General Information


The International A-T Workshops have been held every few years since 1980. The meeting is unique in that it focuses comprehensively on the various facets of A-T, the disease, and ATM function. Meetings have been located in different parts of the world and organized by volunteers from those locations. This serves to recognize their leadership in A-T/ATM research and allows local young investigators to attend and participate who might otherwise not have that opportunity.

Previous International A-T Workshops

Sussex, England, USA    November 5-7, 1980
Solvang, California, USA January 16-20,1984
Newport Beach, California, USA February 22-24,1987
Newport Beach, California, USA May 21-24,1989
Newport Beach, California, USA May 17-20,1992
Birmingham, England March 22-25,1994
Clermont-Ferrand, France   November 22-24,1997
Las Vegas, Nevada, USA February 14-17, 1999
Fraser Island, Queensland, Australia September 10-14, 2003
Belgirate, Lago Maggiore, Italy  June 8-11, 2005
Banff, Alberta, Canada  September 8-12, 2006
Kyoto, Japan April 22-26, 2008

The objectives of ATW2010 are to bring together basic and clinical researchers working on various aspects of the clinical and cellular phenotypes of ATM/atm-deficient models, the role of ATM in neural differentiation, development and pathology, and the DNA damage response, in a comprehensive and stimulating atmosphere that will promote scientific interactions, discussions and cross-disciplinary research collaborations. Our goal is to ultimately arrive at a treatment for A-T that is based on better understanding of the pathogenesis of ATM protein deficiency and to generalize the lessons learned from A-T to the broader areas of other inherited neurological disorders, cancer risk and treatment. Specific areas of focus of the meeting will include the role of ATM in the nervous system, mechanisms of neurodegeneration, the role of other DNA damage proteins in neuropathology, in breast and other human cancers, and the development of new drugs that can correct the specific types of mutations that cause A-T. This will also be the first International A-T Workshop at which a discussion of the logistics of possible clinical trials for A-T can be justified.


The meeting will start on the evening of April 11th (Sunday) with a keynote lecture. All presentations, oral and posters, will take place in the Crowne Plaza Hotel. The hall has seating for 250 people with seating for an additional 100. The venue has excellent audiovisual facilities and a highly efficient staff, who will be in attendance during all sessions. A room will be set aside for speaker preparations. Introductory presentations will be approximately 30 minutes, with most other talks limited to 15 minutes. Each presentation will be followed by 5 minutes of question and answers, and each session will end with a 10-minute general discussion, guided by Focus Topics introduced by each Session Chair. This format will allow for 40-50 oral presentations, largely depending on how the Chairs plan their sessions.

Attendance will be limited to ~250 attendees. Through the generosity of various donors, we are able to provide support for a limited number of participants including Organizing Committee members, Session Chairs/Organizers, Invited Speakers, A-T Clinicians, and Major Sponsors. Other attendees will be charged a registration fee of $500 (Faculty) or $200 (Trainees). These fees help to support meeting costs, including travel and lodging expenses for speakers and poster presenters, conference room and poster board rentals, audiovisual services, printing of abstracts and programs, and some on-site meals. We hope to also waive registration fees for Poster Presenters.

Ataxia-telangiectasia (A-T) is a rare autosomal recessive disorder that affects approximately 1 in 40,000 to 1 in 100,000 live births. All races, as well as religious and ethnic groups are affected. A-T is characterized by progressive cerebellar ataxia, telangiectasia, immunodeficiency, chromosomal instability, radiation sensitivity and increased incidence of lymphoid malignancies. Symptoms of A-T usually manifest in the first few years of life when children exhibit wobbly gait. Loss of neuromuscular control is progressive and, by ten years of age, children are usually confined to a wheel chair. A-T patients usually succumb to infection, pulmonary failure, and/or lymphoid cancer. There are currently no established treatments for the disorder. It has been estimated that 1-6% of the general population carries mutations in one allele of the ATM (ataxia-telangiectasia mutated) gene and that these ATM heterozygotes also have an increased risk of developing breast cancer. The ATM gene encodes a large (369 kDa) serine/threonine kinase, with hundreds of phosphorylation substrates. Cells that lack ATM are highly sensitive to agents, such as ionizing radiation (IR), that produce DNA double strand breaks and are defective in the activation of multiple cell cycle checkpoints in response to such DNA damage. Many other cellular processes are affected, including apoptosis, nonsense mediated decay, oxidative stress responses, mitochondrial function, as well as the development and differentiation of lymphoid and neural cells. Since the discovery of the gene in 1995, it has become apparent that ATM plays a critical role in regulating the cellular response to many DNA damaging agents besides ionizing radiation. It is also now clear that the A-T syndrome provides a prototypic phenotype for diseases of DNA processing and repair of double strand breaks- i.e., such patients share the common features of neurological problems, cancer predisposition, immunodeficiency, and radiosensitivity.

We encourage all interested investigators to submit an abstract by January 15, 2010. We regret that we cannot cover the costs of all participants but everyone is welcome. We hope that your visit to California will be enjoyable and rewarding.

-The Organizers

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