Browsing by Subject "Hyperplasia"

Now showing 1 - 4 of 4
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    Adenomatous hyperplasia of the rete testis. A review and report of new cases
    (Murcia : F. Hernández, 2003) Nistal, M.; Castillo, M.C.; Regadera, J.; García-Cabezas, M.A.
    Adenomatous hyperplasia of the rete testis (AHRT) is an uncommon benign lesion that preferentially involves the septal rete testis and mediastinal rete testis. It is usually an incidental finding in surgical specimens from cryptorchidism and testicular tumour. It can be found in autopsy specimens from patients dying with different chronic diseases and newborns with kidney diseases. Since its first description many articles have been published communicating new cases and putting forward some hypotheses on its aetiology and pathogenic mechanisms. Some authors suggest a role for hormonal changes, tumour invasion and action of chemical agents. We think that AHRT should be categorised into two main aetiological categories: congenital and acquired. The cases associated with different kidney and spermatic duct diseases, most cases associated with cryptorchidic testis and some cases associated with testicular germ cell tumour should be included in the congenital group. The remaining cases associated with chemical agents, some hormonal changes (i.e. androgen blockade) and most of the germ cell tumour cases can be considered as acquired AHRT. Differential diagnosis must be established mainly with metastatic adenocarcinoma of prostate to testis and primary adenocarcinoma of the rete testis. Pseudohyperplasia of the rete testis must also be considered in atrophic testes. Here we review the papers published on this subject and report our recent cases
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    Cooperative role between p21cip1/waf1 and p27kip1 in premature senescence in glandular proliferative lesions in mice
    (F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2014) García-Fernández, R.A.; García-Palencia, P.; Suárez, C.; Sánchez, M.A.; Gil-Gómez, G.; Sánchez, B.; Rollán, E.; Martín-Caballero, J.; Flores, J.M.
    Cellular senescence has been considered a novel target for cancer therapy. It has also been pointed out that p21cip1/waf1 and p27kip1 cyclin-dependent kinase inhibitors (CKIs) play a role in cellular senescence in some tumor types. Therefore, in order to address the possibility of a cooperative role between p21 and p27 proteins in senescence in vivo we analyzed cellular senescence in spontaneous glandular proliferative lesions (adrenal, thyroid and pituitary glands) in a double-KO mice model, using γH2AX, p53, p16, PTEN and Ki67 as senescence markers. The results obtained showed that p21p27 double-null mice had the lowest number of γH2AX positive cells in glandular hyperplasias and benign tumors. Also, in this group, Ki67 proliferation index correlated with a lower immunohistochemical expression of γH2AX and p53. The expression of p16 and PTEN do not seem to cause synergism of senescence in the benign lesions analyzed in p21p27 double-KO mice. These observations suggest an intrinsic cooperation between p21 and p27 CKIs in the activation of stress-induced cellular senescence and tumor progression in vivo, which would be a physiological mechanism to prevent tumor cell proliferation.
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    Maspin expression, subcellular localization and clinicopathological correlation in endometrial hyperplasia and endometrial adenocarcinoma
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Blandamura, Stella; Alessandrini, Lara; Saccardi, Carlo; Giacomelli, Luciano; Fabris, Alberta; Borghero, Angela; Litta, Pietro
    Maspin expression in endometrial hyperplasia and endometrial endometrioid adenocarcinomas was assessed and its correlation with p53 and Ki-67 expressions and clinical outcome, as well as its potential to distinguish typical from atypical endometrial hyperplasia, were assessed in this study. Histological sections from 114 cases of endometrial endometrioid adenocarcinoma, 75 cases of endometrial hyperplasia (typical and atypical), and 23 normal endometrial tissue samples were examined. The most representative hematoxylin-eosin slides were selected and 2-3 micron-thick sections were cut for immunohistochemical staining with maspin, p53, and Ki-67 antibodies. While there was no maspin expression in normal endometrial cells, it was present in 14.5% of the patients with endometrial hyperplasia without atypia. Staining for maspin was positive in atypical hyperplasia and endometrial adenocarcinoma in, respectively, 45% and 49.1% of the cases studied. No statistically significant correlations were found between maspin and Ki-67 antibodies or p53 expression. Our findings showed that maspin expression, which generally correlates with a less aggressive behavior, is significantly higher in atypical hyperplasia and in endometrial endometrioid adenocarcinoma. Maspin positivity in endometrial hyperplasia could be used to identify pseudo-atypical hyperplasia and could be considered a potentially useful prognostic parameter in those cases in which adenocarcinomas are well differentiated.
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    Sustanon induces dose-independent hypertrophy and satellite cell proliferation in slow oxidative fibers of avian skeletal muscle
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Allouh, Mohammed Z.; Jarrar, Ahmad A.; Asfour, Hasan A.; Said, Raed S.; Shaqoura, Emad I.
    Sustanon is a well-known anabolic drug that is used to treat hypogonadism and restore muscle mass and bone density. As research to date has been limited to its effects in glycolytic fibers, this study aimed to investigate the dose-related effects of Sustanon on the oxidative fibers of avian skeletal muscle. Adult female chickens were randomly divided into 4 groups: control (C), received a dose of 100 μl normal saline per injection; and Sustanon-1, -2, and -3 (S1, S2, and S3), that received a dose of 12.5, 25, or 50 mg/kg Sustanon per injection, respectively. Each bird received 4 injections at weekly intervals (1 injection/week). Robust histochemical and immunofluorescent techniques along with morphometric analyses were applied to determine the oxidative activity and morphological variations of the oxidative muscle fibers in all groups. Sustanontreated groups exhibited significant increases in fiber size and numbers of satellite cells and myonuclei compared to the control group. However, no significant variations were found between Sustanon-treated groups in the aforementioned indices. In conclusion, Sustanon induced oxidative fiber hypertrophy that was associated with satellite cell proliferation and myonuclear accretion in avian skeletal muscle. Furthermore, the effects of Sustanon appeared to be dose-independent.