Context: Wnt pathway activation represents a critical step in the etiology of most of colorectal cancer (CRC) and it is commonly due to mutations in the APC gene, which originates the loss of β-catenin regulatory function. It has been suggested that APC inactivation or β-catenin alteration have similar effects in tumor progression in CRC tumorigenesis.
Aims: The aim of this study was to analyze the frequency of β-catenin gene mutation in patients with sporadic CRC and to determine its effect in prognosis.
Background: Deviations in the amount of genomic content that arise during tumorigenesis, called copy number alterations, are structural rearrangements that can critically affect gene expression patterns. Additionally, copy number alteration profiles allow insight into cancer discrimination, progression and complexity. On data obtained from high-throughput sequencing, improving quality through GC bias correction and keeping false positives to a minimum help build reliable copy number alteration profiles.
View Article and Find Full Text PDFAim: The aim of the present study was to determine the relation of EPH tyrosine kinase receptor B2 (EPHB2) A9 region mutation and microsatellite instability (MSI); and to analyze their influence in prognosis of patients with sporadic colorectal cancer (CRC).
Patients And Methods: A total of 481 patients with CRC were examined. MSI (NCI criteria) and EPHB2 were analyzed using PCR and fragment analysis software.
Material And Methods: A prospective study was conducted to determine the value of changes in circulating tumour cell (CTC) levels prior to and after the first cycle of neoadjuvant treatment in early prediction of pathologic response in locally advanced breast cancer (LABC). Two blood samples were obtained from 72 eligible LABC patients to isolate and enumerate CTCs before neoadjuvant chemotherapy started on day 1, and on day 21, immediately before second cycle administration.
Results: Sixty patients (83.
Background And Objective: The aim of this study is the detection and quantification of circulating tumor cells (CTC) in patients diagnosed with colon cancer and to establish whether they are related to the main clinicopathologic variables for this type of carcinoma.
Patients And Method: Twenty-five colon cancer patients and 30 healthy volunteers were analysed. The quantification was performed using the CellSpotter Analyzer (Veridex LLC), that allows immunomagnetic isolation and immunospecific labelling of the cells for their enumeration.
Inflammation and platelet activation are critical phenomena in the setting of acute coronary syndromes. Platelets may contribute to increase ischemic injury by enhancing the inflammatory response of leukocytes and endothelial myocardial cells. Pharmacological inhibition of platelet activation prevents ischemic complications in patients with coronary diseases.
View Article and Find Full Text PDFBackground And Objective: Two different pathways for the development of tumor have been described in colorectal carcinoma: the chromosomic instability, raised by suppressor genes and proto-oncogene alterations, and the microsatellite instability (MSI), caused by alterations in DNA repairing genes.
Patients And Method: The frequency and the clinical meaning of the microsatellites instability pathway were determined in a consecutive prospective cohort of 106 patients who underwent surgical resection of colorectal carcinoma by a single surgeon. Microsatellite instability determination was established according to the criteria proposed by the National Cancer Institute in 1998.
The p16INK4a gene, localized within chromosome 9p21, has been identified as a cyclin-dependent kinase inhibitor and may negatively regulate the cell cycle acting as a tumor suppressor. Genetic alterations involving the 9p21 region are common in human cancers. A consecutive series of 64 untreated patients (median of follow up 53 months) undergoing surgical resection for locally advanced laryngeal squamous-cell carcinomas (LSCCs) has been studied prospectively.
View Article and Find Full Text PDFMultiple endocrine neoplasia type 2A (MEN 2A) is associated with specific germline missense mutations in the RET proto-oncogene. This locus encodes a receptor tyrosine kinase whose activation requires the formation of a multimeric receptor complex including GDNF as a ligand and GFR alpha 1 as a coreceptor. In order to explore the role of RET, GFR alpha 1 and GDNF genes in the variation of phenotypes observed in MEN2A families, we analysed germline mutations of these genes in 4 unrelated Spanish MEN2A families (23 cases studied).
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