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“Determination Of Aurora A Amplification In Colon Cancer By Copy Number Pcr As A Biomarker Of Resistance To Chemotherapy”.

2062 words - 9 pages

Chromosomal instability is a central feature of many tumours and is present in about 85% of colorectal tumours. It is characterised predominantly by frequent chromosomal abnormalities which include translocations, gains, and losses of entire chromosomes or their segments [Grady, 2004; Baba, 2009]. Although the causes of chromosomal instability are still poorly understood it is thought to arise as a result of mutation and amplification of a number of genes including Aurora-A, encoding a serine-threonine kinase. This enzyme is an important regulatory protein involved in mitotic entry, bipolar spindle morphology, centrosome maturation and segregation and regulation of the G2-M transition during ...view middle of the document...

al, 2004; Cammareri et. al, 2010]. With regard to the prophetic role of Aurora-A, its over-expression causes aberrations to bipolar spindle checkpoint formation, thus inducing the cells to become resistant to chemotherapeutic agents such nocodazole, paclitaxel and docetaxol [Santini et. al, 2007; Shimomura et. al, 2007]. The development therefore of small-molecule inhibitors or RNA-mediated interface to knockdown expression of Aurora-A may make it possible to reduce the oncogenic activity of Aurora-A and in addition improve the survival of oncological patients showing resistance to chemotherapeutic agents.

In colorectal cancer, Aurora-A over-expression and amplification have frequently been observed and may therefore provide implications for prognosis/ clinical outcome. It still remains controversial whether the Aurora-A expression levels correlate with malignant phenotype or patient prognosis, with the findings of a number of studies presenting inconsistent data. A recent study by Liang et. al [2012] investigated the expression of Aurora-A in chondrosarcoma tissues by immunohistochemisty and reported patients positively expressing Aurora kinase A had a relatively poor prognosis in comparison to negatively expressing patients via survival analysis. Furthermore, a group led by Nadler et. al [2008] assessed the expression of Aurora-A in breast tumour tissues by AQUA and found that high Aurora-A expression was associated with reduced breast cancer-specific survival within the entire cohort. Moreover, independent studies conducted by Sakakura et. al [2001], Sen et. al [2002] and Landen et. al [2007] evaluating the over-expression of Aurora-A in primary gastric, bladder and ovarian carcinoma tumour cell lines respectively both showed similar findings, reporting that patients who over-expressed Aurora-A had dramatically reduced overall survival compared with patients whose tumours did not overexpress Aurora-A (via Kaplan-Meier analysis). Furthermore, Ogawa et. al [2008] assessed Aurora-A expression in 189 resected non-small-cell lung cancer tissue (NSCLC) and found that patients positively expressing perimembrane Aurora-A showed the poorest postoperative survival, indicating perimembrane Aurora-A status was a significant factor to predict poor prognosis in correlation with increased activation in NSCLC. Recent studies into Aurora-A over-expression in colorectal cancer development have also helped to elucidate its association with high grade tumour and tumour progression. A study by Zhang et. al [2010] collected 134 colorectal adenocarcinoma samples with matched adjacent tissues from a Chinese population and demonstrated a significant increase of DNA copy number gains of Aurora-A in advanced colorectal cancer compared to early stage colorectal cancer. Moreover, this study suggested that copy number gains contributes to colorectal cancer progression and therefore may play a role in tumour aggressiveness. In addition, the group lead by Park et. al...

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