Enhanced expression of insulin-like growth factor II is not a necessary event in Wilms' Tumour progression

Little, Melissa H.; Ablett, G; Smith, Peter J.

doi:10.1093/carcin/8.6.865

Cited by 20 publications

(7 citation statements)

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“…In addition, they show a structural change of the I G F II gene in one Wilms tumour. Although in a recent report [17] some evidence has been presented that I G F II overexpression in Wilms tumour might be a tumour epiphenomenon, we argue that the rearrangement in the I G F II gene or in the vicinity of the gene might be responsible for elevated I G F II gene expression and consecutive tumour growth.…”

Section: Discussioncontrasting

confidence: 66%

Structural alteration of the insulin-like growth factor II-gene in Wilms tumour

et al. 1989

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In this study messenger ribonucleic acid (mRNA) and DNA of five Wilms tumours were investigated. As expected, the level of insulin-like growth factor (IGF) II-mRNA was elevated up to 50 times in tumour tissue as compared to normal adjacent kidney tissue. In addition, genomic DNA was isolated and digested with appropriate restriction enzymes. Southern blots were prepared and hybridized to IGF II-cDNA probes. Additional bands were present in one of the five Wilms tumours compared to normal tissue. The results indicate a rearrangement of the IGF II-gene on one of the two chromosomes. It is speculated, that this change is responsible for the elevated IGF II expression which may be a factor contributing to tumour growth.

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Section: Discussioncontrasting

confidence: 66%

Structural alteration of the insulin-like growth factor II-gene in Wilms tumour

et al. 1989

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“…Selection against such expression in a cell already transformed might be expected if IGF-II has the same suppressive effect on tumour formation in man as in an experimental situation. In support of this Little et al (1987) using xenografts of primary Wilms' tumours, were able to demonstrate that IGF-II expression was selected against during tumour passage, and they suggested that elevated IGF-II mRNA was not an essential component of tumour progression. Additionally, Maitland et al (1989) have reported the selective loss of chromosome 11 during maintenance of cell hybrids between normal human foetal kidney and HeLa cells as grafts in nude mice.…”

Section: Discussionmentioning

confidence: 90%

Tumour suppression associated with expression of human insulin-like growth factor II

Schofield

Lee²,

Hill³

et al. 1991

Br J Cancer

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Recent circumstantial evidence has implicated Insulin-like growth factor II in the genesis of several tumour types, notably developmental tumours (Scott et al., 1985; Schofield & Tate, 1987; Wilkins et al., 1989). This type of tumour, thought to originate during the defective differentiation of organ precursors (Miereau et al., 1987), often expresses greatly elevated levels of mRNA for IGF-II, a known mitogen for these cells and abundantly expressed in their presumed normal counterparts (Scott et al., 1985; Schofield & Tate, 1987; Gray et al., 1987). It has been proposed that continued, inappropriate expression of this gene drives tumour growth by an autocrine mechanism. In order to examine the potential role of IGF-II in the growth of tumour cells an IGF-II cDNA was introduced into a retroviral expression vector, and used to infect a cloned fibroblast cell line. Expression of IGF-II conferred a degree of serum independence of growth in cell culture, however, when cells were injected into nude mice as subcutaneous grafts, clones expressing IGF-II from the retrovirus were found to have a greatly increased (five fold) latency of sarcoma formation. After a prolonged lag all cell lines eventually gave rise to tumours in which the introduced IGF-II genes had either been lost or inactivated, suggesting that in this system IGF-II acts as a tumour suppressor gene. Images Figure 2 Figure 4

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“….00 0. in WT progression (31), the levels of IGF-IR mRNA appear to correlate with the degree of differentiation of the tumor: tumors with heterologous elements and prominent stromal components are generally associated with higher levels of IGF-IR mRNA. This subset of tumors is mostly seen in the WAGR syndrome (1), a condition in which WT is associated with aniridia, genitourinary abnormalities, and mental retardation.…”

Section: Discussionmentioning

confidence: 99%