Clinical laboratory science : journal of the American Society for Medical Technology | Year: 2011
Some clinical laboratories require workers who have basic knowledge in molecular techniques (such as fluorescent in situ hybridization and polymerase chain reaction). Exclusively molecular diagnostic laboratories need workers to be competent in a variety of cutting edge molecular technologies, such as DNA sequencing, array-based comparative genomic hybridization, quantitative polymerase chain reaction, and many other techniques. Having only one certification for molecular biology at the entry level, as newly prescribed by the Board of Certification, doesn't accurately define the two very differently trained types of people these differing types of laboratories require. Creating a second molecular certification, at the specialist level, would address this issue positively.
Hu P.C.,University of Houston |
Hegde M.R.,Emory University |
Modern Clinical Molecular Techniques | Year: 2012
This timely book covers the need to know clinical practices for all those involved in molecular laboratory science. The field of molecular medicine is evolving at an astounding speed. Propelled by the new insights and technologies, advances are being made at an unprecedented rate. With dual measure given to today's breakthroughs, this book is a collection of the most current practices relevant to the clinical molecular laboratorian. It begins with an introductory section on techniques and procedure. It then presents four separate sections on infectious disease, oncology, pre/post-natal, and identity testing, with specific chapters clearly outlining clinical protocols used in daily practice. Modern Clinical Molecular Techniques cuts to the heart of what is essential for the practicing molecular laboratory scientist. It is an outstanding resource for those operating within or looking to set up a clinical molecular laboratory. © 2012 Springer Science+Business Media, LLC. All rights reserved.
Policarpio-Nicolas M.L.C.,University of Texas Health Science Center at San Antonio |
Avery D.L.,PathGroup |
Hartley T.,University of Texas Health Science Center at San Antonio
CytoJournal | Year: 2015
The most common site of metastasis to ascitic fluid in females is from a mullerian (ovarian) primary, whereas in males it is from the gastrointestinal tract. Metastatic Merkel cell carcinoma (MCC) to the ascitic fluid is extremely rare and may present as a diagnostic challenge on effusion cytology. In a review of the literature, there are only two case reports of metastatic MCC in pleural effusion. To the best of our knowledge, we present the first cytological diagnosis of MCC metastatic to the ascitic fluid. We describe the cytologic findings as well as the immunohistochemical stains supportive of the diagnosis. Given the fatal prognosis of this tumor compared to melanoma and rarity of its occurrence in ascitic fluid, awareness of this tumor and use of immunohistochemical stains are critical in arriving at the diagnosis.
Ramirez E.,University of Texas M. D. Anderson Cancer Center |
Singh R.R.,University of Texas M. D. Anderson Cancer Center |
Kunkalla K.,University of Texas M. D. Anderson Cancer Center |
Liu Y.,University of Texas M. D. Anderson Cancer Center |
And 11 more authors.
Leukemia Research | Year: 2012
Hedgehog (Hh) signaling pathway is activated in diffuse large B-cell lymphoma (DLBCL). Genetic abnormalities that explain activation of Hh signaling in DLBCL are unknown. We investigate the presence of amplifications of Hh genes that might result in activation of this pathway in DLBCL. Our data showed few extra copies of GLI1 and SMO due to chromosomal aneuploidies in a subset of DLBCL cell lines. We also showed that pharmacologic inhibition of PI3K/AKT and NF-κB pathways resulted in decreased expression of GLI1 and Hh ligands. In conclusion, our data support the hypothesis that aberrant activation of Hh signaling in DLBCL mainly results from integration of deregulated oncogenic signaling inputs converging into Hh signaling. © 2012 Elsevier Ltd.
Bhaskara S.,Vanderbilt University |
Knutson S.K.,Vanderbilt University |
Jiang G.,Vanderbilt University |
Chandrasekharan M.B.,Vanderbilt University |
And 16 more authors.
Cancer Cell | Year: 2010
Hdac3 is essential for efficient DNA replication and DNA damage control. Deletion of Hdac3 impaired DNA repair and greatly reduced chromatin compaction and heterochromatin content. These defects corresponded to increases in histone H3K9,K14ac; H4K5ac; and H4K12ac in late S phase of the cell cycle, and histone deposition marks were retained in quiescent Hdac3-null cells. Liver-specific deletion of Hdac3 culminated in hepatocellular carcinoma. Whereas HDAC3 expression was downregulated in only a small number of human liver cancers, the mRNA levels of the HDAC3 cofactor NCOR1 were reduced in one-third of these cases. siRNA targeting of NCOR1 and SMRT (NCOR2) increased H4K5ac and caused DNA damage, indicating that the HDAC3/NCOR/SMRT axis is critical for maintaining chromatin structure and genomic stability. © 2010 Elsevier Inc.