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Prevalence and implications of elevated microsatellite alterations at selected tetranucleotides in cancer.

Watson MM, Berg M, Søreide K - Br. J. Cancer (2014)

Bottom Line: Because it is often associated with advanced stages of malignancy, EMAST may be a consequence of rapid cell proliferation and increased mutagenesis.At various tumour sites, EMAST and high-frequency MSI share no clinicopathological features or molecular mechanisms, suggesting their existence as separate entities.In particular, the potential use of EMAST in prognosis and prediction may yield novel types of therapeutic intervention, particularly those involving the immune system.

View Article: PubMed Central - PubMed

Affiliation: 1] Department of Gastrointestinal Surgery, Stavanger University Hospital, Stavanger 4068, Norway [2] Gastrointestinal Surgical Research Unit, Molecular Lab, Hillevåg, Stavanger University Hospital, Stavanger 4068, Norway.

ABSTRACT
Elevated microsatellite alterations at selected tetranucleotides (EMAST), a variation of microsatellite instability (MSI), has been reported in a variety of malignancies (e.g., neoplasias of the lung, head and neck, colorectal region, skin, urinary tract and reproductive organs). EMAST is more prominent at organ sites with potential external exposure to carcinogens (e.g., head, neck, lung, urinary bladder and colon), although the specific molecular mechanisms leading to EMAST remain elusive. Because it is often associated with advanced stages of malignancy, EMAST may be a consequence of rapid cell proliferation and increased mutagenesis. Moreover, defects in DNA mismatch repair enzyme complexes, TP53 mutation status and peritumoural inflammation involving T cells have been described in EMAST tumours. At various tumour sites, EMAST and high-frequency MSI share no clinicopathological features or molecular mechanisms, suggesting their existence as separate entities. Thus EMAST should be explored, because its presence in human cells may reflect both increased risk and the potential for early detection. In particular, the potential use of EMAST in prognosis and prediction may yield novel types of therapeutic intervention, particularly those involving the immune system. This review will summarise the current information concerning EMAST in cancer to highlight the knowledge gaps that require further research.

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Prevalence and main observed features of EMAST in human solid cancers.
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fig1: Prevalence and main observed features of EMAST in human solid cancers.

Mentions: EMAST has been reported in several cancers of solid organs (Figure 1), including the colorectum (Haugen et al, 2008; Devaraj et al, 2010; Lee et al, 2010; Lee et al, 2012), lungs (Ahrendt et al, 2000; Xu et al, 2001; Arai et al, 2013), ovaries (Singer et al, 2004), bladder (Xu et al, 2001; Danaee et al, 2002; Catto et al, 2003; Burger et al, 2006a), prostate (Perinchery et al, 2000; Burger et al, 2006b; Azzouzi et al, 2007), kidney (Xu et al, 2001; Catto et al, 2003), head and neck (Xu et al, 2001; Temam et al, 2004), non-melanoma skin (Danaee et al, 2002) and uterus (Choi et al, 2008). The estimated prevalence of EMAST according to previously reported studies is presented in Table 1. In fact, the reported prevalence and relationship between EMAST and clinicopathological features and molecular mechanisms vary considerably across tumour sites (Figure 1).


Prevalence and implications of elevated microsatellite alterations at selected tetranucleotides in cancer.

Watson MM, Berg M, Søreide K - Br. J. Cancer (2014)

Prevalence and main observed features of EMAST in human solid cancers.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4150258&req=5

fig1: Prevalence and main observed features of EMAST in human solid cancers.
Mentions: EMAST has been reported in several cancers of solid organs (Figure 1), including the colorectum (Haugen et al, 2008; Devaraj et al, 2010; Lee et al, 2010; Lee et al, 2012), lungs (Ahrendt et al, 2000; Xu et al, 2001; Arai et al, 2013), ovaries (Singer et al, 2004), bladder (Xu et al, 2001; Danaee et al, 2002; Catto et al, 2003; Burger et al, 2006a), prostate (Perinchery et al, 2000; Burger et al, 2006b; Azzouzi et al, 2007), kidney (Xu et al, 2001; Catto et al, 2003), head and neck (Xu et al, 2001; Temam et al, 2004), non-melanoma skin (Danaee et al, 2002) and uterus (Choi et al, 2008). The estimated prevalence of EMAST according to previously reported studies is presented in Table 1. In fact, the reported prevalence and relationship between EMAST and clinicopathological features and molecular mechanisms vary considerably across tumour sites (Figure 1).

Bottom Line: Because it is often associated with advanced stages of malignancy, EMAST may be a consequence of rapid cell proliferation and increased mutagenesis.At various tumour sites, EMAST and high-frequency MSI share no clinicopathological features or molecular mechanisms, suggesting their existence as separate entities.In particular, the potential use of EMAST in prognosis and prediction may yield novel types of therapeutic intervention, particularly those involving the immune system.

View Article: PubMed Central - PubMed

Affiliation: 1] Department of Gastrointestinal Surgery, Stavanger University Hospital, Stavanger 4068, Norway [2] Gastrointestinal Surgical Research Unit, Molecular Lab, Hillevåg, Stavanger University Hospital, Stavanger 4068, Norway.

ABSTRACT
Elevated microsatellite alterations at selected tetranucleotides (EMAST), a variation of microsatellite instability (MSI), has been reported in a variety of malignancies (e.g., neoplasias of the lung, head and neck, colorectal region, skin, urinary tract and reproductive organs). EMAST is more prominent at organ sites with potential external exposure to carcinogens (e.g., head, neck, lung, urinary bladder and colon), although the specific molecular mechanisms leading to EMAST remain elusive. Because it is often associated with advanced stages of malignancy, EMAST may be a consequence of rapid cell proliferation and increased mutagenesis. Moreover, defects in DNA mismatch repair enzyme complexes, TP53 mutation status and peritumoural inflammation involving T cells have been described in EMAST tumours. At various tumour sites, EMAST and high-frequency MSI share no clinicopathological features or molecular mechanisms, suggesting their existence as separate entities. Thus EMAST should be explored, because its presence in human cells may reflect both increased risk and the potential for early detection. In particular, the potential use of EMAST in prognosis and prediction may yield novel types of therapeutic intervention, particularly those involving the immune system. This review will summarise the current information concerning EMAST in cancer to highlight the knowledge gaps that require further research.

Show MeSH
Related in: MedlinePlus