Identification of a New Complement Factor H Mutation in a Patient With Pregnancy-Related Acute Kidney Injury

n/

FP846EARLY CMV-SPECIFIC T CELL RESPONSE AND EGFR IDENTIFY PATIENTS AT HIGH RISK OF INFECTION AFTER RENAL TRANSPLANTATION

n/

Prevention, Screening, Treatment and Follow-Up of Gynecological Cancers: State of Art and Future Perspectives

Objective: This study aims to analyze the available data on prevention and early diagnosis in gynecological cancers. Mechanism: A comprehensive search was performed in the PubMed (MEDLINE), EMBASE, SCOPUS and Web of Science databases. Findings in Brief: To date the prevention programmes of all degrees exist exclusively for cervical cancer. Human Papilloma Virus (HPV) vaccination prevents from infection and development of precancerous lesions and contributes significantly to the deflection of the incidence of cervical cancer. Screening for HPV-related lesions is worldwide performed by cervical smear (Pap-test) and HPV test. Finally, tertiary prevention is aimed at the treatment of previously diagnosticated lesions with the aid of surgery, chemotherapy, radiotherapy and immunotherapy. Unfortunately, to date the prevention programmes of other gynecological tumors have not reached a good performance; indeed, the primum movens that leads to the development of such neoplasms has not been identified yet. Actually, no screening programs for the early diagnosis of endometrial cancer are available, however, it is recommended the adoption of a healthy lifestyle and a balanced diet. Diagnostic biomarkers would be helpful for screening asymptomatic high-risk women, but histopatological examinations remain the gold standard for diagnosis of endometrial cancer. Similarly, there are no screening tests for the diagnosis of ovarian cancer. In recent years many steps forward have been made in this field and new perspectives have been presented, however, additional investigation is needed to optimize the duration and timing of treatment, examine its cost-effectiveness, and identify potential tumor or host biologic factors predictive of the efficacy and adverse events. Finally, there are no primary and secondary prevention for vulvar cancer so patients should be invited to self-examination and pay attention to the presence of symptoms. Conclusions: Are the available screening programs for the diagnosis of gynecological carcinomas sufficient? The prevention and the diagnosis of precancerous lesions is the goal to be achieved for all gynecological cancers in order to improve patient outcomes, reduce the costs for managing the disease and prolonged follow up

PPARγ ligands as novel agents able to inhibit breast tumor growth and progression

Dottorato di Ricerca in “Biochimica Cellulare ed Attività dei Farmaci in Oncologia” , XXIV Ciclo, a.a. 2010-2011Università della Calabri

Advances on Prevention and Screening of Gynecologic Tumors: Are We Stepping Forward?

According to 2020 comprehensive global cancer statistics published by the International Agency for Research on Cancer, gynecologic malignancies accounted overall for 16 [...]

The role of L1CAM as predictor of poor prognosis in stage I endometrial cancer: a systematic review and meta-analysis

Introduction: Molecular and genomic profiling in endometrial cancer is increasing popularity. L1 cell adhesion molecule (L1CAM) is frequently mutated in endometrial cancer. In this paper, we aim to evaluate the prognostic role of L1CAM in patients with stage I endometrial cancer. Methods: We performed a systematic review and meta-analysis searching in PubMed (MEDLINE), EMBASE, and Web of Science database to identify studies reporting the expression of L1CAM in endometrial cancer. The primary endpoint measure was to assess and evaluate the impact of L1CAM on survival outcomes. This study was performed according to the Preferred Reporting Items for Systematic review and Meta-Analysis Protocols (PRISMA-P) statement. Results: Five studies were included. The pooled results suggested that L1CAM expression influences survival outcomes in stage I endometrial cancer. High L1CAM expression correlated with worse disease-free survival (HR 4.11, 95% CI 1.02-16.59, p = 0.047) and overall survival (HR 3.62, 95% CI 1.32-9.31, p = 0.012). High L1CAM level was also associated with a more aggressive FIGO grade and with older age. Conclusion: This systematic review supported that L1CAM have a prognostic role in stage I endometrial cancer, thus providing a potential useful tool for tailoring the need of adjuvant therapy

Epigallocatechin gallate inhibits growthand epithelial-to-mesenchymal transition in human thyroid carcinoma cell lines.

Well-differentiated papillary and follicular thyroid carcinoma are the most frequent types of thyroid cancer and the prognosis is generally favorable however, a number of patients develops recurrences. Epigallocatechin-3-gallate (EGCG), a major catechin in green tea, was shown to possess remarkable therapeutic potential against various types of human cancers, although data on thyroid cancer cells are still lacking. The aim of this study was to investigate the effect of EGCG on the proliferation and motility of human thyroid papillary (FB-2) and follicular (WRO) carcinoma cell lines. Our results demonstrate that EGCG (10, 40, 60 μM) treatment inhibited the growth of FB-2 and WRO cells in a dose-dependent manner. These changes were associated with reduced cyclin D1, increased p21 and p53 expression. Furthermore, EGCG suppressed phosphorylation of AKT and ERK1/2. In addition EGCG treatment results in reduction of cell motility and migration. Changes in motility and migration in FB-2 were associated with modulation in the expression of several proteins involved in cell adhesion and reorganization of actin cytoskeleton. After 24 h EGCG caused an increase of the E-cadherin expression and a concomitant decrease of SNAIL, ZEB and the basic helix-loop-helix transcription factor TWIST. Besides expression of Vimentin, N-cadherin and α5-integrin was down-regulated. These data well correlate with a reduction of MMP9 activity as evidenced by gelatin zymography. Our findings support the inhibitory role of EGCG on thyroid cancer cell proliferation and motility with concomitant loss of epithelial-to-mesenchymal cell transition markers

Hysterectomy: Let's Step Up the Ladder of Evidence to Look Over the Horizon

Hysterectomy is one of the most common non-obstetric gynecological surgical procedures carried out in Western countries [...]

Hysterectomy: Let’s Step Up the Ladder of Evidence to Look Over the Horizon

Hysterectomy is one of the most common non-obstetric gynecological surgical procedures carried out in Western countries [...

Exposure to Nerve Growth Factor Worsens Nephrotoxic Effect Induced by Cyclosporine A in HK-2 Cells

<div><p>Nerve growth factor is a neurotrophin that promotes cell growth, differentiation, survival and death through two different receptors: TrkA^NTR and p75^NTR. Nerve growth factor serum concentrations increase during many inflammatory and autoimmune diseases, glomerulonephritis, chronic kidney disease, end-stage renal disease and, particularly, in renal transplant. Considering that nerve growth factor exerts beneficial effects in the treatment of major central and peripheral neurodegenerative diseases, skin and corneal ulcers, we asked whether nerve growth factor could also exert a role in Cyclosporine A-induced graft nephrotoxicity. Our hypothesis was raised from basic evidence indicating that Cyclosporine A-inhibition of calcineurin-NFAT pathway increases nerve growth factor expression levels. Therefore, we investigated the involvement of nerve growth factor and its receptors in the damage exerted by Cyclosporine A in tubular renal cells, HK-2. Our results showed that in HK-2 cells combined treatment with Cyclosporine A + nerve growth factor induced a significant reduction in cell vitality concomitant with a down-regulation of Cyclin D1 and up-regulation of p21 levels respect to cells treated with Cyclosporine A alone. Moreover functional experiments showed that the co-treatment significantly up-regulated human p21promoter activity by involvement of the Sp1 transcription factor, whose nuclear content was negatively regulated by activated NFATc1. In addition we observed that the combined exposure to Cyclosporine A + nerve growth factor promoted an up-regulation of p75 ^NTR and its target genes, p53 and BAD leading to the activation of intrinsic apoptosis. Finally, the chemical inhibition of p75^NTR down-regulated the intrinsic apoptotic signal. We describe two new mechanisms by which nerve growth factor promotes growth arrest and apoptosis in tubular renal cells exposed to Cyclosporine A.</p> </div