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Academic literature on the topic 'PSCA'

Author: Grafiati

Published: 11 March 2023

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Journal articles on the topic "PSCA"

1

Sun, Shi-Qi, Xiang-Tao Liu, Hui-Chen Guo, Shuang-Hui Yin, You-Jun Shang, Xia Feng, Zai-Xin Liu, and Qing-Ge Xie. "Protective immune responses in guinea pigs and swine induced by a suicidal DNA vaccine of the capsid gene of swine vesicular disease virus." Journal of General Virology 88, no. 3 (March 1, 2007): 842–48. http://dx.doi.org/10.1099/vir.0.82504-0.

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A suicidal DNA vaccine based on a Semliki Forest virus (SFV) replicon was evaluated for the development of a vaccine against swine vesicular disease virus (SVDV). The 1BCD gene of SVDV was cloned and inserted into pSCA1, an SFV DNA-based replicon vector. The resultant plasmid, pSCA/1BCD, was transfected into BHK-21 cells and the antigenicity of the expressed protein was confirmed using an indirect immunofluorescence assay. Immunogenicity was studied in guinea pigs and swine. Animals were injected intramuscularly three times with pSCA/1BCD at regular intervals. Anti-SVDV antibodies were detected by ELISA, the lymphocyte proliferation response was tested by the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide method and neutralizing antibodies were measured by microneutralization tests. The data showed that SVDV-specific antibodies, neutralizing antibodies and lymphocyte proliferation were induced in both guinea pigs and swine. Furthermore, after three successive vaccinations with pSCA/1BCD, half of the pigs were protected against challenge with SVDV. These results should encourage further work towards the development of a DNA vaccine against SVDV.

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Arndt, Claudia, Ralf Bergmann, Franziska Striese, Keresztély Merkel, Domokos Máthé, Liliana R. Loureiro, Nicola Mitwasi, et al. "Development and Functional Characterization of a Versatile Radio-/Immunotheranostic Tool for Prostate Cancer Management." Cancers 14, no. 8 (April 14, 2022): 1996. http://dx.doi.org/10.3390/cancers14081996.

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Due to its overexpression on the surface of prostate cancer (PCa) cells, the prostate stem cell antigen (PSCA) is a potential target for PCa diagnosis and therapy. Here we describe the development and functional characterization of a novel IgG4-based anti-PSCA antibody (Ab) derivative (anti-PSCA IgG4-TM) that is conjugated with the chelator DOTAGA. The anti-PSCA IgG4-TM represents a multimodal immunotheranostic compound that can be used (i) as a target module (TM) for UniCAR T cell-based immunotherapy, (ii) for diagnostic positron emission tomography (PET) imaging, and (iii) targeted alpha therapy. Cross-linkage of UniCAR T cells and PSCA-positive tumor cells via the anti-PSCA IgG4-TM results in efficient tumor cell lysis both in vitro and in vivo. After radiolabeling with 64Cu2+, the anti-PSCA IgG4-TM was successfully applied for high contrast PET imaging. In a PCa mouse model, it showed specific accumulation in PSCA-expressing tumors, while no uptake in other organs was observed. Additionally, the DOTAGA-conjugated anti-PSCA IgG4-TM was radiolabeled with 225Ac3+ and applied for targeted alpha therapy. A single injection of the 225Ac-labeled anti-PSCA IgG4-TM was able to significantly control tumor growth in experimental mice. Overall, the novel anti-PSCA IgG4-TM represents an attractive first member of a novel group of radio-/immunotheranostics that allows diagnostic imaging, endoradiotherapy, and CAR T cell immunotherapy.

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Zou, Qiong, Leping Yang, Zhulin Yang, Jiangsheng Huang, and Xi Fu. "PSCA and Oct-4 Expression in the Benign and Malignant Lesions of Gallbladder: Implication for Carcinogenesis, Progression, and Prognosis of Gallbladder Adenocarcinoma." BioMed Research International 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/648420.

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PSCA and Oct-4 have been thought as markers of cancer stem cells. Although overexpression of PSCA and Oct-4 in cancer has been reported, little is known about the clinical and pathological significance with PSCA and Oct-4 expression in gallbladder adenocarcinoma. In this study, overexpression of PSCA and Oct-4 was detected in gallbladder adenocarcinoma (54.6% and 55.6%). Less expression of PSCA and Oct-4 was detected in the pericancerous tissues (19.6% and 21.7%), gallbladder polyps (13.3% and 13.3%), and gallbladder epithelium with chronic cholecystitis (14.3% and 14.3%). The overexpression of PSCA and Oct-4 was significantly associated with differentiation, tumor mass, lymph node metastasis, invasion of gallbladder adenocarcinoma, and decreased overall survival. Our study suggested that overexpression of PSCA and Oct-4 might be closely related to the carcinogenesis, progression, metastasis, or invasive potential and prognosis of gallbladder carcinoma.

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Xiang, Qian, Zhiguo Zhu, Lianmin Luo, Jiamin Wang, Yangzhou Liu, Yihan Deng, Mingda Zhou, and Zhigang Zhao. "The Correlation between PSCA Expression and Neuroendocrine Differentiation in Prostate Cancer." BioMed Research International 2020 (September 24, 2020): 1–9. http://dx.doi.org/10.1155/2020/5395312.

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The prostate stem cell antigen (PSCA), as a predominantly prostate-specific marker, is overexpressed in most prostate cancer specimens, is positively correlated with prostate cancer androgen independence, and has the potential to be treated with castration-resistant prostate cancer (CRPC) as a gene therapy target. Using the typical androgen deprivation therapy, most tumors will progress to CRPC, as well as develop into neuroendocrine prostate cancer (NEPC) characterized by the expression of neuroendocrine markers such as enolase 2 (NSE). Our study was aimed at investigating the expressions of PSCA and NSE and the relationship between the two markers, as well as the correlation between the PSCA and NSE expressions and the clinicopathological parameters in prostate cancer specimens from 118 patients by using immunohistochemistry. Our results demonstrated that the PSCA and NSE protein expressions did not correlate with the prostate cancer patients’ age or the hormone therapy but showed a significant correlation with the pathological tumor stage of prostate cancer, the Gleason score, and the presence of metastasis. There is a positive association between PSCA and NSE but a negative one between the prostate-specific antigen (PSA) and PSCA or between PSA and NSE. High PSCA and NSE expressions correlated with a poor prognosis in prostate cancer patients. PSCA may play an important role in the progression of neuroendocrine prostate cancer (NEPC).

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Garcia-Gonzalez, Ulises, Daniel D. Cavalcanti, Abhishek Agrawal, Robert F. Spetzler, and Mark C. Preul. "Anatomical Study on the “Perforator-free Zone”: Reconsidering the Proximal Superior Cerebellar Artery and Basilar Artery Perforators." Neurosurgery 70, no. 3 (September 6, 2011): 764–73. http://dx.doi.org/10.1227/neu.0b013e3182351f8e.

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Abstract Background: The proximal superior cerebellar artery (pSCA) is often considered a perforator-free area. Precise anatomical knowledge of this region clarifies the pathophysiology underlying posterior fossa ischemic syndromes and helps avoid treatment-related complications. Objective: To anatomically evaluate perforating branches arising from the pSCA and the upper basilar artery (BA). Methods: Forty-four SCAs from 20 cadaveric heads were examined to determine patterns of the pSCA; its morphometry for medial and lateral branches; and frequency, number, diameter, distribution, and vascular territory of perforators arising from the pSCA and rostral BA. Results: SCA arose as a single trunk in 36 sides (90%): mean diameter at origin was 1.38 mm; mean length was 14.± 6 7.9 mm. Ninety-nine pSCA perforator branches were present in 82% of specimens (mean, 2.3 ± 1.6; range, 0-7 perforators/side). Of these, 59% were direct, belonging to the interpeduncular group in 85% of cases; 28% were short circumflex, belonging to lateral and medial pontine group; and 13% were long circumflex, reaching the medullary perforation zone (basal cerebellar group). Median distance to the first perforator was 2.0 mm (range, 0.1–15 mm). There were 132 perforator branches in the last centimeter of the BA. Conclusion: The pSCA should not be regarded as a perforator-free area. Although the pSCA territories likely overlap with the posterior cerebral artery, BA, and anterior inferior cerebellar artery, the pSCA segment cannot be surgically manipulated with impunity.

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Isomoto, Hajime, Takuki Sakaguchi, Tatsuo Inamine, Shintaro Takeshita, Daisuke Fukuda, Ken Ohnita, Tsutomu Kanda, et al. "SNP rs2920280 in PSCA Is Associated with Susceptibility to Gastric Mucosal Atrophy and Is a Promising Biomarker in Japanese Individuals with Helicobacter pylori Infection." Diagnostics 12, no. 8 (August 16, 2022): 1988. http://dx.doi.org/10.3390/diagnostics12081988.

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Helicobacter pylori infection results in gastric cancer (GC) with gastric mucosal atrophy (GMA). Some single-nucleotide polymorphisms (SNPs) in the prostate stem cell antigen gene (PSCA) are associated with GC and duodenal ulcers. However, the relationship of other identified SNPs in PSCA with these diseases remains unclear. Herein, the association between PSCA SNPs and GMA among 195 Japanese individuals with H. pylori infection was evaluated. The definition of GMA or non-GMA was based on serum pepsinogen levels or endoscopic findings. Five tag PSCA SNPs were analyzed using PCR high-resolution melting curve analysis with nonlabelled probes. The frequencies of alleles and the genotypes of each tag SNP were compared between the GMA and non-GMA groups. Subsequently, a genetic test was performed using associated SNPs as biomarkers to detect patients developing GMA. Two tag PSCA SNPs (rs2920280 and rs2294008) were related to GMA susceptibility. Individuals with the rs2920280 G/G genotype or the rs2294008 T/T genotype in PSCA had 3.5- and 2.1-fold susceptibility to GMA, respectively. In conclusion, SNP rs2920280 is a possible biomarker for detecting individuals developing GMA. PSCA polymorphisms may be useful biomarkers for predicting GMA linked to GC risk and a screening endoscopy strategy to detect GC related to early stage H. pylori associated GMA.

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Kim, Sung Han, Weon Seo Park, Sang Jin Lee, Moon Kyung Choi, Seung Min Yeon, Jeong Nam Joo, Ara Ko, et al. "The Quantified Level of Circulating Prostate Stem Cell Antigen mRNA relative to GAPDH Level Is a Clinically Significant Indictor for Predicting Biochemical Recurrence in Prostate Cancer Patients after Radical Prostatectomy." BioMed Research International 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/292454.

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The study quantified the relative absolute PSCA level in relation to the glyceraldehyde 3-phosphate dehydrogenase (GAPDH) level in the peripheral blood of 478 hormone-naive prostate cancer (PC) patients who underwent radical prostatectomy from 2005 to 2012 and evaluated its prognostic significance as a risk factor for predicting biochemical recurrence (BCR), compared to known parameters. Nested real-time polymerase chain reaction (RT-PCR) and gel electrophoresis detected PSCA levels and measured the PSCA/GAPDH ratio. Clinicopathological data from the institutional database were examined to determine the adequate cut-off level to predict postoperative BCR. A total of 110 patients had a positive PSCA result (23.0%) via RT-PCR (mean blood ratio 1.1 ± 0.4). The BCR was significantly higher in the PSCA-positive detection group (p=0.009). A multivariate model was created to show that a PSCA/GAPDH ratio between 1.0 and 1.5 (HR 12.722), clinical T2c stage (HR 0.104), preoperative PSA (HR 1.225), extraprostatic capsule extension (HR 0.006), lymph node dissection (HR 16.437), and positive resection margin (HR 27.453) were significant predictive factors for BCR (p<0.05). The study showed successful quantification of PSCA with its significance for BCR-related risk factor; however, further studies are needed to confirm its clinical predictive value.

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Nejatollahi, Foroogh, Soghra Abdi, and Mahdi Asgharpour. "Antiproliferative and Apoptotic Effects of a Specific Antiprostate Stem Cell Single Chain Antibody on Human Prostate Cancer Cells." Journal of Oncology 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/839831.

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Prostate stem cell antigen (PSCA) is a highly glycosylated cell surface protein which is overexpressed in several malignancies including prostate, pancreas, and urinary bladder cancers. Tumor suppression has been reported by anti-PSCA antibody. Small and high affinity single chain antibodies (scFv) have been introduced as effective agents for cancer immunotargeting approaches. In the present study, we used a phage antibody display library of scFv and selected two antibodies against two immunodominant epitopes of PSCA by panning process. The reactivity of the scFvs for the corresponding epitopes was determined by phage ELISA. The binding specificity of antibodies to PSCA-expressing prostate cancer cell line, DU-145, was analyzed by flow cytometry. The antiproliferative and apoptotic induction effects were evaluated by MTT and Annexin-V assays, respectively. Results represented functional scFv C5-II which could bind specifically to DU-145 cells and significantly inhibited the proliferation of these cells (61%) with no effect on PSCA-negative cells. The antibody also induced apoptosis in the PSCA expressing cells. The percentage of the apoptotic cells after 24 hrs of exposure to 500 scFv/cell was 33.80%. These results demonstrate that the functional anti-PSCA scFv C5-II has the potential to be considered as a new agent for targeted therapy of prostate cancer.

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Hodges, Ron. "How might harmonization influence the future prevalence of public sector creative accounting?" Tékhne 16, no. 1 (November 17, 2018): 3–14. http://dx.doi.org/10.2478/tekhne-2019-0001.

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Abstract This paper considers the significance of future harmonization on public sector creative forms of accounting (PSCA) in the context of both national accounting and government financial reporting. The analysis is carried out through a review of studies provided in the academic and official literatures. Examples are provided of PSCA in a ‘broad’ context of any manipulation of financial information and in a ‘focused’ context, referring to the reporting of deficit / surplus and associated levels of debt. The analysis is related to the influence of harmonization using the classification of information-manipulating behaviour drawn from Birnberg, Turopolec, and Young (1983). There is potential for accounting harmonization to improve the analysability of data to restrict PSCA. However, although many techniques of PSCA have been identified, the drivers and controllers of PSCA remain unclear. Accounting researchers should use their specialist understanding to draw out the differences between apparently consistent frameworks of accounting and to understand the policy effects and social implications of harmonization and related creative forms of accounting. There are relatively few studies of PSCA. This paper represents the first study that seeks to relate PSCA to the increasing tendency towards harmonisation of accounting in the public sector context. An agenda is included to guide researchers towards issues that are worthy of further consideration in this important area of study.

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Plé, Sophie, Viviana Job, Andréa Dessen, and Ina Attree. "Cochaperone Interactions in Export of the Type III Needle Component PscF of Pseudomonas aeruginosa." Journal of Bacteriology 192, no. 14 (May 21, 2010): 3801–8. http://dx.doi.org/10.1128/jb.00117-10.

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ABSTRACT Type III secretion (T3S) systems allow the export and translocation of bacterial effectors into the host cell cytoplasm. Secretion is accomplished by an 80-nm-long needle-like structure composed, in Pseudomonas aeruginosa, of the polymerized form of a 7-kDa protein, PscF. Two proteins, PscG and PscE, stabilize PscF within the bacterial cell before its export and polymerization. In this work we screened the 1,320-Å2 interface between the two chaperones, PscE and PscG, by site-directed mutagenesis and determined hot spot regions that are important for T3S function in vivo and complex formation in vitro. Three amino acids in PscE and five amino acids in PscG, found to be relevant for complex formation, map to the central part of the interacting surface. Stability assays on selected mutants performed both in vitro on purified PscE-PscG complexes and in vivo on P. aeruginosa revealed that PscE is a cochaperone that is essential for the stability of the main chaperone, PscG. Notably, when overexpressed from a bicistronic construct, PscG and PscF compensate for the absence of PscE in cytotoxic P. aeruginosa. These results show that all of the information needed for needle protein stabilization and folding, its presentation to the T3 secreton, and its export is present within the sequence of the PscG chaperone.

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Dissertations / Theses on the topic "PSCA"

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Heinrich, Marie-Christine [Verfasser]. "Die PSCA Expression ist mit günstigen Tumoreigenschaften und reduziertem PSA Rezidiv bei operiertem Prostatakarzinom assoziiert / Marie-Christine Heinrich." Hamburg : Staats- und Universitätsbibliothek Hamburg Carl von Ossietzky, 2020. http://d-nb.info/1221084798/34.

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Nguyen, Minh-Triet [Verfasser]. "PSCA als DNA-Vakzine zur Behandlung des duktalen Pankreaskarzinoms / Minh Triet Nguyen." Bonn : Universitäts- und Landesbibliothek Bonn, 2012. http://d-nb.info/104351094X/34.

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Günes, Serap. "MODIFICATION OF VESICULAR STOMATITIS VIRUS G PROTEIN FOR TARGETED GENE DELIVERY INTO PSCA-POSITIVE TUMOR CELLS." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2007. http://nbn-resolving.de/urn:nbn:de:swb:14-1182861723404-04537.

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Gene therapy is a promising treatment option for cancer. Ideally, a therapeutic gene is delivered specifically into tumor cells sparing the neighboring normal cells. For this purpose gene delivery vectors are designed that can recognize structures, which are exclusively expressed on tumor cells (i.e. the tumor-associated antigens -TAA-). Retroviral vectors are commonly used for gene therapy by modifying the envelope protein responsible for the recognition of the target cell. The Vesicular Stomatitis Virus G protein (VSV-G) is a well-liked choice for pseudotyping the retroviral vectors since it confers on the viral particle stability to allow concentration to high titers necessary for the clinical applications. However, the main drawback of VSV-G, the ubiquitously expressed receptor and thus the broad target range, hinders the use of this protein for targeted gene therapy. In this thesis, we aimed to modify the VSV-G for targeted gene therapy against Prostate Stem Cell Antigen (PSCA) -expressing tumors. Therefore we followed two approaches. The first approach comprised of the fusion of a single-chain antibody fragment against PSCA to the N-terminus of VSV-G. In the second approach the VSV-G was modified by insertion of a small epitope. We could demonstrate that two positions in the N-terminal region of VSV-G protein permit insertion of a ten amino acid long epitope. These mutant VSV-G proteins were successfully assembled into retroviral particles. We demonstrated that the mutant retroviral particles can be used for targeting to PSCA-positive cells using nanobeads. The nanobeads were chemically coupled to antibodies against the epitope in the VSV-G protein and PSCA on the tumor cell. These bispecific nanobeads allowed the recruitment of mutant retroviral particles to the PSCApositive cells. Our results point out the potential of these mutant retroviral particles in targeted gene delivery. Further studies will be necessary to assess the efficiency of in vivo targeted gene therapy using these mutant retroviral particles.

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Michen, Susanne. "Armierung von NK-Zellen mit den PSCA-spezifischen chimären Antigenrezeptoren NKp46-αPSCA und NKp46-KiBAP-αPSCA." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-160333.

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Bei den konventionellen Krebstherapien kommt es häufig zu einer Wiederkehr des Tumors, da meist einzelne Tumorzellen und abgesiedelte Metastasen im Körper verbleiben. Vor diesem Hintergrund hat die Entwicklung neuer Behandlungsmethoden, die spezifisch die Tumorzellen erkennen und eliminieren und zudem gesunde Körperzellen schonen, eine große Bedeutung in der heutigen Krebsforschung. Eine erfolgsversprechende Strategie ist die Generierung von tumorspezifischen, zytotoxischen Immuneffektorzellen, zum Beispiel T-Lymphozyten und Natürlichen Killerzellen, durch die genetische Modifikation mit einem chimären Antigenrezeptor (CAR). Dabei gibt es bereits weitreichende Studien mit T-Lymphozyten, so dass sich nun das Forschungsinteresse immer mehr auf die NK-Zellen richtet. Im Gegensatz zu CAR-armierten T-Lymphozyten sind sie in der Lage ihr antitumorales Potenzial nicht nur gegen Antigen-positive sondern auch MHC-Klasse I-negative Tumorzellen zu richten. Mögliche Zielstrukturen der CAR sind tumorassoziierte Antigene, wie das Prostata-spezifische Stammzellantigen (PSCA). Es wird auf über 94 % der humanen primären Prostatakarzinome und deren Knochenmetastasen verstärkt exprimiert, jedoch kaum auf Normalgewebe. PSCA ist somit ideal für eine Immuntherapie geeignet. Die bisher in Studien verwendeten CAR-armierten NK-Zellen wiesen eine feststehende Spezifität gegenüber einem bestimmten Tumorantigen auf. Allerdings ist die Expression von Tumorantigenen innerhalb des Tumors sehr heterogen oder wird durch Tumorevasionsmechanismen herunterreguliert. Dies begrenzt die Reaktivität CAR-armierter NK-Zellen. Durch die Generierung eines CAR, dessen Spezifität gegenüber einem Tumorantigen ausgetauscht werden kann, wäre der universelle Einsatz CAR-armierter NK-Zellen in der adjuvanten Immuntherapie von Tumorerkrankungen möglich. Im Hauptteil dieser Arbeit wurden die permanente NK-Zelllinie YTS und primäre humane NK-Zellen mittels lentiviralen Gentransfers mit einem PSCA-spezifischen CAR, bestehend aus dem gegen PSCA gerichteten Einzelkettenantikörper αPSCA und dem aktivierenden NK-Zellrezeptor NKp46, armiert. Die generierten NK-Zellen wiesen eine über längere Zeiträume stabile Oberflächenexpression des CAR αPSCA-NKp46 auf. Die Kreuzvernetzung des CAR mit seinem Antigen führte zunächst zu keiner selektiven Immunantwort der CAR-armierten YTS und primären NK-Zellen gegenüber histogenetisch verschiedenen, PSCA-exprimierenden Tumorzelllinien. Erst nach gleichzeitiger Überexpression des mit NKp46 assoziierten Signaladaptermoleküls CD3-ζ wurde eine Aktivierung der Effektorfunktionen der YTS NK-Zellen induziert. Dies zeigte sich zum einen in der Expression von CD107a als Degranulationsmarker sowie der Freisetzung des inflammatorischen Zytokins IFN-γ. Zum anderen wiesen die CAR-armierten und CD3-ζ-exprimierenden YTS NK-Zellen eine spezifische Zytotoxizität gegenüber MHC-Klasse I- und PSCA-exprimierenden Tumorzellen auf. Im anschließenden Teil der Arbeit wurde ein modular aufgebauter CAR generiert, bei dem der Einzelkettenantikörper und folglich die Spezifität gegenüber Tumorantigenen austauschbar ist. Dazu wurden YTS NK-Zellen durch lentiviralen Gentransfer mit dem biotinylierbaren NKp46-NK-Zellrezeptor NKp46-KiBAP modifiziert, der über mehrere Monate stabil auf der Oberfläche exprimiert wurde. Die exogene als auch endogene Biotinylierung des Rezeptors wurde mittels einer Biotinproteinligase demonstriert. Unter Ausnutzung der sehr starken Biotin-Avidin-Bindung wurde die Assoziation mit einem Einzelkettenantikörper nachgewiesen. Dafür wurde exemplarisch der gegen PSCA gerichtete, biotinylierbare Einzelkettenantikörper αPSCA-BAP verwendet. Diese Arbeit zeigt, dass eine spezifische Erkennung und effiziente Lyse von PSCA-exprimierenden Tumorzellen durch die generierten CAR-armierten NK-Zellen erfolgte, wobei zum ersten Mal NKp46 als Bestandteil eines CAR verwendet wurde. Zudem wurde ein modular aufgebauter CAR generiert, dessen Spezifität gegenüber Tumorantigenen austauschbar ist. Diese neuartige Strategie ermöglicht erstmalig eine flexible Armierung von NK-Zellen und stellt damit einen wesentlichen Vorteil bei der Behandlung verschiedener Krebserkrankungen dar.

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Günes, Serap. "Modifikation of vesicular stomatitis virus G protein for targeted gene delivery into PSCA-positive tumor cells." [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:swb:14-1182861723404-04537.

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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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Leyton, Victor Jeffrey. "Engineered antibody fragments for the targeting and imaging of prostate stem cell antigen (PSCA)- expressing xenografts in vivo by microPET." Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1624118821&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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Quinaud, Manuelle. "Étude structurale et fonctionnelle de PscE : PscF : PscG? un hétérotimère nécessaire à la biogenèse de l'aiguille de sécretion de type III de Pseudomonas aeruginosa." Grenoble 1, 2007. http://www.theses.fr/2007GRE10138.

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Le système de sécrétion de type III est présent chez plusieurs pathogènes à Gram négatif chez qui cette véritable nanomachine est impliquée dans le transport de molécules de virulence directement des bactéries vers le cytoplasme des cellulescible. Ce système de sécrétion est composé d'une base ancrée dans la membrane bactérienne et d'une structure creuse en forme d'aiguille qui pointe vers l'extérieur de la bactérie. Pseudomonas aeruginosa, bactérie dont l'aiguille de sécrétion de type III est étudiée dans cette thèse, est responsable de nombreuses maladies nosocomiales ainsi que d'infections chez les patients atteints de mucoviscidose. Dans le cytoplasme bactérien, la protéine PscF qui forme l'aiguille de type III chez P. Aeruginosa est stabilisée avant sa sécrétion par 2 chaperonnes distinctes; PscE et PscG. Ceci est nécessaire à la fonctionnalité du système de sécrétion de type III. La structure cristallographique à 2. 0 A de résolution du complexe hétérotrimérique PscE:PscF55-85_PscG révèle que le domaine C-terminal de la protéine de l'aiguille B PscF, impliqué dans le processus de polymérisation, est enfoui dans une cavité hydrophobe de la protéine PscG. La rupture des interactions spécifiques entre PscG et PscF entraîne une forte baisse de la cytotoxicité de la bactérie envers une lignée de macrophages, ce qui indique que cet hétérotrimère essentiel, qui possède des homologues chez une grande variété de pathogènes, est une cible thérapeutique attractive pour le développement de nouveaux médicaments
Type III secretion systems are found in several Gram-negative bacteria. These nanomachines are involved in the transport of virulence effectors directly into the cytoplasm of Target cells. Pseudomonas aeruginosa, whose type III secretion needle is studied here, is the causative agent of a large number of nosocomial and chronic infections in cystic fibrosis patients. This system is composed of a base anchored in the double bacterial membrane and a hollow needle formed by a single polymerized protein (PscF in Pseudomonas aeruginosa). Within the bacterial cytoplasm, PscF requires two distinct chaperones for stabilisation before its secretion, without which the entire system is nonfunctionnal. The 2. 0 A X-ray crystal structure orthe PscE:PscF55-85 :PscG ternary complex reveals that the C-terminus of the needle protein PscF, which is essential for needle polymerisation, is engulfed within the hydrophobic groove of the TPR-like molecule PscG. This indicates that the macromolecular scaffold necessary to stabilize the needle protein is totally distinct from T chaperoned complexes between pilus- or flagellum- forming molecules. Disruption of specific PscG:PscF interactions leads to impairement of bacterial cytotoxicity toward macrophages, indicating that This essential heterotrimer, which possesses homologs in a wide variety of pathogens, is an attractive therapeutic Target for the development of novel drugs

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Michen, Susanne [Verfasser], Hanns Achim [Akademischer Betreuer] Temme, and Gerold [Akademischer Betreuer] Barth. "Armierung von NK-Zellen mit den PSCA-spezifischen chimären Antigenrezeptoren NKp46-αPSCA und NKp46-KiBAP-αPSCA / Susanne Michen. Gutachter: Hanns Achim Temme ; Gerold Barth. Betreuer: Hanns Achim Temme." Dresden : Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2015. http://d-nb.info/1069093149/34.

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Morgenroth, Agnieszka. "Herstellung chimärer Rezeptoren zur tumorspezifischen Armierung polyklonaler, zytotoxischer T-Lymphozyten." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2005. http://nbn-resolving.de/urn:nbn:de:swb:14-1134590060614-48883.

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Abstract:

Die Effizienz einer Tumortherapie durch einen Transfer von ex vivo aktivierten Tumor-spezifischen zytotoxischen T-Lymphozyten wird durch zahlreiche Faktoren wie geringe Anzahl der isolierten spezifischen T-Zellen, schnelles Abklingen der Aktivität und kurzzeitige Persistenz der transferierten Effektorzellen im Empfängerorganismus stark limitiert. Eine Möglichkeit zur Überwindung dieser Einschränkungen bietet die Entwicklung einer neuen Strategie zur Armierung der zytotoxischen T-Lymphozyten mit Tumor-spezifischen chimären Rezeptoren. Ziel dieser Arbeit war es, die Grundlagen für eine solche immuntherapeutische Strategie zu erarbeiten. Da das Prostatakarzinom die am meisten diagnostizierte maligne Erkrankung und die dritt häufigste Todesursache des Mannes ist, wurde das auf der Oberfläche von Prostatakarzinomzellen exprimierte PSCA (prostataspezifisches Stammzellantigen) als Zielantigen gewählt. Neben der therapierefraktären Spätstadien des Prostatakarzinoms bedürfen die früh entstehenden Mikrometastasen (minimale Resterkrankung) einer neuen adjuvanten Behandlungsoption. Das PSCA ist ein membranständiges Tumor-assoziiertes Antigen, das in mehr als 80 % der primären Prostatakarzinome überexprimiert wird. PSCA wird als besonders aussichtsreiches Zielantigen einer Immuntherapie bei fortgeschrittenen Prostatakarzinomen angesehen, weil sein Expressionsniveau mit der Tumorprogression und der Entwicklung zum androgenunabhängigen Wachstum ansteigt. In der vorgelegten Arbeit wurde zunächst ein neuer monoklonaler PSCA-spezifischer Antikörper generiert, der als Grundlage für die Konstruktion eines Einzelkettenantikörpers (scFv) verwendet wurde. Aus einem Hybridomklon, der sich durch sehr hohe Bindungsstärke auszeichnete, wurden mittels degenerierter Primer die kodierenden Sequenzen für die variablen VH und VL Domänen des Antikörpers amplifiziert. Durch die Verbindung der beiden VH und VL Domänen mittels eines Linkers wurde der PSCA-spezifische Einzelkettenantikörper generiert. Die mit gereinigtem scFv durchgeführten Bindungsanalysen bestätigten die Funktionalität des rekombinanten Proteins und seine Anwendbarkeit zur Chimerisierung eines membranständigen Rezeptors. Nach dem ?Zwei-Signal-Modell? benötigen T-Zellen für eine effiziente Antigen-spezifische Aktivierung neben dem T-Zell-Rezeptorsignal ein zusätzliches kostimulatorisches Signal. Daher wurden chimäre Rezeptoren auf der Basis der Beta-Kette des T-Zell-Rezeptors und des CD28-Moleküls generiert. Bei der Konstruktion des chimären T-Zell-Rezeptors wurde die konstante Domäne der Beta-Kette mit der CD3 &#61562;-Kette fusioniert. Neben einer starken Oberflächenexpression des Rezeptors wurde auch die effiziente Bindung von löslichem PSCA nachgewiesen. Die Bindung des Rezeptors an das PSCA führte zur Phosphorylierung der ITAM-Sequenzen der heterodimeren &#61562;-Kette, was die Funktionalität des chimären Rezeptors bestätigte. Die Stimulation der Zellen über den anti-CD3 Antikörper resultierte ebenfalls in der Phosphorylierung der heterodimeren &#61562;-Kette, was ein Hinweis auf eine mögliche Interaktion der chimären Kette mit dem endogenen CD3-Komplex lieferte. Um die kostimulatorische Wirkung über das selbe Antigen zu erzielen, wurde das CD28 Molekül N-terminal ebenfalls mit dem Einzelkettenantikörper modifiziert. Die durch Bindung des löslichen Proteins induzierte Phosphorylierung der Akt-Kinase bewies die Funktionalität der chimären CD28 Kette als PSCA-spezifischer Rezeptor. Diese Arbeit demonstriert die Generierung eines hochaffinen PSCA-spezifischen Einzelkettenantikörpers als eine Antigen-erkennende Struktur eines chimären Rezeptors. Die Armierung polyklonaler zytotoxischer T-Lymphozyten mit den funktionsfähigen chimären Rezeptoren stellt den ersten Schritt einer neuen Strategie zur Eliminierung hormon-refrektärer und metastasierender Prostatakarzinomzellen dar.

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Books on the topic "PSCA"

1

Boleng, Didimus Tanah. Laporan penelitian studi tentang tanggapan masyarakat terhadap pelaksanaan surveilans acute flaccid paralysis dalam upaya pemantauan kasus poliomyelitis psca [i.e. pasca] PIN tahun 1997. Samarinda: Lembaga Penelitian, Universitas Mulawarman, 2001.

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Antunes, Arnaldo. Psia. 3rd ed. São Paulo, Brasil: Iluminuras, 1991.

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Justicia, Programa Sociedad Civil y. Acceso a. la. PSCAJ, memoria. La Paz, Bolivia?]: Programa Sociedad Civil y Acceso a la Justicia, 2005.

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Magdalena, Moltzan-Małkowska, and Prószyński Media, eds. Psia story. Warszawa: Prószyński Media, 2015.

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Štrelinger, Peter. Psia demokracia: Bájky. Bratislava: Goldpress Publishers, 1993.

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Maria, Goudiss, ed. PSSA reading coach. 2nd ed. New York, N.Y: Educational Design, 2001.

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Ivančević, Olja Savičević. Nasmijati psa. Zagreb: AGM, 2007.

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Ivančević, Olja Savičević. Nasmijati psa. Zagreb: AGM, 2007.

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Begeja, Ksanthipi. The family in the PSRA. New York: Albania Report, 1985.

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Cikuli, Zisa. Health service in the PSRA. New York: Albania Report, 1985.

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Book chapters on the topic "PSCA"

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Wente, M. N., A. Jain, P. O. Berberat, T. Giese, H. A. Reber, R. E. Reiter, H. Friess, and M. W. Büchler. "Blockade des Prostata-Stammzellen-Antigens PSCA hemmt das Wachstum des Pankreaskarzioms." In Zurück in die Zukunft, 505–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55611-1_323.

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Wente, M. N., A. Jain, P. O. Berberat, T. Giese, H. A. Reber, R. E. Reiter, H. Friess, and M. W. Büchler. "Blockade des Prostata-Stammzellen-Antigens PSCA hemmt das Wachstum des Pankreaskarzinoms." In Deutsche Gesellschaft für Chirurgie, 157–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-19024-7_44.

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Oh-oka, Hirozo, Saki Kakutani, Shoichiro Kamei, Hiroshi Matsubara, Masayo Iwaki, and Shigeru Itoh. "Photoactive Reaction Center (PscA/Cytochrome c 551)2 Complex of Chlorobium limicola." In Photosynthesis: from Light to Biosphere, 1061–64. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-009-0173-5_250.

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Mehlhorn, Heinz. "PSAC." In Encyclopedia of Parasitology, 2281. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_4214.

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Mehlhorn, Heinz. "PSAC." In Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_4214-1.

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Pichler, Robert, Johannes Wolfsgruber, Ferdinando Calabria, Orazio Schillaci, and Andreas Dunzinger. "68Ga-PSMA." In Radiopharmaceuticals, 211–25. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-27779-6_12.

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Gulley, James L. "PSA." In Cancer Therapeutic Targets, 451–58. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_31.

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Gulley, James L. "PSA." In Cancer Therapeutic Targets, 1–8. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6613-0_31-4.

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van Balen, J. A. M., A. A. Demeulemeester, M. Frölich, K. Mohrmann, L. M. Harms, W. C. H. van Helden, L. J. Mostert, and J. H. M. Souverijn. "PSA." In Memoboek, 173. Houten: Bohn Stafleu van Loghum, 2012. http://dx.doi.org/10.1007/978-90-313-9129-5_102.

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Braun-Falco, Markus, Henry J. Mankin, Sharon L. Wenger, Markus Braun-Falco, Stephan DiSean Kendall, Gerard C. Blobe, Christoph K. Weber, et al. "PSC." In Encyclopedia of Molecular Mechanisms of Disease, 1740. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6791.

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Conference papers on the topic "PSCA"

1

Tran, Chau P., Scott Knowles, Tove Olafsen, Eric J. Lepin, Anna M. Wu, and Robert E. Reiter. "Abstract 4283: Evaluation of PSCA-specific minibody for in vivo imaging." 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.am2011-4283.

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Matsuda, Koichi, Chizu Tanikawa, and Yusuke Nakamura. "Abstract 5063: PSCA as a potential therapeutic and prognostic biomarker for common cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5063.

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Moore, Miranda L., Shuai Tang, Mark C. Willingham, and Purnima Dubey. "Abstract B37: PSCA haploinsufficiency enhances prostate tumor growth in prostate-specific Pten knockout mice." In Abstracts: First AACR International Conference on Frontiers in Basic Cancer Research--Oct 8–11, 2009; Boston MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.fbcr09-b37.

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Bergmann, R., C. Arndt, D. Máthé, N. Berndt, LR Loureiro, N. Kovács, D. Szöllösi, et al. "Copper-64/Actinium-225-human anti-PSCA-IgG4 theranostics of a prostate cancer model." In NuklearMedizin 2021 – digital. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1726705.

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Tsai, Wen-Ting K., Kirstin A. Zettlitz, Richard Tavaré, Felix B. Salazar, Robert E. Reiter, and Anna M. Wu. "Abstract 1856: Dual-modality immunoPET/fluorescence imaging of prostate cancer utilizing89Zr- or124I-Cy5.5-anti-PSCA cys-minibody." 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.am2017-1856.

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Ito, Hidemi, Isao Oze, Satoyo Hosono, Miki Watanabe, Hideo Tanaka, and Keitaro Matsuo. "Abstract 2210: Cumulative risks of gastric cancer by PSCA polymorphism, Helicobacter Pylori infection and smoking history in Japan." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2210.

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Hess, T., L. Hamann, YK Vashist, K. Butterbach, T. Schmidt, I. Krasniuk, A. Höblinger, et al. "Evidence for PTGER4, PSCA and MBOAT7 as risk genes for gastric cancer on the genome and transcriptome level." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1604759.

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Galindo, Hector G., Milind Suraokar, Carmen Behrens, Denise M. Woods, Neda Kalhor, Kenneth D. Aldape, Junya Fujimoto, Roy S. Herbst, Heidi S. Erickson, and Ignacio I. Wistuba. "Abstract 5166: Identification of prostate stem cell antigen (PSCA) as a potential marker for lung cancer brain metastasis." 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.am2011-5166.

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Abate-Daga, Daniel, Kiran H. Lagisetty, Luca Gattinoni, Zhiya Yu, Nicholas P. Restifo, Steven A. Rosenberg, and Richard A. Morgan. "Abstract 3966: Development of a fully-human chimeric antigen receptor against PSCA for the treatment of pancreatic cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3966.

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Navas, Tony, Trisha Haubrich, Jenny Llamas, Hector Avina, Zhang Chunying, Myra Perez, Linnette Capo, et al. "Abstract 4566: AGS-1C4D4: A fully human anti-PSCA antibody inhibits tumor formation and metastasis in orthotopic models of pancreatic cancer." 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.am2011-4566.

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Reports on the topic "PSCA"

1

Reiter, Robert E. Mechanisms and Refinements of PSCA Directed Antibody Therapy. Fort Belvoir, VA: Defense Technical Information Center, January 2003. http://dx.doi.org/10.21236/ada413309.

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Reiter, Robert E. Mechanisms and Refinements of PSCA Directed Antibody Therapy. Fort Belvoir, VA: Defense Technical Information Center, March 2004. http://dx.doi.org/10.21236/ada426030.

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Reiter, Robert. A PSCA Promoter Based Avian Retroviral Transgene Model of Normal and Malignant Prostate. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada429113.

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Reiter, Robert. A PSCA Promoter Based Avian Retroviral Transgene Model of Normal and Malignant Prostate. Fort Belvoir, VA: Defense Technical Information Center, April 2006. http://dx.doi.org/10.21236/ada460465.

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Reiter, Robert E. Prostate stem Cell Antigen (PSCA): A Promising Marker and Therapeutic Target in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada412761.

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Reiter, Robert E. Prostate Stem Cell Antigen (PSCA): A Promising Prognostic Marker and Therapeutic Target in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada419393.

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Nair, Smita. Prostate Cancer Immunotherapy by Targeting Dendritic Cells In Vivo Using Receptor-Specific Aptamer Conjugated to Prostate Stem Cell Antigen (PSCA)-Encoding RNA. Fort Belvoir, VA: Defense Technical Information Center, August 2011. http://dx.doi.org/10.21236/ada551308.

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Bochert, Monika. PSCR Impact Assessment:. Gaithersburg, MD: National Institute of Standards and Technology, 2023. http://dx.doi.org/10.6028/nist.gcr.23-038.

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Muljadi, E., M. Singh, and V. Gevorgian. PSCAD Modules Representing PV Generator. Office of Scientific and Technical Information (OSTI), August 2013. http://dx.doi.org/10.2172/1096111.

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Nadeau, Lou, Melanie Sands, Douglas Lyons, and Clara Berger. NIST PSCR: Economic Impact Analysis. National Institute of Standards and Technology, June 2021. http://dx.doi.org/10.6028/nist.gcr.21-031.

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