Panizo, A. (Ángel)

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    Identification of TNF-alpha and MMP-9 as potential baseline predictive serum markers of sunitinib activity in patients with renal cell carcinoma using a human cytokine array
    (Nature Publishing Group, 2009) Gil-Bazo, I. (Ignacio); Prior, C. (Celia); Perez-Gracia, J.L. (Jose Luis); Gonzalez-Hernandez, A. (Alvaro); Gurpide, A. (Alfonso); Guillen-Grima, F. (Francisco); Melero, I. (Ignacio); Panizo, A. (Ángel); Grande-Pulido, E. (E.); Segura, V. (Víctor); Calvo-González, A. (Alfonso)
    BACKGROUND: Several drugs are available to treat metastatic renal-cell carcinoma (MRCC), and predictive markers to identify the most adequate treatment for each patient are needed. Our objective was to identify potential predictive markers of sunitinib activity in MRCC. METHODS: We collected sequential serum samples from 31 patients treated with sunitinib. Sera of six patients with extreme phenotypes of either marked responses or clear progressions were analysed with a Human Cytokine Array which evaluates 174 cytokines before and after treatment. Variations in cytokine signal intensity were compared between both groups and the most relevant cytokines were assessed by ELISA in all the patients. RESULTS: Twenty-seven of the 174 cytokines varied significantly between both groups. Five of them (TNF-alpha, MMP-9, ICAM-1, BDNF and SDF-1) were assessed by ELISA in 21 evaluable patients. TNF-alpha and MMP-9 baseline levels were significantly increased in non-responders and significantly associated with reduced overall survival and time-to-progression, respectively. The area under the ROC curves for TNF-alpha and MMP-9 as predictive markers of sunitinib activity were 0.83 and 0.77. CONCLUSION: Baseline levels of TNF-alpha and MMP-9 warrant further study as predictive markers of sunitinib activity in MRCC. Selection of patients with extreme phenotypes seems a valid method to identify potential predictive factors of response.
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    Utilización de células madre en terapia regenerativa cardíaca
    (Servicio de Publicaciones de la Universidad de Navarra, 2002) Herreros, J. (Jesús); Hernández, M. (M.); Rifon, J. J. (Jose J.); Rocha, E. (Eduardo); Cosin, J. (Juan); Inoges, S. (Susana); Perez-Calvo, J. (Javier); Rabago, G. (Gregorio); Panizo, A. (Ángel); Prosper-Cardoso, F. (Felipe); Perez, A. (Ana)
    One of the most important challenges in modern medicine is the use of stem cells for the treatment of human disease such as diabetes, Parkinson ́s disease or isquemic cardiomyopathy. A number of problems need to be solved before stem cells can be applied clinically. In this paper we will review some concepts related to the potential of stem cells, focusing on adult stem cells as they have recently been described by the group of Catherine Verfaillie. We will also present our initial clinical results using adult stem cells for cardiac regenerative therapy. In the studies mentioned above, autologous muscle stem cells (satelite cells) were infused directly in the periphery of the scar tissue of the infarct. We describe the technique for ex vivo expansion and purification of muscle stem cells.
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    Quiste del cuarto arco branquial en la membrana tirohioidea: un difícil diagnóstico diferencial con el laringocele mixto
    (Ediciones Universidad de Navarra, 2007) Noguera, J.J. (José J.); Fernández-González, S. (Secundino); Panizo, A. (Ángel); Villanueva, A. (Alberto)
    We present a case of a 62-year-old female patient with a right latero-cervical mass and an enlarged arytenoepiglottic fold, that caused voice disturbances. Computed tomography of the neck depicted an unilocular and homogeneous well-defined cyst located in the right parapharyngeal space that extended through the thyrohyoid membrane. It was initially diagnosed of mixed laryngocele. During surgical resection, no connexion between the lesion and laryngeal ventricle was detected, so the final diagnosis was branchial cyst. We discuss the pathogenicity and clinical, radiological and histological findings that facilitate differential diagnosis between mixed laryngocele and branchial cysts, mainly those derived from the second and fourth clefts. The radiological and histological findings in both lesions may be similar, so only the communication with the larynx, or its absence, can solve diagnostic doubts, course.
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    Quinapril decreases myocardial accumulation of extracellular matrix components in spontaneously hypertensive rats
    (Nature publishing group, 1995) Diez-Martinez, J. (Javier); Hernandez, M. (Milagros); Panizo, A. (Ángel); Pardo, J. (Javier); Galindo, M.F. (María F.); Cenarruzabeitia, E. (Edurne)
    n genetic and acquired hypertension, a structural remodeling of the nonmyocyte compartment of myocardium, including the accumulation of fibrillar collagen and other components of the extracellular matrix (ECM) within the interstitium, represents a determinant of pathologic hypertrophy that leads to ventricular dysfunction. Therefore, to evaluate the potential benefit of the angiotensin converting enzyme (ACE) inhibitor quinapril in reversing the interstitial remodeling in spontaneously hypertensive rats (SHR) with established left ventricular hypertrophy (LVH), we treated 16-week-old male SHR with oral quinapril (average dose, 10 mg/kg body weight/day) for 20 weeks. Interstitial fibrosis was determined morphometrically using an automatic image analyzer. The amount of collagen was evaluated by measuring myocardial hydroxyproline concentration. Myocardial deposition of collagen molecules (types I, III, and IV) and other ECM components (fibronectin, laminin) was analyzed by immunohistochemical techniques using specific monoclonal antibodies. The activity of ACE was measured in left ventricular tissue by a fluorometric assay. In quinapril-treated SHR compared with 36-week-old untreated SHR and age- and sex-matched Wistar-Kyoto (WKY) controls, we found 1) a lesser degree of LVH and a lesser level of blood pressure, 2) a lesser degree of interstitial fibrosis, represented by less interstitial collagen volume fraction (5.73 +/- 0.45% v 3.42 +/- 0.28%, P < .05; WKY, 3.44 +/- 0.66%), 3) a lower hydroxyproline concentration (1.09 +/- 0.05 mumol/L/g dry weight/100 g body weight to 0.81 +/- 0.05 mumol/L/g dry weight/100 g body weight, P < .05; WKY, 0.96 +/- 0.06 mumol/L/g dry weight/100 g body weight), 4) a lesser presence of collagen fibers, and 5) a lesser presence of collagen IV, fibronectin, and laminin.(ABSTRACT TRUNCATED AT 250 WORDS)
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    Is the regulation of apoptosis altered in smooth muscle cells of adult spontaneously hypertensive rats?
    (American heart association, 1997) Diez-Martinez, J. (Javier); Hernandez, M. (Milagros); Panizo, A. (Ángel); Pardo, J. (Javier)
    Whereas the protein product of the Bcl-2 gene inhibits apoptosis, the protein product of the Bax gene acts as a promoter of apoptosis. To gain insight into the regulation of apoptosis in vascular smooth muscle cells in arterial hypertension, we investigated the expression of the proteins Bcl-2 and Bax in small intramyocardial arteries of 36-week-old normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). In addition, 16-week-old SHR were treated for 20 weeks with the angiotensin-converting enzyme inhibitor quinapril and killed at 36 weeks of age. We measured the percentages of smooth muscle cells expressing these proteins using monoclonal antibodies and the avidin-biotin immunoperoxidase method. Compared with WKY, untreated SHR exhibited increased (P<.001) Bcl-2 expression and similar Bax expression. Values of Bcl-2 measured in quinapril-treated SHR were significantly lower than values measured in untreated SHR and similar to values measured in WKY. Quinapril-treated SHR showed higher (P<.001) Bax expression than WKY and untreated SHR. Bcl-2 expression was directly correlated with systolic pressure. Inverse correlations were found between the expression of Bax and the activities of both cardiac and circulating angiotensin-converting enzyme. These findings suggest that smooth muscle cell apoptosis might be inhibited in small arteries of adult SHR as a consequence of an excess of the protein Bcl-2. In addition, our results suggest that chronic angiotensin-converting enzyme inhibition might restore the susceptibility to apoptosis in these cells through stimulation of the protein Bax.
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    Biología molecular del carcinoma de tiroides de estirpe folicular (II). Aplicaciones clínicas
    (Ediciones Universidad de Navarra, 2003) Panizo, A. (Ángel); Salvador, J. (Javier); Calleja, A. (Amparo); Galofre, J.C. (Juan Carlos)
    The great advance of molecular medicine over the last few years gives us an attractive vision of the new possibilities in diagnosis and therapeutics of thyroid cancer and helps us to understand its biological behaviour. The clinical application of the growing understanding of gene alterations involved in thyroidal oncogenesis is becoming a reality. Such knowledge might contribute to greater diagnostic accuracy, by helping us characterise malignant or benign cells, predict tumour outcome or state its origin. Likewise it might be useful to know the response to conventional therapies or the future implications of pharmacogenetics. In addition molecular medicine applications ought to be considered in determining the prognosis of spontaneous and familiar carcinomas. Such information can significantly improve current clinical-pathologic prognostic methods.
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    Adenoma nefrogénico prostático. A propósito de un caso
    (2011) Romero, L.M. (L.M.); Barba-Abad, J.F. (Javier Fermín); Tienza, A. (Antonio); Panizo, A. (Ángel); Berian-Polo, J.M. (José María); Algarra, R. (Rubén)
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    Serum markers of collagen type I metabolism in spontaneously hypertensive rats: relation to myocardial fibrosis
    (American heart association, 1996) Diez-Martinez, J. (Javier); Hernandez, M. (Milagros); Panizo, A. (Ángel); Gil, M.J. (María José); Monreal, J.I. (José Ignacio); Pardo, J. (Javier)
    BACKGROUND: The assay of serum peptides of extracellular collagen synthesis and degradation could provide an indirect estimate of the rate of fibrillar turnover. This study was designed to investigate whether serum peptides of collagen type I synthesis and degradation are altered in spontaneously hypertensive rats (SHR) with left ventricular hypertrophy and whether these serum collagen-derived peptides are related to myocardial fibrosis. METHODS AND RESULTS: We measured serum levels of carboxyterminal propeptide of procollagen type I (PIP) as a marker of collagen I synthesis and serum levels of the pyridinoline crosslinked telopeptide domain of collagen type I (CITP) as a marker of fibrillar collagen I degradation in ten 36-week-old normotensive Wistar-Kyoto (WKY) rats, ten 36-week-old SHR, and ten 16-week-old SHR treated with the angiotensin-converting enzyme inhibitor quinapril (10 mg /kg body wt per day, orally) for 20 weeks. PIP and CITP were determined by specific radioimmunoassays. Histomorphometric and immunohistochemical studies of the left ventricle were performed in all rats. In untreated SHR compared with WKY rats, we found a more extensive interstitial and perivascular fibrosis, an increased (P<.01) collagen volume fraction, a more marked deposition of collagen type I, an increased (P<.01) serum concentration of PIP, and a similar serum concentration of CITP. In quinapril-treated SHR compared with untreated SHR, we found an absence of left ventricular hypertrophy, a marked decrease of fibrosis, a lower (P<.01) collagen volume fraction, a diminished deposition of collagen type I, a decreased (P<.01) concentration of PIP, and a similar concentration of CITP. A direct correlation was found between the collagen volume fraction and serum PIP (r=.753, P<.05) in untreated SHR. CONCLUSIONS: These results suggest that tissue metabolism of collagen type I is abnormal in SHR and can be normalized by treatment with quinapril. On the basis of our findings, we propose that serum PIP may be a marker of collagen type I-dependent myocardial fibrosis in rats with genetic hypertension.
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    Toward the biochemical assessment of myocardial fibrosis in hypertensive patients
    (Elsevier, 1995) Diez-Martinez, J. (Javier); Laviades, C. (Concepción); Panizo, A. (Ángel); Gil, M.J. (María José); Monreal, J.I. (José Ignacio); Pardo, J. (Javier)
    The serum concentrations of amino-terminal procollagen type III and carboxy-terminal procollagen type I-derived peptides, which have been proposed as useful markers of the tissue synthesis of collagen types III and type I, respectively, were abnormally increased in patients with essential hypertension and became normal after angiotensin-converting enzyme (ACE) inhibition. An association was found between baseline serum concentrations of these peptides and left ventricular hypertrophy, diastolic dysfunction, and ventricular arrhythmias in hypertensive patients. On the other hand, increased serum concentration of the carboxy-terminal procollagen type I-derived peptide was found in spontaneously hypertensive rats compared with normotensive Wistar-Kyoto control rats. An association was found between the serum concentration of this peptide and the extent of myocardial fibrosis and the hydroxyproline concentration in the left ventricle of spontaneously hypertensive rats. It is proposed that procollagen-derived peptides in serum may be markers of exaggerated collagen tissue synthesis involved in hypertensive myocardial fibrosis.
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    Biología molecular del carcinoma de tiroides de estirpe folicular. Bases moleculares en la oncogénesis tiroidea
    (Servicio de Publicaciones de la Universidad de Navarra, 2002) Panizo, A. (Ángel); Salvador, J. (Javier); Calleja, A. (Amparo); Galofre, J.C. (Juan Carlos)
    Existen datos que nos permiten afirmar que probablemente, en gran parte de los casos, no existe una solución de continuidad entre las diferentes neoplasias tiroideas de estirpe folicular. Cabe pensar que el proceso evolutivo comienza con una serie de alteraciones moleculares que condicionan la aparición del adenoma folicular (AF). Cambios posteriores propiciarán el desarrollo de un carcinoma folicular (CF). La aparición del carcinoma papilar (CP) tiene probablemente un itinerario similar sin que esté demostrado que tenga su origen en AF. Ulteriores cambios genéticos, tanto en el CP como en el CF encaminarán hacia la indiferenciación celular y con ello el desarrollo del carcinoma indiferenciado (CI). Esta sucesión de alteraciones moleculares condiciona un empeoramiento en el pronóstico de la neoplasia tiroidea. Por ello, las neoplasias tiroideas constituyen un excelente modelo para el estudio de la cronología de los cambios moleculares que condicionan la evolución desde la benignidad a la malignidad. Se ha comprobado que en algunas neoplasias de tiroides existe inestabilidad genética que favorece dichos cambios moleculares. Como fenómeno inicial es frecuente observar alteraciones en los protooncogenes mientras que las mutaciones en los genes supresores de tumor suelen ser un evento tardío. La aparición de agresividad o invasividad de la neoplasia también se puede investigar mediante el estudio de cambios moleculares. La aplicación clínica de dichos hallazgos comienza a ser una realidad, lo que facilitará la precisión diagnóstica y con ello una terapéutica más eficaz.