@article {zhang_beta-interferon_2015,
	title = {Beta-interferon exposure and onset of secondary progressive multiple sclerosis},
	journal = {European Journal of Neurology},
	volume = {22},
	number = {6},
	year = {2015},
	pages = {990{\textendash}1000},
	abstract = {<p>Background and purpose Beta-interferons (IFNβ) are the most widely prescribed drugs for patients with multiple sclerosis (MS). However, whether or not treatment with IFNβ can delay secondary progressive MS (SPMS) onset remains unknown. Our aim was to examine the association between IFNβ exposure and SPMS onset in patients with relapsing-remitting MS (RRMS). Methods A retrospective cohort study using British Columbia (Canada) population-based clinical and health administrative data (1985{\textendash}2008) was conducted. RRMS patients treated with IFNβ (n\&nbsp;=\&nbsp;794) were compared with untreated contemporary (n\&nbsp;=\&nbsp;933) and historical (n\&nbsp;=\&nbsp;837) controls. Cohort entry was the first clinic visit during which patients became eligible for IFNβ treatment (baseline). The outcome was time from baseline to SPMS onset. Cox regression models with IFNβ as a time-dependent exposure were adjusted for sex, and baseline age, disease duration, disability, *socioeconomic status and *comorbidities (*available for the contemporary cohorts only). Additional analyses included propensity score adjustment. Results The median follow-up for the IFNβ-treated, untreated contemporary and historical controls were 5.7, 3.7 and 7.3\&nbsp;years, and the proportions of patients reaching SPMS were 9.2\%, 11.8\% and 32.9\%, respectively. After adjustment for confounders, IFNβ exposure was not associated with the risk of reaching SPMS when either the contemporary or the historical untreated cohorts were considered (hazard ratio 1.07; 95\% confidence interval 0.93{\textendash}1.48, and hazard ratio 1.04; 95\% confidence interval 0.74{\textendash}1.46, respectively). Further adjustments and the propensity score yielded results consistent with the main analysis. Conclusions Amongst patients with RRMS, use of IFNβ was not associated with a delayed onset of SPMS.</p>
},
	keywords = {beta-interferon, cohort study, multiple sclerosis, progression},
	doi = {10.1111/ene.12698},
	url = {http://onlinelibrary.wiley.com/doi/10.1111/ene.12698/abstract},
	author = {Zhang, T and Shirani, A and Zhao, Y and Karim, ME and Gustafson, P and Petkau, J and Evans, C and Kingwell, E and van der Kop, M and Zhu, F and Oger, J and Tremlett, H and BC MS Clinic Neurologists}
}
@article {poh_unique_2012,
	title = {Unique FISH Patterns Associated with Cancer Progression of Oral Dysplasia},
	journal = {Journal of Dental Research},
	volume = {91},
	number = {1},
	year = {2012},
	month = {jan},
	pages = {52{\textendash}57},
	abstract = {Subgroups of patients with oral pre-malignant lesions (OPLs) are at extremely high risk for developing invasive cancer in spite of surgical excision. The objective of this study was to evaluate the utility of specific genes and their associated centromeres as markers to stratify OPLs for their cancer risk. Samples used in this study included 35 oral dysplasia with known outcome and 20 normal oral mucosa. Of the dysplasias, 20 were from an ongoing longitudinal study showing progression. The remaining 15 cases (2 of which progressed) were chosen from the population-based, provincial BC Oral Biopsy Service (OBS). Copy number alterations at EGFR, CEP7, CCND1, and CEP11 were evaluated by fluorescent in situ hybridization (FISH). There was no significant difference in demographics between progressors and non-progressors. Specific FISH profiles at these genes and their corresponding centromeres were associated with progression. High gene gain of CCND1 was associated with an 8-fold elevated risk of progression compared with those with no gain in time-to-progression analysis. Numerical alterations of EGFR and CCND1 and their centromeres might be an effective means for identifying OPLs at risk. Future studies will expand on this analysis and set the stage for application of this approach in routine clinical practice.},
	keywords = {CCND1, chromosomal instability, EGFR, fluorescent in situ hybridization, oral dysplasia, progression},
	issn = {0022-0345, 1544-0591},
	doi = {10.1177/0022034511425676},
	url = {http://jdr.sagepub.com/content/91/1/52},
	author = {Poh, C. F. and Zhu, Y. and Chen, E. and Berean, K. W. and Wu, L. and Zhang, L. and Rosin, M. P.}
}
