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  • 1
    Language: English
    In: Clinical cancer research, 2008-01-01, Vol.14 (1), p.123-129
    Description: Purpose: The CD133 antigen has been identified as a putative stem cell marker in normal and malignant brain tissues. In gliomas, it is used to enrich a subpopulation of highly tumorigenic cancer cells. According to the cancer stem cell hypothesis, CD133-positive cells determine long-term tumor growth and, therefore, are suspected to influence clinical outcome. To date, a correlation between CD133 expression in primary tumor tissues and patients' prognosis has not been reported. Experimental Design: To address this question, we analyzed the expression of the CD133 stem cell antigen in a series of 95 gliomas of various grade and histology by immunohistochemistry on cryostat sections. Staining data were correlated with patient outcome. Results: By multivariate survival analysis, we found that both the proportion of CD133-positive cells and their topological organization in clusters were significant ( P 〈 0.001) prognostic factors for adverse progression-free survival and overall survival independent of tumor grade, extent of resection, or patient age. Furthermore, proportion of CD133-positive cells was an independent risk factor for tumor regrowth and time to malignant progression in WHO grade 2 and 3 tumors. Conclusions: These findings constitute the first conclusive evidence that CD133 stem cell antigen expression correlates with patient survival in gliomas, lending support to the current cancer stem cell hypothesis.
    Subject(s): stem cells ; glioma ; prognosis ; CD133 ; Neurology ; Biological and medical sciences ; Medical sciences ; Tumors of the nervous system. Phacomatoses ; Antineoplastic agents ; Pharmacology. Drug treatments ; Immunohistochemistry ; Glioma - mortality ; Prognosis ; Peptides ; Antigens, CD - biosynthesis ; Humans ; Middle Aged ; Brain Neoplasms - pathology ; Kaplan-Meier Estimate ; Male ; Stem Cells - metabolism ; AC133 Antigen ; Brain Neoplasms - metabolism ; Glioma - metabolism ; Glycoproteins - biosynthesis ; Disease-Free Survival ; Glioma - pathology ; Survival Analysis ; Adult ; Female ; Brain Neoplasms - mortality ; Index Medicus
    ISSN: 1078-0432
    E-ISSN: 1557-3265
    Source: HighWire Press (Free Journals)
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 2
    Language: English
    In: Cancers, 2019-12, Vol.11 (12), p.1826
    Description: :The epidermal growth factor receptor (EGFR) family contains four transmembrane tyrosine kinases (EGFR1/ErbB1, Her2/ErbB2, Her3/ErbB3 and Her4/ErbB4) and 13 secreted polypeptide ligands. EGFRs are overexpressed in many solid tumors, including breast, pancreas, head-and-neck, prostate, ovarian, renal, colon, and non-small-cell lung cancer. Such overexpression produces strong stimulation of downstream signaling pathways, which induce cell growth, cell differentiation, cell cycle progression, angiogenesis, cell motility and blocking of apoptosis.The high expression and/or functional activation of EGFRs correlates with the pathogenesis and progression of several cancers, which make them attractive targets for both diagnosis and therapy. Several approaches have been developed to target these receptors and/or the EGFR modulated effects in cancer cells. Most approaches include the development of anti-EGFRs antibodies and/or small-molecule EGFR inhibitors. This review presents the state-of-the-art and future prospects of targeting EGFRs to treat breast cancer.
    Subject(s): antibody ; chimeric antigen receptors t cells ; TRASTUZUMAB ; epidermal growth factor receptor ; MONOCLONAL-ANTIBODY ; TYROSINE KINASES ; COMBINATION ; CHEMOTHERAPY PLUS ; GROWTH-FACTOR RECEPTOR ; RANDOMIZED PHASE-II ; antibody drug conjugate ; tyrosine kinase inhibitor ; HER2 ; EXPRESSION ; ERBB RECEPTORS ; Review
    ISSN: 2072-6694
    E-ISSN: 2072-6694
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: Directory of Open Access Journals
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 3
    Language: English
    In: Bioconjugate chemistry, 2018-11-21, Vol.29 (11), p.3586-3594
    Description: Antibody-based diagnostic and therapeutic reagents armed with effector molecules such as dyes and drugs offer hope in the battle against cancer. Several site-specific conjugation methods have been developed to equip antibodies with such effector molecules, but they tend to be expensive and involve multiple reaction steps. The conjugation of two different effector molecules to a single antibody also remains a major challenge. Here we describe a simple, controlled, and robust method for the dual site-specific conjugation of an antibody with two effector molecules in a single-pot reaction using the self-labeling SNAP and CLIP protein tags. We verified the principle of the method by labeling an epidermal growth factor receptor (EGFR)-specific single-chain antibody fragment (scFv-425) simultaneously with IRDye700 and Alexa-Fluor647. This dual-labeled antibody bound to EGFR+ ovarian cancer cell lines and tissue samples with high specificity, and its phototherapeutic efficacy was confirmed by the selective killing of EGFR+ cells in vitro.
    Subject(s): Recombinant Fusion Proteins - immunology ; ErbB Receptors - metabolism ; Humans ; Ovarian Neoplasms - pathology ; Recombinant Fusion Proteins - chemistry ; Immunoconjugates - chemistry ; Microscopy, Confocal ; Flow Cytometry ; ErbB Receptors - immunology ; Cell Line, Tumor ; Protein Binding ; Female ; Protein Conformation ; Single-Chain Antibodies - chemistry ; Single-Chain Antibodies - immunology ; Coloring Agents - chemistry
    ISSN: 1043-1802
    E-ISSN: 1520-4812
    Source: Hellenic Academic Libraries Link
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  • 4
    Language: English
    In: The Journal of pathology, 2014-01, Vol.232 (1), p.16-22
    Description: There is debate as to whether peritoneal implants associated with serous borderline tumours/atypical proliferative serous tumours (SBT/APSTs) of the ovary are derived from the primary ovarian tumour or arise independently in the peritoneum. We analysed 57 SBT/APSTs from 45 patients with advanced‐stage disease identified from a nation‐wide tumour registry in Denmark. Mutational analysis for hotspots in KRAS and BRAF was successful in 55 APSTs and demonstrated KRAS mutations in 34 (61.8%) and BRAF mutations in eight (14.5%). Mutational analysis was successful in 56 peritoneal implants and revealed KRAS mutations in 34 (60.7%) and BRAF mutations in seven (12.5%). Mutational analysis could not be performed in two primary tumours and in nine implants, either because DNA amplification failed or because there was insufficient tissue for mutational analysis. For these specimens we performed VE1 immunohistochemistry, which was shown to be a specific and sensitive surrogate marker for a V600E BRAF mutation. VE1 staining was positive in one of two APSTs and seven of nine implants. Thus, among 63 implants for which mutation status was known (either by direct mutational analysis or by VE1 immunohistochemistry), 34 (53.9%) had KRAS mutations and 14 (22%) had BRAF mutations, of which identical KRAS mutations were found in 34 (91%) of 37 SBT/APST–implant pairs and identical BRAF mutations in 14 (100%) of 14 SBT/APST–implant pairs. Wild‐type KRAS and BRAF (at the loci investigated) were found in 11 (100%) of 11 SBT/APST–implant pairs. Overall concordance of KRAS and BRAF mutations was 95% in 59 of 62 SBT/APST–implant (non‐invasive and invasive) pairs (p 〈 0.00001). This study provides cogent evidence that the vast majority of peritoneal implants, non‐invasive and invasive, harbour the identical KRAS or BRAF mutations that are present in the associated SBT/APST, supporting the view that peritoneal implants are derived from the primary ovarian tumour. Copyright © 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    Subject(s): ovarian neoplasms ; ovarian low‐grade serous carcinoma ; serous borderline tumour ; Immunohistochemistry ; Peritoneal Neoplasms - pathology ; Proto-Oncogene Proteins - metabolism ; ras Proteins - genetics ; Proto-Oncogene Proteins p21(ras) ; Humans ; Ovarian Neoplasms - pathology ; Laser Capture Microdissection ; ras Proteins - metabolism ; Proto-Oncogene Proteins - genetics ; Cystadenocarcinoma, Serous - genetics ; Cystadenocarcinoma, Serous - pathology ; Sequence Analysis, DNA ; DNA, Neoplasm - chemistry ; Ovarian Neoplasms - genetics ; DNA Mutational Analysis ; Peritoneal Neoplasms - genetics ; Proto-Oncogene Proteins B-raf - genetics ; Sensitivity and Specificity ; Denmark ; Female ; DNA, Neoplasm - genetics ; Mutation ; Proto-Oncogene Proteins B-raf - metabolism ; Genetic aspects ; Analysis ; Ovarian cancer ; Index Medicus ; ovarian low-grade serous carcinoma
    ISSN: 0022-3417
    E-ISSN: 1096-9896
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 5
    Language: English
    In: Human pathology, 2017-10, Vol.68, p.87-91
    Description: Activating mutations involving the members of the RAS signaling pathway, including KRAS, NRAS, and BRAF, have been reported in ovarian low-grade serous carcinoma and its precursor lesion, serous borderline tumor (SBT). Whether additional genetic alterations in the RAS oncogene family accumulate during the progression of SBT to invasive low-grade serous carcinoma (LGSC) remains largely unknown. Although mutations of KRAS and BRAF occur at a very early stage of progression, even preceding the development of SBT, additional driving events, such as NRAS mutations, have been postulated to facilitate progression. In this study, we analyzed NRAS exon 3 mutational status in 98 cases that were diagnosed with SBT/atypical proliferative serous tumor, noninvasive LGSC, or invasive LGSC. Of the latter, NRAS Q61R (CAA to CGA) mutations were detected in only 2 of 56 (3.6%) cases. The same mutation was not detected in any of the SBTs (atypical proliferative serous tumors) or noninvasive LGSCs. Mutational analysis for hotspots in KRAS and BRAF demonstrated a wild-type pattern of KRAS and BRAF in one of the NRAS-mutated cases. Interestingly, another LGSC case with NRAS mutation harbored a concurrent BRAF V600L mutation. These findings indicate that, although recurrent NRAS mutations are present, their low prevalence indicates that NRAS plays a limited role in the development of LGSC. Further studies to identify other oncogenic events that drive LGSC progression are warranted. •NRAS mutation is postulated to facilitate the development of low-grade serous carcinoma (LGSC).•NRAS hotspot (Q61R) mutation was detected in only 3.6% cases of LGSCs in this study.•Low prevalence of mutation indicates that NRAS plays a limited role in the development of LGSC.
    Subject(s): NRAS mutation ; Low-grade serous carcinoma ; Oncogenic driver ; RAS signaling ; Ovarian cancer ; Cell Proliferation ; Humans ; Middle Aged ; Ovarian Neoplasms - pathology ; Neoplasms, Cystic, Mucinous, and Serous - genetics ; Ovarian Neoplasms - genetics ; Young Adult ; Neoplasm Grading ; DNA Mutational Analysis ; Aged, 80 and over ; Adult ; Female ; Carcinoma - pathology ; Genetic Predisposition to Disease ; Neoplasms, Cystic, Mucinous, and Serous - pathology ; Membrane Proteins - genetics ; Neoplasm Invasiveness ; Mutation Rate ; Phenotype ; Baltimore ; GTP Phosphohydrolases - genetics ; Proto-Oncogene Proteins B-raf - genetics ; Denmark ; Carcinoma - genetics ; Aged ; Biomarkers, Tumor - genetics ; Mutation ; Neoplasm Staging ; Genetic research ; Genetic aspects ; Carcinoma ; Analysis ; Cancer ; Polymerase chain reaction ; Studies ; Pathology ; Archives & records ; Patients ; Deoxyribonucleic acid--DNA ; Age ; Tumors ; Index Medicus ; Low grade serous carcinoma ; NRAS
    ISSN: 0046-8177
    E-ISSN: 1532-8392
    Source: ProQuest Central
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  • 6
    Language: English
    In: Anti-cancer agents in medicinal chemistry, 2017-09, Vol.17 (10), p.1434-1440
    Description: Background: Targeted imaging and therapy (theranostics) is a promising approach for the simultaneous improvement of cancer diagnosis, prognosis and management. Therapeutic and imaging reagents are coupled to tumor-targeting molecules such as antibodies, providing a basis for truly personalized medicine. However, the development of antibody–drug conjugates with acceptable pharmaceutical properties is a complex process and several parameters must be optimized, such as the controlled conjugation method and the drug-to-antibody ratio. Objective: The major aim of this work is to address fundamental key challenges for the development of versatile technology platform for generating homogenous immunotheranostic reagent. Method: We conjugated the theranostics reagent IRDye700dx to a recombinant antibody fusion protein containing a self-labeling protein (SNAP-tag) which provides a unique reaction site. Results: The resulting conjugate was suitable for the imaging of cancer cells expressing the epidermal growth factor receptor and demonstrated potent phototherapeutic and imaging activities against them. Conclusion: Here, we describe a simple, rapid and robust site-directed labeling method that can be used to generate homogeneous immunoconjugate with defined pharmacological properties.
    Subject(s): Antibodies - therapeutic use ; Receptor, Epidermal Growth Factor - biosynthesis ; Theranostic Nanomedicine ; Antibodies - chemistry ; Humans ; Receptor, Epidermal Growth Factor - analysis ; Structure-Activity Relationship ; Photochemotherapy ; Neoplasms - drug therapy ; Dose-Response Relationship, Drug ; Organosilicon Compounds - chemistry ; Organosilicon Compounds - therapeutic use ; Indoles - therapeutic use ; Molecular Structure ; Indoles - chemistry ; Index Medicus
    ISSN: 1871-5206
    E-ISSN: 1875-5992
    Source: Bentham Science:Eduserv:Complete Collection:2015-2017
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 7
    Language: English
    In: Gynecologic and obstetric investigation, 2012-09, Vol.74 (2), p.171-176
    Description: Primary pulmonary choriocarcinoma is a rare disease with only 31 reported cases in the literature so far. Here, we summarize all published cases, including a recent case of our own clinic. Patients usually presented with symptoms like dyspnea, cough, chest pain, weight loss or hemoptysis. In some cases, the nodule in the lung was found in a routine check-up in asymptomatic patients. In the present case, the patient presented to our clinic because of a positive urine pregnancy test despite taking oral contraceptives. Patients in the analyzed cases were either treated with surgery, chemotherapy, radiotherapy or best supportive care. In the present case, a complete resection of the tumor was possible and the patient has not had any signs of recurrence so far. When looking at the published cases and corresponding outcomes, a slight tendency toward a complete resection followed by chemotherapy or close follow-up examinations seems to give the patients the best survival chances. Nevertheless, the overall prognosis of primary pulmonary choriocarinoma is poor and the 5-year survival rate is below 5%.
    Subject(s): Novel Insights from Clinical Practice ; Choriocarcinoma - surgery ; Ovary - pathology ; Prognosis ; Choriocarcinoma - diagnosis ; Humans ; Middle Aged ; Infant ; Lung Neoplasms - pathology ; Male ; Tomography, X-Ray Computed ; Chorionic Gonadotropin, beta Subunit, Human - urine ; Choriocarcinoma - pathology ; Biopsy ; Adult ; Female ; Lung Neoplasms - surgery ; Aged ; Chemotherapy, Adjuvant ; Endometrium - pathology ; Lung Neoplasms - diagnosis ; Index Medicus
    ISSN: 0378-7346
    E-ISSN: 1423-002X
    Source: Karger Journals Archiv (DFG Nationallizenzen)
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 8
    Language: English
    In: The journal of pathology. Clinical research, 2015-07, Vol.1 (3), p.186-193
    Description: Uterine endometrioid carcinoma is the most common neoplastic disease in the female genital tract and develops from a common precursor lesion, atypical hyperplasia/endometrioid intraepithelial neoplasia (AH/EIN). Although the genomic landscape of endometrioid carcinoma has been recently revealed, the molecular alterations that contribute to tumour progression from AH/EIN to carcinoma remain to be elucidated. In this study, we used immunohistochemistry to determine if loss of expression of two of the most commonly mutated tumour suppressors in endometrioid carcinoma, PTEN and ARID1A, was associated with increased proliferation in AH/EIN. We found that 80 (70%) of 114 cases exhibited decreased or undetectable PTEN and 17 (15%) of 114 cases had focal loss of ARID1A staining. ARID1A loss was focal, while PTEN loss was diffuse, and all specimens with ARID1A loss had concurrent PTEN loss (p = 0.0003). Mapping the distribution of PTEN and ARID1A staining in the same specimens demonstrated that all AH/EIN areas with ARID1A loss were geographically nested within the areas of PTEN loss. A significant increase in the proliferative activity was observed in areas of AH/EIN with concurrent loss of PTEN and ARID1A compared to immediately adjacent AH/EIN areas showing only PTEN loss. In a cell culture system, co‐silencing of ARID1A and PTEN in human endometrial epithelial cells increased cellular proliferation to a greater degree than silencing either ARID1A or PTEN alone. These results suggest an essential gatekeeper role for ARID1A that prevents PTEN inactivation from promoting cellular proliferation in the transition of pre‐cancerous lesions to uterine endometrioid carcinoma.
    Subject(s): proliferation ; endometrioid intraepithelial neoplasia ; tumour suppressor ; atypical hyperplasia ; PTEN ; immunohistochemistry ; ARID1A ; co‐silencing ; in vitro cell culture model ; Cell proliferation ; Immunohistochemistry ; Cell culture ; Immunoglobulins ; Genital tract ; Endometrial cancer ; Epithelial cells ; Cloning ; Hyperplasia ; Cell division ; Genomes ; Pathology ; Uterus ; DNA methylation ; Mutation ; Gene mapping ; PTEN protein ; Deoxyribonucleic acid--DNA ; Endometrium ; Tumors
    ISSN: 2056-4538
    E-ISSN: 2056-4538
    Source: PubMed Central
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 9
    Language: English
    In: Clinical cancer research, 2010-05-15, Vol.16 (10), p.2715-2728
    Description: Stem-like tumor cells comprise a highly tumorigenic and therapy-resistant tumor subpopulation, which is believed to substantially influence tumor initiation and therapy resistance in glioma. Currently, therapeutic, drug-induced differentiation is considered as a promising approach to eradicate this tumor-driving cell population; retinoic acid is well known as a potent modulator of differentiation and proliferation in normal stem cells. In glioma, knowledge about the efficacy of retinoic acid-induced differentiation to target the stem-like tumor cell pool could have therapeutic implications. Stem-like glioma cells (SLGC) were differentiated with all-trans retinoic acid-containing medium to study the effect of differentiation on angiogenesis, invasive growth, as well as radioresistance and chemoresistance of SLGCs. In vivo effects were studied using live microscopy in a cranial window model. Our data suggest that in vitro differentiation of SLGCs induces therapy-sensitizing effects, impairs the secretion of angiogenic cytokines, and disrupts SLGCs motility. Further, ex vivo differentiation reduces tumorigenicity of SLGCs. Finally, we show that all-trans retinoic acid treatment alone can induce antitumor effects in vivo. Altogether, these results highlight the potential of differentiation treatment to target the stem-like cell population in glioblastoma.
    Subject(s): Immunohistochemistry ; Cell Separation ; Neoplastic Stem Cells - drug effects ; Humans ; Brain Neoplasms - pathology ; In Situ Hybridization, Fluorescence ; Brain Neoplasms - drug therapy ; Blotting, Western ; Xenograft Model Antitumor Assays ; Animals ; Flow Cytometry ; Cell Differentiation - drug effects ; Glioma - pathology ; Polymerase Chain Reaction ; Neoplastic Stem Cells - pathology ; Mice, Inbred NOD ; Antineoplastic Agents - pharmacology ; Mice ; Glioma - drug therapy ; Tretinoin - pharmacology ; Index Medicus
    ISSN: 1078-0432
    E-ISSN: 1557-3265
    Source: HighWire Press (Free Journals)
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 10
    Language: English
    In: The American journal of surgical pathology, 2014-12, Vol.38 (12), p.1603-1611
    Description: Serous borderline tumor also known as atypical proliferative serous tumor (APST) is the precursor of ovarian low-grade serous carcinoma (LGSC). In this study, we correlated the morphologic and immunohistochemical phenotypes of 71 APSTs and 18 LGSCs with the mutational status of KRAS and BRAF, the most common molecular genetic changes in these neoplasms. A subset of cells characterized by abundant eosinophilic cytoplasm (EC), discrete cell borders, and bland nuclei was identified in all (100%) 25 BRAF-mutated APSTs but in only 5 (10%) of 46 APSTs without BRAF mutations (P〈0.0001). Among the 18 LGSCs, EC cells were found in only 2, and both contained BRAF mutations. The EC cells were present admixed with cuboidal and columnar cells lining the papillae and appeared to be budding from the surface, resulting in individual cells and clusters of detached cells “floating” above the papillae. Immunohistochemistry showed that the EC cells always expressed p16, a senescence-associated marker, and had a significantly lower Ki-67 labeling index than adjacent cuboidal and columnar cells (P=0.02). In vitro studies supported the interpretation that these cells were undergoing senescence, as the same morphologic features could be reproduced in cultured epithelial cells by ectopic expression of BRAF. Senescence was further established by markers such as SA-β-gal staining, expression of p16 and p21, and reduction in DNA synthesis. In conclusion, this study sheds light on the pathogenesis of this unique group of ovarian tumors by showing that BRAF mutation is associated with cellular senescence and the presence of a specific cell type characterized by abundant EC. This “oncogene-induced senescence” phenotype may represent a mechanism that impedes progression of APSTs to LGSC.
    Subject(s): Immunohistochemistry ; Cellular Senescence - genetics ; ras Proteins - genetics ; Proto-Oncogene Proteins p21(ras) ; Humans ; Ovarian Neoplasms - pathology ; Proto-Oncogene Proteins - genetics ; Cystadenocarcinoma, Serous - genetics ; Cystadenocarcinoma, Serous - pathology ; Ovarian Neoplasms - genetics ; DNA Mutational Analysis ; Proto-Oncogene Proteins B-raf - genetics ; Female ; Mutation ; Cystadenoma, Serous - genetics ; Cystadenoma, Serous - pathology ; Index Medicus
    ISSN: 0147-5185
    E-ISSN: 1532-0979
    Source: Hellenic Academic Libraries Link
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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