RETRACTED ARTICLE: Molecular biology of retinoblastoma

Álvarez, Constantino Sábado

doi:10.1007/s12094-008-0220-y

Cited by 15 publications

(5 citation statements)

References 24 publications

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“…Therefore, we postulated that TET2 hypermethylation might occur. Indeed, it was demonstrated in two (5.9%) patients in this cohort, and hence might be a possible mechanism to result in biallelic gene inactivation, and hence fulfil Knudson's hypothesis, which proposed that both alleles of a tumour suppressor gene have to be inactivated, usually by deletion and/or mutation, for complete abrogation of its function 11. The low frequency of TET2 gene hypermethylation was similar to the finding of absence of TET2 hypermethylation in another cohort of 354 MPN patients 12.…”

Section: Discussionsupporting

confidence: 70%

Methylation of TET2, CBL and CEBPA in Ph-negative myeloproliferative neoplasms

et al. 2010

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A loss-of-function mutation of TET2, CBL and CEBPA has been implicated in the pathogenesis or leukaemic transformation of myeloproliferative neoplasm. As tumour suppressor genes may potentially be inactivated by promoter hypermethylation, the authors studied the methylation status of these genes in three cell lines and diagnostic marrow samples from 45 patients with myeloproliferative neoplasm (MPN) (essential thrombocythaemia, N=34; polycythaemia vera, N=7 and primary myelofibrosis, N=4) by methylation-specific PCR. TET2 was heterozygously methylated in MEG-01 and K562 but completely unmethylated in HEL. On the other hand, both CBL and CEBPA were completely unmethylated in all three cell lines. In the primary marrow samples, methylation of TET2 occurred in two (5.9%) patients with essential thrombocythaemia (4.4% of all patients), both without JAK2 V617 mutation, but not in polycythaemia vera or primary myelofibrosis. There was no association between TET2 methylation with the type of MPN (p=0.713). Hypermethylation of CBL or CEBPA was not detected in any patients. In summary, methylation of TET2, CBL and CEBPA is infrequent in MPN at diagnosis. The role of methylation of these genes at the time of leukaemic transformation warrants further study.

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Section: Discussionsupporting

confidence: 70%

Methylation of TET2, CBL and CEBPA in Ph-negative myeloproliferative neoplasms

et al. 2010

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“…Beyond retinoblastoma, RB1 is also frequently mutated in osteosarcoma and small-cell lung cancer, and patients heterozygous for RB1 have significantly increased risk for developing these cancers (Sábado Alvarez, 2008; Kansara and Thomas, 2007). Indeed, tumors derived from TKO and RB1 −/− MEFs contained cells resembling spindle cell sarcomas.…”

Section: Discussionmentioning

confidence: 99%

Mouse Fibroblasts Lacking RB1 Function Form Spheres and Undergo Reprogramming to a Cancer Stem Cell Phenotype

et al. 2009

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SUMMARY Activation of the RB1 pathway triggers the cell-cycle arrest that mediates cell-cell contact inhibition. Accordingly, mutation of all three RB1 family members leads to loss of contact inhibition and outgrowth of fibroblasts into spheres where cell-cell contacts predominate. We present evidence that such outgrowth triggers reprogramming to generate cells with properties of cancer stem cells. Fibroblasts with only a single RB1 mutation remain contact inhibited; however, if this contact inhibition is bypassed by forcing the RB1−/− cells to form spheres in suspension, cells with properties of cancer stem cells are also generated. These cells not only form tumors in nude mice but also generate differentiated cells. We propose that contact inhibition imposed by the RB1 pathway performs an unexpected tumor suppressor function by preventing cell outgrowth into structures where cells with properties of cancer stem cells can be generated from differentiated somatic cells in advancing cancers.

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“…Based on these theories, gene therapies that can either modify the host responses to a tumor or directly inhibit tumor cell growth have attracted increasing attention and interest of researchers. To date, several molecular targets have been studied for treatment of lung cancer, including Rb1 gene and p53 gene replacement, Bcl-2 down-regulation, the FAS/CD95 receptor system and TRAIL, and inhibition of NF-kappa B [5, 6]. However, as multiple molecular alterations may be involved in the development of lung cancer [7], there is still a lot of work to be done to find more promising and effective therapeutic targets.…”

Section: Introductionmentioning

confidence: 99%

Expression of NDRG2 in human lung cancer and its correlation with prognosis

Wang

et al. 2013

Med Oncol

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We had reported that N-myc downstream–regulated gene (NDRG2) regulates colorectal cancer, breast cancer, clear cell renal cell carcinoma, pancreatic cancer, thyroid cancer and esophageal squamous cell proliferation, development, and apoptosis. The goal of this study was to determine the expression pattern of NDRG2 in human lung cancer and its correlation with prognosis. Immunohistochemistry, RT-PCR and western blot were used to explore the expression of NDRG2 in 185 human lung cancer patients. The correlation of NDRG2 expression with patients’ survival rate was assessed by Kaplan–Meier and Cox regression. Results showed that the expression level of NDRG2 was decreased in human lung cancer tissues, and NDRG2 was positively correlated with depth of invasion (P = 0.038), vascular invasion (P = 0.036), tumor grade (P = 0.039), and tumor size (P = 0.026). Both RT-PCR and Western blots demonstrated that NDRG2 mRNA and protein levels were lower in lung cancer compared to the adjacent normal tissue from the same individual, and NDRG2 level was negatively correlated with UICC stage. Additionally, survival time of lung cancer patients with high expression of NDRG2 was longer than those with low expression during the 5-year follow-up period (P = 0.001). Meanwhile, COX regression analysis indicated that low expression of NDRG2, ≥pT3, pM1, ≥pN1 and vascular invasion were independent, poor prognostic factors of lung cancer patients. These data showed that NDRG2 may play an important role in human lung cancer tumourigenesis, and NDRG2 might serve as a novel prognostic marker in human lung cancer.

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RETRACTED ARTICLE: Molecular biology of retinoblastoma

Cited by 15 publications

References 24 publications

Methylation of TET2, CBL and CEBPA in Ph-negative myeloproliferative neoplasms

Methylation of TET2, CBL and CEBPA in Ph-negative myeloproliferative neoplasms

Mouse Fibroblasts Lacking RB1 Function Form Spheres and Undergo Reprogramming to a Cancer Stem Cell Phenotype

Expression of NDRG2 in human lung cancer and its correlation with prognosis

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