Characterization of chromosome 1 abnormalities in malignant melanomas

Smedley, Damian; Sidhar, Sanjiv; Birdsall, Sandra; Bennett, Dorothy C.; Herlyn, Meenhard; Cooper, Christopher S.; Shipley, Janet

doi:10.1002/(sici)1098-2264(200005)28:1<121::aid-gcc14>3.0.co;2-o

Cited by 77 publications

(47 citation statements)

References 19 publications

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“…However, its involvement, curiously associated with activation of the MUC1 gene, has been demonstrated in lymphomas and malignant melanoma. [27][28][29] A nonrandom involvement of chromosome 15 was also demonstrated in this study with breakpoints at 15q15 and 15q22. As far as we know, there is no description of genes linked to Barrett's adenocarcinoma in these particular regions.…”

Section: Discussionsupporting

confidence: 69%

Chromosomal analysis of Barrett's cells: demonstration of instability and detection of the metaplastic lineage involved

et al. 2007

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Barrett's esophagus is lined by columnar and goblets cells with gastric and intestinal characteristics. Despite the association between goblet elements and malignancy, it was not demonstrated that other columnar cells lineages are not related to neoplasia. Chromosomal abnormalities were described in metaplasia adjacent to Barrett's neoplasia, but it is unknown which metaplastic lineages are involved. This work assessed the frequency and the type of chromosomal abnormalities in Barrett's esophagus without neoplasia and performed the identification of the metaplastic cells carrying chromosomal gains. Barrett's esophagus biopsies were collected and processed for short-term cell culture and cytogenetic analysis. Combined immunofluorescence/ fluorescence in situ hybridization was performed in cases exhibiting chromosomal gains by using antisera against intestinal (MUC2) and gastric (MUC5AC and MUC6) apomucins and chromosome pericentromeric alpha satellite DNA probes for the chromosomes involved. Each case was scored for the number of spots (0, 1, 2, 42) in 200 nonoverlapping nuclei. Columnar and goblet cells were separately assessed. Short-term cell cultures were achieved in 40/60 cases (67%). There were clonal abnormalities in 27/40 cases (68%) and tetraploid (4n) clones in 10/40 (25%). Structural alterations were detected in 14/40 (35%) with recurrent breakpoints at 1q21, 15q15 and 15q22. Numerical changes (trisomies 7 and 18 and loss of Y) occurred in 16/40 (40%). Gains of chromosomes 7 and 18 were more frequent in columnar than in goblet cells (9.8% vs 0.7% (Po0.05)) and (7.9 vs 1.9% (Po0.05)) respectively. These alterations were detected in cells exhibiting gastric as well as intestinal features and were more frequent in cells without apomucin production. Conclusions: (1) chromosomal instability is a common finding in Barrett's esophagus without neoplasia. (2) The two metaplastic populations are committed, chromosomal gains being more frequent in columnar nongoblet than in goblet cells. (3) The two metaplastic phenotypes, gastric and intestinal, are equally involved.

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Section: Discussionsupporting

confidence: 69%

Chromosomal analysis of Barrett's cells: demonstration of instability and detection of the metaplastic lineage involved

et al. 2007

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“…Human GAS5 is encoded at 1q25, a locus that has been associated with abnormalities in several types of cancer, including melanoma (Smedley et al, 2000), prostate (Nupponen and Carpten, 2001) and breast (Stange et al, 2006;Morrison et al, 2007). Chromosomal rearrangements involving GAS5 have been reported recently in a human B-cell lymphoma (Nakamura et al, 2008) as well as in radiation-induced murine thymic lymphoma TL10 (Tsuji et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

GAS5, a non-protein-coding RNA, controls apoptosis and is downregulated in breast cancer

et al. 2008

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Effective control of both cell survival and cell proliferation is critical to the prevention of oncogenesis and to successful cancer therapy. Using functional expression cloning, we have identified GAS5 (growth arrest-specific transcript 5) as critical to the control of mammalian apoptosis and cell population growth. GAS5 transcripts are subject to complex post-transcriptional processing and some, but not all, GAS5 transcripts sensitize mammalian cells to apoptosis inducers. We have found that, in some cell lines, GAS5 expression induces growth arrest and apoptosis independently of other stimuli. GAS5 transcript levels were significantly reduced in breast cancer samples relative to adjacent unaffected normal breast epithelial tissues. The GAS5 gene has no significant protein-coding potential but expression encodes small nucleolar RNAs (snoRNAs) in its introns. Taken together with the recent demonstration of tumor suppressor characteristics in the related snoRNA U50, our observations suggest that such snoRNAs form a novel family of genes controlling oncogenesis and sensitivity to therapy in cancer.

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“…Previous studies indicate that the genetic aberrations of GAS5 have relationship with many types of tumors including melanoma, breast and prostate cancers (Smedley et al, 2000;Nupponen and Carpten, 2001;Morrison et al, 2007). As a most common urological cancer, whether the abnormal expression of GAS5 is associated with RCC carcinogenesis has not yet been reported.…”

Section: Discussionmentioning

confidence: 99%

“…Breast cancers show a significantly lower GAS5 expression compared with normal breast epithelial tissues (Mourtada-Maarabouni et al, 2009). In addition, genetic aberrations of the GAS5 locus have been found in many types of tumors including melanoma, breast and prostate cancers but their functional significance still needs to be established (Smedley et al, 2000;Nupponen and Carpten, 2001;Morrison et al, 2007).…”

Section: Long Non-coding Rna Gas5 Functions As a Tumor Suppressor In mentioning

confidence: 99%

Long Non-coding RNA GAS5 Functions as a Tumor Suppressor in Renal Cell Carcinoma

Qiao¹,

Gao²,

Huo³

et al. 2013

Asian Pacific Journal of Cancer Prevention

213

152

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Background: Renal cell carcinoma (RCC) is a malignancy with a poor prognosis. We aimed to explore whether the expression of Long Non-Coding RNA (LncRNA) growth arrest-specific transcript 5 (GAS5) is associated with RCC genesis. Methods: We selected twelve clinical samples diagnosed for renal clear cell carcinoma and found that the LncRNA GAS5 transcript levels were significantly reduced relative to those in adjacent unaffected normal renal tissues. Results: In addition, expression of GAS5 was lower in the RCC cell line A498 than that in normal renal cell line HK-2. Furthermore, using functional expression cloning, we found that overexpression of GAS5 in A498 cells inhibited cell proliferation, induced cell apoptosis and arrested cell cycling. At the same time, the migration and invasion potential of A498 cells were inhibited compared to control groups. Conclusion: Our study provided the first evidence that a decrease in GAS5 expression is associated with RCC genesis and progression and overexpression of GAS5 can act as a tumor suppressor for RCC, providing a potential attractive therapeutic approach for this malignancy.

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Characterization of chromosome 1 abnormalities in malignant melanomas

Cited by 77 publications

References 19 publications

Chromosomal analysis of Barrett's cells: demonstration of instability and detection of the metaplastic lineage involved

Chromosomal analysis of Barrett's cells: demonstration of instability and detection of the metaplastic lineage involved

GAS5, a non-protein-coding RNA, controls apoptosis and is downregulated in breast cancer

Long Non-coding RNA GAS5 Functions as a Tumor Suppressor in Renal Cell Carcinoma

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