View clinical trials related to Carcinogenesis.
Filter by:In the context of breast cancer, in case of an indication for chemotherapy, anthracycline-based protocols make it possible to improve the overall survival of patients most at risk. The frequency of anthracycline-related cardiac toxicities (ARCT) increases with the cumulative dose of anthracyclines administered and explains, at least in part, the increased risk of cardiovascular (CV) mortality in patient populations treated for breast cancer. The numerous indications for anthracycline-based protocols have made it possible to describe ARCT, among which heart failure with reduced left ventricular ejection fraction (LVEF) remains one of the most comorbid. In addition to left ventricular dysfunction, anthracyclines have been associated with endothelial dysfunction, microvascular damage and myocardial ischemia responsible for dilated cardiomyopathy. Different approaches have attempted to better understand and prevent these ARCT. However, apart from the notion of limit cumulative doses of anthracyclines, few of them have made it possible to screen patients at risk and prevent the onset of cardiac dysfunction. The search for biological markers (Troponin I, BNP) or ultrasound markers (Longitudinal Strain) warning of subclinical cardiac damage is still struggling to assert its interest due in particular to significant inter- and intra-observer variability. Therapeutically, ACE inhibitors and beta-blockers have shown a significant improvement in the incidence rate of LVEF reduction during adjuvant treatment of breast cancer. However, despite equivalent signals in other cancers, the studies conducted to date are insufficiently powered and the role of these treatments is limited to secondary prevention or the treatment of objective heart failure. It remains necessary to determine new biological markers that can identify patients most at risk of ARCT and thus adapt our therapeutic prevention strategies. To do this, it is first necessary to better understand the pathophysiology underlying these ARCT. The objective of this study is to determine whether expression of the receptor among endothelium and circulating cells, SGLT2, is associated with an additional risk of presenting cardiovascular toxicity following treatment with anthracycline. If this association is demonstrated, it will then be possible to better screen and prevent these cardiovascular complications.
The goal of this observational study is to draw the characteristic maps of imaging omics, genomics, transcriptome, proteomics, pathological omics, metabolomics, etc. of the dynamic evolution of endometrial carcinogenesis in 100 patients with normal endometrium, 100 patients with atypical endometrial hyperplasia, and 100 patients with endometrial cancer; and then to explore the underlying molecular mechanism, and establish the database system for the dynamic evolution of endometrial carcinogenesis.
Colo rectal cancer is one of the greatest ,mutual malignancies worldwide ,accounting for an estimated 1.3 million new cases and >500,000 mortality ⁄ year . is the fourth leading cause of cancer-associated mortality worldwide with speedily ,cumulative ,occurrence rate in the worldwide
Cancer is a devastating disease, presenting an immense disease burden to affected individuals and their families as well as health care systems with 10.9 million new cases and 6.7 million deaths per year. Approximately 12% of human cancers worldwide are caused by oncoviruses infection with more than 80% of cases occurring in the developing world. Tumor viruses can be classified into two groups based on their genetic material; 1. DNA tumor viruses: 1. Small DNA tumor viruses (Papilloma viruses, Polyoma viruses and adenoviruses). 2. Complex DNA tumor viruses (Herpes viruses and Hepatitis B viruses). 2. RNA tumor viruses ( Hepatitis C viruses and human T-cell leukemia virus "HTLV"). There are around 100 types of HPV, with different variations in their genetic and oncogenic potential [5]. Thus, HPV genotypes are divided into 2 groups based on their vulnerability; High risk HPV (HR-HPV) and low risk HPV (LR-HPV). The HPV genome encodes several oncoproteins [5]. E6 and E7 are the main genes responsible for cell transformation mediated by HR-HPV, and they modulate the activities of cellular proteins that regulate the cell cycle. Thus, the presence of E6/E7 can be a specific marker for diagnosing precancerous lesions by HPV. Knowledge of the etiology of virus-mediated carcinogenesis, the networking of pathways involved in the transition from infection to cancer and the risk factors associated with each type of cancer, all suggest prophylactic and therapeutic strategies that may reduce the risk of virus-mediated cancer.
To clarify the critical role of glycosyltransferases, altered Mucins, and RTKs in human ovarian and endometrial neoplasms, the study will examine the immunohistochemical expression profiles of glycosyltransferases, Mucins and receptor tyrosin kinases (RTKs) family in various stages and/or histologic subtypes of human ovarian and endometrial neoplasms and tissue microarrays.