Poster: Gregory Stachelek
Human cancers are often characterized by deficiencies in DNA repair arising either from loss of heterozygosity at DNA repair gene loci or from DNA repair gene silencing.
Poster: Ben Taylor
B. Frazier Taylor, Agnes Keh, Connor Clairmont, and Joann B. Sweasy
Poster: Denise Hegan
3E10 is a cell penetrating non-toxic anti-DNA antibody. We have previously found that 3E10 sensitizes cancer cells to doxorubicin and sensitizes both cancer cells and human tumor xenografts to ionizing radiation. We recently found that 3E10 sensitizes cancer cells to cisplatin as well.
Poster: Ahmed Farouk Salem Abdalla
Radiation therapy often is delivered concurrently with conventional chemotherapy and biologics, which can result in either additive or supra-additive (i.e., synergistic) effects on local tumor control, a phenomenon referred to as radiosensitization.
Poster: Dawit Kidane
/Helicobacter pylori/ infection of the human stomach is associated with disease-causing inflammation that elicits DNA damage in both bacterial and host cells. To investigate base excision repair (BER) as the first line of defense against DNA damage that is induced by bacterial infection,
Poster: Jamie Towle-Weicksel
DNA Polymerase Beta (Pol β) is involved in base excision repair and several variants of Pol β have been identified in numerous cancers. One of these variants is E295K, which was identified in gastric and colon cancers.
Poster: Alireza Senejani
DNA polymerase β (pol β) is known to be a key player in the base excision repair pathway and mice devoid of DNA pol β do not live beyond a few hours after birth. Y265C pol β variant has been shown to be a strong mutator polymerase as well as a slow DNA polymerase.
Poster: Yuhong Lu
Transcriptional silencing of the DNA mismatch repair (MMR) gene, /MLH1,/ is one of the main causes of microsatellite instability in sporadic cancers of the colon and other sites.
Poster: Antonia Nemec
DNA Polymerase β (Pol β) is the main gap-filling polymerase involved in base excision repair (BER), a pathway responsible for the repair of small base lesions in the genome.
Poster: Dorina Saro
FANCM is a Fanconi anemia nuclear core complex protein required for the functional integrity of the FA-BRCA pathway of DNA damage response and repair. FANCM is a highly conserved protein that belongs to the SF2 superfamily of helicases/translocases.
Poster: Simonne Longerich
FANCD2 and 15 other proteins whose deficiency leads to Fanconi anemia (FA) function in a common network to repair crosslinked DNA. DNA damage stimulates monoubiquitination of FANCD2 and FANCI (the ID complex).
Poster: Weixing Zhao
The meiosis-specific Hop2-Mnd1 complex functions in homologous recombination with the RAD51 and DMC1 recombinases. Hop2-Mnd1 stabilizes recombinase filaments formed on ssDNA and promotes the capture of the dsDNA partner by the recombinase filaments to assemble the synaptic complex.
Poster: Drew Murphy
DNA polymerase beta (Pol Beta) is mutated in 40% of colorectal tumors, and these mutations may drive carcinogenesis. This work examines the S229L variant found in our previous study in a Stage 3 tumor. Pol Beta S229L was predicted to be damaging and is 50-fold slower than the wild-type polymera