CARLOS JOSE CARRERA, M.D.
Osteopathic Medicine at Arbor Dr, San Diego, CA

6576420, Jun 10, 2003

Jun 17, 1999

09/335231

Dennis A. Carson - Del Mar CA
Mathias Schmid - Bollingen, DE
Carlos J. Carrera - San Diego CA

Regents of the University of California - Oakland CA

C12Q 168

435 6, 435 912, 435 792, 536 231, 536 241, 536 242, 536 243, 536 2433

The invention provides a method for diagnosis of, and determining a prognosis for, cancer causatively associated with derangements of chromosome 9p21. Underlying the invention is the discovery that such derangements have their genesis in deletions occurring centromeric to STS 3. 21, most often including breakpoints in exon 8 and/or between exons 4 and 5 of the gene which codes for methylthioadenosine phosphorylase. As the cancer and tumor development advance, deletions in 9p21 progress centromerically from the genesis point toward the gene encoding p16. Thus, the method of the invention is performed by determining whether (a) portions of the 9p21 region including and telomeric to STS 3. 21 are deleted; and (b) portions of the 9p21 region centromeric to STS 3. 21 are deleted; wherein a positive finding in step (a) and a negative finding in step(b) are indicative of a cancer in an early stage of tumor development and a positive finding in step (b) is indicative of a cancer in an advanced stage of tumor development.

2003017, Sep 18, 2003

Dec 20, 2002

10/326681

Dennis Carson - Del Mar CA, US
Mathias Schmid - Bollingen, DE
Carlos Carrera - San Diego CA, US

REGENTS OF THE UNIVERSITY OF CALIFORNIA - Oakland CA

C12Q001/68, C07H021/04

435/006000, 536/024300

The invention provides a method for diagnosis of, and determining a prognosis for, cancer causatively associated with derangements of chromosome 9p21. Underlying the invention is the discovery that such derangements have their genesis in deletions occurring centromeric to STS 3.21, most often including breakpoints in exon and/or between exons and of the gene which codes for methylthioadenosine phosphorylase. As the cancer and tumor development advance, deletions in 9p21 progress centromerically from the genesis point toward the gene encoding p16. Thus, the method of the invention is performed by determining whether (a) portions of the 9p21 region including and telomeric to STS 3.21 are deleted; and (b) portions of the 9p21 region centromeric to STS 3.21 are deleted; wherein a positive finding in step (a) and a negative finding in step (b) are indicative of a cancer in an early stage of tumor development and a positive finding in step (b) is indicative of a cancer in an advanced stage of tumor development.

6210917, Apr 3, 2001

Oct 23, 1997

8/956657

Dennis A. Carson - Del Mar CA
Carlos J. Carrera - San Diego CA

The Regents of the University of California - Oakland CA

C12Q 134, C12Q 146

435 18

Methods for treating and preventing the onset and maintainance of multiple drug resistance (MDR) in animals undergoing chemotherapy for cancer are provided. According to the methods, target cells are depleted of adenosine 5'-monophosphate (AMP) and adenosine 5'-triphosphate (ATP) such that the cells are unable to support P-glycoprotein activity. According to one method, a population of target cells is obtained from a host and assayed for loss of methylthioadenosine phosphorylase (MTAse) activity. MTAse catabolizes methylthioadenosine to adenine for endogenous salvage incorporation into the intracellular AMP pool. MTAse deficient cells are treated with a purine synthesis inhibitor, such as L-alanosine, which starves the cells of adenine and suppresses P-glycoprotein activity. MTAse competent cells are also treated for MDR with purine synthesis inhibitors. In conjunction with treatment according to the invention, MTAse competent and deficient cells are also treated for malignancy with other anti-cancer drugs.

6214571, Apr 10, 2001

Nov 24, 1998

9/199137

Carlos J. Carrera - San Diego CA
Dennis A. Carson - Del Mar CA
Howard B. Cottam - Escondido CA
Tsutomu Nobori - Mie, JP

The Regents of the University of California - Oakland CA

C12Q 134, C12Q 142, C12Q 148

435 18

An in vivo method for depleting mammalian cells of adenosine 5'-monophosphate (AMP) useful in the treatment of certain cancers is provided. According to the method, a population of cells is obtained from a host and assayed for loss of methylthioadenosine phosphorylase (MTAse) activity. MTAse catabolizes methylthioadenosine to adenine for endogenous salvage incorporation into the intracellular AMP pool. The preferred method for assaying loss of MTAse activity is a hybridization technique for detection of a homozygous loss of the gene which encodes MTAse. Hosts having MTAse deficient tumors are treated with a therapeutically effective amount of an agent which inhibits the activity of adenylsuccinate synthetase, which converts inosine 5-monophosphate to AMP, thus depleting the tumor cells of substrates for de novo AMP production. L-alanosine is the preferred ASS inhibitory agent for use in the method of the invention.

5541164, Jul 30, 1996

Apr 26, 1994

8/233056

Dennis A. Carson - Del Mar CA
Carlos J. Carrera - San Diego CA

The Scripps Research Institute - La Jolla CA

A61K 3170

514.004600

Novel adenine derivatives whose structures are represented by Formula I, are disclosed, as are methods of using those compounds and others of Formula II to treat monocyte-mediated disorders such as rheumatoid arthritis and multiple sclerosis.

5106837, Apr 21, 1992

Jan 3, 1990

7/460351

Dennis A. Carson - Del Mar CA
Carlos J. Carrera - San Diego CA

The Scripps Research Institute - La Jolla CA

A61K 3170

514 46

Novel adenine derivatives whose structures are represented by Formula I, are disclosed, as are methods of using those compounds and others of Formula II to treat monocyte-mediated disorders and autoimmune diseases.