The patent badge is an abbreviated version of the USPTO patent document. The patent badge does contain a link to the full patent document.
The patent badge is an abbreviated version of the USPTO patent document. The patent badge covers the following: Patent number, Date patent was issued, Date patent was filed, Title of the patent, Applicant, Inventor, Assignee, Attorney firm, Primary examiner, Assistant examiner, CPCs, and Abstract. The patent badge does contain a link to the full patent document (in Adobe Acrobat format, aka pdf). To download or print any patent click here.
Patent No.:
Date of Patent:
Apr. 14, 2020
Filed:
Dec. 07, 2017
The Johns Hopkins University, Baltimore, MD (US);
Duke University, Durham, NC (US);
Bert Vogelstein, Baltimore, MD (US);
Kenneth W. Kinzler, Baltimore, MD (US);
Chetan Bettegowda, Baltimore, MD (US);
Nishant Agrawal, Baltimore, MD (US);
Nickolas Papadopoulos, Towson, MD (US);
Darell Bigner, Mebane, NC (US);
Hai Yan, Chapel Hill, NC (US);
Roger McLendon, Durham, NC (US);
The Johns Hopkins University, Baltimore, MD (US);
Duke University, Durham, NC (US);
Abstract
Oligodendrogliomas are the second most common malignant brain tumor in adults. These tumors often contain a chromosomal abnormality involving a pericentromeric fusion of chromosomes 1 and 19, resulting in losses of the entire short arm of the former and the long arm of the latter. To identify the molecular genetic basis for this alteration, we performed exomic sequencing of seven anaplastic oligodendrogliomas with chromosome 1p and 19q losses. Among other changes, we found that that CIC (homolog of thegene capicua) on chromosome 19q was somatically mutated in six of the seven cases and that FUBP1 (far upstream element (FUSE) binding protein) on chromosome 1p was somatically mutated in two of the seven cases. Examination of 27 additional oligodendrogliomas revealed 12 and 3 more tumors with mutations of CIC and FUBP1, respectively, 58% of which were predicted to result in truncations of the encoded proteins. These results suggest a critical role for these genes in the biology and pathology of oligodendrocytes.