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.

Date of Patent:
May. 22, 2018

Filed:

Jun. 22, 2012
Applicants:

Bert Vogelstein, Baltimore, MD (US);

Kenneth W. Kinzler, Baltimore, MD (US);

Jian Wu, Baltimore, MD (US);

Luis Diaz, Ellicott City, MD (US);

Nickolas Papadopoulos, Towson, MD (US);

Hanno Matthaei, Bonn, DE;

Ralph Hruban, Baltimore, MD (US);

Anirban Maitra, Baltimore, MD (US);

Inventors:

Bert Vogelstein, Baltimore, MD (US);

Kenneth W. Kinzler, Baltimore, MD (US);

Jian Wu, Baltimore, MD (US);

Luis Diaz, Ellicott City, MD (US);

Nickolas Papadopoulos, Towson, MD (US);

Hanno Matthaei, Bonn, DE;

Ralph Hruban, Baltimore, MD (US);

Anirban Maitra, Baltimore, MD (US);

Assignee:

The Johns Hopkins University, Baltimore, MD (US);

Attorney:
Primary Examiner:
Int. Cl.
CPC ...
C12Q 1/68 (2018.01); C12P 19/34 (2006.01);
U.S. Cl.
CPC ...
C12Q 1/6886 (2013.01); C12Q 2600/112 (2013.01); C12Q 2600/156 (2013.01);
Abstract

To help reveal the pathogenesis of these lesions, we purified the DNA from Intraductal Papillary Mucinous Neoplasm (IPMN) cyst fluids from 19 patients and searched for mutations in 169 genes commonly altered in human cancers. We identified recurrent mutations at codon 201 of GNAS. We found that GNAS mutations were present in 66% of IPMNs and that either KRAS or GNAS mutations could be identified in 96%. In eight cases, we could investigate invasive adenocarcinomas that developed in association with IPMNs containing GNAS mutations. In seven of these eight cases, the GNAS mutations present in the IPMNs were also found in the invasive lesion. GNAS mutations were not found in other types of cystic neoplasms of the pancreas or in invasive adenocarcinomas not associated with IPMNs. These data suggest that GNAS mutations can inform the diagnosis and management of patients with cystic pancreatic lesions.


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