Biography

Allister Fagg completed a Bachelor of Biomedical Science (Honours Class I) at the University of Queensland in 2015. He completed his Honours year under the supervision of Dr Patricia Carreira and Prof Geoff Faulkner in the Genome Plasticity and Disease group. His research focused on LINE-1 retrotransposition in Ovarian Cancer. Allister now works as a Research Assistant in the laboratory.
Research Links:
Publications:
2018 |
Nguyen, Thu H M; Carreira, Patricia E; Sanchez-Luque, Francisco J; Schauer, Stephanie N; Fagg, Allister C; Richardson, Sandra R; Davies, Claire M; Jesuadian, Samuel J; Kempen, Marie-Jeanne H C; Troskie, Robin-Lee; James, Cini; Beaven, Elizabeth A; Wallis, Tristan P; Coward, Jermaine I G; Chetty, Naven P; Crandon, Alexander J; Venter, Deon J; Armes, Jane E; Perrin, Lewis C; Hooper, John D; Ewing, Adam D; Upton, Kyle R; Faulkner, Geoffrey J L1 Retrotransposon Heterogeneity in Ovarian Tumor Cell Evolution (Journal Article) Cell Reports, 23 (13), pp. 3730–3740, 2018, ISSN: 2211-1247. @article{nguyen_l1_2018, title = {L1 Retrotransposon Heterogeneity in Ovarian Tumor Cell Evolution}, author = {Thu H M Nguyen and Patricia E Carreira and Francisco J Sanchez-Luque and Stephanie N Schauer and Allister C Fagg and Sandra R Richardson and Claire M Davies and Samuel J Jesuadian and Marie-Jeanne H C Kempen and Robin-Lee Troskie and Cini James and Elizabeth A Beaven and Tristan P Wallis and Jermaine I G Coward and Naven P Chetty and Alexander J Crandon and Deon J Venter and Jane E Armes and Lewis C Perrin and John D Hooper and Adam D Ewing and Kyle R Upton and Geoffrey J Faulkner}, url = {http://www.sciencedirect.com/science/article/pii/S2211124718308714}, doi = {10.1016/j.celrep.2018.05.090}, issn = {2211-1247}, year = {2018}, date = {2018-06-01}, urldate = {2018-08-28}, journal = {Cell Reports}, volume = {23}, number = {13}, pages = {3730--3740}, abstract = {Summary LINE-1 (L1) retrotransposons are a source of insertional mutagenesis in tumor cells. However, the clinical significance of L1 mobilization during tumorigenesis remains unclear. Here, we applied retrotransposon capture sequencing (RC-seq) to multiple single-cell clones isolated from five ovarian cancer cell lines and HeLa cells and detected endogenous L1 retrotransposition in vitro. We then applied RC-seq to ovarian tumor and matched blood samples from 19 patients and identified 88 tumor-specific L1 insertions. In one tumor, an intronic de novo L1 insertion supplied a novel cis-enhancer to the putative chemoresistance gene STC1. Notably, the tumor subclone carrying the STC1 L1 mutation increased in prevalence after chemotherapy, further increasing STC1 expression. We also identified hypomethylated donor L1s responsible for new L1 insertions in tumors and cultivated cancer cells. These congruent in vitro and in vivo results highlight L1 insertional mutagenesis as a common component of ovarian tumorigenesis and cancer genome heterogeneity.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Summary LINE-1 (L1) retrotransposons are a source of insertional mutagenesis in tumor cells. However, the clinical significance of L1 mobilization during tumorigenesis remains unclear. Here, we applied retrotransposon capture sequencing (RC-seq) to multiple single-cell clones isolated from five ovarian cancer cell lines and HeLa cells and detected endogenous L1 retrotransposition in vitro. We then applied RC-seq to ovarian tumor and matched blood samples from 19 patients and identified 88 tumor-specific L1 insertions. In one tumor, an intronic de novo L1 insertion supplied a novel cis-enhancer to the putative chemoresistance gene STC1. Notably, the tumor subclone carrying the STC1 L1 mutation increased in prevalence after chemotherapy, further increasing STC1 expression. We also identified hypomethylated donor L1s responsible for new L1 insertions in tumors and cultivated cancer cells. These congruent in vitro and in vivo results highlight L1 insertional mutagenesis as a common component of ovarian tumorigenesis and cancer genome heterogeneity. |
2016 |
Carreira, Patricia E; Ewing, Adam D; Li, Guibo; Schauer, Stephanie N; Upton, Kyle R; Fagg, Allister C; Morell, Santiago; Kindlova, Michaela; Gerdes, Patricia; Richardson, Sandra R; Li, Bo; Gerhardt, Daniel J; Wang, Jun; Brennan, Paul M; Faulkner, Geoffrey J Evidence for L1-associated DNA rearrangements and negligible L1 retrotransposition in glioblastoma multiforme (Journal Article) Mob. DNA, 7 (1), pp. 21, 2016. @article{Carreira2016-vr, title = {Evidence for L1-associated DNA rearrangements and negligible L1 retrotransposition in glioblastoma multiforme}, author = {Patricia E Carreira and Adam D Ewing and Guibo Li and Stephanie N Schauer and Kyle R Upton and Allister C Fagg and Santiago Morell and Michaela Kindlova and Patricia Gerdes and Sandra R Richardson and Bo Li and Daniel J Gerhardt and Jun Wang and Paul M Brennan and Geoffrey J Faulkner}, url = {http://dx.doi.org/10.1186/s13100-016-0076-6}, year = {2016}, date = {2016-01-01}, journal = {Mob. DNA}, volume = {7}, number = {1}, pages = {21}, abstract = {LINE-1 (L1) retrotransposons are a notable endogenous source of mutagenesis in mammals. Notably, cancer cells can support unusual L1 retrotransposition and L1-associated sequence rearrangement mechanisms following DNA damage. Recent reports suggest that L1 is mobile in epithelial tumours and neural cells but, paradoxically, not in brain cancers.}, keywords = {}, pubstate = {published}, tppubtype = {article} } LINE-1 (L1) retrotransposons are a notable endogenous source of mutagenesis in mammals. Notably, cancer cells can support unusual L1 retrotransposition and L1-associated sequence rearrangement mechanisms following DNA damage. Recent reports suggest that L1 is mobile in epithelial tumours and neural cells but, paradoxically, not in brain cancers. |
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