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Добірка наукової літератури з теми "Pancreatic cancer stem cell"

Автор: Grafiati
Опубліковано: 11 березня 2023

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Статті в журналах з теми "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 (June 10, 2008): 2806–12. http://dx.doi.org/10.1200/jco.2008.16.6702.

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Анотація:
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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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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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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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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Анотація:
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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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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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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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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Анотація:
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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Більше джерел

Дисертації з теми "Pancreatic cancer stem cell"

1

Sasaki, Naoya. "Alpha-fetoprotein-producing pancreatic cancer cells possess cancer stem cell characteristics." Kyoto University, 2012. http://hdl.handle.net/2433/157414.

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2

Zheng, Xuehai. "Role of stem cell protein PIWIL4 in the tumorigenesis of human pancreatic cancer." [Huntington, WV : Marshall University Libraries], 2008. http://www.marshall.edu/etd/descript.asp?ref=.

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3

Zhao, Yue. "Characterization and targeted therapy of stem cell-like side population cells in pancreatic cancer and esophageal cancer." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-168236.

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4

Roshan, Moniri Mani. "Pancreatic ductal-derived mesenchymal stem cells : their distribution, characterization and cytotoxic effect on pancreatic cancer cells." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/43529.

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Анотація:
Mesenchymal stem cells (MSCs) have attracted significant attention in cancer research as a result of their accessibility, tumor-oriented homing capacity, and the feasibility of auto-transplantation. This study detected the sensitivity of pancreatic cancer cell lines (PCCs) to pancreatic-derived, engineered MSCs under different culture conditions. Pancreatic ductal tissue was extracted from adult human pancreas. MSCs were derived and expanded ex-vivo and verified to fulfil criteria for human MSCs according to the guidelines of the International Society for Cellular Therapy. MSCs were analyzed for distribution and migratory capacity to the site of pancreas and PCCs in in vivo and in vitro models, and found to have homing capacity to the pancreas and towards PCCs (MSCs were attracted to all PCCs compared to normal human A1F8 cells and they displayed significant attraction to the media obtained from cancer cells compared to normal media (p<0.05)). PCCs (BXPC3, ASPC1, Panc-1, TRM6 and HP62) were analyzed by FACS for TNF-α Related Apoptosis Inducing Ligand (TRAIL) receptors. MSCs engineered with non-secreting TRAIL (MSCnsTRAIL) and secreting TRAIL (MSCstTRAIL) and PTEN (MSCPTEN) were used for both direct and indirect co-cultures. TRAIL/PTEN expression was assessed by both ELISA and western blot analysis; higher molecular weight was observed in the MSCnsTRAIL (56kDA) compared with MSCstTRAIL (26kDa). The TRAIL content of supernanatats from MSCstTRAIL was significantly higher than MSCnsTRAIL (p<0.05). PTEN-RFP fusion protein showed a higher molecular weight of 74 kDa in comparison with endogenous PTEN (47 kDa). A real time detection of MSCs cytotoxicity on PCCs displayed proportional cancer cell death to the ratio of conditioned media used from MSCnsTRAIL, MSCstTRAIL, and MSCPTEN. Naive MSCs exhibit intrinsic cytotoxic effect on pancreatic cancer cells and this effect was potentiated by TRAIL/PTEN-engineering. This study provides a practical platform for the development of MSC-based therapy for pancreatic cancer.
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5

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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Анотація:
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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Zhao, Yue [Verfasser], and Peter [Akademischer Betreuer] Nelson. "Characterization and targeted therapy of stem cell-like side population cells in pancreatic cancer and esophageal cancer / Yue Zhao. Betreuer: Peter Nelson." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2013. http://d-nb.info/1049393317/34.

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7

Maruno, Takahisa. "Visualization of stem cell activity in pancreatic cancer expansion by direct lineage tracing with live imaging." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/265166.

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Анотація:
京都大学
新制・論文博士
博士(医学)
乙第13427号
論医博第2231号
新制||医||1053(附属図書館)
京都大学大学院医学研究科医学専攻
(主査)教授 松田 道行, 教授 渡邊 直樹, 教授 川口 義弥
学位規則第4条第2項該当
Doctor of Medical Science
Kyoto University
DFAM
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Karim, Karzan Khowaraham. "Investigating the effects of curcumin and resveratrol on pancreatic cancer stem cells." Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/33155.

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Анотація:
Anti-proliferative and cancer stem-cell targeting abilities of curcumin and resveratrol individually have been shown in different cancers. This project aimed to assess the activity of these compounds, alone and in combination in pancreatic cancer cell lines (PCCLs) and stellate cells. Anti-proliferation assays were performed for curcumin and resveratrol alone and in combination, combined with end point markers of activity including apoptosis and cell cycle arrest. Pancreatic cancer stem cell populations were defined using the cell surface markers CD44, CD24, ESA, CD133, ALDH-1 activity or sphere forming ability, and finally Nanog expression was assessed. The intracellular uptake of curcumin and its metabolites was analysed by HPLC. The PCCLs were more sensitive to curcumin than resveratrol, and combinations of these compounds showed anti-proliferative efficacy through apoptosis and cell cycle arrest at low, clinically achievable concentrations (CACs) in 2 out of 4 cell lines. Capan-1 cells exhibited the highest sensitivity to curcumin, which was able to enhance the effectiveness of resveratrol treatments in targeting cancer stem-like populations. Spheroid growth was significantly inhibited by curcumin and resveratrol combinations in Capan-1 cells, correlating with decreased ALDH1 activity and Nanog expression. In human pancreatic cancer tissue, various stem-like populations were identified based on expression of ALDH1 or CD24+/CD44+, which may provide a suitable target in vivo. Capan-1 cells metabolised curcumin to detectable amounts of curcumin glucuronide. However, curcumin metabolites did not show any significant activity at CACs. Curcumin alone may have activity against pancreatic cancer stem cells, and enhances efficacy at low concentrations when in combination with resveratrol. Capan-1 cells are able to internalise curcumin, and this cell line exhibited the greatest sensitivity to treatment. Overall, the results suggest that curcumin and resveratrol warrant further investigation as combination therapies for targeting cancer stem-like cells and stellate cells responsible for the dense stroma observed in pancreatic cancer.
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CREMONESE, Giorgia. "Prostate Stem Cell Antigen (PSCA): a putative target for immunotherapy and diagnosis in prostate, pancreatic and bladder carcinoma." Doctoral thesis, Università degli Studi di Verona, 2010. http://hdl.handle.net/11562/342880.

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L’immunoterapia basata sull’utilizzo di anticorpi non coniugati, coniugati a tossine o radiomarcati, che riconoscono antigeni associati a tumore, è promettente per la cura di tumori solidi o ematici. Un possibile target per l’immunoterapia potrebbe essere il prostate stem cell antigen (PSCA), un antigene appartenente alla famiglia delle “GPIanchored protein”. Il PSCA è un antigene di superficie espresso a bassi livelli nel tessuto prostatico sano ed over espresso nel tumore prostatico, pancreatico e della vescica. L’espressione di PSCA è inoltre correlata positivamente a “Gleason score” e allo stadio della patologia nel tumore prostatico. Il presente lavoro di tesi descrive la generazione e caratterizzazione di un anticorpo monoclonale murino anti PSCA (mAb), ottenuta tramite la tecnologia dell’ibridoma, e del suo frammento anticorpale a singola catena (scFv), generato clonando la regione variabile della catena leggera (VL) e della catena pesante (VH) nel vettore di espressione pHEN-2. Tramite citofluorimetria è stato dimostrato che l’anticorpo monoclinale possiede una buona affinità e specificità di legame all’antigene. Il potenziale diagnostico dell’anticorpo è stato dimostrato tramite Western Blot su lisati di tessuti neoplastici di prostrata e pancreas, in cui l’anticorpo è in grado di legare l’antigene denaturato e glicosilato, e tramite ELISA, in cui l’anticorpo si lega all’antigene espresso da cellule precedentemente fissate. Il potenziale terapeutico dell’anticorpo è stato valutato tramite saggio di proliferazione: l’anticorpo da solo non è in grado di indurre morte cellulare tramite un meccanismo diretto, mentre in seguito a coniugazione chimica con la catena A della ricina (RTA) rivela effetto citotossico su cellule PC-3 hPSCA con IC50 (concentrazione in grado di inibire la massima proliferazione cellulare del 50%) pari a 1.3x10-9, valore 100 volte più piccolo di quello ottenuto con la sola tossina RTA. Il frammento scFv è stato prodotto nel ceppo batterico E. Coli. Mediante analisi citofluorimetrica su cellule PSCA positive e saggio immunoenzimatico sull’antigene ricombinante è stato verificato che il frammento anticorpale mantiene le stesse caratteristiche di specificità di legame all’antigene dell’anticorpo monoclinale parentale, ma possiede affinità minore. Quando l’ scFv viene reso bivalente, tramite il cross-linking dei monomeri utilizzando un anticorpo anti-myc, l’affinità raggiunge quasi quella dell’anticorpo parentale. Successivamente l’scFv è stato unito attraverso fusione genetica al dominio enzimatico della tossina batterica Pseudomonas aeruginosa exotoxin A (PE40). L’immunotossina risultante è espressa nel ceppo batterico E. Coli e si accumula nei corpi d’inclusione. L’analisi citofluorimetrica su cellule PSCA positive fatta utilizzando i corpi d’inclusione rinaturati e contenenti l’immunotossina di fusione ha confermato che l’interazione tra l’scFv e l’antigene viene conservata in seguito alla fusione con la tossina PE40. L’effetto citotossico dell’immunotossina purificata scFv-PE40 verrà valutata prima in vitro su linee cellulari PSCA positive e negative e poi in modelli in vivo che permetteranno di valutare anche eventuali effetti collaterali.
Antibody-based therapy using unconjugated, toxin-conjugated or radiolabeled immunoglobulins recognizing tumor-associated antigens has proven beneficial for solid and hematolymphoid neoplasms. A suitable target could be prostate stem cell antigen (PSCA), a member of the “GPI-anchored protein”. PSCA is a cell surface-antigen expressed at low levels in normal prostate tissue and over expressed in prostate, pancreatic and bladder carcinomas. Moreover PSCA expression is positively correlated with Gleason score and with pathologic stage in prostate cancer. The present thesis describes the generation and characterization of the murine anti PSCA monoclonal antibody (mAb), obtained by hybridoma technology, and its fragment single chain (scFv), generated by cloning the variable heavy (VH) and light (VL) chain sequences in the expression vector pHEN-2. The mAb showed the ability to recognize with good affinity and specificity the native PSCA by flow cytometry. The diagnostic potential of the mAb was demonstrated by Western Blot performed with prostate and pancreatic neoplastic tissue lysates, showing the binding to denaturated and glycosylated PSCA, and by ELISA performed with fixed cells. The mAb was also assessed for its possible use in the therapeutic approach: the cell-proliferation assay demonstrated that the antibody alone is not able to induce cell death through a direct mechanism, while when it is conjugated to the ricin A chain toxin (RTA) by chemical linkage it can poison PC-3 hPSCA cells with an IC50 (i.e. concentration inhibiting 50% of the maximal cell proliferation) of 1.3x10-9 M, value 100 fold lower than the IC50 of the RTA toxin alone. The scFv was produced in E. Coli bacteria; flow cytometric analysis on PSCA-positive cells and immunoenzymatic assay on the recombinant antigen proved that the antibody fragment maintains the binding specificity of the parental monoclonal antibody. The affinity of the scFv is lower than the affinity of mAb but it is partially recovered making the scFv divalent by cross-linking the scFv monomers via an antibody-mediated myc- Tag interaction. To create a fusion immunotoxin (IT) the scFv was later genetically fused to the enzymatic domain of Pseudomonas aeruginosa exotoxin A (PE40). The resulting IT was expressed in E. Coli bacteria and it is accumulated in the inclusion bodies. The flow cytometric analysis on PSCA-positive cells performed with the whole refolded inclusion bodies extract containing the fusion IT confirmed that the interaction of scFv with the PSCA is preserved after fusion to PE40. The efficacy of purified scFv-PE40 will be analyse in vitro on positive and negative cell lines and subsequently in vivo models which also will be useful to study the side effects of this new drug.
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Capodanno, Ylenia. "Identifying therapeutic implications of cancer stem cells in human and canine insulinoma." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31175.

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Pancreatic neuroendocrine tumours (PNETs) are the most common neuroendocrine tumours diagnosed in humans and dogs. Due to the highly heterogeneous nature of these tumours, definitive data are still lacking over the molecular mechanisms involved in their cancerous behaviour. This study focused on insulinoma (INS), as it is the most commonly diagnosed PNET in human and veterinary oncology. INS is an insulin-producing tumour that causes a hypoglycaemic syndrome related to the excessive insulin production. In humans, it is often a small benign neoplasm readily curable by surgical resection whereas, in dogs, INS is often malignant. Despite current treatment modalities, malignant canine and human INS have a poor prognosis as patients tend to develop metastases in liver and lymph nodes that do not respond to current therapies. From a comparative oncology perspective, the close resemblance of canine and human malignant INS makes canine INS an interesting study model for human INS. Cancer stem cells (CSCs) are critical for the engraftment and chemoresistance of many tumours. Although CSCs have been isolated from a range of solid tumours, a comprehensive characterisation of INS CSCs has not yet been reported. In this study, it was confirmed that INS CSCs can be enriched and are potential targets for novel INS therapies. Highly invasive and tumourigenic human and canine INS CSCs were successfully isolated and exhibited greater resistance to chemotherapy, which may play a significant role in the poor prognosis of this disease. To date, the mechanisms by which tumours spread and the clinical causes of chemoresistance remain only partially understood. Here, RNA-sequencing analysis was performed over a small set of canine INS tumour samples in order to identify mechanisms involved in INS carcinogenesis through different stages of the disease. Preliminary data showed that distinct gene profiles characterised early and late stage of canine INS. Interestingly, differential gene expression and gene pathways analysis, highlighted that sets of genes involved in pancreatic embryogenesis and insulin secretion were overexpressed in canine primary INS lesions compared with normal pancreas. The Notch pathway is fundamental in pancreatic embryogenesis and it has been previously associated with carcinogenesis of neuroendocrine tumours and with the CSC phenotype. Protein analysis showed that the Notch pathway is activated in both human and canine INS CSCs, particularly when treated with chemotherapy, indicating that the Notch pathway may be involved in chemoresistance. Additionally, it was demonstrated that inhibition of the Notch pathway decreased INS CSCs' survival and chemoresistance, both in vitro and in vivo. These findings provide preclinical evidence that anti-Notch therapy may improve outcomes for patients with malignant INS.
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Книги з теми "Pancreatic cancer stem cell"

1

service), SpringerLink (Online, ed. Pancreatic Stem Cells. Totowa, NJ: Humana Press, 2009.

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2

Shah, Khalid, ed. Stem Cell Therapeutics for Cancer. Hoboken, NJ: John Wiley & Sons, Inc, 2013. http://dx.doi.org/10.1002/9781118660423.

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3

Peter, Gale Robert, Juttner Christopher, and Henon P. R, eds. Blood stem cell transplants. Cambridge, [U.K.]: Cambridge University Press, 1994.

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4

Pavlovic, Mirjana, and Bela Balint. Bioengineering and Cancer Stem Cell Concept. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-25670-2.

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5

Scatena, Roberto, Alvaro Mordente, and Bruno Giardina, eds. Advances in Cancer Stem Cell Biology. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-0809-3.

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6

Scatena, Roberto, Alvaro Mordente, and B. Giardina. Advances in cancer stem cell biology. New York: Springer, 2012.

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7

López-Larrea, Carlos. Stem Cell Transplantation. New York, NY: Springer US, 2012.

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8

N, Winter Jane, ed. Blood stem cell transplantation. Boston: Kluwer Academic Publishers, 1997.

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9

Maccalli, Cristina, Matilde Todaro, and Soldano Ferrone, eds. Cancer Stem Cell Resistance to Targeted Therapy. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-16624-3.

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10

Regad, Tarik, Thomas J. Sayers, and Robert C. Rees, eds. Principles of Stem Cell Biology and Cancer. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118670613.

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Частини книг з теми "Pancreatic cancer stem cell"

1

Proctor, Erica N., and Diane M. Simeone. "Pancreatic Cancer Stem Cells." In Advances in Cancer Stem Cell Biology, 197–209. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0809-3_12.

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2

Li, Chenwei, and Diane M. Simeone. "Pancreatic Cancer Stem Cells." In Pancreatic Cancer, 317–31. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-0-387-77498-5_12.

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3

Goodwin, Mackenzie, Ethan V. Abel, Vinee Purohit, and Diane M. Simeone. "Pancreatic Cancer Stem Cells." In Pancreatic Cancer, 349–68. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7193-0_12.

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4

Goodwin, Mackenzie, Ethan V. Abel, Vinee Purohit, and Diane M. Simeone. "Pancreatic Cancer Stem Cells." In Pancreatic Cancer, 1–20. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6631-8_12-2.

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5

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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6

Hendley, Audrey M., and Jennifer M. Bailey. "Stem Cells and Pancreatic Cancer." In Principles of Stem Cell Biology and Cancer, 213–29. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118670613.ch11.

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7

Dosch, Joseph, Cheong Jun Lee, and Diane M. Simeone. "Cancer Stem Cells: Pancreatic Cancer." In Stem Cells and Cancer, 185–97. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-933-8_15.

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8

García-Silva, Susana, and Christopher Heeschen. "Stem Cells and Pancreatic Cancer." In Cancer Stem Cells, 209–22. Hoboken, NJ: John Wiley & Sons, 2014. http://dx.doi.org/10.1002/9781118356203.ch16.

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9

Simeone, Diane M. "Pancreatic Cancer Stem Cells." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_4359-4.

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Simeone, Diane M. "Pancreatic Cancer Stem Cells." In Encyclopedia of Cancer, 3417–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-46875-3_4359.

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Тези доповідей конференцій з теми "Pancreatic cancer stem cell"

1

Takano, Shigetsugu, Maximilian Reichert, Hideyuki Yoshitomi, Basil Bakir, Koushik K. Das, Steffen Heeg, Shingo Kagawa, et al. "Abstract B30: Prrx1 isoforms regulate pancreatic cancer stem cell functions during pancreatic cancer progression." In Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; May 12-15, 2016; Orlando, FL. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.panca16-b30.

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2

Matsuda, Yoko, Kazuya Yamahatsu, Kiyoko Kawahara, Taeko Suzuki, Takenori Fujii, Tetsushi Yamamoto, Murray Korc, Zenya Naito, and Toshiyuki Ishiwata. "Abstract 2457: Nestin regulates pancreatic cancer stem cell functions." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2457.

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3

Matsuda, Yoko, Masahito Hagio, Yuji Yanagisawa, Taeko Suzuki, Yoko Kawamoto, Kiyoko Kawahara, Zenya Naito, and Toshiyuki Ishiwata. "Abstract 5200: Nestin regulates stem cell functions of pancreatic cancer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5200.

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Ilmer, Matthias, Jody Vykoukal, and Eckhard Alt. "Abstract 3355: Signaling networks in pancreatic cancer cells with stem cell characteristics." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3355.

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5

Kim, Sun A., Soo Bin Park, and Si Young Song. "Abstract 713: GLRX3, a secretory biomarker of pancreatic cancer based on pancreatic cancer stem cell characteristics." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-713.

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6

Breunig, M., J. Merkle, T. Seufferlein, M. Hohwieler, and A. Kleger. "Designer pancreatic cancer generated from human pluripotent stem cell derived ducts." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695427.

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7

Abel, Ethan V., Masashi Goto, Nikita Ramanathan, Chandan Kumar, Lesa Begley, Michele L. Dziubinski, Lidong Wang, Meghna Waghray, Sumithra Urs, and Diane M. Simeone. "Abstract 2335: Pancreatic cancer stem cell function is regulated by HNF1A." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2335.

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Abel, Ethan V., Masashi Goto, Michele L. Dziubinski, Chandan Kumar, Nikita Ramanathan, and Diane M. Simeone. "Abstract A65: Pancreatic cancer stem cell function is regulated by HNF1A." In Abstracts: AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.panca2014-a65.

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Visús, Carmen, Antonio Lozano-Leon, YangYang Wang, YooJung Chang, David C. Whitcomb, Randall E. Brand, and Albert B. DeLeo. "Abstract 3339: Elimination of cancer stem cells in pancreatic cancer cell lines by a combinatorial therapy." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3339.

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Begum, Asma, Ross McMillan, Yu-tai Chang, Vesselin Penchev, NV Rajeshkumar, Anirban Maitra, Michael G. Goggins, et al. "Abstract 5889: Cancer associated fibroblasts regulate cancer stem cell functions in pancreatic ductal adenocarcinoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5889.

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Звіти організацій з теми "Pancreatic cancer stem cell"

1

Houchen, Courtney W. Tuft Cell Regulation of miRNAs in Pancreatic Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada602496.

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Houchen, Courtney W. Tuft Cell Regulation of miRNAs in Pancreatic Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2014. http://dx.doi.org/10.21236/ada621275.

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Fletterick, Robert J. Inhibition of Pancreatic Cancer Cell Proliferation by LRH-1 Inhibitors. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada599687.

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Watabe, Kounosuke. DCIS-Specific MicroRNA in Cancer Stem Cell. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada554452.

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Karp, Jeffrey, and John Isaacs. Mesenchymal Stem Cell-Based Therapy for Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada612823.

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Watabe, Kounosuke. Identification of Dormant Stem Cell in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2012. http://dx.doi.org/10.21236/ada559377.

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Engler, Adam J., Jing Yang, Spencer Wei, Laurent Fattet, and Matthew Ondeck. Regulation of Breast Cancer Stem Cell by Tissue Rigidity. Fort Belvoir, VA: Defense Technical Information Center, June 2014. http://dx.doi.org/10.21236/ada609393.

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Ponnazhagan, Selvarangan. Regenerative Stem Cell Therapy for Breast Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada612699.

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Ponnazhagan, Selvarangan. Regenerative Stem Cell Therapy for Breast Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada567277.

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Ponnazhagan, Selvarangan. Regenerative Stem Cell Therapy for Breast Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada592352.

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