RONI J. BOLLAG, M.D., PH.D.
Medical Practice at 15 St, Augusta, GA

6410508, Jun 25, 2002

Oct 7, 1999

09/414189

Carlos M. Isales - Augusta GA 30909
Roni J. Bollag - Martinez GA 30907
Howard Rasmussen - Augusta GA 30909

A01N 3718

514 2, 514 3, 514 12, 530303, 530308, 4241841, 4241981, 435 691, 435325, 435243

The examples demonstrate that GIP receptor mRNA and protein are present in normal bone and osteoblastic-like cell lines, and that high-affinity receptors for GIP can be demonstrated by I GIP binding studies. When applied to osteoblast-like cells (SaOS2), GIP stimulated an increase in cellular cAMP content and in intracellular calcium, with both responses being dose dependent. Moreover, administration of GIP results in elevated expression of collagen type I mRNA as well as an increase in alkaline phosphatase activity. Both of these effects reflect anabolic actions of presumptive osteoblasts. These results provide the first evidence that GIP receptors are present in bone and osteoblastic like cells and that GIP modulates the function of these cells. GIP has anabolic actions on remodeling bone, increasing vertebral bone density in a rat model of osteoporosis. GIP at 10 nM inhibits PTH-induced bone resorption in a fetal long bone assay and stimulates the synthesis of type 1 collagen mRNA.

6538108, Mar 25, 2003

Mar 10, 1999

09/265503

Robert M. Liskay - Lake Oswego OR
C. Eric Bronner - Portland OR
Sean M. Baker - Berkeley CA
Roni J. Bollag - Martinez GA
Richard D. Kolodner - San Diego CA

Dana-Farber Cancer Institute - Boston MA
Oregon Health Sciences University - Portland OR

C07K 1600

5303871, 5303881, 5303882, 5303891, 5303897, 5303913

Genomic sequences of human mismatch repair genes and gene products are described, as are methods of detecting mutations and/or polymorphisms in those genes. Also described are methods of diagnosing cancer susceptibility in a subject, and methods of identifying and classifying mismatch-repair-defective tumors. In particular, sequences and methods relating to human mutL homologs, hMLH1 and hPMS1 genes and gene products are provided.

5922855, Jul 13, 1999

Mar 8, 1994

8/209521

Robert M. Liskay - Lake Oswego OR
C. Eric Bronner - Portland OR
Sean M. Baker - Portland OR
Roni J. Bollag - Martinez GA
Richard D. Kolodner - Jamaica Plain MA

Oregon Health Sciences University - Portland OR
Dana-Farber Cancer Institute - Boston MA

C07H 2104

536 235

We have discovered two human genes, hMLH1 and hPMS1, each of which apparently encodes for a protein involved in DNA mismatch repair. The hMLH1 gene encodes for a protein which is homologous to the bacterial DNA mismatch repair protein MutL, and is located on human chromosome 3p21. 3-23. We believe that mutations in the hMLH1 gene cause hereditary non-polyposis colon cancer (HNPCC) in some individuals based upon the similarity of the hMLH1 gene product to the yeast DNA mismatch repair protein MLH1, the coincident location of the hMLH1 gene and the HNPCC locus on chromosome 3, and hMLH1 missense mutations in affected individuals from a chromosome 3-linked HNPCC family. The human hPMS1 gene is homologous to the yeast DNA mismatch repair gene PMS1, and is located on human chromosome 7q. We believe that the hPMS1 gene is a strong candidate for HNPCC testing because the yeast proteins MLH1 and PMS1 have been shown to be involved in the same DNA repair pathway and because hMLH1 and hMSH2 have both been implicated in HNPCC families. The most immediate use for hMLH1 and hPMS1 will be in screening tests on individuals who are members of families which exhibit high frequencies of early onset cancer.

6165713, Dec 26, 2000

Oct 31, 1997

8/961810

Robert M. Liskay - Lake Oswego OR
C. Eric Bronner - Portland OR
Sean M. Baker - Portland OR
Roni J. Bollag - Martinez GA
Richard D. Kolodner - Jamaica Plain MA

Oregon Health Sciences University - Portland OR
Dana-Farber Cancer Institute - Boston MA

C12Q 168, C07H 2104, C12P 1934

435 6

Genomic sequences of human mismatch repair genes are described, as are methods of detecting mutations and/or polymorphisms in those genes. Also described are methods of diagnosing cancer susceptibility in a subject, and methods of identifying and classifying mismatch-repair-defective tumors. In particular, sequences and methods relating to human mutL homologs, hMLH1 and hPMS1 genes are provided.

6191268, Feb 20, 2001

Dec 9, 1994

8/352902

Robert M. Liskay - Lake Oswego OR
C. Eric Bronner - Portland OR
Sean M. Baker - Portland OR
Roni J. Bollag - Martinez GA
Richard D. Kolodner - Jamaica Plain MA

Dana-Farber Cancer Institute - Boston MA
Oregon Health Sciences University - Portland OR

C07H 2104

536 235

Genomic sequences of human mismatch repair genes are described, as are methods of detecting mutations and/or polymorphisms in those genes. Also described are methods of diagnosing cancer susceptibility in a subject, and methods of identifying and classifying mismatch-repair-defective tumors. In particular, sequences and methods relating to human mutL homologs, hMLH1 and hPMS1 genes are provided.

2003022, Dec 4, 2003

Jan 22, 2003

10/349607

Robert Liskay - Lake Oswego OR, US
C. Bronner - Portland OR, US
Sean Baker - Berkeley CA, US
Roni Bollag - Martinez GA, US
Richard Kolodner - San Diego CA, US

G01N033/574, C07K016/30

435/007230, 530/388800

Genomic sequences of human mismatch repair genes and gene products are described, as are methods of detecting mutations and/or polymorphisms in those genes. Also described are methods of diagnosing cancer susceptibility in a subject, and methods of identifying and classifying mismatch-repair-defective tumors. In particular, sequences and methods relating to human mutL homologs, hMLH1 and hPMS1 genes and gene products are provided.