A single nucleotide polymorphism in the E-cadherin gene promoter modifies the risk of prostate cancer

Verhage, Bas A.J.; Houwelingen, Kjeld van; Ruijter, Emiel; Kiemeney, Bart; Schalken, Jack A.

doi:10.1016/s1569-9056(02)80018-5

Cited by 21 publications

(38 citation statements)

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“…Our results also confirm findings from the first investigation 1 into the importance of C/A SNP as a novel risk factor for PCa. Our results differ from the results of Verhage et al 1 concerning their finding that heterozygote genotype (CA) is at higher risk compared to a high risk homozygote (AA). It was also not possible to confirm the magnitude of allele A influence, which may be due to the larger data set used in our present study.…”

contrasting

confidence: 99%

“…Polymorphism Ϫ160 C/A was reported to have a direct effect on E-cadherin gene transcriptional regulation, 3 and that the loss of the adhesive function of E-cadherin may be a critical step in the promotion of epithelial cells to a more malignant phenotype. This expectation was not confirmed in our study or the study of Verhage et al 1 Similar findings (increased frequency of AA in cancer patients and no association with progression or metastasis), have been reported for other cancers. 4,5 An open question remains the inverse relation (AA as protective or risk genotype) between cancer and controls comparing PCa (the study of Verhage et al 1 and our study) and gastric cancer studies.…”

contrasting

confidence: 63%

“…This expectation was not confirmed in our study or the study of Verhage et al 1 Similar findings (increased frequency of AA in cancer patients and no association with progression or metastasis), have been reported for other cancers. 4,5 An open question remains the inverse relation (AA as protective or risk genotype) between cancer and controls comparing PCa (the study of Verhage et al 1 and our study) and gastric cancer studies. 5,6 The TaqMan assay on demand proved robust and useful.…”

contrasting

confidence: 63%

“…Family history of PCa was excluded by interview, although some elderly patients may not recall diseases of their firstdegree relatives correctly. We believe that this does not affect the validity of our results because Verhage et al 1 evaluated this aspect and did not find differences in the frequencies of the concerned polymorphism between patients with sporadic and familial PCa. This is further supported by recent findings of no differences in clinical presentation and epidemiological features when comparing familial and sporadic PCa, indicating that the 2 entities are the same disease.…”

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confidence: 61%

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E‐cadherin polymorphism −160 C/A and prostate cancer

Hajdinjak

Toplak

2004

Intl Journal of Cancer

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confidence: 99%

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confidence: 63%

contrasting

confidence: 63%

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confidence: 61%

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E‐cadherin polymorphism −160 C/A and prostate cancer

Hajdinjak

Toplak

2004

Intl Journal of Cancer

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“…Besides decreased expression of E-cadherin, various studies were directed to the role of E-cadherin gene (CDH1) polymorphisms (Bonilla et al 2006;Li et al 2006;Verhage et al 2002). A -160 C/A single nucleotide polymorphism was found in allele A.…”

Section: E-cadherinmentioning

confidence: 99%

New experimental markers for early detection of high-risk prostate cancer: role of cell–cell adhesion and cell migration

Mól

Geldof

Meijer

et al. 2007

J Cancer Res Clin Oncol

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Today's treatment and diagnosis of prostate cancer still exhibit major limitations. The search for new and additional prognostic markers is therefore still an actual Weld of interest. Potential markers involved in numerous biological processes in the tumor cell have been investigated intensively. For therapeutic interventions it is important to distinguish between harmless and aggressive disease in an early stage. Therefore the subject of this review is limited to markers associated with those functional processes, which discriminate early stage aggressive, metastatic cancer from harmless disease. Important processes in this respect are: altered cell adhesion and cellular migration. E-cadherin, N-cadherin, -catenin, integrins, focal adhesion kinase, connexins and matrix metalloproteinases all appear promising biological markers associated with the early stage metastatic process in prostate cancer. Here we discuss their potential to become valid biological markers based on literature data. Thus far, none of these markers proved to be a valid individual marker by itself due to prostate cancer heterogeneity and transient expression. Analyzing a combination of the potential markers discussed in this review is expected to be a better approach toward discriminating high-from low-risk tumors in an early stage of prostate cancer.

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Effects of age on prognosis with imatinib mesylate therapy for patients with Philadelphia chromosome‐positive chronic myelogenous leukemia

Cortés

Talpaz

O’Brien

et al. 2003

Cancer

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BACKGROUNDOlder age is a consistent poor prognostic factor in patients with Philadelphia chromosome (Ph)‐positive chronic myelogenous leukemia (CML). Whether this is related to an intrinsic worse disease biology or to inadequate drug delivery or excessive treatment‐associated toxicity is unknown. The availability of imatinib mesylate, a selective, Bcr‐Abl‐targeted therapy that is administered orally with minimal side effects, may clarify whether older age would remain an adverse factor (thus, implying a different age‐related CML biology).METHODSSeven hundred forty‐seven patients in different phases of Ph‐positive CML who were treated with imatinib from 1999 until the time of last follow‐up were evaluated. Among them, 187 patients had newly diagnosed, early chronic phase CML; 351 patients had chronic phase CML after interferon α (IFN) failure; 133 patients had accelerated phase CML; and 76 patients had blastic phase CML. The imatinib daily dose varied from 400 mg to 800 mg orally, according to the protocol design. Patients were categorized into a group of older patients (age 60 years or older) or younger patients (age younger than 60 years). Their characteristics, responses to therapy, and survival were compared by univariate and multivariate analyses.RESULTSOne hundred eighty‐seven patients had newly diagnosed CML, and 49 patients (26%) were in the older age group. Older patients had similar cytogenetic response rates and survival compared with younger patients. Among 351 patients with late chronic phase CML after IFN failure, 120 patients (34%) were in the older age group. Although the older patients had a lower incidence of achievement of complete cytogenetic response (Ph, 0%) by univariate analysis (56% vs. 44%; P = 0.05), age was not found to be an independent poor prognostic factor in the multivariate analysis. Similarly, older age was not an adverse poor prognostic factor for survival. Forty‐two of 133 patients (32%) with accelerated phase CML were older. The incidence of any cytogenetic response was lower in older patients (53% vs. 33%; P = 0.04), but age was not significant in the multivariate analysis. Older patients also had a trend toward worse survival (P = 0.09) that was not significant in the multivariate analysis. Twenty‐eight of 76 patients (37%) evaluated in blastic phase were older. Older age was not a significant prognostic factor either for achieving response or for survival.CONCLUSIONSWith imatinib therapy, older age appears to have lost much of its prognostic relevance. This suggests that the previous poor prognosis observed with older age was related to treatment‐associated factors (e.g., toxicity with allogeneic transplantation or with IFN therapy) rather than to an intrinsic, different disease biology of CML in older patients. Cancer 2003;98:1105–13. © 2003 American Cancer Society.DOI 10.1002/cncr.11629

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A single nucleotide polymorphism in the E-cadherin gene promoter modifies the risk of prostate cancer

Cited by 21 publications

References 0 publications

E‐cadherin polymorphism −160 C/A and prostate cancer

E‐cadherin polymorphism −160 C/A and prostate cancer

New experimental markers for early detection of high-risk prostate cancer: role of cell–cell adhesion and cell migration

Effects of age on prognosis with imatinib mesylate therapy for patients with Philadelphia chromosome‐positive chronic myelogenous leukemia

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