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:
Feb. 28, 2017

Filed:

May. 23, 2006
Applicants:

Donald William Parsons, Ellicott City, MD (US);

Tian-li Wang, Baltimore, MD (US);

Yardena Samuels, Baltimore, MD (US);

Alberto Bardelli, Turin, IT;

Christopher Lengauer, Noisy-le-Roi, FR;

Victor Velculescu, Dayton, MD (US);

Kenneth W. Kinzler, Bel Air, MD (US);

Bert Vogelstein, Baltimore, MD (US);

Inventors:

Donald William Parsons, Ellicott City, MD (US);

Tian-li Wang, Baltimore, MD (US);

Yardena Samuels, Baltimore, MD (US);

Alberto Bardelli, Turin, IT;

Christopher Lengauer, Noisy-le-Roi, FR;

Victor Velculescu, Dayton, MD (US);

Kenneth W. Kinzler, Bel Air, MD (US);

Bert Vogelstein, Baltimore, MD (US);

Assignee:

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

Attorney:
Primary Examiner:
Int. Cl.
CPC ...
C12Q 1/62 (2006.01); G01N 33/574 (2006.01); C07K 16/40 (2006.01); C12Q 1/68 (2006.01); C12Q 1/48 (2006.01); G01N 33/50 (2006.01);
U.S. Cl.
CPC ...
C12Q 1/6883 (2013.01); C12Q 1/485 (2013.01); G01N 33/5044 (2013.01); G01N 33/57419 (2013.01); C12Q 2600/136 (2013.01); C12Q 2600/156 (2013.01);
Abstract

Given the important role of protein kinases in pathways affecting cellular growth and invasion, we have analyzed 340 serine/threonine kinases for genetic mutations in colorectal cancers. Mutations in eight genes were identified, including three members of the phosphatidylinositol-3-kinase (PI3K) pathway; the alterations in the latter genes each occurred in different tumors and did not overlap with mutations in PIK3CA or other non-serine-threonine kinase (STK) members of the PI3K pathway, suggesting that mutations in any of these genes had equivalent tumorigenic effects. These data demonstrate that the PI3K pathway is a major target for mutational activation in colorectal cancers and provide new opportunities for therapeutic intervention.


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