Aggelos Laliotis

Dr. Aggelos Laliotis

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Research Focus & Metrics

Academic Career Length

22Years (2005-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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14 October 2017 in Healthcare
Verified
Journal Article
Open access
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DDanae Sfantou
Danae Sfantou
ALAggelos Laliotis
Aggelos Laliotis
ATHINA PATELAROUATHINA PATELAROU
ATHINA PATELAROU
Dimitra Sifaki- PistollaDimitra Sifaki- Pistolla
Dimitra Sifaki- Pistolla
MMMichail Matalliotakis
Michail Matalliotakis
EPEvridiki Patelarou
Evridiki Patelarou
Effective leadership of healthcare professionals is critical for strengthening quality and integration of care. This study aimed to assess whether there exist an association between different leadership styles and healthcare quality measures. The search was performed in the Medline (National Library of Medicine, PubMed interface) and EMBASE databases for the time period 2004–2015. The research question that guided this review was posed as: “Is there any relationship between leadership style in healthcare settings and quality of care?” Eighteen articles were found relevant to our research question. Leadership styles were found to be strongly correlated with quality care and associated measures. Leadership was considered a core element for a well-coordinated and integrated provision of care, both from the patients and healthcare professionals.

22 September 2016 in Journal of Educational Evaluation for Health Professions
Verified
Journal Article
Open access
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KKKonstantinos G Kyriakoulis
Konstantinos G Kyriakoulis
ATHINA PATELAROUATHINA PATELAROU
ATHINA PATELAROU
ALAggelos Laliotis
Aggelos Laliotis
AWAndrew C Wan
Andrew C Wan
MMMichail Matalliotakis
Michail Matalliotakis
EPEvridiki Patelarou
Evridiki Patelarou
Purpose: The aim of this systematic review was to find best teaching strategies for teaching evidence-based practice (EBP) to undergraduate health students that have been adopted over the last years in healthcare institutions worldwide. Methods: The authors carried out a systematic, comprehensive bibliographic search using Medline database for the years 2005 to March 2015 (updated in March 2016). Search terms used were chosen from the USNLM Institutes of Health list of MeSH (Medical Subject Headings) and free text key terms were used as well. Selected articles were measured based on the inclusion criteria of this study and initially compared in terms of titles or abstracts. Finally, articles relevant to the subject of this review were retrieved in full text. Critical appraisal was done to determine the effects of strategy of teaching evidence-based medicine (EBM). Results: Twenty articles were included in the review. The majority of the studies sampled medical students (n=13) and only few conducted among nursing (n=2), pharmacy (n=2), physiotherapy/therapy (n=1), dentistry (n=1), or mixed disciplines (n=1) students. Studies evaluated a variety of educational interventions of varying duration, frequency and format (lectures, tutorials, workshops, conferences, journal clubs, and online sessions), or combination of these to teach EBP. We categorized interventions into single interventions covering a workshop, conference, lecture, journal club, or e-learning and multifaceted interventions where a combination of strategies had been assessed. Seven studies reported an overall increase to all EBP domains indicating a higher EBP competence and two studies focused on the searching databases skill. Conclusion: Followings were deduced from above analysis: multifaceted approach may be best suited when teaching EBM to health students; the use of technology to promote EBP through mobile devices, simulation, and the web is on the rise; and the duration of the interventions varying form some hours to even months was not related to the students’ EBP competence.

5 June 2015 in Molecular Oncology
Verified
Journal Article
Open access
George NotasGeorge Notas
George Notas
VPVassiliki Pelekanou
Vassiliki Pelekanou
MKMarilena Kampa
Marilena Kampa
KAKonstantinos Alexakis
Konstantinos Alexakis
SSStelios Sfakianakis
Stelios Sfakianakis
ECElias Castanas
Elias Castanas
Tamoxifen is the treatment of choice in estrogen receptor alpha breast cancer patients that are eligible for adjuvant endocrine therapy. However, ∼50% of ERα‐positive tumors exhibit intrinsic or rapidly acquire resistance to endocrine treatment. Unfortunately, prediction of de novo resistance to endocrine therapy and/or assessment of relapse likelihood remain difficult. While several mechanisms regulating the acquisition and the maintenance of endocrine resistance have been reported, there are several aspects of this phenomenon that need to be further elucidated. Altered metabolic fate of tamoxifen within patients and emergence of tamoxifen‐resistant clones, driven by evolution of the disease phenotype during treatment, appear as the most compelling hypotheses so far. In addition, tamoxifen was reported to induce pluripotency in breast cancer cell lines, in vitro. In this context, we have performed a whole transcriptome analysis of an ERα‐positive (T47D) and a triple‐negative breast cancer cell line (MDA‐MB‐231), exposed to tamoxifen for a short time frame (hours), in order to identify how early pluripotency‐related effects of tamoxifen may occur. Our ultimate goal was to identify whether the transcriptional actions of tamoxifen related to induction of pluripotency are mediated through specific ER‐dependent or independent mechanisms. We report that even as early as 3 hours after the exposure of breast cancer cells to tamoxifen, a subset of ERα‐dependent genes associated with developmental processes and pluripotency are induced and this is accompanied by specific phenotypic changes (expression of pluripotency‐related proteins). Furthermore we report an association between the increased expression of pluripotency‐related genes in ERα‐positive breast cancer tissues samples and disease relapse after tamoxifen therapy. Finally we describe that in a small group of ERα‐positive breast cancer patients, with disease relapse after surgery and tamoxifen treatment, ALDH1A1 (a marker of pluripotency in epithelial cancers which is absent in normal breast tissue) is increased in relapsing tumors, with a concurrent modification of its intra‐cellular localization. Our data could be of value in the discrimination of patients susceptible to develop tamoxifen resistance and in the selection of optimized patient‐tailored therapies.

1 October 2005 in Chest
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Journal Article
Closed access
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AKAlexandros Kafetzakis
Alexandros Kafetzakis
GKGeorge Kochiadakis
George Kochiadakis
ALAggelos Laliotis
Aggelos Laliotis
IPIoannis Peteinarakis
Ioannis Peteinarakis
ETEmmanouel Touloupakis
Emmanouel Touloupakis
AKAsterios Katsamouris
Asterios Katsamouris

21 June 2010 in International Journal of Dermatology
Verified
Journal Article
Closed access
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Eelco De BreeEelco De Bree
Eelco De Bree
ALAggelos Laliotis
Aggelos Laliotis
AMAndreas Manios
Andreas Manios
DTDimitris D. Tsiftsis
Dimitris D. Tsiftsis
JMJohn Melissas
John Melissas

1 February 2013 in The Breast
Verified
Journal Article
Open access
ALAggelos Laliotis
Aggelos Laliotis
TVThomas Vrekoussis
Thomas Vrekoussis
MKMaria Kafousi
Maria Kafousi
ESElias Sanidas
Elias Sanidas
JAJohn Askoxilakis
John Askoxilakis
ESEfstathios N. Stathopoulos
Efstathios N. Stathopoulos
Recently an increased interest on Elk1 protein and its role in breast cancer evolution has been noted. This protein is an element of the Ets family of transcription factors and it has been involved in a number of important cell processes through the activation of different genes, in a number of normal tissues as well as in many malignancies. One hundred and seventy (n = 170) cases of operable breast cancer (invasive ductal, lobular and mixed type breast carcinomas) were randomly selected and investigated for the expression of pElk-1, Ki-67 and Cyclin D1 using immunohistochemistry. Our findings were correlated with tumors' clinicopathologic data and biologic profile. Activated Elk1 is positively associated with ER (p-value: 0.018) and also shows a positive association of with Cyclin D1 (p-value: <0.001). No relationship was noted between pElk1 and Ki67 (p-value: 0.213). Luminal A and B Her-2 negative breast cancer subtypes were showing greater pElk-1 immunoreactivity compared to Her-2 and Basal breast cancer subtypes, and also a higher staining intensity. No association of the molecule with other clinicopathologic characteristics (tumor size, stage, histological type or lymph node metastases) or disease adverse events (local recurrence, metastasis or death) was evidenced. Our findings offer a new perspective for the role of pElk-1 in breast neoplasia suggesting a direct relation of this molecule to tumor biology and a putative target of personalized breast cancer therapies, although its prognostic/discriminant role is not supported.