Surface Enhanced Raman Spectroscopy (SERS) for the Multiplex Detection of Braf, Kras, and Pik3ca Mutations in Plasma of Colorectal Cancer Patients.
Adult; Female; Humans; Male; Middle Aged; Aged; *colorectal cancer; *gene; *mutation; *Mutation; *PCR; *surface enhanced Raman scattering; Class I Phosphatidylinositol 3-Kinases/blood/*genetics; Cluster Analysis; Colorectal Neoplasms/blood/*diagnosis/genetics/pathology; DNA Primers/chemistry; Exons; Multiplex Polymerase Chain Reaction/methods/standards; Neoplasm Staging; Proto-Oncogene Proteins B-raf/blood/*genetics; Proto-Oncogene Proteins p21(ras)/blood/*genetics; Biomarkers; Spectrum Analysis; Raman/methods/*standards; Tumor/blood/*genetics
In this paper, we discuss the use of a procedure based on polymerase chain reaction (PCR) and surface enhanced Raman spectroscopy (SERS) (PCR-SERS) to detect DNA mutations. Methods: This method was implemented by first amplifying
Li Xiaozhou; Yang Tianyue; Li Caesar Siqi; Song Youtao; Lou Hong; Guan Dagang; Jin Lili
Theranostics
2018
1905-07
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.7150/thno.22502" target="_blank" rel="noreferrer noopener">10.7150/thno.22502</a>
A splicing mutation in the cytochrome b5 gene from a patient with congenital methemoglobinemia and pseudohermaphrodism.
*DNA; *Mutation; Base Sequence; Cytochromes b5/*genetics; Disorders of Sex Development/*enzymology/genetics; DNA Primers/chemistry; Gene Deletion; Humans; Leukocytes/metabolism; Male; Messenger/metabolism; Methemoglobinemia/*congenital/*enzymology; Molecular Sequence Data; Polymerase Chain Reaction; Recombinant; Reticulocytes/metabolism; RNA
We have analyzed reticulocyte and leukocyte mRNAs isolated from a patient with congenital methemoglobinemia and pseudohermaphrodism. The cytochrome b5 cDNA sequences were amplified using specific oligonucleotide primers and the polymerase chain reaction (PCR). DNA sequencing indicated that there was a 16-bp deletion in the cDNA leading to a new, in-frame stop signal and resulting in a truncated protein of 45 amino acids. Genomic DNA was analyzed, and the molecular lesion was shown to be an AG–\textgreaterGG alteration in the 3' splicing junction of intron 1. The splice site alteration leads to the usage of the nearest AG as an alternative splice site, resulting in a 16-bp deletion in the mRNA. All of the studies on reticulocyte mRNA and genomic DNA indicated that the patient was homozygous for the lesion.
Giordano S J; Kaftory A; Steggles A W
Human genetics
1994
1994-05
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1007/bf00202825" target="_blank" rel="noreferrer noopener">10.1007/bf00202825</a>