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Richard A. Gatti, MD


Richard Gatti, MD

UCLA Physician Richard Gatti, MD specializes in Anatomic Pathology & Clinical Pathology.
Preferred Name
Richard A. Gatti
Anatomic Pathology & Clinical Pathology
Language Spoken
English, Italian
Hospital Affiliation
Ronald Reagan UCLA Medical Center
State License Number
(310) 825-7618 Information and referral
(310) 825-7200 Lab
Fax Number
(310) 825-7618
Email Address

UCLA Pathology & Lab Medicine
10833 Le Conte Ave, 13-188 CHS
Los Angeles, CA 90095

Pediatrics, American Board of Pediatrics, 1970
Tumor Biology, Karolinska Institutet, 1972 - 1974
Clinical Immunology & Immunogenetics, University of Minnesota Medical School, 1968 - 1972
Pediatrics, Children's Memorial Medical Center, 1963 - 1966
Pediatrics, Children's Memorial Medical Center, 1962 - 1963
MD, St. Louis University School of Medicine, 1962
Research Interest
molecular genetics, cancer genetics, immunology, DNA repair
Additional Information

Gatti is interested in translational research, including both the development of diagnostic assays and finding new drugs to treat genetic disorders. His research focuses on DNA repair disorders, using ataxia-telangiectsia (A-T) as the primary working model. The lab collaborates with investigators in many other countries. Ongoing projects include: 1) identification of genes that cause hypersensitivity to ionizing radiation, 2) identification of chemicals that correct the effects of specific types of mutations in the ATM gene, 3) better diagnostic assays for A-T, and 4) identification of chemicals that might be useful in combating a "dirty bomb" attack in a major city. The Gatti lab was the first at UCLA to localize a gene to a particular chromosome by linkage analysis (1988). This was the gene for A-T. An international consortium was then formed to fine map the region of interest on chromosome 11q22-23. Seven years later the Israeli members of the consortium successfully cloned the ATM gene from within this region. The ATM protein is a serine/threonine kinase that phosphorylates over 700 substrates, impacting primarily on cell cycle checkpoints and DNA repair signaling cascades. These findings have accounted for the pleiotropic A-T syndrome, which includes cancer susceptibility, radiation sensitivity, immunodeficiency, a progressive loss of balance, and specific chromosome translocations. The lab identifies ~30 new A-T patientsper year, and has characterized the majority of the ~700 unique ATM mutations (www.LOVD.nl/ATM). The team is now trying to characterize drugs that induce the expression of full length, functional ATM protein in A-T cells lacking the protein due to nonsense-type mutations and in others that carry splicing mutations. A novel high throughput screen was developed and ~70,000 chemicals were tested to identify small molecule readtrhrough (SMRT) compounds. These drugs promise to impact upon the treatment of most genetic diseases and perhaps upon cancer-prone individuals as well. The lab has the largest repository of cell lines from A-T patients, an important resource for these ongoing studies.

More Information
Diagnostic Testing Information


Link to my PubMed publications.

Recent publications include: Lange et al. Localization of an ataxia-telangiectasia gene to a ~500 kb interval on chromosome 11q23.1: linkage analysis of 176 families in an international consortium. Amer J Hum Genet 57: 112-119, 1995. Savitsky et al. A single ataxia telangiectasia gene with a product similar to PI-3 kinase. Science 268: 1749-1753, 1995. [Accompanying Research News article by R. Nowak: Discovery of AT gene sparks biomedical research bonanza. Science 268: 1700-1701, 1995.] Pan-Hammarstrom et al. ATM is not required in somatic hypermutation of VH, but is involved in the introduction of mutations in the switch u region. J. Immunol. 170:3707-3716, 2003 Lai et al. Correction of ATM gene function by aminoglycoside-induced readthrough of premature termination codons. Proc Natl Acad Sci.101: 15676-81, 2004. Birrell et al. ATM mutations, haplotype analysis, and immunological status of Russian patients with ataxia telangiectasia. Hum Mutation 25: 593m 2005. Nahas et al. Post-irradiation phosphorylation of structural maintenance chromosome 1 (SMC1) is independent of the Fanconi protein pathway. Intl J Rad Oncol Biol. Physics 61: 1167-72, 2005. Cavalieri et al. ATM mutations in Italian families with ataxia-telangiectasia include two distinct large genomic deletiions. Hum Mutation 27:1061-71, 2006 Du L, Pollard J, Gatti RA. Correction of prototypic ATM splicing mutation and aberrant ATM function with antisense morpholino oligonucleotides. PNAS 104: 6007-6012, 2007.

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