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Articles by J MacLeod
Total Records ( 2 ) for J MacLeod
  J Tang , S Le , L Sun , X Yan , M Zhang , J MacLeod , B LeRoy , N Northrup , A Ellis , T. J Yeatman , Y Liang , M. E Zwick and S. Zhao
 

Human colorectal cancer (CRC) is one of the better-understood systems for studying the genetics of cancer initiation and progression. To develop a cross-species comparison strategy for identifying CRC causative gene or genomic alterations, we performed array comparative genomic hybridization (aCGH) to investigate copy number abnormalities (CNAs), one of the most prominent lesion types reported for human CRCs, in 10 spontaneously occurring canine CRCs. The results revealed for the first time a strong degree of genetic homology between sporadic canine and human CRCs. First, we saw that between 5% and 22% of the canine genome was amplified/deleted in these tumors, and that, reminiscent of human CRCs, the total altered sequences directly correlated to the tumor's progression stage, origin, and likely microsatellite instability status. Second, when mapping the identified CNAs onto syntenic regions of the human genome, we noted that the canine orthologs of genes participating in known human CRC pathways were recurrently disrupted, indicating that these pathways might be altered in the canine CRCs as well. Last, we observed a significant overlapping of CNAs between human and canine tumors, and tumors from the two species were clustered according to the tumor subtypes but not the species. Significantly, compared with the shared CNAs, we found that species-specific (especially human-specific) CNAs localize to evolutionarily unstable regions that harbor more segmental duplications and interspecies genomic rearrangement breakpoints. These findings indicate that CNAs recurrent between human and dog CRCs may have a higher probability of being cancer-causative, compared with CNAs found in one species only.

  M Hickman , V Hope , B Coleman , J Parry , M Telfer , J Twigger , C Irish , J Macleod and H. Annett
  Background

We report on an exercise to estimate the prevalence of injecting drug use (IDU) and associated harms in a single primary care trust.

Methods

Covariate capture–recapture methods to estimate (i) IDU prevalence; respondent driven sampling to measure (ii) prevalence of HCV and HIV and record linkage to measure (iii) mortality risk.

Results

(i) The overall estimated number of IDU was 5540 (95% confidence interval, CI: 4710–6780) for all cases and 3280 (95% CI: 1940–4610) for cases matched to primary care register, i.e. a prevalence of 2.2 and 1.3% aged 15–54, respectively. (ii) The prevalence of HCV, hepatitis B and HIV was: 53, 32 and 0.7%. Over 70% of IDU in Bristol reported having at least one vaccination for HBV; more than half of those who were HCV positive were undiagnosed. (iii) The all-cause and overdose mortality rates for IDU were 0.75 and 0.4% respectively; and the standardized mortality ratio was 7.8 (95% CI: 5.4–10.8).

Conclusion

Locally specific and useful intelligence on injecting and its health consequence can be generated to inform local public health action, and may contribute information to validate national prevalence estimates.

 
 
 
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