The 1st international conference on drug design and discovery

Ingvarsson, S. (Participant)

Faculty of Medicine

Activity: Participating in or organising an event › Organising a conference, workshop, ...

Period	4 Feb 2008 → 8 Feb 2008
Event type	Conference
Location	Dubai, United Arab EmiratesShow on map
Degree of Recognition	International

Documents & Links

Dubai2008
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Ingvarsson2008Dubai
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Dubai2008ChairInvitation
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The ICDDD 2008 was the first major international conference and exhibition of this series, which aimed to present cutting edge advances in various disciplines of drug design and discovery that have been recently achieved. Over 400 leading industrial and academic experts presented their findings in the form of lectures and poster presentations at this four-day conference. The ICDDD 2008 offered an in-depth assessment of the challenges involved in the dynamic and fast moving field of drug discovery and development. It brought together leading chemists, pharmacologists, biotechnologists, and other allied professionals to discuss and present the latest important developments in drug design and discovery. The major topics of discussion related to drug design and discovery included: Cancer; Cardiovascular Diseases; CNS; Pharmacogenomics; Protein & Peptides; Inflammation & Allergy; Drug Delivery & Safety; Drug Discovery Informatics; Drug Metabolism; Medicinal and Combinatorial Chemistry; Nanotechnology; Emerging Biomarkers & Drug Targets; Case Studies of Successful Drug Discovery and Development. Dubai, the host city, is the region's business and tourism centre which is connected to all international markets. The city is also famous as the regional trading hub and gateway to the rest of the Middle East. The visitors coming to Dubai can enjoy a whole range of different experiences which includes elements of adventure, contrast, discovery and surprise. Dubai World Trade Center, the venue of the conference, offers a comprehensive range of facilities catering to all types of meetings and major international conventions.
https://icddt.com/2008/
https://icddt.com/2008/sciprog.htm
https://icddt.com/2008/conprog.htm
The presence of numerical and structural chromosome aberrations is a common characteristic of tumor cells. Accumulation of these aberrations leads to dramatic changes within the genome. These changes have tumor type and stage specific pattern of segmental losses and gains, resulting in gene losses and gene copy number imbalances. Tumor development and progression is driven by sequential acquisition of specific gene alterations, and chromosome aberrations contribute to these processes. Genomic instability in tumors can be classified as chromosome instability (CIN) and microsatellite instability (MIN). MIN is in general less frequent in tumors than CIN, but is rather frequent in some tumors of the digestive tract. This is mainly due to germline mutations in mismatch repair genes associated with the HNPCC cancer syndrome, but can also be due to somatic mutations and epigenetic mechanism. While MIN is rare in breast tumors, CIN is demonstrated in the majority of breast tumors (about 70%) by aneuploidy, deletions, amplifications and rearrangements. Although the reasons for CIN in breast tumors are not well understood, explanations can partly be obtained from deficient control of genes controlling cell proliferation, apoptosis, DNA repair or chromosome segregation. Among these genes are TP53, MYC, AURKA, BRCA1 and BRCA2. TP53 is relatively well studied and is believed to be a guardian of genome integrity. Myc seems to affect tumor pathogenesis in several ways, including increased proliferation and immortalization of the cancer cells and induction of CIN. The STK15 gene encodes the aurora A kinase, which has been shown to bind to centrosomes and is important in controlling their number and the segregation of correct chromosomes to the daughter cells during mitosis. Genomic instability is high in some hereditary breast cancer, particularly in tumors of BRCA1 and BRCA2 mutation carriers, a finding which is in line with the role of the gene products in DNA repair. Some recent developments in drug therapy are based on molecular and genomic findings about breast cancer pathogenesis. Defects in checkpoint control generate CIN and are believed to facilitate tumorigenesis, but additional disabling of checkpoint signaling is a possible anticancer strategy.
https://icddt.com/2008/confAbstractssss.htm
https://icddt.com/2008/authIndex.htm