Progression through the mammalian cell cycle is regulated by cyclin-cyclin-dependent kinase (CDKs) complexes that are activated throughout the cell cycle. Alteration in cell cycle control could lead to proliferation and tumourogenesis. This study was designed to analyse, at messenger RNA (mRNA) level, cyclins and CDKs involved in the retinoblastoma pathway, as well as cell division cycle 25a phosphatase (CDC25a), which activates some of the CDKs that were analysed. The aim of the study was to determine the possible prognostic relevance of these molecules in 73 women with peri- and post-menopausal breast cancer. Cyclins A, D1 and E; CDKs 2, 4 and 6 and phosphatase CDC25a expression status were analysed in primary tumours at mRNA level, by reverse transcriptase polymerase chain reaction analysis in paraffin-embedded primary breast cancers. High expression levels of CDK2, CDK4 and CDC25a were related to tumour recurrence. Over-expression of CDK2 and CDC25a was also associated with reduced overall survival; moreover, the CDK2 expression level was able to define a short-living cohort of patients with tumour-positive lymph nodes. CDK2, CDK4 and CDC25a can be used as reliable biomarkers to predict prognosis in women with peri- and post-menopausal breast cancer.
Skin melanoma represents one of the most common and lethal solid tumor. It usually develops on the skin but it can occur in any tissues with melanine- containing-cells (extracutaneous malignant melanoma). Only 4-5% of malignant melanomas originate in extracutaneous tissues, and they have an extremely lethal behavior (1). These non-skin malignant melanomas are rare but extremely aggressive. Primary melanoma of the genitourinary tract accounts for less than 0.2% of all melanomas. To date only 28 cases of primary bladder melanoma (PMM) are described. We report a rare case of PMM of the bladder in a 72 years old man treated with radical cystectomy and immunotherapy with Nivolumab.
Aims-The spectrum of microscopic lesions resulting from the chronic use of non-steroidal anti-inflammatory drugs (NSAIDs), known as chemical gastritis, remains unclear, and the variable prevalence reported in diVerent studies makes this issue a matter of lively debate. The aim of this study was to evaluate the prevalence and importance of chemical gastritis in patients regularly taking NSAIDs. Owing to the high prevalence of Helicobacter pylori infection, particularly in subjects over 60 years of age, and in view of a possible association with damage, the presence of H pylori infection in the same tissue sample was also determined in all patients. Methods-One hundred and ninety seven subjects were enrolled, 118 of whom were receiving chronic treatment with NSAIDs and 79 of whom were controls, pair matched for age, sex, and clinical symptoms (ulcer-like dyspepsia or upper digestive tract haemorrhage). Antral biopsies taken during upper gastroduodenal endoscopy were assessed for chemical gastritis according to a modified version of Dixon's score, and for helicobacter correlated chronic active gastritis, according to the updated Sydney system. Results-Chemical gastritis was identified in 11 patients taking NSAIDs (9%) and in four controls (5%) (p < 0.05). Helicobacter pylori was detected in 53 patients taking NSAIDs (45%) and in 34 controls (43%). Patients taking NSAIDs had a significantly higher number of erosions and ulcers and worse endoscores than controls. The presence of H pylori did not appear to increase histological damage, ulcer prevalence, or haemorrhagic events. Conclusions-Chemicalgastritis is present in a limited number of patients regularly taking NSAIDs, and is not strongly correlated with NSAID induced damage. In many cases of peptic ulcer or upper gastrointestinal bleeding in patients taking NSAIDs, the presence of chemical gastritis or H pylori infection cannot solely account for the development of mucosal damage. The chronic use of non-steroidal antiinflammatory drugs (NSAIDs) is a common cause of gastroduodenal erosions and peptic ulcers resulting, in many cases, in fatal haemorrhage.
The ability to predict the recurrence risk in breast cancer patients is not available for the individual. It is commonly accepted that the different clinical course of tumours with identical histology and stage are the result of differences at the molecular level. This case study of 80 patients affected by breast cancer looked at the messenger ribonucleic acid expression level of 22 genes, by using quantitative reverse transcriptase-polymerase chain reaction. Our results showed that a panel of seven genes is associated to patients' survival. Moreover, the combination of two couples of genes is able to define short-and longliving cohorts of patients. In particular, our findings strongly demonstrate that retinoblastoma (RB) and cyclindependent kinase 2 (CDK2) on one side and cytokeratin 8 (CK8) and epidermal growth factor receptor 2 (HER2) on the other may affect the clinical course of the disease in 56% of patients. Groups characterised by low RB and high CDK2 as with low CK8 and high HER2 have a higher risk of recurrences and death in 5 years. The identification of these sub-groups of patients with higher risk of early relapse could have further involvement in the selection of the cases to submit to therapy against HER2 or CDK2 as a possible therapy target.
Primary cryptococcal infection is thought to arise in the lungs, whereas secondary lesions may be found anywhere in the body. Because intestinal involvement is rare, especially in nonimmunocompromised patients, little is known about this localization. Nevertheless, the intestinal tract has long been suggested a possible portal of entry of Cryptococcus neoformans, although the hypothesis has never been sufficiently documented. We report an isolated cryptococcosis of the sigmoid colon mimicking an adenomatous polyp. The lesion has an endoscopic interest, being the first of its kind reported in the literature, and a more important pathogenic interest, as it highlights a further pathway of cryptococcal infection, one of major importance in immunocompromised patients.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.