JAMES RICHARD ESHLEMAN
Medical Practice in Lutherville Timonium, MD

2012011, May 10, 2012

Sep 3, 2009

13/060453

Bert Vogelstein - Baltimore MD, US
Kenneth W. Kinzler - Baltimore MD, US
D. Williams Parsons - Ellicott City MD, US
Sian Jones - Baltimore MD, US
Xiaosong Zhang - Baltimore MD, US
Jimmy Cheng-Ho Lin - Baltimore MD, US
Rebecca J. Leary - Baltimore MD, US
Philipp Angenendt - Hamburg, DE
Nickolas Papadopoulos - Towson MD, US
Victor Velculescu - Dayton MD, US
Giovanni Parmigiani - Brookline MA, US
Rachel Karchin - Towson MD, US
Scott Kern - Hunt Valley MD, US
Ralph Hruban - Baltimore MD, US
James R. Eshleman - Lutherville MD, US
Michael Goggins - Baltimore MD, US
Alison Klein - Baltimore MD, US

THE JOHNS HOPKINS UNIVERSITY - Baltimore MD

C12Q 1/68, C40B 20/00, C07H 21/04

506 2, 435 611, 536 2431, 536 2433

There are currently few therapeutic options for patients with pancreatic cancers and new insights into the pathogenesis of this lethal disease are urgently needed. To this end, we performed a comprehensive analysis of the genes altered in 24 pancreatic tumors. First, we determined the sequences of 23,781 transcripts, representing 20,583 protein-encoding genes, in DNA from these tumors. Second, we searched for homozygous deletions and amplifications using microarrays querying ˜one million single nucleotide polymorphisms in each sample. Third, we analyzed the transcriptomes of the same samples using SAGE and next-generation sequencing-by-synthesis technologies. We found that pancreatic cancers contain an average of 63 genetic alterations, of which 49 are point mutations, 8 are homozygous deletions, and 6 are amplifications. Further analyses revealed a core set of 12 regulatory processes or pathways that were each genetically altered in 70% to 100% of the samples. The data suggest that dysregulation of this core set of pathways is responsible for the major features of pancreatic tumorigenesis.

2012013, May 31, 2012

Sep 28, 2011

13/247366

James R. Eshleman - Lutherville MD, US
Antony R. Parker - Eastbourne, GB

C12N 5/02, C07H 21/04

435375, 536 245

An oligonucleotide based therapeutic strategy, called anti-gene locks, is described which specifically kills cells based on their genotype. The strategy employs oligonucleotides with arms and a backbone that are complementary to both strands of the gene target. Anti-gene locks bind in vitro in a sequence dependent fashion and inhibit DNA synthesis. In bacterial cells containing an episome target, they cause elimination of the extra-chromosomal DNA structure. When the target is present in the bacterial or human genome, they selectively kill the majority of these cells.

2003021, Nov 27, 2003

Nov 8, 2002

10/291205

James Eshleman - Lutherville MD, US
Kathleen Murphy - Baltimore MD, US

C12Q001/68, G06F019/00, G01N033/48, G01N033/50

435/006000, 702/020000

Methods for the simultaneous sequencing of multiple nucleic acid molecules are provided. Preferred methods include simultaneous single-direction sequencing of multiple genes or forward and reverse sequencing from a single gene, within a single reaction vessel. Additional methods of the invention include combined amplification and sequencing of nucleic acids, from a variety of sources, within a single reaction and wherein nucleic acid products also can be simultaneously analyzed, and where the reaction can be either bidirectional or long unidirectional. Additional methods encompass combined amplification and sequencing of multiple nucleic acid molecules simultaneously.

2006011, May 25, 2006

Feb 24, 2003

10/505308

James Eshleman - Lutherville MD, US
Antony Parker - Eastbourne, GB

The John Hopkins University - Baltimore MD

A61K 48/00

514044000

An oligonucleotide based therapeutic strategy, called anti-gene locks, is described which specifically kills cells based on their genotype. The strategy employs oligonucleotides with arms and a backbone that are complementary to both strands of the gene target. Anti-gene locks bind in vitro in a sequence dependent fashion and inhibit DNA synthesis. In bacterial cells containing an episome target, they cause elimination of the extra-chromosomal DNA structure. When the target is present in the bacterial or human genome, they selectively kill the majority of these cells.

2007017, Aug 2, 2007

Mar 22, 2005

10/590541

James Eshleman - Lutherville MD, US
Chanjuan Shi - Lutherville MD, US
Susan Eshleman - Lutherville MD, US

C12Q 1/70, C12Q 1/68

435005000, 435006000

The invention provides methods permitting the detection of small amounts of different nucleic acids in the presence of an excess amount of wild-type nucleic acids. Also provided herein are method so detecting infectious disease minority variants, methods of forensic identification, methods of diagnosing cancer and monitoring disease progress.

2012003, Feb 9, 2012

Mar 5, 2010

13/254610

Bert Vogelstein - Baltimore MD, US
Kenneth W. Kinzler - Baltimore MD, US
D. Williams Parsons - Ellicott City MD, US
Sian Jones - Baltimore MD, US
Scott Kern - Hunt Valley MD, US
Ralph Hruban - Baltimore MD, US
James R. Eshleman - Lutherville MD, US
Michael Goggins - Baltimore MD, US
Alison Klein - Baltimore MD, US
Manuel Hidalgo - Baltimore MD, US
Victor E. Velculescu - Dayton MD, US

THE JOHNS HOPKINS UNIVERSITY - Baltimore MD

A61K 33/24, A61P 35/00, C40B 20/08, G01N 33/577, G01N 33/566, C12Q 1/68

424649, 435 723, 435 612, 435 611, 506 6

The present invention provides a method for detecting mutations in the PALB2 gene in pancreatic cancer patients and in individuals having a family history of pancreatic cancer. Methods are also provided for diagnosing a predisposition to pancreatic cancer, for predicting a patient's response to pancreatic cancer therapies, and for treating pancreatic cancer, based on presence of a PALB2 mutation or abberant PALB2 gene expression in a patient.