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Providers > Researchers > Jing Wang
Genomic instability and cancer development: Internal or external insults can cause chromosomal breaks. Incorrect juxtaposition of different pieces of chromosomes during the repair process leads to chromosomal translocation, which can promote cancer. Cancer type-specific translocations are frequently identified in leukemia and lymphomas, and increasingly found in solid tumors. However, the mechanisms underlying the generation and specificity of translocations are poorly understood. Our goal is to understand the molecular mechanisms that promote translocations and cancer development in B lymphocytes. We are investigating how DNA double strand breaks (DSBs) response factors suppress oncogenic translocations. Furthermore, we are elucidating how cancer-type specific translocations are generated at the molecular level, and how mechanistic factors including DSB frequency, spatial proximity of target loci and DNA repair pathways influence translocation frequency and spectrum.
Tumor cells evolve two distinct features, unlimited growth and metastasis, which are the major causes for cancerous patient mortality. Our interests focus on how tumor cells acquire the ability to metastasize. Metastasis is a complicated process that includes multiple steps of tumor cells detaching from primary lesion, entering, circulating and exiting from blood or lymphatic vessels, and eventually localizing and growing in distal organs. We hypothesize that genomic instability induced by an uncharacterized somatic mutation process in cancer cells may lead to oncogene activation, which in turn endows tumor cells with metastatic potential. We are interested in identifying the molecular pathways that initiate the mutational process and contribute to tumor cell metastasis. Our current project is to investigate whether aberrant expression of some cell adhesion molecules in certain types of tumor cells is caused by genomic instability. We are also studying whether and how these cell adhesion molecules function in tumor metastasis.
Molecular mechanism of somatic hypermutation and class switch recombination: In responses to antigen, activated B cells undergo somatic hypermutation (SHM) and class switch recombination (CSR) to enhance antibody diversity and specificity. Both SHM and CSR require activation induced deaminase (AID). AID causes point mutations in the variable regions of the immunoglobulin (Ig) genes. These mutations lead to increased antibody affinity for specific antigens. AID induces DSBs in the repetitive switch regions of the Ig heavy chain locus to mediate CSR. CSR assigns antigen-appropriate effector functions to antibody molecules. We are interested in elucidating the molecular mechanisms that regulate AID targeting specificity and efficiency. Furthermore, AID-initiated DSBs can lead to chromosomal breaks and translocations if they are not properly repaired. Thus, we are also investigating how AID contributes to genomic instability and cancer development in B cells.
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