conference (CCC). IEEE, 2016. http://dx.doi.org/10.1109/chicc.2016.7554844.

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De Gaetano, Andrea, Claudio Gaz, Claudio Gori Giorgi, and Pasquale Palumbo. "An islet population model of pancreatic insulin production." In 2013 IEEE 52nd Annual Conference on Decision and Control (CDC). IEEE, 2013. http://dx.doi.org/10.1109/cdc.2013.6760396.

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Gong, Haijun, Paolo Zuliani, Qinsi Wang, and Edmund M. Clarke. "Formal analysis for logical models of pancreatic cancer." In 2011 50th IEEE Conference on Decision and Control and European Control Conference (CDC-ECC 2011). IEEE, 2011. http://dx.doi.org/10.1109/cdc.2011.6161052.

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Geng, Yuchen, and Weimin Zhou. "Image Super-Resolution Reconstruction of Pancreatic Carcinoma Based on Edge Repair Generative Adversarial Network." In 2022 41st Chinese Control Conference (CCC). IEEE, 2022. http://dx.doi.org/10.23919/ccc55666.2022.9901818.

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Bossard, Carine, Nathalia Cruz, Brian Eastman, Chi-Ching Mak, K. C. Sunil, Betty Tam, Gail Bucci, Josh Stewart, Timothy Phalen, and Steven Cha. "Abstract A02: SM08502, a novel, small-molecule CDC-like kinase (CLK) inhibitor, downregulates the Wnt signaling pathway and demonstrates antitumor activity in pancreatic cancer cell lines and in vivo xenograft models." In Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; September 6-9, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.panca19-a02.

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Bossard, Carine, Igor Astsaturov, Nathalia Cruz, Brian Eastman, Chi-Ching Mak, K. C. Sunil, Betty Tam, et al. "Abstract C09: Inhibition of tumor growth and post-treatment regrowth by SM08502, a novel, small-molecule CDC-like kinase (CLK) inhibitor, in combination with standard of care in pancreatic cancer models." In Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; September 6-9, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.panca19-c09.

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You might also be interested in the extended bibliographies on the topic 'Pancreatic CSC' for particular source types:
Journal articles
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