{"id":18031,"date":"2022-02-16T17:27:35","date_gmt":"2022-02-16T22:27:35","guid":{"rendered":"http:\/\/www.bumc.bu.edu\/ppb\/?post_type=profile&p=18031"},"modified":"2023-09-26T11:11:43","modified_gmt":"2023-09-26T15:11:43","slug":"rachel-litman-flynn-ph-d","status":"publish","type":"profile","link":"https:\/\/www.bumc.bu.edu\/ppb\/profile\/rachel-litman-flynn-ph-d\/","title":{"rendered":"Rachel Litman Flynn, Ph.D."},"content":{"rendered":"

Section of Hematology and Medical Oncology<\/strong><\/span><\/h4>\n

Research Interests<\/h4>\n

The focus of the Laboratory of Genomic Instability and Cancer Therapeutics is to understand the mechanisms regulating mammalian telomere maintenance and to understand how defects in this process contribute to premature aging and cancer progression. \u00a0The hope is that these studies will allow us to gain the mechanistic insight necessary to define novel targets and\/or strategies in the treatment of human disease.<\/p>\n

In my lab we use a combination of biochemical and cell biological approaches to study the function of mammalian telomeres. \u00a0Telomeres cap the ends of linear chromosomes and provide a molecular barrier for the human genome. \u00a0 Following each cell division, progressive telomere shortening erodes that barrier and compromises the stability of the genome. \u00a0Critically short, or dysfunctional telomeres induce replicative senescence and\/or cell death and ultimately, lead to cellular aging. \u00a0Cancer cells, however, overcome the replicative senescence associated with critically short telomeres by exploiting mechanisms of telomere elongation. \u00a0Reactivation of the enzyme telomerase or activation of the Alternative Lengthening of Telomeres (ALT) pathway accounts for cellular immortalization in the majority of all human cancers. \u00a0Clinical trials are currently underway to test the efficacy of telomerase inhibitors in the treatment of telomerase-positive cancers; however, there are no known treatments for ALT-positive cancers. \u00a0By gaining a better mechanistic understanding of how normal telomeres are maintained, and how dysfunctional telomeres bypass replicative senescence, we hope to identify novel therapeutic approaches in the treatment of both premature aging syndromes and cancer.<\/p>\n

Lab Page<\/a><\/span><\/h4>\n

Publications<\/span><\/a><\/h4>\n

Recent News<\/h4>
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