Similar regions of human chromosome 3 are eliminated from or retained in human/human and human/mouse microcell hybrids during tumor growth in severe combined immunodeficient (SCID) mice

Yang, Ying; Kost‐Alimova, Maria; Ingvarsson, Sigurður; Qiu, Qianhui; Kiss, Hajnalka; Szeles, Anna; Kholodnyuk, Irina; Cuthbert, Andrew; Klein, George; Imreh, Stefan

doi:10.1073/pnas.98.3.1136

Cited by 29 publications

(35 citation statements)

References 32 publications

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“…The tumors were analysed in comparison with corresponding MCHs. The results suggested that the human/human MCH-based elimination test identifies similar eliminated and retained regions on chromosome 3 as the human/murine MCH-based test (Yang et al, 2001a). From these data it was proposed that this region may contain genes antagonizing tumor growth.…”

Section: Rbm5 and Rbm6mentioning

confidence: 84%

Tumor suppressor genes on chromosome 3p involved in the pathogenesis of lung and other cancers

Zabarovsky¹,

2002

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Loss of heterozygosity (LOH) involving several chromosome 3p regions accompanied by chromosome 3p deletions are detected in almost 100% of small (SCLCs) and more than 90% of non-small (NSCLCs) cell lung cancers. In addition, these changes appear early in the pathogenesis of lung cancer and are found as clonal lesions in the smoking damaged respiratory epithelium including histologically normal epithelium as well as in epithelium showing histologic changes of preneoplasia. These 3p genetic alterations lead to the conclusion that the short arm of human chromosome 3 contains several tumor suppressor gene(s) (TSG(s)). Although the first data suggesting that 3p alterations were involved in lung carcinogenesis were published more than 10 years ago, only recently has significant progress been achieved in identifying the candidate TSGs and beginning to demonstrate their functional role in tumor pathogenesis. Some of the striking results of these findings has been the discovery of multiple 3p TSGs and the importance of tumor acquired promoter DNA methylation as an epigenetic mechanism for inactivating the expression of these genes in lung cancer. This progress, combined with the well known role of smoking as an environmental causative risk factor in lung cancer pathogenesis, is leading to the development of new diagnostic and therapeutic strategies which can be translated into the clinic to combat and prevent the lung cancer epidemic. It is clear now that genetic and epigenetic abnormalities of several genes residing in chromosome region 3p are important for the development of lung cancers but it is still obscure how many of them exist and which of the numerous candidate TSGs are the key players in lung cancer pathogenesis. We review herein our current knowledge and describe the most credible candidate genes.

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Section: Rbm5 and Rbm6mentioning

confidence: 84%

Tumor suppressor genes on chromosome 3p involved in the pathogenesis of lung and other cancers

Zabarovsky¹,

2002

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“…By comparing the functional impact of the transferred exogeneous chromosome and the tumorigenic potential of different microcell hybrids (MCHs), critical regions (CRs), important for tumorigenic suppression, can be identified. Several CRs in chromosome 3 were previously reported for other cancers including the 3p21.3 and 3p21.2-p14 regions in renal cell carcinoma (Yang et al, 2001), 3p21.3 in nasopharyngeal carcinoma (NPC) (Cheng et al, 1998), and 3p21.3, 3p25, and 3p13 in oral squamous cell carcinoma (Uzawa et al, 1998). Our lab recently identified 9q33-34 and 14q32 as CRs for tumorigenic suppression in ESCC Yang et al, 2005).…”

Section: Introductionmentioning

confidence: 95%

Identification of a tumor suppressive critical region mapping to 3p14.2 in esophageal squamous cell carcinoma and studies of a candidate tumor suppressor gene, ADAMTS9

Leung

Kwok

et al. 2006

Oncogene

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“…⌿, pseudogene. The gray arrows point to the positions of mouse gene duplications (m dupl) and human pseudogene insertions (h ins) (41), and the black arrows point to cancer-associated breakpoints (deletions and inversion in human and mouse tumors: h del, h inv, and m del) (16,40). At the bottom, positions of sequence-tagged site markers used for the analysis of YACs covering CER1 are shown.…”

Section: Deletions In Yeast Artificial Chromosomes (Yacs)mentioning

confidence: 99%

“…To analyze these losses we have generated monochromosomal human chr 3 hybrids by using a tumorigenic mouse fibrosarcoma or a human nonpapillary renal cell carcinoma as recipients. We found that an Ϸ1.4-Mb segment, designated as the common eliminated region (CER)1, was missing from all derived tumors (15,16).…”

mentioning

confidence: 99%

“…Two more regions identified in our system (16,17) and four well characterized deletion hot-spot regions found in tumor biopsies and cell lines (6,7,18,19) are located at 3p12-22 (see Table 1, which is published as supporting information on the PNAS web site, www.pnas.org). Comparing human and mouse genomic sequences assembled by the Celera Discovery System, we found that CBRs localize preferentially within the tumorassociated deletions in this chromosomal segment.…”

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confidence: 99%

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Coincidence of synteny breakpoints with malignancy-related deletions on human chromosome 3

Kost‐Alimova¹,

Kiss²,

Fedorova³

et al. 2003

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

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We have found previously that during tumor growth intact human chromosome 3 transferred into tumor cells regularly looses certain 3p regions, among them the Ϸ1.4-Mb common eliminated region 1 (CER1) at 3p21.3. Fluorescence in situ hybridization analysis of 12 mouse orthologous loci revealed that CER1 splits into two segments in mouse and therefore contains a murine͞human conservation breakpoint region (CBR). Several breaks occurred in tumors within the region surrounding the CBR, and this sequence has features that characterize unstable chromosomal regions: deletions in yeast artificial chromosome clones, late replication, gene and segment duplications, and pseudogene insertions. Sequence analysis of the entire 3p12-22 revealed that other cancer-associated deletions (regions eliminated from monochromosomal hybrids carrying an intact chromosome 3 during tumor growth and homozygous deletions found in human tumors) colocalized nonrandomly with murine͞human CBRs and were characterized by an increased number of local gene duplications and murine͞human conservation mismatches (single genes that do not match into the conserved chromosomal segment). The CBR within CER1 contains a simple tandem TATAGA repeat capable of forming a 40-bp-long secondary hairpin-like structure. This repeat is nonrandomly localized within the other tumor-associated deletions and in the vicinity of 3p12-22 CBRs.

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Similar regions of human chromosome 3 are eliminated from or retained in human/human and human/mouse microcell hybrids during tumor growth in severe combined immunodeficient (SCID) mice

Cited by 29 publications

References 32 publications

Tumor suppressor genes on chromosome 3p involved in the pathogenesis of lung and other cancers

Tumor suppressor genes on chromosome 3p involved in the pathogenesis of lung and other cancers

Identification of a tumor suppressive critical region mapping to 3p14.2 in esophageal squamous cell carcinoma and studies of a candidate tumor suppressor gene, ADAMTS9

Coincidence of synteny breakpoints with malignancy-related deletions on human chromosome 3

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