Alejandro Ismael Lorenzo Pouso

Dr. Alejandro Ismael Lorenzo Pouso

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Research Focus & Metrics

Academic Career Length

10Years (2017-Present)

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

Representative Publications

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FSFábio França Vieira e Silva
Fábio França Vieira e Silva
MPMaria Elena Padín-Iruegas
Maria Elena Padín-Iruegas
VCVITO CARLO ALBERTO CAPONIO
VITO CARLO ALBERTO CAPONIO
APAlejandro Ismael Lorenzo Pouso
Alejandro Ismael Lorenzo Pouso
PSPaula Saavedra-Nieves
Paula Saavedra-Nieves
Mario Pérez-SayánsMario Pérez-Sayáns
Mario Pérez-Sayáns
Head and neck cancer (HNC) is an ascending and agressive disease. The search for new molecular markers is emerging to solve difficulties in diagnosis, risk management, prognosis and effectiveness of treatments. Proteins related to apoptotic machinery have been identified as potential biomarkers. Caspase 3 is the main effector caspase and has a key role in apoptosis. The objective of this systematic review and meta-analysis is to review studies that analyze changes in Caspase 3 and Cleaved Caspase 3 expression both in oral premalignant disorders (OPMD) as well as in head and neck cancer (HNC). This study also proposes to review the prognostic values associated with HNC according to the expression of Caspase 3. Medline (via PubMed), EMBASE, Scopus, Cochrane, Web of Science and Grey Literature Database were screened from inception to june of 2022 and 18 studies were selected and 8 were included in the prognostic meta-analysis. Results related to the comparison of Caspase 3 expression demonstrated similar expression of Caspase 3 in HNC, with an average of 51.9% (9.5–98.1) showing high/moderate expression compared to 45.7% (14.6–84.7) in OPMD. Of interest, Cleaved Caspase 3 resulted incresed in HNC when compared with OPMD, being 73.3% (38.6–88.3) versus 22.9% (7.1–38.7). Pooled Fixed effect of HR values (95% CI) for OS related to Caspase 3 IHC expression in HNC patients was 1.48 (95% CI 0.95–2.28); also, the rate of heterogeneity was low, as revealed by I2 = 31%. For DFS was 1.07 (95% CI 0.79–1.45) with I2 = 0% and DSS showed a HR of 0.88 (95% CI 0.69–1.12) with I2 = 37%. Caspase 3 and Cleaved Caspase 3 expression could be linked with malignancy progression, but the expression of Caspase 3 did not influence the prognosis of patients with HNC.

7 November 2019 in Journal of Clinical Medicine
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Mario Pérez-SayánsMario Pérez-Sayáns
Mario Pérez-Sayáns
CCCintia Chamorro
Cintia Chamorro
APAlejandro Ismael Lorenzo Pouso
Alejandro Ismael Lorenzo Pouso
EIElena Padín Iruegas
Elena Padín Iruegas
ABAndrés Blanco-Carrión
Andrés Blanco-Carrión
AGAbel Garcia-Garcia
Abel Garcia-Garcia
The aim of this present study was to comprehensively describe somatic DNA alterations and transcriptional alterations in the last extension of the HNSCC subsets in TCGA, encompassing a total of 528 tumours. In order to achieve this goal, transcriptional analysis, functional enrichment assays, survival analysis, somatic copy number alteration analysis and somatic alteration analysis were carried out. A total of 3491 deregulated genes were found in HNSCC patients, and the functional analysis carried out determined that tissue development and cell differentiation were the most relevant signalling pathways in upregulated and downregulated genes, respectively. Somatic copy number alteration analysis showed a “top five” altered HNSCC genes: CDKN2A (deleted in 32.03% of patients), CDKN2B (deleted in 28.34% of patients), PPFIA1 (amplified in 26.02% of patients), FADD (amplified in 25.63% of patients) and ANO1 (amplified in 25.44% of patients). Somatic mutations analysis revealed TP53 mutation in 72% of the tumour samples followed by TTN (39%), FAT1 (23%) and MUC16 (19%). Another interesting result is the mutual exclusivity pattern that was discovered between the TP53 and PIK3CA mutations, and the co-occurrence of CDKN2A with the TP53 and FAT1 alterations. On analysis to relate differential expression genes and somatic copy number alterations, some genes were overexpressed and amplified, for example, FOXL2, but other deleted genes also showed overexpression, such as CDKN2A. Survival analysis revealed that overexpression of some oncogenes, such as EGFR, CDK6 or CDK4 were associated with poorer prognosis tumours. These new findings help us to develop new therapies and programs for the prevention of HNSCC.

7 November 2018 in Disease Markers
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APAlejandro Ismael Lorenzo Pouso
Alejandro Ismael Lorenzo Pouso
Mario Pérez-SayánsMario Pérez-Sayáns
Mario Pérez-Sayáns
SLSusana Belen Bravo López
Susana Belen Bravo López
Pia Lopez-JornetPia Lopez-Jornet
Pia Lopez-Jornet
MGMaría García-Vence
María García-Vence
AGAbel Garcia-Garcia
Abel Garcia-Garcia
The Global Burden of Oral Diseases affects 3.5 billion people worldwide, representing the number of people affected by the burden of untreated dental caries, severe periodontal disease, and edentulism. Thus, much more efforts in terms of diagnostics and treatments must be provided in the fight of these outcomes. In this sense, recently, the study of saliva as biological matrix has been identified as a new landmark initiative in the search of novel and useful biomarkers to prevent and diagnose these conditions. Specifically, saliva is a rich reservoir of different proteins and peptides and accessible due to recent advances in molecular biology and specially in targeted and unbiased proteomics technologies. Nonetheless, emerging barriers are an obstacle to the study of the salivary proteome in an effective way. This review aims at giving an overall perspective of salivary biomarkers identified in several oral diseases by means of molecular biology approaches.

12 October 2019 in Journal of Oral Pathology & Medicine
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APAlejandro Ismael Lorenzo Pouso
Alejandro Ismael Lorenzo Pouso
Mario Pérez-SayánsMario Pérez-Sayáns
Mario Pérez-Sayáns
CCCintia Chamorro
Cintia Chamorro
Pilar Gandara Gandara-VilaPilar Gandara Gandara-Vila
Pilar Gandara Gandara-Vila
Pia Lopez-JornetPia Lopez-Jornet
Pia Lopez-Jornet
AGAbel García‐García
Abel García‐García

28 December 2020 in Acta Odontologica Scandinavica
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APAlejandro Ismael Lorenzo Pouso
Alejandro Ismael Lorenzo Pouso
PCPablo Castelo-Baz
Pablo Castelo-Baz
SZSamuel Rodríguez Zorrilla
Samuel Rodríguez Zorrilla
Mario Pérez-SayánsMario Pérez-Sayáns
Mario Pérez-Sayáns
PVPablo Vega
Pablo Vega
The aim of this systematic review was to investigate the association between periodontal disease (PD) and inflammatory bowel disease (IBD), and its two major forms Crohn’s disease (CD) and ulcerati...

17 October 2022 in Journal of Fungi
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APAlejandro Ismael Lorenzo Pouso
Alejandro Ismael Lorenzo Pouso
APAlba Pérez-Jardón
Alba Pérez-Jardón
VCVITO CARLO ALBERTO CAPONIO
VITO CARLO ALBERTO CAPONIO
FSFrancesca Spirito
Francesca Spirito
CCCintia Chamorro
Cintia Chamorro
Mario Pérez-SayánsMario Pérez-Sayáns
Mario Pérez-Sayáns
Chronic hyperplastic candidiasis (CHC) is a prototypical oral lesion caused by chronic Candida infection. A major controversy surrounding CHC is whether this oral lesion owns malignant transformation (MT) potential. The aim of the present study was to evaluate current evidence on the MT of CHC and to determine the variables which have the greatest influence on cancer development. Bibliographical searches included PubMed, Embase, Web of Science, Scopus and LILACS. The cohort studies and case series used to investigate the MT of CHC were deemed suitable for inclusion. The quality of the enrolled studies was measured by the Joanna Briggs Institute scale. Moreover, we undertook subgroup analyses, assessed small study effects, and conducted sensitivity analyses. From 338 studies, nine were finally included for qualitative/quantitative analysis. The overall MT rate for CHC across all studies was 12.1% (95% confidential interval, 4.1–19.8%). Subgroup analysis showed that the MT rate increased when pooled analysis was restricted to poor quality studies. It remains complex to affirm whether CHC is an individual and oral, potentially malignant disorder according to the retrieved evidence. Prospective cohort studies to define the natural history of CHC and a consensus statement to clarify a proper set of diagnostic criteria are strongly needed. PROSPERO ID: CRD42022319572.