The evolution of molecular diagnosis using digital polymerase chain reaction to detect cancer via cell-free DNA and circulating tumor cells.

Cancer is one of the most important causes of death worldwide. The onset of cancer may be initiated due to a variety of factors such as environment, genetics or even due to personal lifestyle choices. To counteract this tremendous increase, the demand for a new technology has risen. By this means, the use of digital polymerase chain reaction (dPCR) has been shown to be a promising methodology in the early detection of many types of cancers. Furthermore, several researchers confirmed that the use of tumor cell-free DNA (cfDNA) and circulating tumor cells (CTC) in peripheral blood is essential in revealing an early prognosis of such diseases. Besides this, it was established that dPCR might be used in a much more efficient, accurate, and reliable manner to amplify a variety of genetic material up to the identification of mutations in hematological diseases. Therefore, this article demonstrates the differences between conventional PCR and dPCR as a molecular technique to detect the early onset of cancer. Furthermore, CTC and cfDNA were officially approved by the Food and Drug Administration as new biological biomarkers in cancer development and monitoring.

Adoptive Transfer of Bone Marrow-Derived Monocytes Ameliorates Schistosoma mansoni -Induced Liver Fibrosis in Mice.

Liver diseases are a major health problem worldwide leading to high mortality rates and causing a considerable economic burden in many countries. Cellular therapies as potential treatments for liver diseases have proven beneficial in most of the conditions. In recent years, studies involving therapy with bone marrow cells have been implemented to promote liver regeneration and to reduce hepatic fibrosis, however identifying the cell population present in the bone marrow that is responsible for hepatic improvement after therapy is still necessary. The aim of the present study was the evaluation of the therapeutic efficacy of monocytes obtained from bone marrow in fibrosis resulting from S. mansoni infection in C57BL/6 mice. Monocytes were isolated by immunomagnetic separation and administered to the infected animals. The effects of treatment were evaluated through morphometric, biochemical, immunological and molecular analyzes. Monocyte therapy promoted reduction of liver fibrosis induced by S. mansoni infection, associated with a decrease in production of inflammatory and pro-fibrogenic mediators. In addition, monocyte infusion caused downregulation of factors associated with the M1 activation profile, as well as upregulation of M2reg markers. The findings altogether reinforce the hypothesis that the predominance of M2reg macrophages, producers of immunosuppressive cytokines, may favor the improvement of hepatic fibrosis in a preclinical model, through fibrous tissue remodeling, modulation of the inflammatory response and fibrogenesis.

Acute coronary syndrome: Relationship between genetic variants and TIMI risk.

Acute Coronary Syndrome (ACS) is a multifactorial disease, including the genetic factor, caused by coronary artery obstruction by atheroma. Some genetic variants have been described as risk factors for this disease. Its early diagnosis and stratification of risk of death by Thrombolysis in Myocardial Infarction (TIMI) are important. Therefore, we evaluated variants in the IL6R (c950-1722C>T), TNFa (c.-488G>A), LEPR (c.2673+1118C>T) and IL1b (c.-598T>C) genes in relation to TIMI risk, cytokine serum levels, and risk factors for ACS. We selected 200 patients with ACS, 50 without ACS from the Real Hospital Português, Recife - PE, and 295 blood donors at the Fundação de Hematologia e Hemoterapia de Pernambuco (Hemope). Variants were determined by DNA sequencing or enzymatic cleavage. Cytokine levels were measured by ELISA. The most frequent risk factors found in the patients were dyslipidemia and hypertension, this latter associated with high TIMI risk (p = 0.003). Genotype frequencies of IL6R and TNFa differed between patients with ACS and the blood donors (p = 0.0002 and p = 0.01, respectively), and TNF-α levels differed between genotypes. The TT genotype of the IL6R gene is as a possible protective factor for ACS because it was significantly more present in blood donors (32.2%) than in patients with ACS (18.0%), and was more frequent in low TIMI risk (22.9%) than in the intermediate (20.2%) or high (4.9%). In patients with ACS, the TT genotype in IL6R was related to a lower concentration of c-reactive protein (p = 0.03) and troponin (p = 0.02), showing a less inflammatory reaction and tissue damage. The differences in the frequencies of variants in genes of medical interest among the groups show the importance of studies in specific populations groups to establish the relationship between genes and diseases.