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Molecular biology of cholesteatoma Alma Maniu, Oana Harabagiu, Maria Perde Schrepler, Andreea Catana, Bogdan Fanuta, Carmen Aurelia Mogoanta Cholesteatoma is a non-neoplastic, keratinizing lesion, characterized by the proliferation of epithelium with aberrant micro-architecture into the middle ear and mastoid cavity.

The exact pathogenic molecular mechanisms behind the formation and propagation of cholesteatoma remain unclear. Immunohistochemical examinations of the matrix and perimatrix have considerably improved the knowledge of cholesteatoma pathogenesis.

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In this review, the current concepts of cholesteatoma pathogenesis are discussed. Currently, the most widely acknowledged pathogenesis of acquired cholesteatoma is the theory that negative pressure, dysfunction of the Eustachian tube, causes a deepening retraction pocket that, when obstructed, desquamated keratin cannot be cleared from the recess, and a cholesteatoma results.

Aggressive variants of prostate cancer - Are we ready to apply specific treatment right now? Cancer Treat Rev. In most cases, prostate cancer essentially depends on androgen receptor signaling axis, even in castration-resistant setting, and hence may be targeted by second generation hormonal therapy. However, a subset of patients bears androgen-independent cancer biology with a short-term response to hormonal treatment, early and extensive visceral metastases, low PSA levels and poor outcomes. Identification and specific management of these rapidly fatal malignancies is of an unmet medical need since their classification and utilized therapeutic regimens vary significantly.

Local infection leads to a disturbance of self-cleaning mechanisms, with cell debris and keratinocytes accumulate inside the retraction pocket, and this is followed by an immigration of immune cells, i.

There is an imbalance and a vicious circle of epithelial proliferation, keratinocyte differentiation and maturation, prolonged apoptosis, and disturbance of self-cleaning mechanisms. The inflammatory stimulus will induce an epithelial proliferation along with expression of lytic enzymes and cytokines.

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Bacteria inside the retraction pocket produce some antigens, which will activate different cytokines and lytic enzymes. These cytokines lead to activation and maturing of osteoclasts with the consequence of degradation of extracellular bone matrix and hyperproliferation, bone erosion and medicamente vierme nume de copii progression of the disease. Further research is necessary cancer highly aggressive a better understanding of the pathogenetic mechanisms and to expand the spectrum of therapeutic options.

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Most cases are represented by the aggressive histological type diffuse large B-cell lymphoma. Aim: Identification of factors with potential prognosis impact in the aggressive primary gastric lymphoma and the prognosis profile of the patient with impact on the response to therapy and overall survival. Patients cancer highly aggressive Methods: The study group is composed of 49 patients diagnosed with primary gastric diffuse large-cell non-Hodgkin's malignant lymphoma at "Fundeni" Hematology Clinic of Bucharest and at the Hematology Clinic of Cancer highly aggressive, Romania, in the period Conclusions: Identifying prognostic factors is important for personalized therapy approach to obtain optimal response with minimal adverse reaction.

cancer highly aggressive

Acute leukemia with erythroid hyperplasia. Our experience on a series of cases with acute myeloid leukemia Elena-Cristina Selicean, Mariana Patiu, Andrei Cucuianu, Delia Dima, Minodora Dobreanu Diagnosis of myeloid malignancies with erythroid hyperplasia may sometimes confront hematologists with a mathematical dilemma, if cut-off criteria of blast percentage as proposed by the World Health Organization WHO Classification are applied.

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Several questions have been raised regarding differentiation of acute erythroid leukemia AEL from myelodysplastic syndrome with erythroid hyperplasia and some aspects still remain unclear.

This paper discusses the differential diagnosis and presents our own experience in a series of patients with acute myeloid leukemia.

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Although the diagnostic criteria of AEL have been repeatedly refined, it remains a diagnosis primarily based on morphology and on exclusion criteria.

Many of the cases designated before as AEL, actually fit into other disease categories, most often into myelodysplasia related changes - acute myeloid leukemia. Our experience on a series of cases with acute myeloid leukemia PDF 4. Obesity is associated with a high cardiovascular risk, abdominal obesity being the most aggressive form, because it secretes cytokines and hormones in comparison to subcutaneous adipose tissue. Adipocytokines secreted by adipose tissue are mediators of atherosclerosis and endothelial damage.

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Materials and Methods: We studied a total of 80 subjects aged between 40 and 60 years with metabolic syndrome, in which the following adipocytokines cancer highly aggressive were determined: hs-CRP turbidimetric methodIL-6, TNF-alpha, leptin ELISA methodin comparison to a control group.

Results: The values of these adipocytokines were significantly higher in the studied group compared with cancer highly aggressive control group and correlated with increased levels of glucose patients with type II diabetes or increased tolerance test and with hyper-triglyceridemia. Conclusions: Patients with metabolic syndrome had increased levels of proatherogenic adipocytokines, particularly leptin, leptin-resistance representing the pathogenic link of obesity.

The identification as early as possible of the metabolic syndrome patients allows effective monitoring and correction of cardiovascular risk factors, with the opportunity to reduce morbidity and mortality in young ages.

In men, proatherogenic cytokines values presented higher values than in women, which prove the role of abdominal obesity in proatherogenic cytokines cancer highly aggressive.

Cancerul de prostată este cel mai frecvent tip de cancer diagnosticat şi totodată cauza principală de deces prin cancer la bărbaţii europeni. Tratamentul curativ pentru cancerul de prostată clinic localizat poate produce un control oncologic acceptabil al bolii, iar pentru un grup selecţionat de pacienţi poate fi suficient. În ciuda acestui fapt, cancerul de prostată prezintă o variabilitate considerabilă în comportamentul clinic, variind de la formele indolente la boala letală.

Although women have a higher percentage of adipose tissue, this is not primarily abdominal adipose tissue. Materials and Methods: Tissue samples containing tooth buds were removed from the incisor areas of human fetuses in different stages of development weeks, and from the canine and molar areas of weeks fetuses.

The tissue fragments were fixed using formalin and were processed using common histological techniques with paraffin embedding.

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Immunostaining for Ki67, p53 and CD34 has been performed using the dextran method and moist heat antigen retrieval except for CD The resulting slides were photographed and quantitatively evaluated. Results: Ki67 immunoexpression decreases cancer highly aggressive advancement of the developmental stage of the tooth bud: in the inner enamel epithelium, between weeks 9 and 16 IEEin the preameloblasts PB between weeks 13 and 16, in the ameloblasts AB between weeks 21 and 24; outer enamel epithelium OEE ; stratum intermedium SI ; in the dental papilla: between weeks 9 and 10 in the dental papilla DPbetween weeks 13 and 16 in the outer layer of the dental papilla DP1 and in the central layer of the dental papilla DP2.

Likewise, we noted Ki67 expression in the odontoblast layer O and pulp Pbetween weeks 21 and Concerning CD34 expression, we observed a decrease from weeks until weeksfollowed by an increase until weeks of intrauterine life. From weekswe observed a constant decrease of expression until weeksfollowed by an increase during weeks Conclusions: All Ki67, p53 and CD34 have been identified in the tooth bud.

Ki67 expression gradually decreases with the embryonic development of the tooth, while p53 and CD34 expression decreases from weeks to weeks of intrauterine life, followed by an increase until weeks cancer highly aggressive

The Typical Prognosis of Aggressive Renal Cell Cancer