DNA markers predicting benefit from adjuvant fluorouracil in patients with colon cancer: a molecular study

Barratt, PL; Seymour, Michel; Stenning, SP; Georgiades, Izabela B.; Walker, Colin; Birbeck, K; Quirke, Philip

doi:10.1016/s0140-6736(02)11402-4

Cited by 182 publications

(127 citation statements)

References 26 publications

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“…Chromosome 18q LOH has been associated with poor prognosis in colorectal cancer patients lacking lymph nodes or distant metastases at the time of surgery (so-called stage II), as well as in patients who have lymph nodes but no distant metastases at the time of surgery (stage III) (Jen et al, 1994;Ogunbiyi et al, 1998). In other studies, chromosome 18q LOH has also been associated with decreased responsiveness to 5-fluorouracil-based adjuvant chemotherapy regimens in stage III colorectal cancer patients (Watanabe et al, 2001;Barratt et al, 2002). Loss of DCC expression was often associated with poor prognosis and increased risk of metastasis (Shibata et al, 1996;Saito et al, 1999).…”

Section: Role Of Dependence Receptors Unc5h and DCC In Colorectal Tummentioning

confidence: 95%

Role of netrin-1 and netrin-1 dependence receptors in colorectal cancers

Mehlen

Llambi

2005

Br J Cancer

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Although cancer is a multifaceted disease, all cancer types share identical molecular and cellular mechanisms. These mechanisms involve a collection of alterations critical to the normal physiological functioning of cells, such as alterations of growth factor signalling pathways, angiogenesis, cell adhesion signals, DNA replication and apoptotic cell death. Many genes involved in the processes enumerated above are functionally inactive in tumour cells, designating them as putative 'tumour suppressor genes'. Back in the early 1990s, Vogelstein and colleagues suggested that a gene called DCC (for Deleted in Colorectal Cancer) could be a tumour suppressor gene because it was found to be deleted in more than 70% of colorectal cancers, as well as in many other cancers. During the last 15 years, controversial data have failed to firmly establish whether DCC is indeed a tumour suppressor gene. However, the recent observations that DCC triggers cell death and is a receptor for netrin-1, a molecule recently implicated in colorectal tumorigenesis, have prompted a renewal of interest in the role of DCC in tumorigenesis and suggest that the netrin-1/receptor pairs act as novel negative regulators of tumour development.

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Section: Role Of Dependence Receptors Unc5h and DCC In Colorectal Tummentioning

confidence: 95%

Role of netrin-1 and netrin-1 dependence receptors in colorectal cancers

Mehlen

Llambi

2005

Br J Cancer

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“…This conclusion, which is derived from numerous studies that used varying techniques (microsatellite analysis, CGH, CGH array, SNP array, karyotyping), is actually consistent with the observation that 18q loss is also associated with distant metastasis. 40 As indicated in Table 1, 24,26 the loss of 8p 24,34 -39,41 or 17p (the location of TP53 tumor suppressor gene) 33,34,42 is also linked to lower survival rate.…”

Section: Somatic Copy Number Aberrations In Crcsmentioning

confidence: 99%

Gene Dysregulations Driven by Somatic Copy Number Aberrations-Biological and Clinical Implications in Colon Tumors

Bacolod

Barany

2010

The Journal of Molecular Diagnostics

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The majority of colorectal cancer (CRC) cases have chromosomal instability , in which the tumor genome is characterized by gross chromosomal aberrations such as gains in 20q , 13q , 8q , and 7 , and losses in 4, 8p , 18q , and 17p. These somatic copy number changes (gains , losses , and somatic uniparental disomies) are crucial to CRC progression as they drive genes toward cancer-promoting (oncogenic or tumor suppressive) states. Numerous studies have shown that the loss of 18q or 8p is associated with poorer clinical outcome in CRCs. Either chromosomal arm may contain a tumor suppressor gene (or genes), whose deactivation by copy loss (loss of wild-type allele , decreased expression) can be crucial to the later stages of cancer progression. Our own integrated genomic analysis (single nucleotide polymorphism array , expression array) of more than 200 CRC tumor and normal samples indicates that the overall down-regulation of genes within the 8p or 18q arm is associated with lower survival rate. Among the often down-regulated , poor prognosis-associated 8p genes is MTUS1, whose gene product (a mitotic spindleassociated protein) was recently demonstrated to have a tumor suppressive property. Within 18q is ATP5A1 , which codes for the catalytic a component of mitochondrial H ؉ -ATP synthase. Like SMAD4(also in 18q) , the decreased expression of ATP5A1 appears to be a marker of unfavorable clinical outcome in

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“…Its association with prognosis has been reported earlier in breast cancer , although this study included patients treated by adjuvant systemic therapy. The true prognostic value, however, of a given factor should be assessed in patients in the absence of adjuvant treatment (Hayes et al, 1998;Henderson and Patek, 1998;Barratt et al, 2002;Mori et al, 2002). Predictive factors can be used to predict response or lack of response to a particular therapy (Mori et al, 2002).…”

Section: Xmentioning

confidence: 99%

Carbonic anhydrase-9 expression levels and prognosis in human breast cancer: association with treatment outcome

et al. 2003

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Here, we set out to assess CA9 expression levels by real-time quantitative RT -PCR in breast cancer tissue samples obtained from 253 patients, and correlated those with relapse-free (RFS) survival. The median follow-up time was 75 months (range 2 -168 months). CA9 expression was mainly found in high-grade, steroid receptor negative cancer tissues. CA9 levels were not significantly associated with RFS (P ¼ 0.926, hazard ratio (HR) ¼ 0.99, 95% CI ¼ 0.80 -1.22) in the total cohort of 253 patients. In multivariate analysis with other clinicopathological factors, CA9 (P ¼ 0.018, HR ¼ 0.77, 95% CI ¼ 0.62 -0.96), the interaction of adjuvant chemotherapy with CA9 (P ¼ 0.009, HR ¼ 1.31, 95% CI ¼ 1.07 -1.61) and the interaction of adjuvant endocrine therapy with CA9 (Po0.001, HR ¼ 1.41, 95% CI ¼ 1.20 -1.66) all contributed significantly to the final model. These results indicate that patients with low CA9 levels benefit more from adjuvant treatment than do patients with high levels. Thus, the determination of CA9 levels could aid in the selection of patients who will not benefit from adjuvant therapy, and whose prognosis will more likely improve with other treatment modalities.

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DNA markers predicting benefit from adjuvant fluorouracil in patients with colon cancer: a molecular study

Cited by 182 publications

References 26 publications

Role of netrin-1 and netrin-1 dependence receptors in colorectal cancers

Role of netrin-1 and netrin-1 dependence receptors in colorectal cancers

Gene Dysregulations Driven by Somatic Copy Number Aberrations-Biological and Clinical Implications in Colon Tumors

Carbonic anhydrase-9 expression levels and prognosis in human breast cancer: association with treatment outcome

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