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Gene Abnormality clinical trials

View clinical trials related to Gene Abnormality.

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NCT ID: NCT05456048 Completed - Clinical trials for Refractory Acute Myeloid Leukemia

Influence of Molecular Abnormalities on Response of VAH vs. VEN+HMA in RR-AML

Start date: December 3, 2018
Phase:
Study type: Observational

The aim of this study is to reveal the influence of gene mutations on the treatment response of the regimen of HHT combined with Venetoclax plus AZA versus venetoclax plus HMA in the salvage therapy of RR-AML.

NCT ID: NCT05427617 Completed - Clinical trials for Metastatic Breast Cancer

Circulating Tumor DNA (ctDNA)-Guided Late-Line Treatment in Patients With Late-Stage Breast Cancer

ACTDNAGLT
Start date: December 1, 2016
Phase:
Study type: Observational

This is a retrospective, observational, multi-center clinical study of circulating tumor DNA (ctDNA) to guide late-line therapy in late-stage metastatic breast cancer patients.

NCT ID: NCT05079074 Completed - Clinical trials for Metastatic Breast Cancer

Clinical Application of Circulating Tumor DNA (ctDNA) in Patients With Late-stage Breast Cancer

ACTDNA
Start date: December 1, 2016
Phase:
Study type: Observational

This is a retrospective, observational, multi-center clinical study of circulating tumor DNA (ctDNA) application in late-stage breast cancers.

NCT ID: NCT04751058 Completed - Gene Abnormality Clinical Trials

Genetic Profile in Patients With Aortic Syndrome

GEN-AOR
Start date: February 27, 2021
Phase:
Study type: Observational

The overall prevalence has increased significantly in the general population, which may be due in part to advances in diagnostic techniques, such as improved imaging techniques. Aortic dissection (AD) can cause sudden cardiac death (SCD). Approximately 95% of thoracic AAS are clinically "silent" until a life-threatening complication arises in an unpredictable manner and presents as sudden cardiac death. The peak incidence of death caused by aortic dissection occurs within 48 hours, therefore, timely diagnosis is essential and saves lives. We have traditionally associated as risk factors in patients with ASA long-term arterial hypertension, present in 66-75% of cases, smoking, dyslipidemia or atherosclerotic disease. Likewise, any condition that alters the structure of the aorta such as: collagen diseases, aneurysms, bicuspid aorta, and manipulation of the thoracic aorta (cardiac surgery, 18%, or percutaneous intervention that can injure the intima) is involved in ASA. In addition to the well-known hereditary syndromes that affect collagen (Marfan, Elher-Danlos ...) there is a clear familial aggregation: 13-19% of patients without identifiable syndrome have first-degree relatives with thoracic aortic aneurysms or ICD, something that has been called "thoracic aortic dissection and familial aneurysm syndrome." Notable achievements have been made in the discovery of genetic mutations associated with SAA and key regulatory molecules involved, including the extracellular matrix (ECM), cytoskeletal proteins, and the TGF-β signaling pathway. Identification of the causative gene is advantageous for both patients and their families, especially those who do not show symptoms. The specific underlying genotype could benefit the process of diagnosis, surveillance and surgery, with the aim of reducing morbidity and mortality