Breakpoint Junction of Interstitial Homozygous Deletion at Chromosome 2q33 in a Small Cell Lung Carcinoma

Otsuka, Toshiyuki; Inazawa, Johji; Abe, Tatsuo; Yokota, Jun

doi:10.1093/dnares/3.6.421

Cited by 9 publications

(2 citation statements)

References 20 publications

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“…For example, the Sdpr gene is located on chromosome region 2q33, ( 25 ) which undergoes a high incidence of loss of heterozygosity in some lung cancers. ( 49 ) An Sdpr relative called SRBC (sdr‐related gene product that binds to c‐kinase) is also induced by serum deprivation and associates with protein kinase C. ( 50 ) Interestingly, SRBC expression is suppressed in lung and breast cancers, ( 51 ) apparently by gene deletion ( 52 ) or methylation. ( 51 )…”

Section: Discussionmentioning

confidence: 99%

Coordinate suppression of Sdpr and Fhl1 expression in tumors of the breast, kidney, and prostate

Jia

Shen

et al. 2008

Cancer Science

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S rc is a membrane-bound tyrosine kinase(1) that has been implicated in the progression of many human cancers (2,3) including tumors of the breast, (4-6) kidney, (7) and prostate. (8) The Src kinase phosphorylates Cas (Crk-associated substrate) and activates mitogen-activated protein kinase (MAPK) to promote anchorage-independent growth and migration. (9)(10)(11)(12)(13)(14)(15)(16) These fundamental hallmarks of tumor-cell growth are required for metastasis and distinguish most cancer cells from their non-transformed precursors. (17,18) We have recently found that Src utilizes Cas to inhibit Fhl1 (four and a half LIM domains 1) expression, in order to promote non-anchored cell growth and migration. (19) Transfection studies show that Fhl1 specifically blocks non-anchored tumor-cell growth and migration, but does not affect 'normal' anchored cell growth. Therefore, Fhl1 acts as a true tumor suppressor rather than as a general mitotic inhibitor. (19) As the name indicates, Fhl1 consists of 'four and a half LIM domains'. Fhl1 can move between intercellular junctions, (20) focal adhesions, and the nucleus (21) to affect gene expression. (22,23) For example, Fhl1 associates with the recombination signal binding protein for immunoglobulin kappa J region (RBP-J)-DNA binding protein to modulate gene transcription. (22,23)

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Section: Discussionmentioning

confidence: 99%

Coordinate suppression of Sdpr and Fhl1 expression in tumors of the breast, kidney, and prostate

Jia

Shen

et al. 2008

Cancer Science

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show abstract

“…Finally, SDPR relative protein called SRBC (SDR-related gene product that binds to c-kinase) is also induced by serum deprivation and associated with Protein Kinase C [68]. SRBC expression is suppressed in lung and breast cancers [69], apparently by gene deletion [70] or methylation [69].…”

Section: Accepted M Manuscriptmentioning

confidence: 99%

Alterations of the serum peptidome in renal cell carcinoma discriminating benign and malignant kidney tumors

Gianazza

Chinello

Mainini

et al. 2012

Journal of Proteomics

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Common chromosome fragile sites in human and murine epithelial cells and FHIT/FRA3B loss‐induced global genome instability

Hosseini

Horton

Saldivar

et al. 2013

Genes Chromosomes & Cancer

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Chromosomal positions of common fragile sites differ in lymphoblasts and fibroblasts, with positions dependent on the epigenetically determined density of replication origins at these loci. Because rearrangement of fragile loci and associated loss of fragile gene products are hallmarks of cancers, we aimed to map common fragile sites in epithelial cells, from which most cancers derive. Among the five most frequently activated sites in human epithelial cells were chromosome bands 2q33 and Xq22.1, which are not among top fragile sites identified in lymphoblasts or fibroblasts. FRA16D at 16q23 was among the top three fragile sites in the human epithelial cells examined, as it is in lymphoblasts and fibroblasts, while FRA3B at 3p14.2, the top fragile locus in lymphoblasts, was not fragile in most epithelial cell lines tested. Epithelial cells exhibited varying hierarchies of fragile sites; some frequent epithelial cell fragile sites are apparently not frequently altered in epithelial cancers and sites that are frequently deleted in epithelial cancers are not necessarily among the most fragile. Since we have reported that loss of expression of the FRA3B-encoded FHIT protein causes increased replication stress-induced DNA damage, we also examined the effect of FHIT-deficiency on markers of genome instability in epithelial cells. FHIT-deficient cells exhibited increases in fragile breaks and in γH2AX and 53BP1 foci in G1 phase cells, confirming in epithelial cells that the FHIT gene and encompassing FRA3B, is a “caretaker gene” necessary for maintenance of genome stability.

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Breakpoint Junction of Interstitial Homozygous Deletion at Chromosome 2q33 in a Small Cell Lung Carcinoma

Cited by 9 publications

References 20 publications

Coordinate suppression of Sdpr and Fhl1 expression in tumors of the breast, kidney, and prostate

Coordinate suppression of Sdpr and Fhl1 expression in tumors of the breast, kidney, and prostate

Alterations of the serum peptidome in renal cell carcinoma discriminating benign and malignant kidney tumors

Common chromosome fragile sites in human and murine epithelial cells and FHIT/FRA3B loss‐induced global genome instability

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