LOH at 3p correlates with a poor survival in oral squamous cell carcinoma

Partridge, M; Emilion, G; Langdon, John H.

doi:10.1038/bjc.1996.62

Cited by 67 publications

(48 citation statements)

References 10 publications

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“…The existence of a putative tumor suppressor gene masked by allelic deletions is suggested by the correspondence of LOH with clinicopathological factors. LOH on 3p was reported to correlate with poor survival in lung and oral cancer (Mitsudomi et al 1996;Partridge et al 1996). These findings suggest a tumor suppressor gene on 3p involved in the development of several types of tumor.…”

Section: Introductionmentioning

confidence: 52%

Frequent loss of heterozygosity at 3p25-p26 is associated with invasive oral squamous cell carcinoma

et al. 2001

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Recent molecular evidence suggests that allelic deletions of chromosomes are involved in the carcinogenesis of various neoplasms, including oral squamous cell carcinoma (OSCC). To determine the role of 3p deletions in Japanese OSCC and to define the localization of putative tumor suppressor genes, we initially examined loss of heterozygosity (LOH), using nine microsatellite markers in 36 OSCCs and 28 oral epithelial dysplastic lesions (OEDLs). LOH on chromosome 3p was observed at one or more loci in 72% of OSCCs and 18% of OEDLs. Fourteen (61%) of 23 OSCC patients informative at D3S2450 (3pter-p24.2) showed LOH most frequently, in contrast to OEDL, where LOH was never seen at this locus. Interestingly, we found a significant association between an allelic deletion at this locus and the histologic grade of mode of tumor invasion. Therefore, we also examined allelic deletion on chromosome 3p telomeric to where D3S2450 was located. A common deletion region was identified between D3S2450 and D3S3591. Our results provide evidence for the presence of a tumor suppressor gene in a 0.8-cM region bordered by D3S2450 and D3S3591 at 3p25-p26, which may play a role in carcinogenesis and invasion of OSCC.

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Section: Introductionmentioning

confidence: 52%

Frequent loss of heterozygosity at 3p25-p26 is associated with invasive oral squamous cell carcinoma

et al. 2001

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“…54 Overall, studies in HNSCC have shown that deletions at chromosome arms 3p, 4p, 8p and 9p represent early genetic changes and that loss at 18q, 17p and 11qter is associated with neoplastic progression. 33,34,36,45,48,55 Dysplastic regions in the head and neck region that show more LOH seem to be more at risk for neoplastic evolution. 17,18,19,33 There are several reports that LOH is associated with more advanced stage and more aggressive HNSCC tumors, 13,34,36,37,56 and specifically with nodal involvement.…”

Section: Lohmentioning

confidence: 99%

The clinical relevance of microsatellite alterations in head and neck squamous cell carcinoma: a critical review

Schutter¹,

Spaepen²,

Bride

et al. 2007

Eur J Hum Genet

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Triggered by the existing confusion in the field, the current paper aimed to review the current knowledge of both microsatellite instability (MSI) and loss of heterozygosity (LOH) detected by microsatellite markers in head and neck squamous cell carcinoma (HNSCC), and to provide the reader with an assessment of their prognostic and predictive value in this tumor type. For both MSI and LOH, various detection methods were included such as mono-and polynucleotidemarkers and gel-as well as automated analyses. Only studies based on PCR techniques with microsatellite markers were considered. Taking the methodological problems occurring in investigations with microsatellite markers into account, LOH seems to be more common than MSI in HNSCC. Although both types of microsatellite alterations have been correlated with clinicopathological features of this tumor type, only LOH seems to have a clear prognostic value. The predictive value of both MSI and LOH is debatable. More research has to be performed to clearly establish LOH detection as a translational application in the HNSCC field, aiming to predict response to treatments or outcome, and eventually to use as a therapeutic target.

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“…Loss of heterozygosity (LOH) studies using microsatellite markers on head-and-neck malignancies have demonstrated extensive areas of loss. [1][2][3][4][5] Moreover, premalignant lesions studied in the initial description of a genetic progression model revealed the timing of genetic alterations such as LOH as premalignant lesions advance toward malignancy. 6 These specific genetic events can be detected in the saliva and serum of patients with head and neck malignancy, 7,8 opening the door to new strategies for early cancer detection and tumor surveillance.…”

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confidence: 99%

Progression of microsatellite instability from premalignant lesions to tumors of the head and neck

Pilkington

Westra

et al. 2002

Intl Journal of Cancer

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The role of microsatellite alterations other than loss of heterozygosity (LOH) in the progression of benign epithelium to head-and-neck squamous cell cancer (HNSCC) has not been previously described. As the severity of the dysplasia increases at the microscopic level, there is an increase in the prevalence of LOH as defined by microsatellite analysis. Other alterations have been detected in the form of microsatellite instability (MSI), represented by insertions or deletions of base pairs. It is unknown, however, whether the prevalence of these alterations likewise increases during these early stages of tumor progression. Key words: microsatellite instability; head-and-neck squamous cell carcinoma; loss of heterozygosity; hereditary nonpolyposis colon cancerThe molecular progression of head-and-neck squamous cell carcinoma (HNSCC) correlates with the phenotypic spectrum of dysplasia found in premalignant lesions of the upper respiratory tract epithelium. Loss of heterozygosity (LOH) studies using microsatellite markers on head-and-neck malignancies have demonstrated extensive areas of loss. [1][2][3][4][5] Moreover, premalignant lesions studied in the initial description of a genetic progression model revealed the timing of genetic alterations such as LOH as premalignant lesions advance toward malignancy. 6 These specific genetic events can be detected in the saliva and serum of patients with head and neck malignancy, 7,8 opening the door to new strategies for early cancer detection and tumor surveillance. These genetic alterations included LOH and other microsatellite changes, such as simple insertions or deletions of base pairs, referred to as microsatellite instability (MSI).These simple base pair insertions/deletions are dominant features of certain solid tumors with significant mismatch repair (MMR) defects, such as hereditary non-polyposis colon cancer (HNPCC). 9 However, the reduced prevalence of such alterations and the lack of mutations in gene products known to maintain MMR functions in HNSCC do not support classification of HNSCC as a tumor type with a dominant feature of MMR deficiency. Nevertheless, when detected in HNSCC at selected loci, the shifted alleles can be quite useful in detecting the presence of altered clonal populations in body fluids, including saliva and serum. 7,8 It is important to emphasize that the microsatellite markers selected in these studies were known to exhibit LOH and MSI in lung tumors; therefore, identification of MSI in these head-andneck tumors does not implicate HNSCC as an MMR-deficient tumor type.However, MSI has not been studied comprehensively in premalignant lesions of the head and neck. Further definition of the temporal occurrence of such alterations in premalignant lesions in HNSCC should provide insight into the detection of premalignant lesions using analyses of both MSI and LOH.We looked at 5 different categories of head-and-neck lesions, predominantly from the oral cavity: hyperplasia without atypia, mild dysplasia, moderate dysplasia, severe dysplasia/ca...

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LOH at 3p correlates with a poor survival in oral squamous cell carcinoma

Abstract: Summary We analysed chromosome 3p for loss of heterozygosity (LOH)

Cited by 67 publications

References 10 publications

Frequent loss of heterozygosity at 3p25-p26 is associated with invasive oral squamous cell carcinoma

Frequent loss of heterozygosity at 3p25-p26 is associated with invasive oral squamous cell carcinoma

The clinical relevance of microsatellite alterations in head and neck squamous cell carcinoma: a critical review

Progression of microsatellite instability from premalignant lesions to tumors of the head and neck

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