Search for dissertations about: "homologous recombination HR"
Showing result 16 - 20 of 20 swedish dissertations containing the words homologous recombination HR.
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16. Finding synergies for cancer treatment : new ways to modulate DNA damage repair by CX3CR1 and PFKFB3 inhibition
Abstract : The goal of targeted cancer therapy is to selectively kill cancer cells based on their molecular survival mechanisms. DNA repair is as a promising cancer target as many cancers have chronic replication stress and deficiencies in the DNA damage response. READ MORE
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17. Studies of cohesin functions in the yeast and human DNA damage response
Abstract : Maintaining genome stability is critical to cell survival and normal cell growth and most human cancers display some form of genome instability. Genome instability is caused by multiple reasons and the ability to properly recognize, signal and subsequently repair DNA damages is crucial. READ MORE
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18. Emerging roles of PFKFB3 and CX3CR1 in the DNA damage response and their potential as therapeutic targets in cancer
Abstract : Genomic instability in cancer is exploited therapeutically using DNA damaging therapies that cause irreparable lesions above the threshold of tolerable DNA damage levels. Nevertheless, toxic side effects on healthy tissues limit the therapeutic potential of such therapies. READ MORE
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19. Study of the mechanisms behind the additive effect of neoadjuvant castration on radiotherapy for prostate cancer
Abstract : Castration improves responses to radiotherapy (RT) in prostate cancer with unknown mechanism. An understanding of what happens at the cellular and molecular level in prostate cancer cells, while reducing their access to androgens and then exposing them to ionizing radiation (IR), would give us an opportunity to optimize the treatment and may also inspire novel therapeutic approaches. READ MORE
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20. p53-dependent and -independent mechanisms of p53-targeting small molecules
Abstract : Tumor suppressor p53 (Tp53) is mutated in around half of human cancers, while in wild type p53 cells its activity is continuously inhibited by MDM2 through proteasome degradation resulting in the loss of its function. Currently, cancer treatments with small molecules based on reactivation of wild type p53 and restoration of mutant p53 have moved to clinical trials and exhibited promising anti-cancer effects. READ MORE