Frequency of carriers of cystic fibrosis gene among patients with myeloid malignancy and melanoma.

Warren, N.; Holmes, Jordan A.; Al-Jader, Layla N.; West, Robert R.; Lewis, Deri; Padua, Rose Ann

doi:10.1136/bmj.302.6779.760

Cited by 21 publications

(16 citation statements)

References 6 publications

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“…Also, there has been a concern about the risk of various cancers in CF patients and carriers of CFTR mutations (Malats et al, 2001). While a protective role of CFTR has been predicted for breast cancer and melanoma (Warren et al, 1991;Abraham et al, 1996), a significant excess of digestive tract cancer in CF patients has also been reported (Sheldon et al, 1993;Neglia et al, 1995). In the present study, we observed a reduced/negligible expression of CFTR in most (81%) pancreatic cancer cell lines, while it was expressed in cultured pancreatic ductal cells and normal pancreas ( Figure 1a).…”

Section: Discussionmentioning

confidence: 99%

MUC4 expression is regulated by cystic fibrosis transmembrane conductance regulator in pancreatic adenocarcinoma cells via transcriptional and post-translational mechanisms

et al. 2006

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MUC4 mucin is a high molecular weight transmembrane glycoprotein that plays important roles in tumour biology. It is aberrantly expressed in pancreatic adenocarcinoma, while not being detectable in the normal pancreas. Previous studies have demonstrated that the cystic fibrosis transmembrane conductance regulator (CFTR), a chloride channel that is defective in CF, is implicated in multiple cellular functions, including gene regulation. In the present study, using a CFTR-defective pancreatic cancer cell line and its derived subline expressing functional CFTR, we report that MUC4 expression is negatively regulated by CFTR. Short-interfering RNA (siRNA)-mediated silencing of CFTR also leads to an increased expression of MUC4. Additionally, our results suggest that CFTR-mediated regulation of MUC4 is cell densitydependent and is achieved by transcriptional and posttranslational mechanisms. Moreover, in a panel of pancreatic cancer cell lines and normal pancreas, we observed that CFTR was downregulated in pancreatic cancer cells and negatively correlated with MUC4 in most cases. An aberrant expression of MUC4 was also detected in the CF pancreas. Downregulation of CFTR in pancreatic adenocarcinoma and its inverse association with the tumour-linked mucin, MUC4, indicate novel function(s) of CFTR in pancreatic tumour biology and suggest the implication of new signalling pathway(s) in MUC4 regulation.

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Section: Discussionmentioning

confidence: 99%

MUC4 expression is regulated by cystic fibrosis transmembrane conductance regulator in pancreatic adenocarcinoma cells via transcriptional and post-translational mechanisms

et al. 2006

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“…‫,ء‬ deleted alleles. molecular mechanism behind this association is unknown (33). Characterization of additional polymorphic markers and identification of cases similar to patient 23 will allow better understanding of the heterogeneity of molecular lesions associated with anomalies of the proximal 7q31.3 region.…”

Section: Discussionmentioning

confidence: 99%

Molecular anatomy of chromosome 7q deletions in myeloid neoplasms: Evidence for multiple critical loci

Luan

Fairman

Claxton

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

132

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Complete or partial deletions of the long arm of chromosome 7 (7q-and -7) are nonrandom abnormalities seen in primary and therapy-induced myelodysplasia (MDS) and acute myelogenous leukemia (AML). Monosomy 7, occurring as the sole cytogenetic anomaly in a small but significant number of cases, may denote a dominant mechanism involving critical tumor suppressor gene(s). We have determined the extent of allele loss in cytogenetically prescreened MDS and AML patients for microsatellite markers from chromosome 7q22 and 7q31. Whereas >80% of these cases revealed allele loss for the entire region, a rare case of the 7q-chromosome showed allele loss for only the proximal 7q31.1 loci f lanked by the markers D7S486 and D7S2456, and a case of monosomy 7 revealed allele loss for loci at both 7q31 and 7q22 with retention of sequences between these sets of loci. Furthermore, a case of AML with no cytogenetic anomaly of chromosome 7 revealed a submicroscopic allelic imbalance for a third distal locus, D7S677. These findings suggest the presence of three distinct critical loci that may contribute alone or in combination to the evolution of MDS and AML. The data also provide molecular evidence for unbalanced translocation with noncontiguous deletions, as an alternate mechanism underlying monosomy 7.

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“…Meanwhile, mutations and lowpenetrance polymorphisms in the CFTR gene have been found in patients with various cancers, including pancreatic cancer [6][7][8][9][10], melanoma [11,12], breast cancer [12,13], colon cancer [12], and lung cancer [14,15]. Prostate cancer has been reported in CF patients [16] and atypical CF patients [17], and the incidence seemed to be lower than expected [16].…”

Section: Introductionmentioning

confidence: 99%

“…Nonfunctional CFTR has been suggested to suppress tumor growth and proliferation [21]. Mutations and polymorphisms in CFTR gene can cause failure of CFTR, therefore may be involved in the pathogenesis of some cancers [6][7][8][9][10][11][12][13][14][15][16]. It has been suggested that interactions between CFTR polymorphisms and environmental factors might play a role in the development of pancreatic cancer [7,8].…”

Section: Introductionmentioning

confidence: 99%

Cystic fibrosis transmembrane conductance regulator (CFTR) gene 5T allele may protect against prostate cancer: A case-control study in Chinese Han population

Qiao

Liu

et al. 2008

Journal of Cystic Fibrosis

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Frequency of carriers of cystic fibrosis gene among patients with myeloid malignancy and melanoma.

Abstract: Coronarv heart disease and drinking water. A search in two Finnish male cohorts for epidemiologic evidence of a water factor. J Chronic Dis 1975 ;28:259-87.

Cited by 21 publications

References 6 publications

MUC4 expression is regulated by cystic fibrosis transmembrane conductance regulator in pancreatic adenocarcinoma cells via transcriptional and post-translational mechanisms

MUC4 expression is regulated by cystic fibrosis transmembrane conductance regulator in pancreatic adenocarcinoma cells via transcriptional and post-translational mechanisms

Molecular anatomy of chromosome 7q deletions in myeloid neoplasms: Evidence for multiple critical loci

Cystic fibrosis transmembrane conductance regulator (CFTR) gene 5T allele may protect against prostate cancer: A case-control study in Chinese Han population

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