DR. BERT VOGELSTEIN, M.D.
Medical Practice in Baltimore, MD

5330892, Jul 19, 1994

Mar 13, 1991

7/670611

Bert Vogelstein - Baltimore MD
Kenneth W. Kinzler - Baltimore MD
Raymond White - Salt Lake City UT
Yusuke Nakamura - Tokyo, JP

The Johns Hopkins University - Baltimore MD
University of Utah - Salt Lake City UT
The Cancer Institute

C12Q 168, C12P 1934

435 6

A new human gene termed MCC is disclosed. Methods and kits are provided for assessing mutations of the MCC gene in human tissues and body samples. Gross rearrangement and point mutations in MCC are observed in human tumor cells. MCC is expressed in most normal tissues. These results suggest that MCC is a tumor suppressor.

5571905, Nov 5, 1996

Mar 31, 1994

8/220674

Bert Vogelstein - Baltimore MD
Kenneth W. Kinzler - Baltimore MD
Raymond White - Salt Lake City UT
Yusuke Nakamura - Tokyo, JP

The Johns Hopkins University - Baltimore MD
University of Utah - Salt Lake City UT
The Cancer Institute

C07H 2104, C12P 1934, C12Q 168

536 2431

A new human gene termed MCC is disclosed. Methods, primers, probes and kits are provided for assessing mutations of the MCC gene in human tissues and body samples. Gross rearrangement and point mutations in MCC are observed in human tumor cells. MCC is expressed in most normal tissues. These results suggest that MCC is a tumor suppressor.

2012009, Apr 19, 2012

Oct 18, 2011

13/275958

Zhenghe WANG - Baltimore MD, US
Victor VELCULESCU - Dayton MD, US
Kenneth W. KINZLER - Baltimore MD, US
Bert VOGELSTEIN - Baltimore MD, US

THE JOHNS HOPKINS UNIVERSITY - Baltimore MD

A61K 31/7052, C12Q 1/42, A61P 35/00, C12N 15/55, C12N 5/10, C12Q 1/68, C12N 9/16

514 44 R, 435 612, 435 21, 435196, 536 232, 435325, 435375

Tyrosine phosphorylation, regulated by protein tyrosine phosphatases (PTPs) and kinases (PTKs), is important in signaling pathways underlying tumorigenesis. A mutational analysis of the tyrosine phosphatase gene superfamily in human cancers identified 83 somatic mutations in six PTPs (PTPRF, PTPRG, PTPRT, PTPN3, PTPN13, PTPN14), affecting 26% of colorectal cancers and a smaller fraction of lung, breast and gastric cancers. Fifteen mutations were nonsense, frameshift or splice site alterations predicted to result in truncated proteins lacking phosphatase activity. Five missense mutations in the most commonly altered PTP (PTPRT) were biochemically examined and found to reduce phosphatase activity. Expression of wild-type but not a mutant PTPRT in human cancer cells inhibited cell growth. These observations suggest that the tyrosine phosphatase genes are tumor suppressor genes, regulating cellular pathways that may be amenable to therapeutic intervention.

2013029, Nov 7, 2013

Nov 8, 2011

13/884154

Bert Vogelstein - Baltimore MD, US
Kenneth Kinzler - Baltimore MD, US
Nickolas Papadopoulos - Towson MD, US
Donald Williams Parsons - Bellaire TX, US
Rebecca J. Leary - Baltimore MD, US
Meng Li - San Francisco CA, US
Xiaosong Zhang - San Francisco CA, US
Sian Jones - Baltimore MD, US
Gregory J. Riggins - White Hall MD, US
Victor Velculescu - Dayton MD, US

C12Q 1/68

514 44 R, 435 611, 435 71

Medulloblastoma (MB) is the most common malignant brain tumor of children. To identify the genetic alterations in this tumor type, we searched for copy number alterations using high density microarrays and sequenced all known protein-coding genes and miRNA genes using Sanger sequencing. We found that, on average, each tumor had 11 gene alterations, markedly fewer than in common adult cancers. In addition to alterations in the Hedgehog and Wnt pathways, our analysis led to the discovery of genes not previously known to be altered in MBs. Most notably, inactivating mutations of the histone H3K4 trimethylase genes MLL2 or MLL3 were identified in 16% of MB patients. These results demonstrate key differences between the genetic landscapes of adult and childhood cancers, highlight dysregulation of developmental pathways as an important mechanism underlying MBs, and identify a role for a specific type of histone methylation in human tumorigenesis.

5851775, Dec 22, 1998

Mar 20, 1997

8/821355

Nick Barker - Utrecht, NL
Hans Clevers - Ruysdaellaan, NL
Kenneth W. Kinzler - Belair MD
Vladimer Korinek - Prague, CZ
Patrice J. Morin - Columbia MD
Andrew B. Sparks - Baltimore MD
Bert Vogelstein - Baltimore MD

Johns Hopkins University - Baltimore MD
Utrecht University

C12Q 168, G01N 3353

435 6

The APC tumor suppressor protein binds to. beta. -catenin, a protein recently shown to interact with Tcf/Lef transcription factors. Here, the gene encoding a Tcf family member that is expressed in colonic epithelium (hTcf-4) was cloned and characterized. hTcf-4 transactivates transcription only when associated with. beta. -catenin. Nuclei of APC. sup. -/- colon carcinoma cells were found to contain a stable. beta. -catenin-hTCF-4 complex that was constitutively active, as measured by transcription of a Tcf reporter gene. Reintroduction of APC removed. beta. -catenin from hTcf4 and abrogated the transcriptional transactivation. Constitutive transcription of TCF target genes, caused by loss of APC function, may be a crucial event in the early transformation of colonic epithelium. It is also shown here that the products of mutant APC genes found in colorectal tumors are defective in regulating. beta. -catenin/Tcf-4 transcrpitional activation.

6048701, Apr 11, 2000

Sep 9, 1996

8/709784

Kenneth W. Kinzler - BelAir MD
Bert Vogelstein - Baltimore MD
Marilee Burrell - Cambridge MA
David E. Hill - Arlington MA
Fredrick S. Leach - Dallas TX

The Johns Hopkins University - Baltimore MD

G01N 3353

435 71

Antibodies directed to human protein mismatch repair proteins can be used diagnostically to discriminate between proliferating and non-proliferating cells. In addition, they can be used to determine whether cells have a mismatch repair defect caused by a mutation in e. g. , hMSH2, hMLH1, or hPMS2. They can also be used to monitor the efficacy of anti-neoplastic therapies.

6146894, Nov 14, 2000

Apr 14, 1998

9/059461

Nicholas Nicolaides - Boothwyn PA
Bert Vogelstein - Baltimore MD
Kenneth W. Kinzler - BelAir MD

The Johns Hopkins University - Baltimore MD

C12N 1500

435440

Dominant negative alleles of human mismatch repair genes can be used to generate hypermutable cells and organisms. By introducing these genes into cells and transgenic animals, new cell lines and animal varieties with novel and useful properties can be prepared more efficiently than by relying on the natural rate of mutation.

5888735, Mar 30, 1999

Jan 10, 1997

8/781200

Bert Vogelstein - Baltimore MD
Todd Waldman - Bethesda MD
Christoph Lengauer - Columbia MD
Kenneth W. Kinzler - BelAir MD

The Johns Hopkins University - Baltimore MD

C12Q 168

435 6

Checkpoint gene-defective human cells are useful for screening potential anti-tumor agents. Potential therapeutic agents are screened for the ability to cause DNA accumulation or cell death in a checkpoint gene-defective human cell.

5736338, Apr 7, 1998

Feb 17, 1995

8/390517

Marilee Burrell - Cambridge MA
David E. Hill - Arlington MA
Kenneth W. Kinzler - Baltimore MD
Bert Vogelstein - Baltimore MD

The Johns Hopkins University - Baltimore MD

G01N 3353, G01N 33574, C12N 500, C07K 1600

435 71

In certain human tumor cells, the gene encoding MDM2 protein is amplified and expression of MDM2 protein is elevated. Since human MDM2 protein binds to human p53, excess MDM2 protein apparently releases a cell from p53-regulated growth. Detection of elevated amounts of human MDM2 protein thus can be used to diagnose neoplastic disease in a human.

5858976, Jan 12, 1999

Feb 14, 1997

8/801718

Marilee Burrell - Cambridge MA
David E. Hill - Arlington MA
Kenneth W. Kinzler - Baltimore MD
Bert Vogelstein - Baltimore MD

The Johns Hopkins University - Baltimore MD

C07K 14435

514 12

A human gene has been discovered which is genetically altered in human tumor cells. The genetic alteration is gene amplification and leads to a corresponding increase in gene products. Detecting that the gene, designated hMDM2, has become amplified or detecting increased expression of gene products is diagnostic of tumorigenesis. Human MDM2 protein binds to human p53 and allows the cell to escape from p53-regulated growth.