Thirty per cent of all colorectal tumours develop in the rectum. The location of the rectum within the bony pelvis and its proximity to vital structures presents significant therapeutic challenges when considering neoadjuvant options and surgical interventions. Most patients with early rectal cancer can be adequately managed by surgery alone. However, a significant proportion of patients with rectal cancer present with locally advanced disease and will potentially benefit from down staging prior to surgery. Neoadjuvant therapy involves a variety of options including radiotherapy, chemotherapy used alone or in combination. Neoadjuvant radiotherapy in rectal cancer has been shown to be effective in reducing tumour burden in advance of curative surgery. The gold standard surgical rectal cancer management aims to achieve surgical removal of the tumour and all draining lymph nodes, within an intact mesorectal package, in order to minimise local recurrence. It is critically important that all rectal cancer cases are discussed at a multidisciplinary meeting represented by all relevant specialties. Pre-operative staging including CT thorax, abdomen, pelvis to assess for distal disease and magnetic resonance imaging to assess local involvement is essential. Staging radiology and MDT discussion are integral in identifying patients who require neoadjuvant radiotherapy. While Neoadjuvant radiotherapy is potentially beneficial it may also result in morbidity and thus should be reserved for those patients who are at a high risk of local failure, which includes patients with nodal involvement, extramural venous invasion and threatened circumferential margin. The aim of this review is to discuss the role of neoadjuvant radiotherapy in the management of rectal cancer.

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Using microarray analysis of pretreatment FFPE rectal cancer tissues, we identified for the first time a group of miRNA predictors of response to neoadjuvant CRT. This, indeed, can lead to a significant improvement in patient selection criteria and personalized rectal cancer management.

Hepatitis C virus (HCV) infection is the main cause of parenteral non-A, non-B hepatitis. 1-5 HCV consists of a heterogeneous mix of isolates defined by genotype, each of which is further classified into subtypes. A number of factors have been identified as important in predicting the outcome of disease progression. These include age at infection, viral type/subtype, viral load, quasispecies, and mode of infection. [6][7][8][9][10] Clinical heterogeneity in disease progression may reflect either viral heterogeneity or variations in host response. However, the fluctuations in viral load during the natural history of hepatitis C infection are poorly understood. The purpose of the present study was to determine if viral load remains at a steady state or is in dynamic flux during the course of an HCV infection. To avoid heterogeneity of risk factors and confounding variables in viral type/subtype, we studied a unique cohort of individuals all infected by anti-D/ blood product from a single source of HCV 1b. The sole source of the infectious agent was identified as HCV 1b-contaminated anti-D immunoglobulin. The contaminating HCV 1b was derived from a single donor. [11][12][13] The patients were of similar ethnogeographic background and had an absence of other risk factors for liver disease.Serum HCV RNA can be quantitated by a range of different technologies (reverse transcription-polymerase chain reaction [RT-PCR], RT-PCR coupled to different signal amplification systems such as colorimetric assays, and the branched chain technology). [14][15][16][17][18][19][20] The level of sensitivity achieved by the more recent versions of these technologies has improved qualitative assessment of HCV serum status. Clinically relevant sensitivities of 100 viral genomes per mL of serum are now readily achievable.The work reported here used the Roche Monitor system for amplification of the HCV. The high degree of reproducible quantification of viral load and a uniform linear range of amplification between the different versions of the Roche HCV Monitor assays for HCV of genotype 1b provide a means in which quantifications over several generations of assays are suitable for longitudinal studies. In addition, amplification of HCV genotype 1b by the Monitor system does not suffer from the reported difficulties associated with other genotypes. 21